Maffulli2019

Review
Achilles tendinopathy
Nicola Maffullia,b
, Umile Giuseppe Longoc
, Anish Kadakiad
, Filippo Spieziae,
*
a
Department of Musculoskeletal Disorders, University of Salerno School of Medicine, Surgery and Dentistry, Salerno, Italy
b
Centre for Sports and Exercise Medicine, Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Mile End Hospital, 275
Bancroft Road, London, E1 4DG, England, United Kingdom
c
Department of Orthopaedic and Trauma Surgery, Campus Biomedico University, Via Alvaro del Portillo, 200, 00128 Rome, Italy
d
Department of OrthopedicSurgery, NorthwesternUniversity - Feinberg School of Medicine, Chicago, IL 60611, USA
e
Department of Orthopaedic and Trauma Surgery, Ospedale San Carlo, Via Potito Petrone, 85100 Potenza, PZ
A R T I C L E I N F O
Article history:
Received 25 January 2018
Received in revised form 11 December 2018
Accepted 27 March 2019
Available online xxx
Keywords:
Achilles tendinopaty
Injections
Ankle
Tendon
Sports trauma
A B S T R A C T
Background: Achilles Tendinopathy (AT) is essentially a failed healing response with haphazard
proliferation of tenocytes, abnormalities in tenocytes with disruption of collagen fibers, and subsequent
increase in non-collagenous matrix.
Methods: The diagnosis of Achilles tendinopathy is clinical, and MRI and utrasound imaging can be useful
in differential diagnosis. Conservative manegement, open surgery or minimally invasive techniques are
available. Injections and physical therapy are also vauable options.
Results: Eccentric exercises are useful tools to manage the pathology. If the condition does not ameliorate,
shock wave therapy, or nitric oxide patches might be considered. Peritendinous injections or injections at
the interface between the Achilles tendon and Kager’s triangle could be considered if physical therapy
should fail. Surgery is indicated after 6 months of non-operative management.
Conclusions: The clinical diagnosis and management of ATare not straightforward. Hence, patients should
understand that symptoms may recur with either conservative or surgical approaches.
© 2019 European Foot and Ankle Society. Published by Elsevier Ltd. All rights reserved.
Contents
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
2. Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
3. Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4. Conservative management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
4.1. Surgical management of tendinopathy of the main body of the Achilles tendon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
5. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
6. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 00
1. Introduction
Achilles tendinopathy(AT) is characterised by pain, impaired
performance, and swelling in and around the tendon [1]. It can be
categorized as insertional and non insertional, two distinct
disorders with different underlying pathophysiology and manage-
ment options. Other terms used as synonymous of non insertional
tendinopathy include tendinopathy of the main body of the
Achilles tendon and mid-portion AT. The mid-tendon and the
insertion are morphologically, functionally and physiologically
different in the normal state. Also, at the beginning of pathology
cell matrix changes are indistinguishable so that the pathology
appears to be the same. However, despite a similar pathology,
exercise specific for insertional or mid-tendon tendinopathy of AT
provides improved clinical outcomes, probably a reflection of the
loading profiles in different parts of the tendon [2]. Although
scientifically sound epidemiological data are lacking, AT is
common in athletes, accounting for 6–17% of all running injuries
* Corresponding author.
E-mail address: spieziafilippo@gmail.com (F. Spiezia).
https://doi.org/10.1016/j.fas.2019.03.009
1268-7731/© 2019 European Foot and Ankle Society. Published by Elsevier Ltd. All rights reserved.
Foot and Ankle Surgery xxx (2019) xxx–xxx
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FAS 1285 No. of Pages 10
Please cite this article in press as: N. Maffulli, et al., Achilles tendinopathy, Foot Ankle Surg (2019), https://doi.org/10.1016/j.fas.2019.03.009
Contents lists available at ScienceDirect
Foot and Ankle Surgery
journal homepage: www.elsevier.com/locate/fas

[3]. However, it does presents in middle aged overweight non-
athletic patients without a history of increased physical activity
[3]. To date, the incidence and prevalence of AT in other
populations remain non-established, even though the conditions
has been correlated with seronegative arthropathies [4]. Most
studies include more males than females, although a definite
greater prevalence in males has not been shown. It is controversial
whether aging is a riskfactor for tendinopathy [5]. However,
evidences showed that aging also induces aberrant changes in the
expression of various genes and production of various types of
matrix proteins in the tendon, and may consequently lead to
tendon degeneration and impaired healing in aging tendons [6].
The history of a chronic tendinopathic process preceding a
rupture is also controversial, and some of the available literature
demonstrate high association of tendinopathy and rupture, since
pain symptoms represent a late finding of the process, and most
patients with AT are asymptomatic [2,7–10].
The essence of tendinopathy is a failed healing response, with
degeneration and haphazard proliferation of tenocytes, disruption
of collagen fibres, and subsequent increase in non-collagenous
matrix [1]. In tendinopathic samples, there is unequal and irregular
crimping, loosening and increased waviness of collagen fibres,
with an increase in Type III (reparative) collagen [1]. Hypoxic,
hyaline degeneration, mucoid or myxoid, fibrinoid, or lipoid
degeneration, calcification, fibrocartilaginous and bony metaplasia
can coexist [1].
The aetiology of AT remains debated, and is likely caused by
intrinsic and extrinsic factors. Postulated intrinsic factors include
tendon vascularity, weakness as well as lack of flexibility of the
gastrocnemius-soleus complex, pes cavus, and lateral ankle
instability [11]. Excessive loading of the tendon is considered
the major causative factor for AT [12]. Free radical damage
occurring on reperfusion after ischaemia, hypoxia, hyperthermia
and impaired tenocyte apoptosis have been linked with tendin-
opathy. In a case-control study, subjects with chronic painful AT
had a lipid profile characteristic of dyslipidemia [13]. A meta-
analysis of the effects of corticosteroid has shown that published
data are insufficient to determine the risk of rupture following
corticosteroid injections [14]. Evidences from a large population-
based case-control study showed that single case of rupture would
occur for every 5958 persons treated with fluoroquinolones [15].
The corresponding number needed to harm was 979 for patients
who concomitantly use corticosteroids and 1638 for those aged
>60 years [15]. The clinical impact of fluoroquinolone use on the
onset of less severe forms of tendon disorders is actually unknown,
but it is expected to be even higher.
AT is difficult to treat, and results, even after surgery, are
variable. The few studies which reported long-term results
indicated a relatively poor outcome. Also, surgery requires
prolonged rehabilitation, and, depending on the patient's occupa-
tion, a varying period of sick leave from work.
The diagnosis of AT is mainly based on history and clinical
examination [16]. Pain is a late symptom. A common symptom is
morning stiffness or stiffness after a period of inactivity, and a
gradual onset of pain during activity. In athletes, pain typically
occurs at the beginning and end of a training session, with a period
of diminished discomfort in between. As the condition progresses,
pain may occur with even minor exertion, and may interfere with
activities of daily living. In severe cases, pain occurs at rest. In the
acute phase, the tendon is diffusely swollen and edematous, and
tenderness is usually greatest 2–6 cm proximal to the tendon
insertion. A tender, nodular swelling is usually present in chronic
cases. Clinical examination is the best diagnostic tool (Fig. 1A, B)
(Table 1).
Some simple manoeuvres during physical examination and
elements of the history can often distinguish AT from other
conditions which may cause similar symptoms (Table 2).
The Victorian Institute of Sports Assessment - Achilles (VISA-A)
questionnaire specifically measures the severity of AT [17]. It
covers the domains of pain, function, and activity. Scores are
summed to give a total out of 100. An asymptomatic person would
score 100. In clinical care, the VISA-A questionnaire provides a
valid, reliable, and user friendly index of the severity of AT.The
VISA-A-S questionnaire showed good responsiveness in a ran-
domized controlled trial (it was sensitive for clinically important
changes over time with treatment, easy for the patients to fill out,
and the data were easily handled) [18]. It has been cross-culturally
adapted to Swedish [19], Italian [20] and Turkish [21].
2. Imaging
Radiographs may be useful in diagnosing associated or
incidental bony abnormalities. Radiographs are routinely obtained
for patients with symptoms lasting longer than six weeks to rule
out bony abnormalities, and identify the possible presence of
intratendinous calcific deposits and ossification. The presence of a
posterior calcification of the calcaneus (posterior heel spur) is
diagnostic of insertional Achilles tendinopathy.
Fig. 1. Royal London Hospital Test: Once the tester has elicited local tenderness by palpating the tendon with the ankle in neutral position (Fig. 1A), the patient is asked to
actively dorsiflex the ankle and to actively plantarflex it. With the ankle in maximum dorsiflexion and in maximum plantarflexion, the portion of the tendon originally found
to be tender is palpated again (Fig. 1B).
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Ultrasonography, though operator-dependent, correlates well
with histopathologic finding, and, especially in Europe, it is
regarded as the primary imaging method (Fig. 2). A major
advantage of ultrasonography over other imaging modalities is
its interactive capability. Grey scale ultrasonography is associated
with colour or power Doppler to detect neovascularity.
Recently, ultrasound tissue characterization (UTC) has been
introduced as a reliable method to quantify tendon structure [22].
UTC can quantitatively evaluate tendon structure and thereby
discriminate symptomatic and asymptomatic tendons [23].
Structure is an important clinical marker of tendon health; current
standards use qualitative scores that are not reliable, but
quantitative assessments of tendon structure using B-mode
ultrasound could be a reliable tool to diagnose and follow up
Achilles tendinopathy [24].
Only if ultrasonography remains unclear should magnetic
resonance imaging (MRI) imaging be performed.
MRI provides extensive information about the internal mor-
phology of the tendon and surrounding bone as well as other soft
tissue. It allows the surgeon to differentiate between para-
tendinopathy and tendinopathy of the main body of the tendon
(Fig. 3). Additionally, the extent of diseased tissue present, may be
estimated valuable for pre-operative planning. MRI is superior to
ultrasound in detecting incomplete tendon ruptures. However,
given the high sensitivity of MRI, the data should be interpreted
with caution, and correlated to the patient symptoms before
making any recommendations [12].
3. Management
The management of AT lacks evidence-based support, and
tendinopathy sufferers are at risk of long-term morbidity with
unpredictable clinical outcome. The appropriate moment to switch
from conservative to operative therapy remains unknown. In a
prospective observational follow-up study, the 8 year prognosis of
patients with AT was generally favourable, even though 29% of the
patients required surgical intervention during the follow-up
period [25].
In general, non-operative care should be implemented for a
minimum of three to six months prior to considering surgery, since
AT may resolve during this period in up to three quarters of
patients. However, each patient should be evaluated on their own.
4. Conservative management
Several therapeutic options lack hard scientific background
[26]. NSAIDs are commonly used for the management of AT, even
though data from three trials of NSAIDs showed, at best, a modest
effect on acute symptoms in the short term [27].The analgesic
effect of NSAIDs allows patients to ignore early symptoms, possibly
imposing further damage to the affected tendon and delaying
definitive healing. NSAIDs can be effective, to some extent, for pain
control to allow effective eccentric strengthening as well as
gastrocnemius and soleus stretching. Potential harms of NSAIDS
(such as ulcers, hypertension, renal impairment etc, especially in
older people) need to be weighted up for each patient, balancing
potential risks and benefits.
Rest is considered another first-line therapy for AT, but the
strength of recommendation is based on expert opinion [27]. Data
from recent randomized controlled trials showed that patients
with AT can safely continue with their activity of choice [18,28].
Even though cryotherapy is widely used for analgesia, to reduce
the metabolic rate of the tendon, and decrease the extravasation of
blood and protein from new capillaries found in tendon injuries
[29], there is no evidence that this is an effective treatment for AT.
Eccentric exercises have been proposed to promote collagen
fibre cross-link formation within the tendon, thereby facilitating
tendon remodeling [30]. Evidences of histological changes
following a program of eccentric exercise are lacking, and the
mechanisms by which eccentric exercises may help to resolve the
pain of tendinopathy remain unclear. Some groups report excellent
clinical results [31,32]. The results of eccentric training from other
study groups are less convincing, with a 50–60% of good outcome
after a regime of eccentric training both in athletic and sedentary
patients [33]. In general, the overall trend suggests a positive effect
of eccentric exercises, with no reported adverse effects [30].
Combining eccentric training and shock wave therapy produces
higher success rates compared to eccentric loading alone or shock
wave therapy alone [34].
Orthotics are widely used in conservative management, with
heel pads being the most commonly prescribed. There is little
evidence to support their use [35]. An AirHeel brace, which applies
intermittent compression to minimize swelling and promote
circulation, has been proposed as a viable alternative to eccentric
exercises, especially in patient who do not tolerate training
because of pain [36]. No differences between management with
the AirHeel brace and an eccentric training program were found in
patients with chronic Achilles tendon pain [36]. The combination
of eccentric training with the AirHeel Brace does not produce a
synergistic effect [36–39].
Nitric oxide is a small free radical generated by a family of
enzymes, the nitric oxide synthases [40]. A prospective, random-
ized, double-blind, placebo controlled clinical trial in patients with
tendinopathy of the main body of the Achilles evaluated the
efficacy of nitric oxide administration via an adhesive patch [41].
Topical glyceryltrinitrate was effective in chronic noninsertionalAT,
and the treatment benefits continue at 3 years [42]. However, a
more recent study questioned the clinical benefit of topical
glyceryltrinitrate patches [43].
Low-energy shock wave therapy in tendinopathy has been
proposed to stimulate soft tissue healing and inhibit pain
receptors. Low energy shock wave therapy or eccentric training
produced comparable results in a randomized controlled trial [28],
and both management modalities showed outcomes superior to
the wait-and-see policy. The combined use of low-energy shock
wave therapy and eccentric exercises is beneficial [43]. However,
Table 1
Diagnostic tests for Achilles tendinopathy.
Test How to perform it Sensitivity Specificity
Palpation Both legs are exposed from above the knees, and the patient examined while standing and prone. The Achilles
tendon should be palpated for tenderness, heat, thickening, nodule and crepitation.
0.583 (CI 0.393,
0.752) [57]
0.845 (CI 0.745,
0.911) [57]
Painful arc It helps to distinguish between tendon and paratenon lesions. In paratendinopathy, the area of maximum
thickening and tenderness remains fixed in relation to the malleoli from full dorsi- to plantar-flexion; lesions
within the tendon move with ankle motion. There is often a discrete nodule, the tenderness of which markedly
decreases or disappears when the tendon is put under tension [57].
0.525 (CI 0.347,
0.697) [57]
0.833 (CI 0.717,
0.908) [57]
Royal London
Hospital test
The clinician elicits local tenderness by palpating the tendon with the ankle in neutral position or slightly
plantar flexed. The tenderness significantly decreases or becomes totally painless when the ankle is
dorsiflexed [57].
0.542 (CI 0.345,
0.726) [57]
0.912 (CI 0.858,
0.952) [57]
N. Maffulli et al. / Foot and Ankle Surgery xxx (2019) xxx–xxx 3
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Table 2
Differential diagnosis of Achilles tendinopathy.
Diagnosis History Findings
Physical Examination Plain-Film
Radiographic
Assessment
MRI or Ultrasonographic
Examination
Bone scan
Tendinopathy of the main
body of the Achilles
tendon
Pain, impaired function,
and swelling in and
around the Achilles
tendons.
Tender area of intratendinous
swelling that moves with the
tendon and whose tenderness
significantly decreases or
disappears when the tendon is
put under tension.
Normal findings. Focal or diffuse thickening
of the Achilles tendon, with
focal hypoechoic areas.
Normal findings.
Paratenonitis of the Achilles
tendon
Pain in the Achilles
tendon region or
posterior heel region.
The tendon is diffusely swollen
on
palpation, and is tender in the
middle third of the tendon. A
crepitus may be occasionally
palpable in the acute phase.
However, the swelling and
tenderness do not move when
the ankle is dorsiflexed. Areas of
erythema, increased local
warmth, and palpable tendon
nodules or defects
may also be present.
Normal findings. US can be useful only if
adhesions are present
around the Achilles tendon.
In acute
form, US can detect fluid
around the tendon, whereas
paratendinous adhesions
are visualized
as thickening of the
hypoechoicparatenon with
poorly defined borders in
the chronic form.
Normal findings.
Insertional Achilles
tendinopathy
Early morning stiffness,
pain at the insertion of
the Achilles tendon that
deteriorates after
exercise
or climbing stairs,
running on hard surfaces,
or heel running.
Pain, swelling, and tenderness in
the back of the calcaneus. The
pain generally emanates from
the posterior aspect of the heel
and is aggravated by active or
passive motion.
Ossification of
insertion of the Achilles
tendon or a spur
(fishhook osteophyte)
on the superior portion
of the calcaneum.
Insertional calcification.
Moderate to severe variety
in the echo structure of
tendon in the insertional
area.
Normal findings.
Retrocalcaneal bursitis Pain in the posterior heel
region.
Fluctuation at palpation
indicates an
effusion of the retrocalcaneal
bursa.
Normal findings. Hypertrophic bursa. Normal findings.
Sever's (Calcaneal traction
apophysitis)
Patients complain of
activity related pain.
Localized tenderness and
swelling at the site of insertion
of the Achilles tendon.
Avulsion of the of the
calcaneal apophysis.
Avulsion of the of the
calcaneal apophysis.
Normalfindings.
Achilles tendon ossification Pain and difficulty
walking.
May be totally silent. The Royal
London Test is negative.
Areas of ossification
within the Achilles
tendon.
Thickening of the Achilles
tendon, areas of marked
echogenicity with
no through-transmission
(consistent with
ossification). Radiographic
evidence of intratendinous
ossification.
Normalfindings.
Osteomyelitis of tibia and
calcaneus
Pain and difficulty
walking. Temperature.
The Achilles tendon itself is not
involved in the pathology.
provide an anatomic
overview of the region.
MRI: excellent soft-tissue
contrast and
its sensitivity to tissue
oedema and hyperaemia.
Increased uptake.
Neoplasms of tibia and
calcaneus
Nocturnal pain and
difficulty walking.
Temperature.
The Achilles tendon itself is not
involved in the pathology.
provide an anatomic
overview of the region.
The features change
according to the neoplasm
and its location. The Achilles
tendon shows no evident
abnormality.
Increased uptake.
Flexor
hallucislongustendinopathy
Pain on toe-off or forefoot
weigh-bearing,
maximum over the
posteromedial aspect of
the calcaneus around the
sustentaculumtali.
Pain aggravated by resisted
flexion of the first toe or stretch
into full dorsiflexion of the
hallux.
Normal findings. MRI: Abrupt fluid cut-off in
the tendon sheath,
excessive fluid loculated
around a normal-appearing
tendon proximal to the
fibro-osseous canal.
Normal findings.
Posterior tibialis
tendinopathy
Medial ankle pain behind
the medial malleolus and
extending towards the
insertion of the tendon.
Tenderness along the tendon.
Resisted inversion of the ankle
elicits pain and relative
weakness compared with the
contralateral side.
Single heel raise test viewed
from behind reveals lack of
inversion of the hind foot, and, if
severe, the patient may have
difficulty performing a heel
raise. If the pathology is
advanced, loss of the medial
arch, progressive pronation of
the foot, ‘too many toes’ sign.
Normal findings. Increased signal and tendon
thickening.
Normal findings.
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when low energy shock wave therapy is used outwith of the
indications and modalities outlined in the above trials, the results
can be disappointing [44].
Hyperthermia can be another option for the management of
these patients, with the potential to stimulate repair processes,
increase drug activity, allow more efficient relief from pain, help
removal toxic wastes, increase tendon extensibility and reduce
muscle and joint stiffness. Randomized controlled trials seem to
confirm these potential advantages [45].
Ultrasound therapy is widely available and frequently used.
However, systematic reviews and meta-analyses have repeatedly
concluded that there is insufficient evidence to support a beneficial
effect of ultrasound therapy at the current clinical dosages [46]. A
pilot randomized controlled trial showed similar outcome
between heavy eccentric loading and ultrasound for the manage-
ment of AT in subjects with a relatively sedentary lifestyle, with no
adverse effects [47]. These results need to be confirmed in wider
populations.
Several substances have been used for Achilles tendon
injections (Table 3). At present, studies which demonstrate the
superiority of one injection technique or of one substance over
another are few. A recent randomized control trial showed that
treatment with High Volume Injections (steroid, saline, and local
anaesthetic) or Platelet Rich Plasma in combination with eccentric
training in chronic Achilles tendinopathy seems more effective in
Table 2 (Continued)
Diagnosis History Findings
Physical Examination Plain-Film
Radiographic
Assessment
MRI or Ultrasonographic
Examination
Bone scan
Peronealtendinopathy Lateral ankle or heel pain
and swelling which is
aggravated by activity
and relieved by rest.
Local tenderness over the
peroneal tendons
Painful passive inversion and
resisted eversion.
Normal findings. Increased signal and tendon
thickening.
Normal findings.
Ostrigonum syndrome Pain with mild swelling
posterior to the ankle.
Pain is accentuated by resisted
plantar flexion or dorsiflexion
of the great toe.
Tenderness is present anterior to
the Achilles tendon and
posterior to the talus. Positive
posterior impingement sign.
There may be
hypertrophy of the
ossicle or lateral
tubercle.
MR can identify a disruption
of the cartilaginous
synchondrosis by
demonstrating fluid
between the ostrigonum
and the lateral talar process.
Increased uptake
in the region of the
os trigonum in
symptomatic os
trigonum and
ununited posterior
process fractures.
Fig. 2. Ultrasound view showing thickening of the Achilles tendon.
Fig. 3. MRI showing tendinopathy of the main body of the Achilles tendon.
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reducing pain, improving activity level, and reducing tendon
thickness and intratendinous vascularity than eccentric training
alone. High volume injections, also, seem to be more effective in
improving outcomes of chronic Achilles tendinopathy than Platelet
Rich Plasma in the short term [48].
4.1. Surgical management of tendinopathy of the main body of the
Achilles tendon
In 24–45.5% of patients with AT, conservative management is
unsuccessful, and surgery is recommended after at least six
months of conservative methods of management. There is a lack of
trials on surgical management of AT, and therefore the high success
rate reported by some authors needs to be interpreted with
caution. Surgical options range from simple percutaneous tenot-
omy (Fig. 4A, B, C) [49,50] (possibly ultrasound-guided [51]), to
minimally invasive stripping of the tendon (Fig. 5A, B, C) [52], to
open procedures (Fig. 6), (Table 4). During open procedures, if
more than 50% of the tendon is debrided, consideration could be
given to a tendon augmentation or transfer.
Most authorities anecdotally report excellent or good results in
up to 85% of cases. In a systematic review [53], most of the articles
on surgical success rates reported successful results in over 70% of
cases. However, this relatively high success rate is not always
observed in clinical practice. The articles that reported success
rates higher than 70% often had poorer methods scores. Surgery
appears to work better for athletes [27,54] and males [55].
Rehabilitation is focused on early motion and avoidance of
overloading the tendon in the initial healing phase. A period of
initial splinting and crutch walking is generally used to allow pain
and swelling to subside. After 14 days, patients are encouraged to
start daily active and passive ankle range of motion exercises. The
use of a removable walker boot can be helpful during this phase.
Weightbearing is not limited according to the degree of debride-
ment needed at surgery, and early weight bearing is encouraged.
However, extensive debridement and tendon transfers may require
protected weightbearing for 4–6 weeks postoperatively. After 6–8
weeks of mostly range of motion and light resistive exercises,
initial tendon healing will have completed. More intensive
strengthening exercises are started, gradually progressing to
plyometrics and eventually running and jumping
Table 3
Injections for Achilles tendinopathy.
Injections
Corticosteroid injections At present, there is not significant evidence from which to draw firm conclusions on the utility of local steroid treatments for Achilles
tendinopathy. 3 randomized controlled trials [58–60] showed a mixed picture of the effect of local steroids on healing, with 2 studies
reporting some benefit [58,59] and the other detecting none [60]. Meta-analysis of the effects of corticosteroid injections has shown
little benefit [14]. The safety of using corticosteroid injections can be enhanced with the use of imaging as a guide to enter the
peritendinous space [61].
Hyperosmolar dextrose
injections
Sonographically guided intratendinous injection of hyperosmolar dextrose yielded good clinical responses in patients with chronic
Achilles tendinopathy in pilot studies [62,63].
MMPinhibitors Injections of aprotinin (a broad spectrum proteinase inhibitor) have been used for the management of Achilles tendinopathy with
good results [64]. Patients must be warned of the risk of allergy from aprotinin injections for tendinopathy and be prepared to remain
under medical surveillance for 30 to 60 minutes after injection. Because of this risk, aprotinin should be used as second-line therapy
only, for chronic conditions where more basic measures have failed.
Sclerosing injections In patients with chronic painful Achilles tendinopathy, but not in normal pain-free tendons, there is neovascularisation outside and
inside the ventral part of the tendinopathic area [37,38]. Local anaesthetic injected in the area of neovascularisation outside the tendon
resulted in a pain-free tendon, indicating that this area is involved in pain generation. These are the bases for the injection of sclerosing
substances under ultrasonography and colour Doppler-guidance in the area with neovessels outside the tendon.
Injections with the sclerosing substance Polidocanol showed the potential to reduce tendon pain during activity in patients with
chronic painful mid-portion Achilles tendinopathy in a randomized controlled trial [65].
High volume ultrasound guided
injections
High volume ultrasound guided injections aim to produce local mechanical effects causing neo-vessels to stretch, break or occlude
[66]. In this way, the accompanying nerve supply would also be damaged, decreasing the pain in patients with resistant Achilles
tendinopathy. In a pilot study [66], high volume image guided Achilles tendon injection of normal saline in patients with resistant
Achilles tendinopathy decreased the amount of pain perceived by patients, while improving daily functional ankle and Achilles
movements in the short- and long-term.
Fig. 4. High volume injection procedure. Using an aseptic technique, a 21gaugen-
eedleattached to a 30 cm connecting tube is inserted under real-time ultrasound
guidance between the anterior aspect of the AT and Kager’sfatpad. A mixture of
10 ml 0.5% Bupivacaine hydrochloride and 25 mg of Hydrocortisone acetate is
injected, followed by 4 Â10 mL of injectable normal saline. The position of the
needle and flow of fluid is monitored continuously by US during this phase, and the
needle moved gently across the anterior aspect of the tendon.
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Fig. 5. Percutaneous longitudinal tenotomy. The patient lies prone on the examination couch with the feet protruding beyond its edge, and the ankles resting on a sandbag.
The tendon is accurately palpated, and the area of maximum swelling and/or tenderness marked, and checked by US scanning. A number11surgicalscalpelblade (Swann-
Morton, London, United Kingdom) is inserted parallel to the long axis of the tendon fibres in the centre of the area of tendinopathy. The cutting edge of the blade points
caudally and penetrates the whole thickness of the tendon. While keeping the blade still, a full passive ankle flexion is produced. The scalpel blade is then retracted to the
surface of the tendon and inclined 45
on the sagittal axis, and the blade is inserted medially through the original tenotomy. While keeping the blade still, a full passive ankle
flexion is produced. The whole procedure is repeated inclining the blade 45
laterally to the original tenotomy, inserting it laterally through the original tenotomy. While
keeping the blade still, a full passive ankle flexion is produced. The blade is then partially retracted to the posterior surface of the tendo Achillis, reversed 180
, so that its
cutting edge now points caudally, and the whole procedure repeated, taking care to dorsiflex the ankle passively.
Fig. 6. Minimally invasive stripping. The patient is positioned prone with a calf tourniquet which is inflated to 250 mmHg after exsanguination. Four skin incisions are made.
The first two incisions are 0.5 cm longitudinal incisions at the proximal origin of the Achilles tendon, just medial and lateral to the origin of the tendon. The other two incisions
are also 0.5 cm long and longitudinal, but 1 cm distal to the distal end of the tendon insertion on the calcaneus.
A surgical instrument (mosquito) is inserted in the proximal incisions (Fig. 6A), and the AT is freed of the peritendinous adhesions. A Number 1 unmounted Ethibond (Ethicon,
Somerville, NJ) suture thread is inserted proximally, passing through the two proximal incisions. The Ethibond is retrieved from the distal incisions (Fig. 6A), over the posterior
aspect of the Achilles tendon. Using a gentle see-saw motion, similar to using a Gigli saw, the Ethibond suture thread is made to slide posterior to the tendon (Fig. 6C), which is
stripped and freed from the fat of Kager’striangle.
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5. Discussion
The natural history and clinical course of AT are unclear, and the
condition may be self-limiting in many patients. Therefore, it is
important to establish whether the many commonly used treat-
ments, including surgery, really work. Data from randomized,
controlled trials are insufficient to assess the efficacy of
conservative and surgical interventions in the management of
AT. It is still debatable why tendinopathic tendons respond to
surgery. For example, we do not know whether surgery induces
long term re-vascularisation, denervation, healing of the failed
healing response lesion or a combination of all these, resulting in
pain reduction.
Guidelines have been published for the evaluation and
management of AT [56].However, these guidelines have not been
tested in a systematic manner, and are to be regarded at best as
expert opinion.
The clinical diagnosis of AT, even in experienced hands, is not
straightforward. If the patient presents with tendinopathy of the
Achilles tendon with a tender area of intratendinous swelling that
moves with the tendon and whose tenderness significantly
decreases or disappears when the tendon is put under tension,
a clinical diagnosis of tendinopathy can be formulated. In this
instance, further imaging is indicated only for confirmatory, not
diagnostic, purposes, as it is unlikely to change the management of
the patient. It would be reasonable to refer the patient to a physical
therapist to start a programme of eccentric exercises. If the
condition does not respond to these interventions, shock wave
therapy, or nitric oxide patches might be considered, although data
on their efficacy are limited. If the condition does not respond to
these interventions, peritendinous injections or injections at the
interface between the Achilles tendon and Kager’s triangle could
be considered (Fig. 7). The possibility of surgery should be
discussed with the patient after at least three to 6 months of non-
operative management. In well conducted studies in specialist
centres, the percentage of success of surgery is around 75%, and a
Table 4
Options for Achilles Tendon Disorders.
Less invasive More invasive
Paratendinopatghy 1. High volume image guided injection (hvigi) between the achilles
tendon and paratenon.
2. Minimally invasive paratenon stripping.
3. Tendoscopic debridement of paratenon.
1. Open debridement of paratenon.
2. Gastrocnemius recession if isolated contracture is present.
Non-insertional
tendinopathy
1. Percutaneous longitudinal tenotomy.
2. Gastrocnemius recession if isolated contracture is present.
1. Debridement with tubularization if less than 50% resection required.
consider a gastrocnemius recession if an isolated contracture is
present.
2. Debridement with tubularization and concomitant tendon transfer
(flexor hallucis longus or peroneus brevis).
3. Consider a concomitant gastrocnemius recession if an isolated
contracture is present.
Insertional
tendinopathy
1. Gastrocnemius recession if isolated contracture is present. Con-
comitant resection of prominent superior calcaneus is required to
decrease the risk of further impingement following the recession.
1. Debridement and re-attachment if less than 50% resection is required.
Concomitant resection of the postero-superior corner of the calcaneus
should be performed. Consider a gastrocnemius recession if an
isolated contracture is present.
2. Debridement and re-attachment with concomitant tendon transfer
(flexor hallucis longus or peroneus brevis) if greater than 50%
resection is required. Concomitant Haglund’s resection should be
performed.
In cases of severe tendinopathy where no viable Achilles tendon remains:
a. a. Allograft reconstruction.
b. V-Y lengthening with re-attachment.
c. Tenodesis of flexor hallucis longus /peroneus brevis to remaining
Achilles.
d. Isolated flexor hallucis longus /peroneus brevis transfer in lower
demand patients (no impact).
Fig. 7. The paratenon and the Achilles tendon are exposed. The paratenon is
identified and incised. In patients with evidence of co-existing paratendinopathy,
the scarred and thickened tissue is generally excised. A longitudinal tenotomy is
performed. The tendinopathic tissue can be identified as it generally has lost its
shiny appearance, and frequently contains disorganized fibre bundles which have
more of a “crabmeat” appearance. This tissue is sharply excised.
G Model

period of around 6 months will be required before returning to
sports activities.
6. Conclusions
The clinical diagnosis and management of AT, even in
experienced hands, is not straightforward. Hence, patients should
understand that symptoms may recur with either conservative or
surgical approaches. Teaching patients to control the symptoms
may be more beneficial than leading them to believe that AT is fully
curable.
Conflict of interest
We declare that we do not have any conflict of interest by any
means.
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