Keywords
ultrasonography-guided procedures - ankle - Achilles tendon - foot - plantar fascia
Achilles Tendon
Background
Achilles tendinopathy (AT) is a painful overuse injury that is extremely common in
athletes, especially those who participate in running and jumping sports. However,
AT is not purely an athletic injury; 65% of injuries diagnosed in a general practice
setting are not sport related.[1]
The terminology used to describe and diagnose tendon injuries has changed in recent
decades.[2] The term “tendinopathy” describes a clinical syndrome in which two components are present: pain and a histologic diagnosis of tendinosis.
The term “tendinosis” indicates degenerative changes in the thickness of the tendon.
It is not correct to use the term “tendinitis” because there is no inflammatory response
in chronic tendinopathy.[3]
Achilles tendon injuries are classified according to the location of the lesion: insertional
tendinopathy (20–25% of the injuries), midportion tendinopathy (55–65%), and proximal
musculotendinous junction (9–25%) injuries.[4]
Reactive tendinopathy is defined as symptoms lasting 6 weeks, whereas a chronic tendinopathy
lasts ≥ 3 months.[5]
Macroscopically, tendinopathy results in enlargement, disruption of the fibrillar
pattern, and an increase in tendon vascularity. Histopathologically, there is evidence
of disorganized proliferation of tenocytes, disrupted organization of collagen fibers,
an increase in the noncollagenous matrix, and neovascularization. There is usually
no evidence of inflammation, but the cause is considered a failed healing response.[6]
The exact pathophysiology of AT is still unknown; it is thought to have a multifactorial
origin.[5] However, most authors believe repetitive microtrauma from unusual or excessive mechanical
loading is a causative factor. The most common cause of tendinopathy in athletes is
excessive loading with inadequate recovery between training sessions. At the Achilles
tendon insertion, compressive forces on the Achilles tendon and calcaneus from footwear
or activities that place the ankle in dorsiflexion (e.g., uphill running) or an anatomical
abnormality (e.g., Haglund's deformity) may contribute to the development of pain.
Enthesitis is the unifying clinicopathologic feature for all seronegative spondyloarthropathies.
The diagnosis of AT is usually made using clinical findings.[5] Pain and reduced function are the primary symptoms.
Recovery from AT can take a year or more.[1] Treatment initially is nonsurgical. The first advice for AT often consists of temporarily
adjusting or stopping the sports load that probably caused the injury and wait and
see.[5]
If there is still no improvement in patient symptom after 3 months of patient education,
structural exercise therapy, and following loading advice, additional treatment options
should be considered.[7]
Various additional treatments have been described:
-
▶ Extracorporeal shockwave therapy.
-
▶ Injection therapies, including injections with corticosteroid (CS), polidocanol,
lidocaine, autologous blood, platelet-rich plasma (PRP), stromal vascular fraction,
hyaluronic acid, prolotherapy, high-volume image-guided injection (HVIGI), or intratendinous
needling.[5]
If > 6 months of basic management and additional therapies do not improve symptoms,
surgery should be considered.[1]
[5]
The use of imaging-guided injection treatment in recalcitrant cases is controversial.
A 2015 Cochrane review concluded there is insufficient evidence from randomized controlled
trials to support the use of injection therapies.[8] However, different kinds of treatment have been described with promising results.
Imaging-guided interventional procedures in AT can be divided into two subcategories.
The first are procedures in which some substances are injected into the retrocalcaneal
bursa or pre-Achilles fascia, such as anesthesia, steroids, or (HIVGI). The second
are procedures performed directly on the tendon, such as dry needling, prolotherapy,
sclerosing polidocanol injection, or injection with PRP.
HVIGI involves a large volume of saline and local anesthetic with or without steroid injected
into the interface between the midportion of the Achilles tendon and peritendinous
tissue and Kager's fat pad. The high volume is thought to have a mechanical effect
on neurovascular ingrowth and adhesions between the tendon and peritendinous tissue
but may also have effects on pain and local sensitization.[9]
[10]
[11]
[12]
HVIGI seem to be effective at treating AT in the short term. Boesen et al[9] demonstrated that treatment with HVIGI or PRP in combination with eccentric training
in chronic AT seems more effective in reducing pain, improving activity level, and
reducing tendon thickness and intratendinous vascularity than eccentric training alone.
HVIGI may be more effective in improving outcomes of chronic AT than PRP in the short
term (6 and 12 weeks) but not in the medium term (24 weeks) in which the positive
effect of treatment with PRP persists.
PRP is the cellular component of the plasma obtained by centrifuging whole blood, resulting
in a higher platelet concentration, and contains various growth factors that have
the potential to influence tissue regeneration.
Treatment of chronic tendon injuries by needling originated in veterinary medicine,
in a practice known as “pin-firing,”[13] in which veterinarians used a firing iron to burn soft tissue and thus transform
a chronic tendon injury into an acute one, producing an inflammatory state. This cruel
method of treatment is no longer used. However, the idea of changing a chronic nonhealing
injury (such as occurs in tendinosis) into an acute condition that may have greater
healing potential is the basis of PRP treatment.
The goal of PRP injected into areas of tendinopathy is to induce healing via cellular
and humoral mediators.[9]
[14]
[15]
[16]
[17]
[18] The mechanism of PRP injections to treat chronic tendinopathy is believed to be
a variety of growth factors, such as platelet-derived growth factor, transforming
growth factor, and insulinlike growth factor, that promote a healing response. One
of the main advantages is that PRP is autologous; therefore, it has an excellent safety
profile with almost no side effects.[19] Some studies have reported promising results when examining the effect of PRP in
chronic tendinopathies.[16]
[20]
[21]
[22]
[23]
[24]
[25]
In a study comparing PRP with blinded sham saline injections, de Vos[26] and colleagues reported significant improvement in both saline and PRP groups that
slightly favored the PRP subjects but not by a statistically significant margin. However,
saline injection may not be the best control group because it is likely active for
tendinopathy; injecting saline into the tendon alters the pressure–volume relationship
in a given space, thereby disrupting pathologic vascular and neural ingrowth. Injections
into the tendon may induce bleeding, which in turn releases certain growth factors
that stimulate the healing process with a similar mechanism of action as PRP.
(CS) injections are a manufactured version of hormones normally produced by the adrenal glands.
Steroids reduce redness and swelling in the nearby area. The infiltration with steroid
can help relieve pain and stiffness.
Local CS injection is an effective and safe modality to treat plantar fasciitis of
various causes.[8] However, only a few studies have evaluated this modality for the treatment of AT.
Some authors have indicated that ultrasonography (US)-guided local CS retrocalcaneal
injection is an effective and safe modality for refractory Achilles enthesis in patients
with insertional AT and leads to reversion of acute changes at the enthesis site.[27] CS bursal injections rapidly help settle pain and swelling in tissue, restoring
function and allowing individuals to participate in their rehabilitation.[28]
Side effects of steroid injection include local site infection, tendon rupture, skin
depigmentation, and fat pad atrophy in cases of plantar fascia injections.[29] Tendon rupture, the most serious complication, is relatively rare with a reported
incidence of 2.5 to 6.7% for injection for plantar fasciitis and is more associated
with recurrent and blind palpation-guided injections. US guidance significantly decreases
complication rates.[30]
Often combined with local anesthetic, these injections are described as having a diagnostic
(from the anesthetic) and therapeutic (from the steroid) element. Commonly used injectable
steroids in musculoskeletal medicine include triamcinolone acetonide, methylprednisolone
acetate, and betamethasone. The choice depends on local availability and the site
of treatment; for intra-articular injections, triamcinolone or methylprednisolone
is typically used.[31] For the infiltration of the retrocalcaneal bursa CS injection, we prefer to use
betamethasone.
To date, no definitive study has compared the efficacy of different treatment options
in AT, and therefore no definitive superior method has emerged. Therefore, decision
on technique remains a personal decision based on unique patient factors, imaging
findings, and radiologist expertise/comfort level.
We divide the treatment of AT tendinopathy into three parts: HVIGI, PRP, and CS US-guided
injection.
Recommended Clinical Indications
Recommended Clinical Indications
Clinical indications for HVI tendon stripping for tendinopathy (1) PRP injections
for degenerative tendon disease with intrasubstance tearing; or (2) retrocalcaneal
bursa injection for retrocalcaneal bursitis and Achilles enthesitis.
Pretreatment US Tendon Evaluation
Pretreatment US Tendon Evaluation
The Normal Achilles Tendon
The Achilles tendon is the largest and strongest tendon in the body that connects
the calf muscles to the heel. It is ∼ 15 cm in length and begins in the mid-lower
leg. The tendon is formed from the gastrocnemius and soleus muscles and inserts into
the calcaneus. The tendon descends to its insertion on the calcaneus, an enthesis
composed of fibrocartilage with direct meshing of the tendon fibrils into the marrow.
The tendon rotates 90 degrees as it descends, with the soleus fibers twisting from
anterior in the midcalf, to insert medially onto the posterior calcaneus, and thus
the gastrocnemius fibers rotate from their posterior location to insert laterally
into the calcaneus.[32] The Achilles tendon is covered by the paratenon; normally it is not visible on US.
The paratenon is highly vascularized and thus is important in healing the Achilles
tendon. Kager's fat pad (also known as the precalcaneal fat pad) refers to the fat
within Kager's triangle, located in the posterior ankle joint, anterior to the Achilles
tendon. The retrocalcaneal bursa is a synovial-lined structure occupying the space
between the Achilles tendon and calcaneus. The superficial calcaneal bursa is located
between the skin and the Achilles tendon insertion[33] ([Fig. 1]).
Fig. 1 Gross anatomy of the Achilles tendon (AT). (a) Posterior view. The AT is the distal insertion of the triceps surae that consists
of the two heads of the gastrocnemius muscle and soleus muscle. Note the relationship
of the AT with the lateral gastrocnemius (gl) and medial gastrocnemius (gm) muscles.
(b) Sagittal view shows the highly vascularity of the paratenon. Note the relatively
poorly vascularity of the midregion (star). (c) Sagittal section through the calcaneus (C) and distal AT shows the AT enthesis (E)
and the prominent Achilles fat pad (K). Note the retrocalcaneal bursa (arrow) between
the AT and the superior tuberosity of the calcaneus (figures courtesy of Dr. Alfonso
Rodriguez, University of the Balearic Islands).
High-resolution US demonstrates the dimensions and morphology of the tendon. The Achilles
tendon is divided into the body, preinsertional zone (2 cm), and insertional zone.
The fibrillary anatomical architecture can be appreciated as tightly packed thin echogenic
lines on longitudinal scanning and echogenic punctate foci in the axial plane. The
thin paratenon is usually seen surrounding the tendon as a slightly more echogenic
border. The normal tendon shows no vascularity on color Doppler ([Fig. 2]).
Fig. 2 High-resolution ultrasonography (US) demonstrates the dimensions and morphology of
the tendon. (a) Longitudinal and (b) transverse US view of the normal Achilles tendon (AT). The tightly packed thin echogenic
lines on the longitudinal view and echogenic punctate foci in the axial plane indicate
the fibrillary anatomical architecture. The thin paratenon is usually seen surrounding
the tendon as a slightly more echogenic border (b, arrow). Note the distention of
the retrocalcaneal bursa (K) in (a). Note the sural nerve (n) in the axial plane in
(b). C, calcaneus.
Paratenonitis
The inflammatory condition of paratenonitis is one of the most common findings in
patients with a painful Achilles tendon. It is the first symptomatic stage of Achilles
disorders and usually presents in cases of tendon degeneration. On high-resolution
US, these changes appear as a thickened hypoechoic paratenon, mainly posteriorly.
In the acute phase, fluid can be seen between the tendon and paratenon, along with
an increased vascularity. The changes can extend into the local soft tissues around
the tendon, including Kager's fat pad ([Fig. 3]).
Fig. 3 High-resolution ultrasonography (US) of the Achilles tendon (AT) in the axial plane
showing paratenonitis. A thickened hypoechoic paratenon is best appreciated posteriorly.
On US, these changes appear as a thickened hypoechoic paratenon.
Achilles Tendon Injuries
Achilles tendon injuries can be separated into insertional tendinopathy (20–25% of
the injuries), midportion tendinopathy (55–65%), and proximal musculotendinous junction
(9–25%) injuries, according to the location of the pain ([Fig. 4a]).
Fig. 4 (a) Sagittal DP magnetic resonance image of a normal Achilles tendon (AT). AT injuries
can be separated into insertional tendinopathy (blue), midportion tendinopathy (yellow),
and proximal musculotendinous junction (red) injuries. (b) Insertional tendinopathy: The injury is localized within the first 2 cm of the attachment
of the AT to the calcaneus. High-resolution ultrasonography (US) in the longitudinal
plane shows the AT enlarged and hypoechoic with heterogeneous echotexture. Note the
associated prominence of the calcaneus (Haglund's morphology) (white arrow) and the
enthesopathic calcification at the tendon insertion (arrowhead). (c) Noninsertional tendinopathy is the tendinopathy located at the midportion of the
tendon, localized > 2 cm above the distal attachment. High-resolution US in the longitudinal
plane shows the tendon diffusely enlarged.
In insertional tendinopathy, symptoms localize within the first 2 cm of the attachment of the Achilles tendon
to the calcaneus ([Fig. 4b]). There may be a tendinopathy of the Achilles tendon insertion and associated prominence
of the calcaneus (Haglund's morphology) and/or an associated retrocalcaneal bursitis.
Noninsertional tendinopathy is the tendinopathy located at the midportion of the tendon, localized > 2 cm above
the distal attachment ([Fig. 4c]). The distinction between these two subclassifications is also justified because
there seems to be a difference in prognosis during nonsurgical treatment.
On US, imaging findings of AT depend on the stage of tendon degeneration. The pathologic
process usually starts as myxoid or hypoxic intrasubstance degeneration (or a combination),
with an accumulation of mucoid material throughout the affected portion of the tendon.
With tendinosis progression, there is a coalescence of microscopic foci of mucoid
material, collagen fiber separation, and disruption. The degeneration can progress
through the stages of microtears, intrasubstance tears, partial tear, and complete
tear.[32] Mucoid accumulation results in tendon thickening that may be diffuse, fusiform,
or, less commonly, nodular.[32]
[33]
On US evaluation, symptomatic tendinopathy usually shows tendon neovascularization.
Dystrophic calcification can occur in degenerative tendon, often progressing to ossification,
with distinct cortex and trabecula.
Ultrasonography Treatment Procedure
Ultrasonography Treatment Procedure
Patient Positioning
The patient is placed in a prone position, with the leg fully extended and the foot
hanging off the end of the bed table ([Fig. 5]). This exposes the tendon at the posterior aspect of the ankle.
Fig. 5 In the prone position, the knee is fully extended and the foot hangs off the end
of the bed. The injection can be administered with the transducer in a sagittal or
axial orientation over the Achilles tendon, and the needle is introduced using an
in-plane technique. For high-volume image-guided injection, the needle is placed between
the tendon and Kager's fat pad; for platelet-rich plasma injections, it is taken into
the tendon itself.
Skin Antisepsis and US Probe Disinfection
Ordinary antisepsis is generally sufficient to guarantee a safe procedure for both
the patient and operator. Preliminary disinfection of instruments is mandatory before
starting the procedure.[34] For skin cleaning, we use uncolored disinfectant ([Fig. 6]).
Fig. 6 Recommended transducers. (a) Linear, 6–15 MHz. (b) Hockey stick, 8–18 MHz.
We use a sterile probe cover to protect the probe. The use of a sterile lubricating
gel is advisable to optimize the contact between probe and skin.
High-Volume Injection
Equipment Needed
-
A. Transducers: Linear, 6–15 MHz; hockey stick, 8–18 MHz ([Fig. 6])
-
B. Nonsterile materials ([Fig. 7])
-
Nonsterile gloves
-
Bandages
-
Anesthetic spray
-
Lubricating gel
-
Uncolored disinfectant.
-
C. Expendable materials ([Fig. 8a])
-
D. Medications ([Fig. 8b])
Fig. 7 Nonsterile material. Nonsterile gloves. Bandages. Anesthetic spray. Lubricating gel.
Uncolored disinfectant.
Fig. 8 Equipment preparation for high-volume image-guided injection tendon stripping. (a) Expendable material: One 21G needle. One 18G needle. Four to five Cono Luer Lock
(10 mL) syringes, sterile gel, tubing, sterile gloves, gauzes, sterile probe cover,
sterile dressing pack. (b) Medication: sterile saline solution (40 mL), local anesthesia, steroid.
US-guided HVI Procedure
Our US technique is identical to that suggested by other authors.[9]
[10]
[11]
[12]
[35]
[36] In general, a medial-to-lateral approach is preferred to avoid the superficial located
sural nerve. The choice of lateral-to-medial or medial-to-lateral direction depends
on the location of the sural nerve. Under US control we identify the point where we
want to perform the injection and mark the skin with a needle cap and marker.
Using an aseptic technique and helped by an assistant, using a transverse needle approach,
a 21G needle is inserted between the anterior aspect of the Achilles tendon and Kager's
fat pad. The needle is attached to a connecting tube and inserted under real-time
US guidance. A mixture of 8 mL 1% or 2% lidocaine and 2 mL of 12 mg betamethasone
is injected (total: 10 mL), immediately followed by 10 mL injectable normal saline
three to four times depending on the characteristics of each patient (total volume:
40–50 mL). The position of the needle is monitored continuously by US during this
phase, and the needle is moved gently across the anterior aspect of the tendon to
ensure uniform effect over the symptomatic area. The saline is injected in bursts
to maximize potential mechanical effect ([Fig. 9]). Note: Some authors have described using more or less volume and without adding
CS.[37]
Fig. 9 Ultrasonography (US)-guided high-volume image-guided injection. (a) In the axial orientation, the needle is introduced at 15 to 20 degrees using an
in-plane technique from the lateral aspect of the ankle. (b) Needle is inserted in the interface between the anterior aspect of the Achilles
tendon (AT) and Kager's fat pad (K; arrowheads); the needle is attached to a connecting
tube and inserted under real-time US guidance. A total volume of 40 to 50 mL is injected.
Platelet-Rich Plasma Injection
Platelet-Rich Plasma Injection
Equipment Needed
-
A. Transducers: Linear, 6–15 MHz; hockey stick, 8–18 MHz ([Fig. 6])
-
B. Nonsterile materials ([Fig. 7])
-
Nonsterile gloves
-
Bandages
-
Anesthetic spray
-
Lubricating gel
-
Uncolored disinfectant
-
C. Medications ([Fig. 10])
-
PRP (1–3 mL)
-
Lidocaine 1% (10 mL)
-
D. Expendable materials ([Fig. 10])
Fig. 10 Equipment preparation for platelet-rich plasma (PRP). Expendable material and medication:
One 21G needle, one 18G needle, two Cono Luer Lock (10 mL) syringes, sterile gel,
sterile gloves, gauzes, sterile probe cover, sterile dressing pack. Medication: PRP
(1–3 mL), lidocaine 1% (10 mL).
US-guided PRP Procedure
PRP can be obtained by manual procedures (open technique) or disposable kits (closed
technique). According to the platelet concentrations, PRP can be classified as low,
intermediate, or high concentrations. The correct platelet concentration must be ∼
1 million.
Depending on the presence of white blood cells, PRP can be classified into “pure PRP”
without leukocytes and “L-PRP” with leukocytes.
PRP can be liquid without activation but can also be used after activation, resulting
in a gelatinous substance. Platelet-rich fibrin is a solid material and not an injectable
platelet suspension.
The PRP we use is prepared manually by the Hematology Department. The PRP obtained
is nonactivated L-PRP.
Under US control, we identify the point where we want to perform the injection and
mark the skin with a needle cap and marker.
We can optionally use anesthetic spray. In our experience, the procedure is painful,
so we inject anesthesia into the peritendinous level but not into the tendon.
For PRP injections, the Achilles tendon can be viewed in the sagittal plane and the
needle can be introduced intratendinous from the dorsal aspect at 15 to 20 degrees
directly into the tendon ([Fig. 11a]). Alternatively, an axial approach can also be used with the needle again guided
into the tendon itself. We prefer to use the sagittal approach. In both positions,
the PRP can be delivered using a fenestration technique.
Fig. 11 Ultrasonography (US)-guided platelet-rich plasma (PRP). (a) In the sagittal orientation, the needle is introduced from the dorsal aspect at
15 to 20 degrees using an in-plane technique. (b) High-resolution US axial view. Under real-time US guidance, < 5 mL 1% or 2% lidocaine
is injected into the peritendinous level (arrowheads). (c) Then 4 to 5 minutes later, with the needle under US guidance, PRP is injected into
the tendon itself. The PRP can be delivered using a fenestration technique (arrowheads).
AT, Achilles tendon.
Using an aseptic technique and under real-time US guidance, < 5 mL 1% lidocaine is
injected into the peritendinous level ([Fig. 11b]). Then we locate the lesion with US and infiltrate it with the PRP ([Fig. 11c]).
The optimal dose, number, and interval of injections is controversial. We administer
1 to 3 mL PRP depending on the size of the lesion and repeat the procedure 12 weeks
later if necessary. Most recent studies suggest that a single infiltration with 1 mL
PRP is enough.[16]
[22]
[25]
Corticosteroid Injection
Equipment Needed
-
A. Transducers: Linear, 6–15 MHz; hockey stick, 8–18 MHz
-
B. Nonsterile materials ([Fig. 7])
-
Nonsterile gloves
-
Bandages
-
Anesthetic spray
-
Lubricating gel
-
Uncolored disinfectant
-
C. Medications ([Fig. 12])
-
D. Expendable materials ([Fig. 12])
Fig. 12 Equipment preparation for corticosteroid injection. Expendable material: one 21G
needle, one 18G needle, one syringe Cono Luer Lock (5 mL), sterile gel, sterile gloves,
gauzes, sterile probe cover, sterile dressing pack. Medication: local anesthesia and
steroid.
US-guided Retrocalcaneal Bursa Corticosteroid Procedure
In general, a medial-to-lateral approach is preferred to avoid the superficially located
sural nerve. Under US control, we identify the point where we want to perform the
injection and mark the skin with a needle cap and marker.
Using an aseptic technique and with a transverse needle approach, a 21G needle is
inserted in the retrocalcaneal bursa ([Fig. 13]). A mixture of 2 cc betamethasone and 2 cc 1% or 2% lidocaine or 1 cc triamcinolone
acetonide and 2 cc 1% or 2% lidocaine is introduced into the retrocalcaneal bursa.
Fig. 13 Ultrasonography (US)-guided corticosteroid injection. (a) In the axial orientation, the needle is introduced at 15 to 20 degrees using an
in-plane technique from the lateral aspect of the ankle. (b) The needle is inserted in the retrocalcaneal bursa (arrowheads). A mixture of 2 cc
betamethasone and 2 cc 1% or 2% lidocaine or 1 cc triamcinolone acetonide and 2 cc
1% or 2% lidocaine is introduced into the retrocalcaneal bursa.
Postprocedural Treatment
How patients are managed after treatment varies widely.
Patients are allowed to walk on the injected leg immediately but are advised strictly
to refrain from high-impact activity, such as running or jumping for 72 hours. After
72 hours, patients are sent to their referring clinicians for advice about physiotherapy
and returning to sport.
After treatment we suggest that the patient rest for 72 hours. It is recommended not
to locally apply ice. The patient is advised not to take nonsteroidal anti-inflammatory
drugs (NSAIDs) for 1 week before and 2 weeks after the procedure. Finally, a written
recommendation of non-NSAID oral painkillers is given to patients in case of pain.
Patients are asked to avoid weight-bearing for the following 48 hours and to continue
their baseline medications including NSAIDs.
Clinical Effectiveness
Scales used to evaluate the effectiveness treatment of Achilles tendon injuries vary
widely among different authors. The visual analog scale (VAS) is a simple technique
to measure the subjective experience of pain. A score of 0 means “no pain”; a score
of 10 means the “worst pain imaginable.”[38]
The Victorian Institute of Sport Assessment–Achilles questionnaire (VISA-A) is designed
to evaluate pain and symptom severity with activity in patients with AT. The VISA-A
contains eight questions, and scores range from 0 to 100, with 100 indicating no symptoms
and full participation in physical activity.[39]
In cases after HVIGI and CS injection, imaging is not routinely used during follow-up.
After treatment, patients are sent to their referring physician; a short treatment
of physiotherapy is recommended. Patients are instructed to call our department if
fever or pain persist 2 months posttreatment. We then perform US to detect the presence
of complications, and in some cases a second US-guided injection is performed.
In the PRP procedure, we perform a clinical control (VAS and VISA-A questionnaire)
and US 12 weeks after treatment. A second intratendinous infiltration of PRP is sometimes
indicated.
Plantar Fascia
Background
Plantar fasciitis (PF) is the most common cause of plantar pain in the heel of the
foot in adults, ∼ 7% of all foot pain in adults > 65 years of age, and 24% in athletic
individuals.[40] The main stress to the fascia occurs during walking, especially at the heel elevation
phase. It is more common in athletes because of overuse and repetitive impact to the
heel, but in patients > 40 years of age, it is more related to other factors, such
as being overweight; long-standing periods, especially wearing work boots; and systemic
disease such as diabetes and/or rheumatoid and other inflammatory types of arthritis.
It is also related to AT and biomechanical problems.
The plantar fascia has three components: the medial, central, and lateral band. The
most affected part in PF is the central band, a strong and thick aponeurosis attached
to the calcaneus tuberosity and the main support of the plantar arch. The central
band is divided at the level of the Lisfranc joint into five fascicles that cover
the flexor digitorum brevis and more distally help stabilize the flexor tendons, ending
at the base of the proximal phalanges.
The most frequent symptom in PF is pain at the inferomedial part of the heel that
is at its peak in the morning and improves during the day. It worsens with load, sport
activities, and long walks. At the physical examination, patients have selective pain
at the calcaneus origin of the fascia that improves with dorsal flexion and increases
with extension of the foot.
Overuse and biomechanical problems may increase excessive tensile strain within the
plantar fascia, resulting in microscopic tears and chronic inflammation. Overuse rather
than anatomy is thought to be the most common cause in athletes. Although PF presents
with the typical clinical signs of inflammation, such as pain and swelling in acute
cases, the histologic findings do not show inflammation but instead are characterized
by tissue destruction and tissue repair, neovascularization, and fibrosis with infiltration
of macrophages, lymphocytes, and plasma cells. The histologic findings in chronic
PF therefore support a degenerative rather than an inflammatory process. Thus the
term fasciopathy would be more accurate; fasciitis should be used when the condition becomes clinically
significant.[29]
[41]
The diagnosis of PF is usually made with clinical findings. US findings are hypoechoic
thickening (> 4–5 mm) of the insertional or proximal part of the plantar fascia.
The first treatments are rest, avoiding flat shoes, physiotherapy with stretching
of the fascia and the triceps surae muscle, and solving biomechanical problems if
they are present with arch supports and orthotics. PF is normally regarded as a self-limiting
condition and usually resolves within 6 to18 months.[41] But symptoms improve slowly, and there are many intractable cases that need another
treatment, such as US-guided injections or extracorporeal shockwave therapy. When
conservative management fails, US-guided CS injections are often the first option.[42]
Two types of imaging-guided interventional procedures are described in PF. In the
first, a substance like CS is injected around the fascia (either superficial or deep
layers or both). In the second, procedures are performed directly on the tendon, such
as injection with PRP.
Regarding CS injection, no studies have compared the efficacy of the different approaches
around the fascia (superficial or deep of both layers). Therefore the decision on
technique remains a personalized one based on patient factors, imaging findings, and
the radiologist's experience.
A Delphi-based consensus of experts from the European Society of Musculoskeletal Radiology
(ESSR) recently reviewed the literature and concluded that US guidance is strongly
recommended to improve the efficacy of interventional procedures for PF, particularly
using PRP.[8]
There is evidence that US-guided CS injections are more effective than palpation-guided
injections to treat PF, providing significant short-term pain relief, particularly
when combined with strength training and stretching. Both can be recommended as the
first-line treatment in patients with PF.[8]
[43]
[44] Often combined with local anesthetic, these injections are often diagnostic and
therapeutic.
Adverse effects of steroid injection at the site are local infection, tendon rupture,
skin depigmentation, and fat pad atrophy.[26] Tendon rupture, the most serious complication, is relatively rare with a reported
incidence of 2.5 to 6.7% in case of injection for PF and associated more with recurrent
and blind palpation-guided injections. US guidance significantly decreases complication
rates.[27]
For chronic PF, PRP injections provide significant pain relief with better outcome
at mid- and long-term follow-up if compared with CS injections.[45]
[46] Although both PRP and CS can decrease inflammation, PRP may be advantageous over
CS because it may modulate the plantar fascia degeneration due to its biological regenerative
properties. PRP contains an abundance of growth factors and bioactive cytokines that
are believed to influence healing by augmenting cellular migration, improving cellular
proliferation, promoting angiogenesis, and increasing matrix deposition. This results
in increasing fiber organization and tensile strength in soft tissue. PRP also releases
vascular endothelial growth factor that promotes angiogenesis and may facilitate healing
of a degenerative condition by improving neovascularization and repair. By contrast,
CS has no such regenerative capacity, and consequently its effect is solely to reduce
inflammation.[45]
The latest meta-analysis showed significantly lower VAS scores in the PRP group in
the intermediate term (6 months) and long term (12 months) compared with CS injection.
However, in the short term (1 and 3 months), no differences between the two groups
were observed.[47]
In conclusion, PRP injection for PF is an effective and safe treatment option. In
comparison with CS, PRP showed significantly better pain control at intermediate-
and long-term follow-up, so for chronic PF cases, the current clinical evidence suggests
it may lead to a greater improvement in pain and functional outcome. Therefore PRP
could be recommended as a first-line treatment for those patients.[8]
[47]
According to the recent ESSR consensus, the effectiveness of US-guided injections
with ozone, hyaluronic acid, or botulinum toxin type A has not yet been sufficiently
proven to be recommended for PF because no comparative studies are available.[8]
Recommended Clinical Indications
Recommended Clinical Indications
When conservative management is not effective, we recommend CS injections combined
with strength training and stretching and PRP injections for chronic PF.
Pretreatment US Tendon Evaluation
Pretreatment US Tendon Evaluation
The Normal Plantar Fascia
Plantar fascia is a thick and strong aponeurosis that supports the plantar arch ([Fig. 14]). It is a dense collection of collagen fibers on the sole of the foot. These fibers
are mostly longitudinal but also transverse, and the fascia is firmly attached to
the calcaneus tuberosity.
Fig. 14 Gross anatomy of the plantar fascia (PF). (a) Plantar view of the PF. (b) Sagittal view of the PF shows the normal insertion of the fascia and the fat pad
(figures courtesy of Dr. Alfonso Rodriguez, University of the Balearic Islands).
Plantar fat pad is a group of specialized fat pads separated by collagen septa and
elastic fibers that extend from the skin to the calcaneus periosteum. It absorbs heel
impact forces when walking or running.
US demonstrates the normal dimensions and morphology of the fascia and can scan the
insertional and proximal zones but also the thin heads behind the metatarsals. The
fibrillary anatomical architecture can be appreciated as tightly packed thin echogenic
lines on longitudinal scanning, with no vascularity on color Doppler examination ([Fig. 15]).
Fig. 15 Magnetic resonance imaging and high-resolution ultrasonography (US) demonstrate the
dimensions and morphology of the fascia. (a) Longitudinal and (b) transversal US view of the normal plantar fascia (PF).
Plantar Fascia Injuries
PF injuries can be separated into insertional fasciitis and nonproximal/noninsertional
fasciitis ([Fig. 16]). On US, PF is seen as focal hypoechoic thickening and loss of normal echogenicity,
often with fluid around the fascia and calcaneus cortical irregularity or bone spur
([Fig. 16]). It can demonstrate hyperemia on Doppler examination that should be evaluated in
plantar flexion (relaxation of the fascia).
Fig. 16 High-resolution ultrasonography of the plantar fascia (PF) in the sagittal and axial
planes showing fasciitis. A thickened hypoechoic fascia is better appreciated in the
sagittal/longitudinal view and is useful to compare with the contralateral fascia.
(a) Plantar fasciitis. (b) Contralateral normal fascia. (c) Note edema and fluid in the fat pad (arrowhead) and (d) bone spur (white arrow), findings often associated with fasciitis.
US Treatment Procedure
Patient Positioning
The patient is placed in a supine position, with the leg fully extended and external
rotation of the foot ([Fig. 5]).
Skin Antisepsis and US Probe Disinfection
Ordinary antisepsis is generally sufficient to guarantee a safe procedure for both
the patient and operator. Preliminary disinfection of instruments is mandatory before
starting the procedure.[34] For skin cleaning, we use uncolored disinfectant ([Fig. 7]).
We use a sterile probe cover. The use of a sterile lubricating gel is advisable to
optimize the contact between probe and skin.
Corticosteroid Injection
Equipment Needed
-
A. Transducers: Linear, 6–15 MHz; hockey stick, 8–18 MHz
-
B. Nonsterile materials ([Fig. 7])
-
Nonsterile gloves
-
Bandages
-
Anesthetic spray
-
Lubricating gel
-
Uncolored disinfectant
-
C. Medications ([Fig. 12])
-
D. Expendable materials ([Fig. 12])
US-guided Corticosteroid Procedure
In general, an anterior and medial oblique to lateral approach and perifascial injection
is preferred, avoiding intrafascial or fat pad injection. Under US control, we identify
the injection point.
Using an aseptic technique and with a transverse needle approach, a 21G needle is
located close to the fascia ([Fig. 17]). A mixture of 2 cc betamethasone and 2 cc 1% lidocaine or 1 cc triamcinolone acetonide
and 2 cc 1% lidocaine is introduced into the perifascial tissue (superficial or deep
injection or both).
Fig. 17 Ultrasonography-guided corticosteroid injection. (a) In the axial orientation, the needle is introduced at 15 to 20 degrees, using an
in-plane technique from the medial aspect of the heel. (b) The needle is inserted close to the superficial layer of the plantar fascia (PF;
arrowheads) (arrowheads). A mixture of 2 cc betamethasone and 2 cc 1% or 2% lidocaine
or 1 cc triamcinolone acetonide and 2 cc 1% or 2% lidocaine is introduced around the
fascia.
Platelet-Rich Plasma Injection
Platelet-Rich Plasma Injection
Equipment Needed
-
A. Transducers: Linear, 6–15 MHz; hockey stick, 8–18 MHz ([Fig. 6])
-
B. Nonsterile materials ([Fig. 7])
-
Nonsterile gloves
-
Bandages
-
Anesthetic spray
-
Lubricating gel
-
Uncolored disinfectant
-
C. Medications ([Fig. 10])
-
PRP (1–3 mL)
-
Lidocaine 1% (10 mL)
-
D. Expendable materials ([Fig. 10])
US-guided PRP Procedure
We use nonactivated L-PRP prepared manually by the Hematology Department. Under US
control we identify the point where we want to perform the injection and mark the
skin with a needle cap and marker.
We can optionally use anesthetic spray. In our experience, the procedure is painful,
so we inject anesthesia into the perifascial level but not into the fascia.
For PRP injections, the approach is the same as the CS injection, but the needle should
be introduced directly into the fascia into the most hypoechoic/degenerative area
and can be delivered using a fenestration technique ([Fig. 18]).
Fig. 18 Ultrasonography (US)-guided platelet-rich plasma (PRP) injection. (a) In the transversal orientation, the needle is introduced from the medial aspect,
using an in-plane technique. (b) High-resolution US axial view. Under real-time US guidance, < 5 mL 1% or 2% lidocaine
is injected into the soft tissues around the plantar fascia (PF) (arrowheads). (c) Then 4 to 5 minutes later, using the needle with US as a guide, PRP is injected
into the fascia itself. The PRP can be delivered using a fenestration technique (arrowheads)
(figures courtesy of Dr. Javier Fernández-Jara, Hospital Fundación Jiménez Díaz/Sanitas,
La Zarzuela, Madrid, Spain).
Using an aseptic technique and under real-time US guidance, < 5 mL 1% lidocaine is
injected into the perifascial level. Then with US we localize the lesion and infiltrate
it with the 2 to 3 mL PRP. We can repeat the procedure 12 weeks later, if necessary,
but there is no consensus about the optimal timing and number of PRP injections.
Postprocedural Treatment
There is wide heterogeneity in how patients are managed after treatment. After a CS
injection, patients are asked to avoid weight-bearing for 48 hours and to continue
their baseline medications including NSAIDs.
After treatment with a PRP injection, we recommend the patient rest for 72 hours.
It is recommended not to apply ice. The patient is advised not to take NSAIDs for
1 week before and 2 weeks after the procedure. Finally, a written recommendation for
oral non-NSAID painkillers is given to the patients in case of pain.
Clinical Effectiveness
Two scales are often used to evaluate the effectiveness treatment of PF injuries in
the literature. The VAS is a simple technique for measuring subjective experience
of pain, as described earlier.
The American Orthopaedic Foot and Ankle Society (AOFAS) is a standardized evaluation
of the clinical status of the ankle and hindfoot. It incorporates both subjective
and objective information. Patients report their pain, and physicians assess alignment.
The patient and physician work together to complete the functional portion. Scores
range from 0 to 100, with healthy ankles receiving 100 points.[48]
With CS injection, imaging is not routinely used during follow-up. After treatment,
patients are sent to their referring physician, and a short treatment of physiotherapy
is recommended. Patients are instructed to call our department in case of fever or
if pain persists at 2 months posttreatment. In this case, we perform US to detect
the presence of complications, and in some patients, a second US-guided injection
is performed.
After a PRP procedure, we perform a clinical control (VAS and AOFAS questionnaire)
and US 12 weeks after treatment. In some cases, a second intrafascial infiltration
of PRP is indicated.
Conclusion
US-guided injections in patients with Achilles tendon injuries has been shown to be
a safe and feasible. These injections are quick, low cost, and minimally invasive.
To date, no study has compared the efficacy of the different treatments, and therefore
no definitive superior method has been established.
HVIGI seems to be effective to treat AT. The goal of PRP injected into areas of tendinopathy
is to induce healing via cellular and humoral mediators. It seems to be effective
for degenerative tendon disease with intrasubstance tearing. Local US-guided CS injection
of the retrocalcaneal bursa improves bursitis symptoms.
US-guided injections in patients with PF injuries has been shown to be a safe and
effective treatment. US-guided CS injections are quick, low cost, and minimally invasive.
US-guided PRP injection showed significantly better pain control at intermediate-
and long-term follow-up compared with CS. We can recommend PRP for chronic PF following
the current clinical evidence because it has a regenerative capacity, facilitating
healing of a degenerative condition by improving neovascularization and repair.
