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Achilles tendinopathy: new insights in cause of pain, diagnosis and management
van Sterkenburg, M.N.
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Citation for published version (APA):van Sterkenburg, M. N. (2012). Achilles tendinopathy: new insights in cause of pain, diagnosis andmanagement.
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Download date: 25 Aug 2019
Achilles tendinopathyNew insights in cause of pain,
diagnosis and management
M.N. van Sterkenburg
Achilles tendinopathy: new insights in cause of pain, diagnosis and management
Maayke van Sterkenburg
PhD thesis, University of Amsterdam, the Netherlands
©2012, M.N. van Sterkenburg, Amsterdam, the Netherlands
This thesis was prepared at the Orthopaedic Research Center Amsterdam, Academical Medi-
cal Center, University of Amsterdam, the Netherlands
This thesis was supported by Stichting Steun Orthopaedie AMC
The publication of this thesis was supported by Nederlandse Orthopaedische Vereniging,
Anna Fonds, Universiteitsfonds Universiteit van Amsterdam, Department of Orthopaedic
Surgery AMC, DJO Global, Biomet, Arthrex, Smith& Nephew, Pro- Motion Orthopedics,
Bauerfeind Benelux B.V., Astra Tech Benelux B.V., Penders Voetzorg
ISBN 978-94-6169-210-8
Cover illustration:Maayke van Sterkenburg & Optima Grafische Communicatie
Layout and Printing: Optima Grafische Communicatie
Achilles tendinopathy
New insights in cause of pain, diagnosis and management
ACADEMISCH PROEFSCHRIFT
Ter verkrijging van de graad van doctor
aan de Universiteit van Amsterdam
op gezag van de Rector Magnificus
Prof. dr. D.C. van den Boom
ten overstaan van een door het college
voor promoties ingestelde commissie,
in het openbaar te verdedigen
in de Aula der Universiteit
op woensdag 4 april 2012, te 11:00 uur
door
Maayke Nadine van Sterkenburg
geboren te Leiderdorp
Promotiecommissie
Promotor Prof. dr. C.N. van Dijk
Copromotor Dr. G.M.M.J. Kerkhoffs
Overige leden Prof. dr. J.C. Goslings
Prof. dr. R.J. Oostra
Prof. dr. R.J.P.M. Scholten
Prof. dr. F.J.G. Backx
Prof. dr. R.L. Diercks
Dr. M. Maas
Faculteit der Geneeskunde
CONTENTS
PART I GENERAL INTRODUCTION 9
PART II TERMINOLOGY AND OUTCOME MEASURES 27
Chapter 1 Terminology for Achilles tendon related disorders CN van Dijk, MN van Sterkenburg, JI Wiegerinck, J Karlsson, N Maffulli. Knee Surgery Sports Traumatol Arthrosc 2011;19:835-841
29
Chapter 2 Outcome measures and assessment tools K Gravare Silbernagel, MN van Sterkenburg, A Brorsson, J Karlsson. Achilles tendinopathy:current concepts 2009:205-212
41
Chapter 3 Reliability and validity of the Dutch VISA-A questionnaire and applicability to non-athletes MN van Sterkenburg, IN Sierevelt, JL Tol, IV van Dalen, D Haverkamp, CN van Dijk. Submitted
53
PART III MIDPORTION ACHILLES TENDINOPATHY: CAUSE OF PAIN AND TREATMENT MODALITIES
67
Chapter 4 Less promising results with sclerosing Ethoxysclerol injections for Achilles tendinopathy: a retrospective study MN van Sterkenburg, MC de Jonge, IN Sierevelt, CN van Dijk. Am J Sports Med 2010; 38: 2226-2232
69
Chapter 5 Tendoskopie am Sprunggelenk und Fuß MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Artroskopie 2009; 22: 132-140
85
Chapter 6 The plantaris tendon and a potential role in midportion Achilles tendinopathy: an observational anatomical study MN van Sterkenburg, GMMJ Kerkhoffs, RP Kleipool, CN van Dijk. J Anat 2011; 218: 336-341
107
Chapter 7 Good outcome after stripping the plantaris tendon in patients with chronic midportion Achilles tendinopathy MN van Sterkenburg, GMMJ Kerkhoffs, CN van Dijk. Knee Surg Sports Traumatol Arthrosc 2011;19:1362-1366
121
Chapter 8 Midportion Achilles tendinopathy: why painful? An evidence based philosophy MN van Sterkenburg, CN van Dijk Knee Surg Sports Traumatol Arthrosc 2011;19:1367-1375
131
Part IV RETROCALCANEAL BURSITIS: DIAGNOSIS AND TREATMENT 149
Chapter 9 Appearance of the weight-bearing lateral radiograph in retrocalcaneal bursitis MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. Acta Orthop 2010;81 387-390
151
Chapter 10 Endoscopic Calcaneoplasty Chapter in ‘Minimally invasive foot and ankle surgery’ MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Accepted for publication 2010
159
Chapter 11 Optimization of Portal Placement for Endoscopic Calcaneoplasty MN van Sterkenburg, M Groot, IN Sierevelt, GMMJ Kerkhoffs, CN van Dijk. Arthroscopy 2011;27:1110-1117
175
Part V GENERAL DISCUSSION 189
Part VI 207
SUMMARY 211
Samenvatting 221
Addendum 229
PArt iGeNerAL iNtroDUctioN
General introduction
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BAckGroUND
The Achilles tendon was weak, small or absent in the great ape, but is one of the hallmarks
of bipedal man. It possibly originated soon after the divergence of chimpanzee and human
lineages4. Its origination may be related to the greater relative length of the tarsal bones
in man. The name ‘Achilles tendon’ is derived from the Iliad by Homer. Achilles was made
invulnerable in infancy by his mother the goddess Thetis, who plunged him into the river
Styx. As he was held by one heel, this part was not bathed and so remained unprotected.
This heel was the site where Achilles was mortally wounded by a poisoned arrow launched
from the bow of Paris during the Trojan War. The ‘Achilles heel’ is currently used as an idiom
to express one’s principal weakness. In 1693 the Dutch surgeon Philip Verheyen changed the
concept ‘tendo magnus of Hippocrates’, the anatomical connection between the calcaneus
and triceps surae muscle, to ‘Achilles tendon’23.
The human body is built for movement. However, over the years we have become progres-
sively less active in daily life. The prevalence of obesity in the Western World has been rising,
and as a reaction keeping fit is increasingly advocated in recent years. Healthy nourishment,
physical discipline, and fitness occupy a considerable part of the cultural space. Endurance
sports like triathlons and long distance running have gained popularity. Although scientific
evidence supports the notion that humans evolved to be runners, with the ability to outrun
almost any animal when it comes to long distances28, overuse injuries have become promi-
nent in daily practice.
General inactivity during the week in an office-setting for many years, followed by
extreme and extensive exercise in the weekend without decent build-up in training program
allow for these types of injury to occur. Thirty to fifty percent of all sports injuries are due to
overuse, and overuse tendon injury has become an important issue in both recreational and
competitive athletes. Chronic Achilles tendon pathology is one of the most frequently occur-
ring problems in sports involving running and jumping. In elite long-distance runners there
even is a lifetime risk of 52% of sustaining an Achilles tendon injury24. However, the injury is
not always related to excessive physical activity. Thirty percent of patients have a sedentary
lifestyle, which may suggest that physical activity might exacerbate symptoms rather than
cause them3.
Recalcitrant Achilles tendons may cause pain for years and are often resistant to any form
of treatment. In the end, chronic Achilles tendon complaints may be self-limiting, since they
have been described to quench after an average of 8 years43. Doctors and athletes will not
consent with this prospect. Unfortunately, the cause of pain has not yet been clarified and
therefore its treatment is challenging and often unsatisfactory.
14
TerminologyThe terminology of chronic Achilles tendon disorders has been confusing. Maffulli and
co-workers proposed ‘Achilles tendinopathy’, the combination of Achilles tendon pain,
swelling, and impaired performance as standard terminology for chronic midportion prob-
lems, including the histopathological entities tendinosis and peritendinitis33. Terminology is
still confusing for problems around the insertion: retrocalcaneal bursitis, insertional spurs,
Haglund’s syndrome, - disease, - exostosis, pumpbump, cucumber heel and many more are
used interchangeably.
AnatomyThe Achilles tendon consists of the fibers of two muscle units in the superficial compartment
of the posterior leg: the gastrocnemius muscle (medial and lateral head) and the soleus
muscle. The gastrocnemius muscle crosses the knee and ankle joints (ankle and subtalar);
originating from the posterior surface of condylus medialis and -lateralis femoris and insert-
ing onto the calcaneus. The soleus muscle lies anterior to the gastrocnemius muscle and
originates from each side of the anterior aponeurosis attached to the tibia and fibula, and
from the posterior surfaces of the head of the fibula and its proximal quarter, as well as the
middle third of the medial border of the tibia. The soleus muscle only crosses the 2 ankle
joints. Distally, both the gastrocnemius and soleus muscles form an aponeurosis, from each
of which a tendon originates. At about the level where the soleus contributes fibers to the
Achilles tendon, rotation of the tendon begins and becomes more marked in the distal 5-6
cm. The gastrocnemius fibers rotate to lateral and the soleus fibers are positioned medial to
the insertion41. The Achilles tendon inserts crescent-shaped halfway the posterior tuberosity
of the calcaneus29. Just anterior to the distal portion of the Achilles tendon and posterior to
the posterosuperior calcaneal prominence the retrocalcaneal bursa is situated.
Unlike other tendons in the leg, the Achilles tendon lacks a synovial sheath. Instead, it
has a paratenon, which is an array of thin, fibrous tissue containing blood vessels49. Together
with the bone- tendon- and the muscle-tendon junction the paratenon forms the sole vas-
cular supply of the Achilles tendon. Within the paratenon, the plantaris tendon runs with
the Achilles tendon. The plantaris tendon is believed to be rudimentary. Absence in 7-20%
human lower limbs has been reported6, 7, 12, 39, 51.
The muscle of the plantaris muscle-tendon complex is triangularly shaped and lies poste-
rior to the knee joint, originating from the inferior part of the lateral supracondylar line of the
femur. The tendon travels inferomedially, posterior to the soleus muscle and anterior to the
medial gastrocnemius muscle. The tendon crosses the calf relatively proximal, running medial
from, and parallel with the Achilles tendon from the midportion of the calf; in the majority
of cases inserting medially onto the calcaneus7, 16. The plantaris tendon is considered to
function as a weak ankle- and knee flexor and ankle invertor.
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Clinical assessment of chronic Achilles tendon pathologyThe most common clinical diagnosis of chronic Achilles tendon problems is paratendinopathy
with or without tendinopathy (55-65%) (midportion tendinopathy), followed by insertional
problems such as retrocalcaneal bursitis and insertional spurs or calcifications (20-25%)17-19,
27. This thesis focuses on midportion Achilles tendinopathy and retrocalcaneal bursitis.
Midportion Achilles tendinopathy
General symptoms of midportion Achilles tendinopathy include painful swelling typically 2-7
centimeter (cm) proximal to the insertion, and stiffness especially when getting up after a
period of rest. Pain is often most prominent on the medial side of the tendon52.
Tendinopathy and paratendinopathy often co-exist. In isolated paratendinopathy, there is
local thickening of the paratenon. Paratendinopathy can be acute or chronic. Acute isolated
paratendinopathy manifests itself as peritendinous crepitation as the tendon tries to glide
within the inflamed covering. Areas of increased erythema, local heat, and palpable tendon
nodules or defects may also be present at clinical examination. In chronic Achilles paraten-
dinopathy, exercise-induced pain is still the cardinal symptom while crepitation and swelling
diminish. The area of swelling does not move with dorsiflexion and plantarflexion of the
ankle, where it does in tendinopathy35,55,60. In addition, ankle instability and malalignment
of the lower extremity, especially in the foot, should be looked for in patients with Achilles
tendon complaints.
Retrocalcaneal bursitis
Retrocalcaneal bursitis is caused by repetitive impingement of the bursa between Achilles
tendon and posterosuperior calcaneus. Differentiation between midportion and insertional
tendinopathy can be made on thorough history taking and physical examination. In case
of a retrocalcaneal bursitis, patients complain of pain after a day of strenuous activity or
when starting to walk after a period of rest. Wearing shoes with rigid heel counters is often
avoided. Physical examination reveals swelling on both sides of the Achilles tendon at the
level of the posterosuperior calcaneal prominence. Pain is aggravated by palpating this area
just medial and lateral to the Achilles tendon. Retrocalcaneal bursitis can be accompanied
by insertional tendinopathy. In case of insertional tendinopathy, there is pain at the bone-
tendon junction, which gets worse after exercise. The area of maximum tenderness is often
located in the central part of the insertion.
In clinical practice overuse injuries often do have features of more than one patho-
physiological entity, however in most cases thorough history taking and physical examination
should provide with the correct diagnosis.
16
ImagingStandard lateral and anteroposterior (AP) weight-bearing radiographs of the foot should
routinely be made even when soft tissue pathology is suspected, to exclude bony pathology
and assess foot deformities. Calcifications and bone spurs can be detected in case of inser-
tional tendinopathy. A posterosuperior calcaneal prominence can be seen and may cause
retrocalcaneal bursitis, but is not conclusive of the diagnosis. In case of a clinical diagnosis of
midportion tendinopathy or retrocalcaneal bursitis, additional investigations such as ultraso-
nography (US) or magnetic resonance imaging (MRI) can be helpful.
In midportion Achilles tendinopathy, US may reveal discontinuity of tendon fibers, focal
hypoechoic intratendinous areas, fusiform tendon swelling, and neovascularisation. In the
acute phase of paratendinopathy, there is fluid surrounding the tendon. Peritendinous adhe-
sions can be seen as thickening of the hypo-echoic paratenon with poorly defined borders.
In case of a retrocalcaneal bursitis fluid can be detected in the retrocalcaneal space, and an
insertional problem provides a hyperechoic signal.
US is a cost-effective and accurate measure to evaluate disorders of the Achilles tendon
and has the advantage of dynamic assessment, but is operator-dependent and often not
accessible by the orthopedic surgeon. Moreover, it is nowadays often superseded by contrast
enhanced MRI. Although MRI is expensive and time-consuming, its ability to acquire images
from multiple planes is an advantage, and is especially important for pre-operative planning.
The tendon proper may show expansion on T1- weighted images and central enhancement
of the signal within the tendon. In the acute phase of Achilles paratendinopathy, MRI is the
most useful imaging modality and shows high signal around the Achilles tendon on the STIR-
and T2 images. In the chronic phase the paratenon is thickened. In case of a retrocalcaneal
bursitis a high signal is seen on T2 and STIR in the retrocalcaneal space.
Outcome measuresMany studies have been published on different treatment modalities for Achilles tendinopathy.
Important in the evaluation of treatment outcome are standardized outcome measures46. A
patient’s subjective assessment of treatment outcome is increasingly appreciated. Criteria as
pain, functional ability and satisfaction fulfill the criteria of being valid, reliable and sensitive
to change if gathered by a correctly designed and tested patient-centered questionnaire8.
Response bias is minimized since the investigator has minimal influence on the scoring5, 56.
The Victorian Institute of Sports Assessment- Achilles (VISA-A) questionnaire was created
in 2001. It is a self- administered valid and reliable questionnaire evaluating symptoms and
their effect on physical activity46. Subjective scoring systems can be used in all countries after
translation and validation for specific language and population13, 14, 38.
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Management
Midportion tendinopathy
A wide range of conservative treatment measures is available for Achilles tendinopathy. An
eccentric training schedule is currently the treatment of first choice, preferably combined
with avoidance of painful activities, correction of malalignments of the foot, stretching and
use of NSAIDs when an acute element is present or just for pain relief. With compliance
this program is described to render good results in up to 90% of patients1,11,36,42,48,53. If it
fails, many other conservative measures can be applied, with varying results. An effective
treatment algorithm has not been developed yet. Independent of the levels of evidence, at 6
months after the start of treatment, 75-80% of patients report to be able to return to their
previous sporting activities. For the remaining patients surgical treatment can be considered.
Surgical measures can be divided into minimally invasive and open procedures, but also into
treatment for paratendinopathy, tendinopathy of the main body, and a combination of both.
Open debridement of the Achilles tendon is the most commonly performed procedure. After
removal of pathological tissue often enough tendon remains to achieve side-to-side closure.
When more than 50% of the tendon is degenerative, augmentation with a turn-down flap
and/or plantaris tendon can be performed, but larger defects require tendon transfer. When
the paratenon is involved, open adhesiolysis with or without resection of the paratenon can
be performed20,25,32,40,47. Aftertreatment for open debridement often consists of immobili-
zation in cast; modern postoperative strategies consist of bracing in walkers or the use of
heel raises and functional treatment. Return to sport tends to be at around the 6- month
mark but should be individualized. Because of the long time to recovery, minimally invasive
procedures have been developed to reduce per- and postoperative morbidity, rehabilitation
and time to normal activity. For isolated tendinopathy of the main body, percutaneous longi-
tudinal tenotomies can be performed34, 57; for paratendinopathy percutaneous stripping of
the paratenon and Achilles tendoscopy have been invented31, 55.
Success rates for the surgical management of non-insertional Achilles tendinopathy are
reported to be in the order of 75-100%26, 40, 44, 50. However, these results cannot be matched
with day-to-day clinical practice. These long-term difficulties in assessing the methods and
outcome of surgery are probably caused by a lack of understanding the pathology37.
Retrocalcaneal bursitis
Multiple conservative treatment options have been described to manage retrocalcaneal bur-
sitis, including avoidance of tight shoe heel counters, cast immobilization, NSAIDs, activity
modification, padding, shock wave treatment, physical therapy and injection of corticoste-
roids into the retrocalcaneal space. When these measures fail, surgical treatment can be
18
considered. Mostly open procedures performed through a lateral, medial or transverse Achil-
les tendon incision. The retrocalcaneal area is debrided and an osteotomy of the posterosu-
perior calcaneus is performed. These open procedures are invasive, have high complication
rates and rehabilitation is extensive7,20,31,32,42,47. Therefore, an endoscopic approach was
developed by Van Dijk et al.59. In this ‘endoscopic calcaneoplasty’ two portals are created,
just lateral and medial to the Achilles tendon, directly proximal to the superior part of the cal-
caneus. During the procedure, the retrocalcaneal bursa, posterosuperior calcaneus tuberosity
and local synovitis are addressed.
Current concepts on the cause of pain in midportion tendinopathyThe cause of complaints in midportion Achilles tendinopathy has not yet been unraveled;
however extensive research over the past three decades has led to the formulation of gener-
ally two different theories; (1) mechanical overuse and (2) neovascularisation. The first theory
hypothesizes that repetitive tensional loading with repeated strains below acute tendon injury
threshold induces microdamage. When matrix composition and organization is repaired and
mechanical strain continues on transiently weak tissue, tendon damage accumulates. Since
there is no time for proper repair due to overuse, degeneration develops. The poor vascu-
larisation and low metabolism contribute to the pathology. However, this theory does not
explain pain associated with tendinopathy, nor the cause of complaints in 30% of sedentary
patients45,54. Degeneration is believed to be associated with aging. Tendons become stiffer,
blood flow declines and responsiveness of cells to loading decreases45,54. Disuse is closely
connected to ageing; a disused tendon has similar changes as an aged tendon43. Neverthe-
less, degeneration does not seem to be an inevitable consequence of aging. Synergism of
overuse and ageing in the development of Achilles tendinopathy has been proposed54,58.
Several studies have reported intratendinous changes in up to 34% of cadaver specimens
and MRI images of patients without complaints10,15,21,22. A long-term follow-up study was
published by Alfredson et al. revealing persistent structural abnormalities and thickening
of the tendon 13 years after intratendinous surgery for Achilles tendinopathy, whereas all
patients were satisfied with the results and went back to Achilles tendon loading activities
without restrictions2. These studies imply that an area of intratendon abnormality of the
Achilles tendon proper is not necessarily the cause of pain.
The second, more recent theory on the cause of tendinopathy is the increased irregular
vascular and neurogenic ingrowth into the tendon proper as a contributory factor to the
pain in patients with symptomatic midportion tendinopathy. Pain-free normal tendons are
sparsely vascularised, which is even less at the two hypovascular regions at the insertion and
midportion area, commonly associated with pathology. Blood flow declines with ageing and
mechanical loading. Although the role of neovascularisation is poorly understood, and may
even be part of a healing response, treatment with Doppler ultrasound guided injection of
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Polidocanol (Ethoxysclerol) into these neovessels is described as a successful invasive conser-
vative treatment modality in different publications1-4,19,60.
Aims AND oUtLiNe of this thesis
This thesis aims at elucidating the cause of pain, and optimizing current diagnostic and
management methods in midportion Achilles tendinopathy and retrocalcaneal bursitis. A
better understanding will have positive consequences for the patients.
The terminology for chronic Achilles tendon pathology has become inconsistent and con-
fusing. Eponyms have been introduced but their definitions vary. Some terms represent a
disease, some an anatomic location, pathology, or a generic name. For proper research and
assessment of diagnosis and management, a uniform and clear terminology is necessary.
The objective of Chapter 1 is to provide a clear and uniform terminology for Achilles ten-
dinopathy. It comprises anatomic location, symptoms, clinical findings, and histopathology.
Chapter 2 reviews the currently available outcome measures and assessment tools for the
evaluation of complaints and outcome of interventions.
Validated outcome measures are essential in the evaluation of complaints and effective-
ness of treatment in both the clinical setting and research. The VISA-A has successfully been
translated into Swedish, German and Italian30, 38, 53. The aim of chapter 3 is to translate
and validate the Dutch version of the VISA-A subjective outcome measure for Achilles tendi-
nopathy (VISA-A-NL). It was hypothesized that the translated version would be a reliable and
valid tool in the subjective evaluation of complaints in patients with Achilles tendinopathy.
Another hypothesis was that the questions on activity could be deleted when applied to
non-athletes.
In Chapter 4 the aim was to evaluate the short- and midterm outcome of Ethoxysclerol
injections as a conservative measure for Achilles tendinopathy. This treatment was intro-
duced in 2003 by Alfredson et al. and was based on the findings of enhanced vascularisation
around degenerative tendons. Ethoxysclerol obliterates neovessels by destroying the intima
as is done in the treatment of varicose veins. We hypothesized that sclerosing Etoxysclerol
injections would not yield good results in the majority of patients.
When conservative measures fail, surgery can be considered. Also for operative interven-
tions many options are available. Minimally invasive treatment is preferable, and has proved
to cause less postoperative morbidity, to facilitate shorter rehabilitation and quicker sport
resumption when compared to open surgery. Amongst Achilles tendon endoscopy, ‘Achilles
tendoscopy’, chapter 5 describes the endoscopic approach and outcome of tendon prob-
lems around the ankle.
20
The exact pathophysiological mechanism causing midportion Achilles tendinopathy has not
yet been clarified. Obviously this is the main reason that the optimal treatment modality has
not yet been found. Pain is often located on the medial side of the Achilles tendon, where the
plantaris tendon accompanies the Achilles tendon. Also, most ultrasonographically detected
midportion disorders are found in the medial segment of the tendon9. In a healthy situation
the plantaris tendon is attached to the calcaneus or Achilles tendon at its insertion, but is
separate from the Achilles tendon at its midportion in 95%7. During Achilles tendoscopy it
is found that the plantaris tendon is fixed to the Achilles tendon at the level of complaints55.
The aim of chapter 6 is to evaluate the anatomic relations of the plantaris muscle and distal
tendon origins. We hypothesized that in chronic Achilles tendinopathy adhesions between
Achilles- and plantaris tendon are formed and so could seriously contribute to patient’s symp-
toms. In chapter 7 the results of stripping the plantaris tendon in 3 patients with midportion
Achilles tendinopathy are analyzed. It was hypothesized that stripping the plantaris tendon
would relate to a good outcome. In chapter 8, the cause of pain in midportion Achilles
tendinopathy is re-evaluated. We hypothesized that the tendon proper is not the cause of
complaints, but the process of scarring and adhesion of the paratenon onto the Achilles and
plantaris tendon that comes with the inflammatory response. This theory is elucidated using
the available evidence on the cause and treatment of midportion Achilles tendinopathy.
As described earlier, chronic Achilles tendon problems also occur around the tendon’s inser-
tion onto the calcaneus. Chronic retrocalcaneal bursitis is diagnosed at physical examination
as a prominent palpable swelling is palpable lateral and medial from the Achilles tendon just
proximal to the calcaneus. Standard lateral and anteroposterior radiographs of the ankle are
made to assess foot deformities or any bony abnormalities. In order to confirm the diagnosis
chronic retrocalcaneal bursitis, ultrasound, MRI or even bone scans are performed. These are
expensive and time consuming. Chapter 9 evaluates the usefulness of a visible soft tissue
swelling in the retrocalcaneal recess on standard lateral weight-bearing radiographs on the
ankle in diagnosing a retrocalcaneal bursitis. It was hypothesized that the retrocalcaneal
recess on radiography would be a useful and reliable tool in the diagnosis of a chronic
retrocalcaneal bursitis.
Primary treatment of choice consists of a number of conservative treatment options
including avoidance of tight shoe heel counters, cast immobilization, NSAIDs, activity modi-
fication, padding, shock wave treatment and physical therapy. When conservative treatment
fails, endoscopic calcaneoplasty can be performed. In chapter 10 this surgical procedure
is described. Adequately determining the location of landmarks can be difficult due to the
anatomy and swelling. Portals are positioned too far proximal and as a consequence the
posterosuperior part of the calcaneus cannot be reached properly resulting in a suboptimal
procedure or, when the problem is recognized, a need to re-incise or lengthen the incisions.
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For this reason, we aimed to standardize portal placement in chapter 11. It was hypothesized
that the landmark of the fibula tip in standard 2-portal hindfoot endoscopy was usable, and
that in patients with flat feet portals should be placed more proximal to this landmark.
22
refereNce List
1. Alfredson H, Pietila T, Jonsson P, Lorentzon R.
Heavy-load eccentric calf muscle training for
the treatment of chronic Achilles tendinosis.
Am J Sports Med 1998; 26(3): 360-366.
2. Alfredson H, Zeisig E, Fahlstrom M. No
normalisation of the tendon structure and
thickness after intratendinous surgery for
chronic painful midportion Achilles tendino-
sis. Br J Sports Med 2009; 43: 948-949.
3. Ames PR, Longo UG, Denaro V, Maffulli
N. Achilles tendon problems: not just an
orthopaedic issue. Disabil Rehabil 2008;
30(20-22): 1646-1650.
4. Bramble DM, Lieberman DE. Endurance
running and the evolution of Homo. Nature
2004; 432(7015): 345-352.
5. Coleman BD, Khan KM, Maffulli N, Cook JL,
Wark JD. Studies of surgical outcome after
patellar tendinopathy: clinical significance of
methodological deficiencies and guidelines
for future studies. Victorian Institute of
Sport Tendon Study Group. Scand J Med Sci
Sports 2000; 10(1): 2-11.
6. Danforth CH. The Heredity of Unilateral
Variations in Man. Genetics 1923; 9: 199-
210.
7. Daseler EH. The Plantaris Muscle: An Ana-
tomical Study of 750 Specimens. J Bone
Joint Surg 1943; 25: 822-827.
8. Dawson J, Carr A. Outcomes evaluation in
orthopaedics. J Bone Joint Surg Br 2001;
83(3): 313-315.
9. de Vos RJ, Heijboer MP, Weinans H, Verhaar
JA, van Schie HT. Tendon Structure is Not
Related to Clinical Outcome Following
Eccentric Exercises in Chronic Mid-Portion
Achilles Tendinopathy. Unpublished results.
10. Emerson C, Morrissey D, Perry M, Jalan
R. Ultrasonographically detected changes
in Achilles tendons and self reported
symptoms in elite gymnasts compared with
controls - An observational study. Man Ther
2010; 15(1): 37-42.
11. Fahlstrom M, Jonsson P, Lorentzon R, Alfred-
son H. Chronic Achilles tendon pain treated
with eccentric calf-muscle training. Knee
Surg Sports Traumatol Arthrosc 2003; 11(5):
327-333.
12. Freeman AJ, Jacobson NA, Fogg QA. Ana-
tomical variations of the plantaris muscle
and a potential role in patellofemoral pain
syndrome. Clin Anat 2008; 21(2): 178-181.
13. Guillemin F. Cross-cultural adaptation and
validation of health status measures. Scand J
Rheumatol 1995; 24(2): 61-63.
14. Guillemin F, Bombardier C, Beaton D. Cross-
cultural adaptation of health-related quality
of life measures: literature review and
proposed guidelines. J Clin Epidemiol 1993;
46(12): 1417-1432.
15. Haims AH, Schweitzer ME, Patel RS, Hecht
P, Wapner KL. MR imaging of the Achilles
tendon: overlap of findings in symptomatic
and asymptomatic individuals. Skeletal
Radiol 2000; 29(11): 640-645.
16. Harvey FJ, Chu G, Harvey PM. Surgical avail-
ability of the plantaris tendon. J Hand Surg
Am 1983; 8(3): 243-247.
17. Järvinen M. Epidemiology of tendon injuries
in sports. Clin Sports Med 1992; 11(3): 493-
504.
18. Järvinen TA, Kannus P, Maffulli N, Khan
KM. Achilles tendon disorders: etiology and
epidemiology. Foot Ankle Clin 2005; 10(2):
255-266.
19. Järvinen TA, Kannus P, Paavola M, Jarvinen
TL, Jozsa L, Jarvinen M. Achilles tendon
injuries. Curr Opin Rheumatol 2001; 13(2):
150-155.
20. Jozsa L, Kannus P. Human Tendons:
Anatomy, Physiology, and Pathology. Human
Kinetics 1997.
21. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73(10): 1507-1525.
Part 1G
eneral in
trod
uctio
n
23
22. Khan KM, Forster BB, Robinson J et al. Are
ultrasound and magnetic resonance imag-
ing of value in assessment of Achilles tendon
disorders? A two year prospective study. Br J
Sports Med 2003; 37(2): 149-153.
23. Kirkup J. Mythology and History. In: Helal
B, Wilson D, editors. The Foot. Churchill
Livingstone; 1988: 1-8.
24. Kujala UM, Sarna S, Kaprio J. Cumulative
incidence of achilles tendon rupture and
tendinopathy in male former elite athletes.
Clin J Sport Med 2005; 15(3): 133-135.
25. Kvist H, Kvist M. The operative treatment of
chronic calcaneal paratenonitis. J Bone Joint
Surg Br 1980; 62(3): 353-357.
26. Kvist H, Kvist M. The operative treatment of
chronic calcaneal paratenonitis. J Bone Joint
Surg Br 1980; 62(3): 353-357.
27. Kvist M. Achilles tendon injuries in athletes.
Sports Med 1994; 18(3): 173-201.
28. Lieberman DE, Bramble DM. The evolution of
marathon running : capabilities in humans.
Sports Med 2007; 37(4-5): 288-290.
29. Lohrer H, Arentz S, Nauck T, Dorn-Lange NV,
Konerding MA. The Achilles tendon inser-
tion is crescent-shaped: an in vitro anatomic
investigation. Clin Orthop Relat Res 2008;
466(9): 2230-2237.
30. Lohrer H, Nauck T. Cross-cultural adaptation
and validation of the VISA-A questionnaire
for German-speaking Achilles tendinopathy
patients. BMC Musculoskelet Disord 2009;
10(1): 134.
31. Longo UG, Ramamurthy C, Denaro V,
Maffulli N. Minimally invasive stripping for
chronic Achilles tendinopathy. Disabil Reha-
bil 2008; 30(20-22): 1709-1713.
32. Maffulli N, Binfield PM, Moore D, King JB.
Surgical decompression of chronic central
core lesions of the Achilles tendon. Am J
Sports Med 1999; 27(6): 747-752.
33. Maffulli N, Khan KM, Puddu G. Overuse
tendon conditions: time to change a confus-
ing terminology. Arthroscopy 1998; 14(8):
840-843.
34. Maffulli N, Testa V, Capasso G, Bifulco G,
Binfield PM. Results of percutaneous longi-
tudinal tenotomy for Achilles tendinopathy
in middle- and long-distance runners. Am J
Sports Med 1997; 25(6): 835-840.
35. Maffulli N, Walley G, Sayana MK, Longo UG,
Denaro V. Eccentric calf muscle training in
athletic patients with Achilles tendinopathy.
Disabil Rehabil 2008; 1-8.
36. Mafi N, Lorentzon R, Alfredson H. Superior
short-term results with eccentric calf muscle
training compared to concentric training in
a randomized prospective multicenter study
on patients with chronic Achilles tendinosis.
Knee Surg Sports Traumatol Arthrosc 2001;
9(1): 42-47.
37. Matheson GO. Nonoperative treatment of
midportion Achilles tendinopathy: a review.
Clin J Sport Med 2010; 20(1): 72-73.
38. Mathias SD, Fifer SK, Patrick DL. Rapid
translation of quality of life measures for
international clinical trials: avoiding errors
in the minimalist approach. Qual Life Res
1994; 3(6): 403-412.
39. Moss ALH. Is There an Association Between
an Absence of Palmaris Longus Tendon and
an Absence of Plantaris Tendon? Eur J Plast
Surg 1988; 11: 32-34.
40. Nelen G, Martens M, Burssens A. Surgical
treatment of chronic Achilles tendinitis. Am
J Sports Med 1989; 17(6): 754-759.
41. O’Brien M. The anatomy of the Achilles ten-
don. Foot Ankle Clin 2005; 10(2): 225-238.
42. Ohberg L, Lorentzon R, Alfredson H. Eccen-
tric training in patients with chronic Achilles
tendinosis: normalised tendon structure and
decreased thickness at follow up. Br J Sports
Med 2004; 38(1): 8-11.
43. Paavola M, Kannus P, Paakkala T, Pasanen M,
Jarvinen M. Long-term prognosis of patients
with achilles tendinopathy. An observational
8-year follow-up study. Am J Sports Med
2000; 28(5): 634-642.
44. Paavola M, Orava S, Leppilahti J, Kannus
P, Jarvinen M. Chronic Achilles tendon
overuse injury: complications after surgical
24
treatment. An analysis of 432 consecutive
patients. Am J Sports Med 2000; 28(1):
77-82.
45. Rees JD, Wilson AM, Wolman RL. Current
concepts in the management of tendon
disorders. Rheumatology (Oxford) 2006;
45(5): 508-521.
46. Robinson JM, Cook JL, Purdam C et al. The
VISA-A questionnaire: a valid and reliable
index of the clinical severity of Achilles
tendinopathy. Br J Sports Med 2001; 35(5):
335-341.
47. Rolf C, Movin T. Etiology, histopathology,
and outcome of surgery in achillodynia. Foot
Ankle Int 1997; 18(9): 565-569.
48. Roos EM, Engstrom M, Lagerquist A,
Soderberg B. Clinical improvement after 6
weeks of eccentric exercise in patients with
mid-portion Achilles tendinopathy -- a ran-
domized trial with 1-year follow-up. Scand J
Med Sci Sports 2004; 14(5): 286-295.
49. Saxena A, Bareither D. Magnetic resonance
and cadaveric findings of the “watershed
band” of the achilles tendon. J Foot Ankle
Surg 2001; 40(3): 132-136.
50. Schepsis AA, Jones H, Haas AL. Achilles
tendon disorders in athletes. Am J Sports
Med 2002; 30(2): 287-305.
51. Schwalbe, Pfitzner. Varietäten-Statistik und
Anthropologie. Deutsche Med Wchnschr
1894; XXV(3): 459.
52. Segesser B, Goesele A, Renggli P. [The
Achilles tendon in sports]. Orthopäde 1995;
24(3): 252-267.
53. Silbernagel KG, Thomee R, Thomee P,
Karlsson J. Eccentric overload training for
patients with chronic Achilles tendon pain--a
randomised controlled study with reliability
testing of the evaluation methods. Scand J
Med Sci Sports 2001; 11(4): 197-206.
54. Smith RK, Birch HL, Goodman S, Heinegard
D, Goodship AE. The influence of age-
ing and exercise on tendon growth and
degeneration--hypotheses for the initiation
and prevention of strain-induced tendinopa-
thies. Comp Biochem Physiol A Mol Integr
Physiol 2002; 133(4): 1039-1050.
55. Steenstra F, van Dijk CN. Achilles tendos-
copy. Foot Ankle Clin 2006; 11(2): 429-38.
56. Tallon C, Coleman BD, Khan KM, Maffulli
N. Outcome of surgery for chronic Achilles
tendinopathy. A critical review. Am J Sports
Med 2001; 29(3): 315-320.
57. Thermann H, Benetos IS, Panelli C, Gavriilidis
I, Feil S. Endoscopic treatment of chronic
mid-portion Achilles tendinopathy: novel
technique with short-term results. Knee
Surg Sports Traumatol Arthrosc 2009;
17(10): 1264-1269.
58. Tuite DJ, Renstrom PA, O’Brien M. The aging
tendon. Scand J Med Sci Sports 1997; 7(2):
72-77.
59. van Dijk CN, van Dyk GE, Scholten PE, Kort
NP. Endoscopic calcaneoplasty. Am J Sports
Med 2001; 29(2): 185-189.
60. Williams JG. Achilles tendon lesions in sport.
Sports Med 1993; 16(3): 216-220.
PArt ii termiNoLoGY AND
oUtcome meAsUres
Chapter 1
Terminology for Achilles tendon related disorders
Time for a change
CN van Dijk
MN van Sterkenburg
JI Wiegerinck
J Karlsson
N Maffulli
Knee Surgery Sports Traumatol Arthrosc 2011;19: 835-841
30
ABstrAct
The terminology of Achilles tendon pathology has become inconsistent and confusing
throughout the years. For proper research, assessment and treatment, a uniform and clear
terminology is necessary. A new terminology is proposed; the definitions hereof encompass
the anatomic location, symptoms, clinical findings and histopathology.
It comprises the following definitions: Midportion Achilles tendinopathy: a clinical
syndrome characterized by a combination of pain, swelling and impaired performance. It
includes, but is not limited to, the histopathological diagnosis of tendinosis. Achilles para-
tendinopathy: an acute or chronic inflammation and/or degeneration of the thin membrane
around the Achilles tendon. There are clear distinctions between acute paratendinopathy
and chronic paratendinopathy, both in symptoms as in histopathology. Insertional Achilles
tendinopathy: located at the insertion of the Achilles tendon onto the calcaneus, bone spurs
and calcifications in the tendon proper at the insertion site may exist. Retrocalcaneal bursitis:
an inflammation of the bursa in the recess between the anterior inferior side of the Achilles
tendon and the posterosuperior aspect of the calcaneus (retrocalcaneal recess). Superficial
calcaneal bursitis: inflammation of the bursa located between a calcaneal prominence or the
Achilles tendon and the skin.
Finally, it is suggested that previous terms as Haglund’s disease; Haglund’s syndrome;
Haglund’s deformity; pump bump (calcaneus altus; high prow heels; knobbly heels; cucum-
ber heel), are no longer used.
Ch
apter 1
Termin
olo
gy fo
r Ach
illes tend
on
related d
isord
ers
31
iNtroDUctioN
Overuse injuries of the Achilles tendon can be either insertional or non-insertional. As there
is no evidence available for chronic inflammation in patients with “tendinitis”, the term
tendinosis has been proposed instead1. In 1998, Maffulli et al. proposed to use the term
“tendinopathy” for the clinical syndrome characterized by a combination of pain, swelling
and impaired performance23. In Haglund’s syndrome, the pain is located at the postero-
superior calcaneal prominence. Originally, Haglund described pain in the hindfoot caused
by a prominent postero-superior corner of the calcaneus in combination with wearing a
rigid low-back shoe2,10. Today, when using the term Haglund’s exostosis, physicians are usu-
ally referring to a clinical situation of pain and tenderness at the postero-lateral aspect of
the calcaneus, where a calcaneal prominence can often be palpated. This is also known as
“pump-bump”, with alternative names as calcaneus altus, high prow heels, knobbly heels,
and cucumber heel.
A distinction between Haglund’s disease and other conditions such as a superficial Achilles
bursitis must be made. Haglund’s disease must be differentiated from Haglund’s syndrome,
which involves a painful swelling of an inflamed retrocalcaneal bursa, sometimes combined
with insertional tendinopathy of the Achilles tendon. It must also be distinguished from
Haglund’s disease, which is the term of osteochondrosis of the accessory navicular bone.
No doubt that all this is confusing: in reality, many different names and terms are used in
the literature. The purpose of this paper is to propose a terminology which includes the
combination of anatomic location, symptoms, clinical findings and pathological changes for
each entity.
historicAL PersPective
Midportion Achilles tendinopathy Philip Verheyen, a Dutch surgeon, was the first in 1693 to actually name the Achilles tendon
after the Greek hero Achilles16. Previously, it was known as “tendo magnus of Hippocrates”.
In 1883, Raynal described the first case of “cellulite peritendineuse of the Achilles tendon”32.
Other cases of “cellulite peritendineuse” of the Achilles tendon followed shortly2,17.
In 1905, Schanz was the first to describe a traumatic inflammation of the Achilles ten-
don: He described a patient who experienced ‘a chronic strain’ after mountain climbing36.
He entitled this “tendinitis Achillea traumatica”36. The inflammation was presumed to be
located in the Achilles tendon itself, instead of the insertion into the calcaneus, contrary to
the standard or ideas of the time1,34.
32
The terminology has changed more or less constantly, often without any evident scientific
reason throughout the 20th century. In 1950, Lipscomb proposed new definitions for inflam-
matory processes of tendons. He defined “paratendinitis” as an inflammatory process of
tendons or portions of tendons without a tendon sheath; “tenosynovitis” was implemented
to refer to inflammatory processes of tendons with a sheath. Additionally, he proposed
“peritendinitis” as a general term to refer to either “tenosynovitis” or “paratendinitis”20.
Since the 1970’s, increased effort was put in categorising Achilles tendon pathology, related
to subgroups. In 1976, Perugia et al. introduced new terminology on inflammatory problems
of the Achilles tendon30. They based their definitions on histological findings. Perugia et
al. differentiated between pure peritendinitis, peritendinitis associated with tendinosis, and
pure tendinosis. Peritendinitis was characterised by the presence of inflammation of the
peritendinous sheaths, without any pathological changes in the tendon itself. Peritendinitis
associated with tendinosis involved degenerative features of the tendon associated with
inflammation of the sheaths. Pure tendinosis was said to be characterized by degenerative
phenomena exclusively, often associated with foci of osteo-cartilaginous metaplasia. Later in
the same year, Puddu et al. published a paper clarifying the new terms introduced by Perugia
et al30,31. Tendinosis implied tendon degeneration, without any clinical or histological signs
of intratendinous inflammation.
Throughout the years, the discussion continued on the terminology of the location and on
the actual nomenclature of Achilles tendon disorders9,39. It took, however, until 1992 for
Clain and Baxter to divide the definitions of Achilles “tendinitis” in insertional and non-
insertional6.
In 1998, Maffulli et al.23 suggested to change the confusing terminology concerning overuse
tendon conditions. They proposed to use the terms “tendinosis”15, “paratendinitis”, and
“tendinitis” only after excision biopsy had been examined by a pathologist as these imply
specific, histopathologically proven conditions, with inflammatory cells23. They advised not
to use the aforementioned terms in clinical practice when discussing overuse tendon injuries.
The term “partial tear” should be reserved to acute partial tendinous lesions. In fact, this
term may be questioned altogether whether it does exist or not. “Achillodynia” is a purely
descriptive term, referring to pain in the region of the Achilles tendon1,24,34. Finally, Maf-
fulli et al. proposed to name the clinical syndrome of pain, swelling (diffuse or localised),
and impaired performance as tendinopathy. Depending on the involved tissues, the terms
tendinopathy, paratendinopathy, and pantendinopathy should be used23. Maffulli et al`s
publication has greatly helped to reduce the confusion in clinical terminology; the proposal
was broadly accepted, but it was not, however, implemented universally. Terminology has
therefore remained confusing27,40.
Ch
apter 1
Termin
olo
gy fo
r Ach
illes tend
on
related d
isord
ers
33
Pathology around the Achilles tendon insertionAlbert1 was the first to describe ‘Achillodynia’ in 1893, but the underlying pathology was
not determined, however25. In 1895, Rössler34 found that the cause of this Achillodynia
was an inflammation of the bursa between the insertion of the Achilles tendon and the
postero-superior tuberosity of the calcaneus. Three years later, Painter published his histo-
logical findings after resection of the post-calcaneal exostosis causing the inflammation of
the post-calcaneal bursa28. He concluded the exostoses were most probably manifestations
of an osteoarthritic process. In Patrick Haglund’s opinion, the term Achillodynia was too
general, and he divided patients into three groups: ‘Achillotendinitis ossificans’, ‘Bursitis
Achillea’, and children with growth problems of the epiphysis of the calcaneus. In terms
of “bursitis Achillea”, he noted there were 2 bursae: one located between the calcaneus
and the skin (bursa Achillea infero-posterior), and one between the Achilles tendon and
the calcaneus (bursa Achillea supero-anterior). In his opinion, the superficial bursitis was
caused by incorrect shoe-wear for ‘Kulturmenschen’ (culture people), and the other (deep
bursitis) by either acute or chronic trauma. The inferior posterior bursitis had, in his opinion,
no clinical relevance, but the superior anterior bursitis, caused by impingement between the
Achilles tendon and a bony prominence, on the calcaneus caused clinically relevant signs
and symptoms. This condition can be treated surgically by resecting the postero-superior
bony prominence of the calcaneus in case conservative measures fail10,28. In 1954, the term
‘pump bump’ arose. Dickinson et al. described the ‘pump bump’ as an enlargement of
the posterolateral aspect of the heel at the site of the insertion of the Achilles tendon and
Achilles tendon bursitis, mostly associated with wearing high heel shoes. When conservative
treatment failed, patients were treated surgically by excision of the posterosuperior corner
of the calcaneus7.
Until 1982, inflammation of the retro-calcaneal bursa caused by impingement between the
anterior aspect of the Achilles tendon and the posterior part of the calcaneus was named
retrocalcaneal bursitis. In that year, Pavlov et al. first described the ‘Haglund’s syndrome’,
defined as a frequent cause of posterior heel pain, characterized by a painful soft tissue
swelling at the level of the Achilles tendon insertion. Using a lateral heel radiograph, they
described a prominent calcaneal bursal projection, retro-calcaneal bursitis, thickening of the
Achilles tendon, and a convexity of the superficial soft tissues at the level of the Achilles
tendon insertion, a ‘pump bump’29. This is the first publication in which the authors used the
name ‘Haglund’. Haglund’s deformity was then described by Vega et al. as a tender swelling
in the region of the Achilles tendon with visible prominence of the postero-lateral aspect of
the calcaneus. In their opinion, the superficial Achilles bursa and/or the retrocalcaneal bursa
reflected the enlarged prominence. Then, in 1990 and 1991 ‘analogies’ for Haglund’s defor-
mity were described: Haglund’s syndrome, achillobursitis, achillodynia, and retro-calcaneal
bursitis were mentioned18,33. In 1993, Haglund’s disease was added to this list3, although
34
it was earlier described as being an osteochondrosis of the accessory navicular bone (or os
tibiale externum)5,18,42.
Sella et al.38 thought that all these names were confusing, and proposed separate definitions
for Haglund’s disease, Haglund’s syndrome, and Haglund’s deformity. Haglund’s disease was
referred to as osteochondrosis of the accessory navicular; Haglund’s deformity as a chronic,
sometimes painful distortion of the postero-superior and lateral portion of the calcaneus;
and the term Haglund’s syndrome was used when symptoms were present with/without the
deformity, and may involve the retro-calcaneal bursa as well as the Achilles tendon and the
superficial Achilles bursa38. This proposal was, however, not commonly adapted, and many
publications kept using terms interchangeably 4,11-13,19,21,22,26,37.
In 1998, the Federative Committee on Anatomical Terminology and the International
Federation of Associations of Anatomists published a general anatomic terminology8. This
“Terminologia Anatomica” defines the retrocalcaneal bursa as “bursa tendinis calcanei” and
the superficial calcaneal bursa is termed the “bursa subcutanea calcanea”8.
ProPoseD termiNoLoGY for AchiLLes teNDoN reLAteD DisorDers
Examining the evolution of the terminology over the years, the efforts and the struggle are
obvious. Some terms represent a disease, some an anatomic location, a pathology, or a
generic name. The reasoning behind a change in terminology is unclear; it appears largely
to be susceptible to fashion. In the 19th century, the terminology was mainly based on
anatomy1; later, it was based on histopathology30; others have proposed a ‘history’-based
terminology3,29,38.
Five leading anatomy journals were contacted, and asked for information on which terminol-
ogy they demanded from their authors. Based on the answers, it can be concluded that,
concerning anatomy, there is no such thing as a “standard terminology”. Some stated that
the authors were expected to use “widely accepted terminology”.
The definitions for Achilles tendon disorders should comprise anatomic location, symptoms,
clinical findings, and histopathology. The term to represent the entity must be neutral yet
descriptive, uniform and clear. The aforementioned lack of consistency should be avoided as
much as possible. The following definitions are therefore proposed (Table 1).
Ch
apter 1
Termin
olo
gy fo
r Ach
illes tend
on
related d
isord
ers
35
Tab
le 1
. Ter
min
olog
y fo
r A
chill
es t
endo
n re
late
d di
sord
ers,
incl
udin
g th
e an
atom
ic lo
catio
n, s
ympt
oms,
clin
ical
find
ings
his
topa
thol
ogy.
For
rad
iogr
aphi
c fin
ding
s,
see
tabl
e2
Term
An
ato
mic
loca
tio
nSy
mp
tom
sC
linic
al fi
nd
ing
sH
isto
pat
ho
log
y
Mid
po
rtio
n A
chill
es
ten
din
op
ath
y2-
7 cm
fro
m t
he in
sert
ion
onto
the
cal
cane
usA
com
bina
tion
of p
ain,
sw
ellin
g an
d im
paire
d pe
rfor
man
ce
Diff
use
or lo
caliz
ed
swel
ling
incl
udes
, but
is n
ot li
mite
d to
, the
his
topa
thol
ogic
al
diag
nosi
s of
ten
dino
sis:
impl
ies
hist
opat
holo
gica
l dia
gnos
is
of t
endo
n de
gene
ratio
n w
ithou
t cl
inic
al o
r hi
stol
ogic
al s
igns
of
intr
aten
dino
us in
flam
mat
ion,
not
nec
essa
rily
sym
ptom
atic
Para
ten
din
op
ath
yA
cute
Ch
ron
ic
arou
nd t
he m
id-p
ortio
n A
chill
es t
endo
n
arou
nd t
he m
id-p
ortio
n A
chill
es t
endo
n
Edem
a an
d hy
pere
mia
Exer
cise
-indu
ced
pain
palp
able
cre
pita
tions
, sw
ellin
g
crep
itatio
ns a
nd s
wel
ling
less
pro
noun
ced
edem
a an
d hy
pere
mia
of
para
teno
n, w
ith in
filtr
atio
n of
in
flam
mat
ory
cells
, pos
sibl
y w
ith p
rodu
ctio
n of
a fi
brin
ous
exsu
date
tha
t fil
ls t
he s
pace
bet
wee
n te
ndon
she
ath
and
tend
on.
para
teno
n th
icke
ned
as a
res
ult
of fi
brin
ous
exud
ate,
pr
omin
ent
and
wid
espr
ead
prol
ifera
tion
of (m
yo)fi
brob
last
s,
form
atio
n of
new
con
nect
ive
tissu
e an
d ad
hesi
ons
betw
een
tend
on, p
arat
enon
, and
cru
ral f
asci
a
Inse
rtio
nal
Ach
illes
te
nd
ino
pat
hy
inse
rtio
n of
Ach
illes
ten
don
onto
cal
cane
us, m
ost
ofte
n w
ith f
orm
atio
n of
bon
e sp
urs
and
calc
ifica
tions
in
tend
on p
rope
r at
inse
rtio
n si
te
Pain
, stif
fnes
s,
som
etim
es a
(sol
id)
swel
ling
Pain
ful t
endo
n in
sert
ion
at t
he m
id-p
ortio
n of
the
po
ster
ior
aspe
ct o
f th
e ca
lcan
eus,
sw
ellin
g m
ay
be v
isib
le a
nd a
bon
y sp
ur
may
be
palp
able
ossi
ficat
ion
of e
nthe
sial
fibr
ocar
tilag
e, a
nd s
omet
imes
sm
all
tend
on t
ears
occ
urrin
g at
ten
don-
bone
junc
tion
Ret
roca
lcan
eal b
urs
itis
Burs
a in
the
rec
ess
betw
een
the
ante
rior
infe
rior
side
of
the
Ach
illes
ten
don
and
the
post
eros
uper
ior
aspe
ct o
f th
e ca
lcan
eus
(ret
roca
lcan
eal r
eces
s)
Pain
ful s
wel
ling
supe
rior
to c
alca
neus
pa
infu
l sof
t tis
sue
swel
ling,
med
ial a
nd
late
ral t
o th
e A
chill
es
tend
on a
t th
e le
vel o
f th
e po
ster
osup
erio
r ca
lcan
eus
Fibr
o-ca
rtila
gino
us b
ursa
l wal
ls s
how
deg
ener
atio
n an
d/or
ca
lcifi
catio
n, w
ith h
yper
trop
hy o
f th
e sy
novi
al in
fold
ings
and
ac
cum
ulat
ion
of fl
uid
in t
he b
ursa
. A
ltern
ativ
ely,
the
bur
sa
may
be
prim
arily
invo
lved
by
infla
mm
ator
y or
infe
ctio
us
burs
itis
due
to a
n in
flam
mat
ory
arth
ropa
thy
Sup
erfi
cial
cal
can
eal
bu
rsit
isbu
rsa
loca
ted
betw
een
ca
lcan
eal p
rom
inen
ce o
r th
e A
chill
es t
endo
n an
d th
e sk
in
visi
ble,
pai
nful
, sol
id
swel
ling
post
erol
ater
al
calc
aneu
s (o
ften
as
soci
ated
with
sho
es
with
rig
id p
oste
rior
port
ion)
Vis
ible
, pai
nful
, sol
id
swel
ling
and
disc
olor
atio
n of
ski
n. M
ost
ofte
n lo
cate
d at
pos
tero
late
ral
calc
aneu
s; s
omet
imes
po
ster
ior
or p
oste
rom
edia
l
an a
cqui
red
adve
ntiti
ous
burs
a, d
evel
opin
g in
res
pons
e to
fric
tion.
Whe
n in
flam
ed, l
ined
by
hype
rtro
phic
syn
ovia
l tis
sue
and
fluid
.
36
Tab
le 2
. Rad
iolo
gic
findi
ngs
in A
chill
es t
endo
n di
sord
ers
Term
/Im
agin
gPl
ain
Radi
ogra
phy
Ultr
asou
ndC
TM
RI
Mid
po
rtio
n A
chill
es
ten
din
op
ath
yD
evia
tion
of s
oft
tissu
e co
ntou
rs is
usu
ally
pre
sent
. In
rar
e ca
ses
calc
ifica
tions
ca
n be
fou
nd
Tend
on la
rger
tha
n no
rmal
in b
oth
cros
s-se
ctio
nal a
rea
and
ante
ro-p
oste
rior
diam
eter
. H
ypoe
choi
c ar
eas
with
in t
he t
endo
n,
disr
uptio
n of
fibr
illar
pat
tern
, inc
reas
e in
te
ndon
vas
cula
rity
(Ech
o-D
oppl
er) m
ainl
y in
ve
ntra
l per
itend
inou
s ar
ea
In c
ase
(mas
sive
) cal
cific
atio
n ar
e se
en o
n pl
ain
radi
ogra
phy.
C
T im
agin
g ca
n be
hel
pful
in
pre
-ope
rativ
e pl
anni
ng,
show
ing
the
exac
t si
ze a
nd
loca
tion
of t
he c
alci
ficat
ions
Fat-
sat
urat
ed T
1 or
T2
imag
es: f
usifo
rm
expa
nsio
n ,c
entr
al
enha
ncem
ent
cons
iste
nt
with
intr
aten
dino
us
neov
ascu
lariz
atio
n
Para
ten
din
op
ath
yA
cute
Ch
ron
ic
-A
nor
mal
Ach
illes
ten
don
with
ci
rcum
fere
ntia
l hyp
oech
ogen
ic h
alo
A t
hick
ened
hyp
oech
oic
para
teno
n w
ith
poor
ly d
efine
d bo
rder
s m
ay s
how
as
a si
gn
of p
erite
ndin
ous
adhe
sion
s; in
crea
se in
te
ndon
vas
cula
rity
(Ech
o-D
oppl
er) m
ainl
y in
ve
ntra
l per
itend
inou
s ar
ea
-Pe
riphe
ral e
nhan
cem
ent
on
fat-
satu
rate
d T1
or
on T
2 im
ages
Inse
rtio
nal
Ach
illes
te
nd
ino
pat
hy
May
sho
w o
ssifi
catio
n or
a
bone
spu
r at
the
ten
don’
s in
sert
ion;
pos
sibl
y de
viat
ion
of s
oft
tissu
e co
ntou
rs
Cal
cane
al b
ony
abno
rmal
ities
Bone
for
mat
ion
at in
sert
ion.
CT
scan
is in
dica
ted
mai
nly
for
pre-
oper
ativ
e pl
anni
ng. I
t sh
ows
the
exac
t lo
catio
n an
d si
ze o
f th
e ca
lcifi
catio
ns a
nd s
purs
Bone
for
mat
ion
and/
or o
n ST
IR (s
hort
tau
inve
rsio
n re
cove
ry) h
yper
inte
nse
sign
al
at t
endo
n in
sert
ion
Ret
roca
lcan
eal b
urs
itis
A p
oste
rosu
perio
r ca
lcan
eal
prom
inen
ce c
an b
e id
entifi
ed; r
adio
-opa
city
of
the
retr
ocal
cane
al r
eces
s;
poss
ibly
dev
iatio
n of
sof
t tis
sue
cont
ours
Flui
d in
the
ret
roca
lcan
eal a
rea/
burs
a (h
yper
echo
ic)
-H
yper
inte
nse
sign
al in
re
troc
alca
neal
rec
ess
on T
2 w
eigh
ed im
ages
Sup
erfi
cial
cal
can
eal
bu
rsit
isPo
ssib
ly d
evia
tion
of s
oft
tissu
e co
ntou
rs
Flui
d be
twee
n sk
in a
nd A
chill
es t
endo
n-
Hyp
erin
tens
e si
gnal
bet
wee
n A
chill
es t
endo
n an
d su
bcut
aneo
us t
issu
e on
T2
wei
ghed
imag
es
Ch
apter 1
Termin
olo
gy fo
r Ach
illes tend
on
related d
isord
ers
37
Midportion Achilles tendinopathy Achilles tendinopathy is a clinical syndrome characterized by a combination of pain, swelling
and impaired performance. The swelling can be diffuse or localized. Typically, the nodular
swelling is located at 2-7 cm from the insertion onto the calcaneus. This part of the tendon
has also been described as the “main body of the Achilles tendon”. This entity involves
isolated pathology of the tendon proper, and includes, but is not limited to, the histopatho-
logical diagnosis of tendinosis23.
Tendinosis implies histopathological diagnosis of tendon degeneration without clinical
or histological signs of intratendinous inflammation, and is not necessarily symptomatic14.
However, it should be kept in mind that, although the histological term ‘tendinosis’ is also
widely used, the essential lesion of tendinopathy is not, strictu sensu, of a degenerative
nature: it has the features of a failed healing response, in which the tendon attempts to heal,
but, for some reason, including, possibly, continuous inappropriate mechanical stimuli, the
healing process appears non-finalised.
Achilles paratendinopathyParatendinopathy is defined by acute or chronic inflammation and/or degeneration of the
thin membrane around the Achilles tendon. Exercise-induced pain and local swelling around
the tendon’s midportion are the most important symptoms.
Histopathologically, acute paratendinopathy is characterized by edema and hyperemia of
the paratenon, with infiltration of inflammatory cells, possibly with production of a fibrinous
exsudate that fills the space between the tendon sheath and the tendon, causing palpable
crepitations on physical examination. In chronic Achilles paratendinopathy, exercise-induced
pain is the major symptom, while crepitations and swelling are less pronounced. Histopatho-
logically, the paratenon becomes thickened as a result of fibrinous exsudate, prominent and
widespread proliferation of (myo)fibroblasts, formation of new connective tissue and adhe-
sions between tendon, paratenon, and the crural fascia27.
Insertional Achilles tendinopathyInsertional Achilles tendinopathy is located at the insertion of the Achilles tendon onto the
calcaneus, possibly with the formation of bone spurs and calcifications in the tendon proper
at the insertion site. Patients complain of pain and stiffness and sometimes (a solid) swelling.
On physical examination, the tendon insertion (at the midportion of the posterior aspect of
the calcaneus) is painful. A swelling may be visible and a bony spur may be palpable. Histo-
pathologically, there is ossification of enthesial fibrocartilage, and sometimes small tendon
tears occurring at the tendon-bone junction35.
38
Retrocalcaneal bursitis An inflammation of the bursa in the recess between the anterior inferior side of the Achilles
tendon and the posterosuperior aspect of the calcaneus (retrocalcaneal recess) results in a
visible and painful soft tissue swelling, medial and lateral to the Achilles tendon at the level
of the posterosuperior calcaneus. Frequently, a posterosuperior calcaneal prominence can
be identified at plain radiography. Histopathologically, the fibro-cartilaginous bursal walls
show degeneration and/or calcification, with hypertrophy of the synovial infoldings and
accumulation of fluid in the bursa itself41. Alternatively, the bursa may be primarily involved
by inflammatory or infectious bursitis due to an inflammatory arthropathy.
Superficial calcaneal bursitis An inflammation of the bursa located between a calcaneal prominence or the Achilles ten-
don and the skin resulting in a visible, painful, solid swelling and discoloration of the skin. It
is most often located at the posterolateral aspect of the calcaneus. It is frequently associated
with shoes with a rigid posterior portion. The Achilles tendon is usually not involved, how-
ever. Histopathologically, the subcutaneous bursa is an adventitious bursa, which is acquired
after birth, and develops in response to friction. It is lined by hypertrophic synovial tissue and
fluid. A superficial calcaneal bursitis can be further specified by its location, i.e. posterior,
posterolateral, or posteromedial.
Achilles tendinopathy and paratendinopathy often co-exist. Retro-calcaneal bursitis is often
seen in combination with insertional tendinopathy. Other combinations are possible, but
occur less frequently.
coNcLUsioN
An inconsistent and erroneous change in nomenclature of disorders of the Achilles tendon
throughout the years has resulted in a large pool of confusing definitions and terms. A
uniform and clear terminology is necessary for proper research, diagnostics and treatment.
Proposed are new definitions, based on the anatomic location, symptoms, clinical findings
and histopathology. In addition it is proposed that Haglund’s disease, Haglund’s syndrome,
Haglund’s deformity, pump bump (calcaneus altus; high prow heels; knobbly heels; cucum-
ber heel), tendinitis are no longer used.
One of the following, depending on pathology, should be used instead: Midportion Achil-
les tendinopathy; Achilles paratendinopathy; insertional Achilles tendinopathy; retrocalcaneal
bursitis and superficial calcaneal bursitis.
Ch
apter 1
Termin
olo
gy fo
r Ach
illes tend
on
related d
isord
ers
39
refereNce List
1. Albert E. Achillodynie. Wien Med Presse
1893; 34: 41-43.
2. Baracz V. Tendonitis achillea arthritica als
eine besondere Form der Achillessehnener-
krankung. Zcntrafbt Chir 1906.
3. Biyani A, Jones DA. Results of excision of
calcaneal prominence. Acta Orthop Belg
1993; 59(1): 45-49.
4. Brunner J, Anderson J, O’Malley M, Bohne
W, Deland J, Kennedy J. Physician and
patient based outcomes following surgical
resection of Haglund’s deformity. Acta
Orthop Belg 2005; 71(6): 718-723.
5. Caffey J. Pediatric X-ray Diagnosis. 4th ed.
Chicago: Year Book Medical; 1962.
6. Clain MR, Baxter DE. Achilles tendinitis. Foot
Ankle 1992; 13(8): 482-487.
7. Dickinson PH, Coutts MB, Woodward EP,
Handler D. Tendo Achillis bursitis. Report
of twenty-one cases. J Bone Joint Surg Am
1966; 48(1): 77-81.
8. Federative Committee on Anatomical Termi-
nology. Terminologia Anatomica. Stuttgart-
New York: Thieme; 1998.
9. Fry HJH. Overuse Syndrome, alias Tenosy-
novitis/Tendinitis: The Terminological Hoax.
Plast Recons Surg 1986; 78(3): 414-417.
10. Haglund P. Beitrag zur Klinik der Achil-
lessehne. Zeitschr Orthop Chir 1928; 49:
49-58.
11. Harris CA, Peduto AJ. Achilles tendon imag-
ing. Australas Radiol 2006; 50(6): 513-525.
12. Jerosch J, Nasef NM. Endoscopic calcane-
oplasty--rationale, surgical technique, and
early results: a preliminary report. Knee Surg
Sports Traumatol Arthrosc 2003; 11(3): 190-
195.
13. Jerosch J, Schunck J, Sokkar SH. Endoscopic
calcaneoplasty (ECP) as a surgical treatment
of Haglund’s syndrome. Knee Surg Sports
Traumatol Arthrosc 2007; 15(7): 927-934.
14. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73(10): 1507-1525.
15. Khan KM, Bonar F, Desmond PM et al.
Patellar tendinosis (jumper’s knee): findings
at histopathologic examination, US, and MR
imaging. Victorian Institute of Sport Tendon
Study Group. Radiology 1996; 200(3): 821-
827.
16. Kirkup J. Mythology and History. In: Helal
B, Wilson D, editors. The Foot. Churchill
Livingstone; 1988: 1-8.
17. Kirmission. Cellulite peritendineuse du
tendon d’Achille. Arch Gen Med 1884; 1:
100-105.
18. Le TA, Joseph PM. Common exostectomies
of the rearfoot. Clin Podiatr Med Surg 1991;
8(3): 601-623.
19. Leitze Z, Sella EJ, Aversa JM. Endoscopic
decompression of the retrocalcaneal space.
J Bone Joint Surg Am 2003; 85-A(8): 1488-
1496.
20. Lipscomb PR. Tendons: Nonsuppurative
tenosynovitis and paratendinitis. Instr
Course Lect 1950; 7: 254-261.
21. Lohrer H, Nauck T, Dorn NV, Konerding MA.
Comparison of endoscopic and open resec-
tion for Haglund tuberosity in a cadaver
study. Foot Ankle Int 2006; 27(6): 445-450.
22. Ly JQ, Bui-Mansfield LT. Anatomy of and
abnormalities associated with Kager’s fat
Pad. AJR Am J Roentgenol 2004; 182(1):
147-154.
23. Maffulli N, Khan KM, Puddu G. Overuse
tendon conditions: time to change a confus-
ing terminology. Arthroscopy 1998; 14(8):
840-843.
24. Movin T, Kristoffersen-Wiberg M, Shalabi
A, Gad A, Aspelin P, Rolf C. Intratendinous
alterations as imaged by ultrasound and
contrast medium-enhanced magnetic reso-
nance in chronic achillodynia. Foot Ankle Int
1998; 19(5): 311-317.
40
25. Nielson AL. Diagnostic and Therapeutic
Point in Retrocalcanean Bursitis. J Am Med
Assoc 1921; 77(6): 463.
26. Ortmann FW, McBryde AM. Endoscopic
bony and soft-tissue decompression of
the retrocalcaneal space for the treatment
of Haglund deformity and retrocalcaneal
bursitis. Foot Ankle Int 2007; 28(2): 149-153.
27. Paavola M, Jarvinen TA. Paratendinopathy.
Foot Ankle Clin 2005; 10(2): 279-292.
28. Painter C.F. Inflammation of the post-
calcaneal bursa associated with exostosis. J
Bone Joint Surg Am 1898; s1-11: 169-180.
29. Pavlov H, Heneghan MA, Hersh A, Goldman
AB, Vigorita V. The Haglund syndrome:
initial and differential diagnosis. Radiology
1982; 144(1): 83-88.
30. Perugia L, Ippolitio E, Postacchini F. A new
approach to the pathology, clinical features
and treatment of stress tendinopathy of
the Achilles tendon. Ital J Orthop Traumatol
1976; 2(1): 5-21.
31. Puddu G, Ippolito E, Postacchini F. A clas-
sification of Achilles tendon disease. Am J
Sports Med 1976; 4(4): 145-150.
32. Raynal E. Cellulite peritendineuse du tendon
d’Achille. Arch Gen Med 1883; 11(2): 677-
689.
33. Reinherz RP, Smith BA, Henning KE.
Understanding the pathologic Haglund’s
deformity. J Foot Surg 1990; 29(5): 432-435.
34. Rössler. Zur Kenntniss der Achillodynie.
Deutsch Ztschr f Chir 1895; 52: 274-291.
35. Rufai A, Ralphs JR, Benjamin M. Structure
and histopathology of the insertional region
of the human Achilles tendon. J Orthop Res
1995; 13(4): 585-593.
36. Schanz A. Eine typische Erkrankung der
Achillessehne. Zentralblatt für Chirurgie
1905; 32: 1289-1291.
37. Schunck J, Jerosch J. Operative treatment
of Haglund’s syndrome. Basics, indications,
procedures, surgical techniques, results and
problems. Foot Ankle Surg 2005; 11: 123-
130.
38. Sella EJ, Caminear DS, McLarney EA.
Haglund’s Syndrome. J Foot Ankle Surg
1997; 37(2): 110-114.
39. Smith DC. Tendinitis- or peri tendinitis. Brit
Med J 1960; 5183: 1429.
40. Sorosky B, Press J, Plastaras C, Rittenberg
J. The practical management of Achilles
tendinopathy. Clin J Sport Med 2004; 14(1):
40-44.
41. Stephens MM. Haglund’s deformity and
retrocalcaneal bursitis. Orthop Clin North
Am 1994; 25(1): 41-46.
42. Vega MR, Cavolo DJ, Green RM, Cohen RS.
Haglund’s deformity. J Am Podiatry Assoc
1984; 74(3): 129-135.
Chapter 2
Outcome measures and assessment tools
K Grävare Silbernagel
MN van Sterkenburg
A Brorsson
J Karlsson
Achilles tendinopathy: current concepts 2009: 205-212
42
iNtroDUctioN
Tallon and co-workers75 published a review of the outcome after surgery in patients with
chronic Achilles tendinopathy and pointed at the deficiencies in outcome assessment and
criteria. They recommended the use of outcome measures that were condition-specific, reli-
able, sensitive, and correlated with clinical severity.
oUtcome scores – qUestioNNAires
Many research studies have not used specific outcome measures validated for Achilles tendi-
nopathy. Instead, many studies use patient-reported pain (on a Visual Analogue Scale) with
tendon loading activity as a main outcome measure to determine the success of treatment.
Sometimes, the investigators have graded the success of treatment based on patient-reported
improvements1,41,45,51,76.
To minimize the response bias, which can affect the patients’ reports of pain and symp-
toms, it is important to use outcome assessments in which the investigator has a minimal
influence on the scoring12,75. In many of the above-mentioned studies, it is difficult to judge
how much the investigator could have influenced the results. Many studies include question-
naires relating to symptoms, physical activity, other treatments and previous injuries, but they
are rarely specific standardized questionnaires. The lack of standardized outcome measures
for Achilles tendinopathy caused previously difficulties when comparing treatment studies75.
A performance test protocol and scoring scale for the evaluation of ankle injuries by Kaik-
konen and co-workers has been used in a follow-up study of patients with Achilles tendi-
nopathy25,49,50. It includes both objective and subjective measurements and has been shown
to have good reliability in healthy individuals and to be able to distinguish patients with
ankle ligament injury from healthy individuals. However, its validity on patients with Achilles
tendinopathy has not been evaluated.
Stanish and co-workers73 designed a system for tendon symptom classification (Table 1). This
classification system has not been evaluated for reliability and validity, but it has been used
as an outcome measure after surgery in patients with ‘achillodynia’56.
The VISA-A questionnaireIn 2001, Robinson and co-workers55 developed a questionnaire as an index of the clinical
severity of Achilles tendinopathy, the Victorian Institute of Sports Assessment – Achilles
questionnaire (VISA-A). This questionnaire is based on a similar questionnaire for patellar
tendinopathy79,80. The VISA-A questionnaire is the first outcome measure designed specifi-
cally for Achilles tendinopathy. It has also been evaluated and shown to have good reliability
Ch
apter 2
Ou
tcom
e measu
res and
assessmen
t too
ls
43and validity38,55,72. A factor analysis of the Swedish version of the VISA-A questionnaire
(VISA-A-S) revealed that the questionnaire evaluated the two factors pain/symptoms and
physical activity72. The VISA-A-S questionnaire also has been shown to have a large effect
size indicating that it is responsive to clinically relevant changes71. The high responsiveness
(as indicated by an effect size of 2.1) also indicates that the VISA-A-S questionnaire can be
useful as an outcome measure in scientific studies.
When reviewing the literature we found that the VISA-A questionnaire had been used
as an outcome measure in 19 studies on treatment for patients with Achilles tendinopa-
thy9-11,15-17,39, 40, 53, 54, 57-59,65,69-71,77,78. Furthermore, the VISA-A questionnaire had been
translated to Italian and Swedish, and these versions were also shown to be reliable and
valid38,72.
The VISA-A is a self-administered questionnaire and provides an index of the clinical sever-
ity, which is easily followed over time, for patients with Achilles tendinopathy. The score
ranges between 0-100, and a lower score indicates worse symptoms and greater limitation
on physical activity. It can be used to compare different populations with Achilles tendinopa-
thy and to facilitate comparisons between studies. In the clinic, the VISA-A questionnaire can
be used to assess the clinical severity of the patient’s symptoms and provide a guideline for
treatment, as well as for monitoring the effect of treatment. This score might be less valid for
sedentary persons suffering from Achilles tendinopathy.
The Foot and Ankle Outcome ScoreThe Foot and Ankle Outcome Score (FAOS) is a questionnaire that assesses patients’ symp-
toms, function and foot- and ankle-related quality of life60. The FAOS content is based on
the Knee injury and Osteoarthritis Outcome Score (KOOS) and has been shown to have
good content validity and reliability in patients with ankle injury60. It has, however, not been
validated for patients with Achilles tendinopathy. When used as an outcome measure for
patients with Achilles tendinopathy, it has been shown to be responsive to changes over time
with treatment 60,28,61.
Table 1. Classification system for the effect of pain on athletic performance (Stanish et al 2000)
Level Description of pain Level of sports performance
1 No pain Normal
2 Pain only with extreme exertion Normal
3 Pain with extreme exertion and 1 to 2 hours afterwards Normal or slightly decreased
4 Pain during and after vigorous activities Somewhat decreased
5 Pain during activity and forcing termination Markedly decreased
6 Pain during daily activities Unable to perform
44
fUNctioNAL AssessmeNt
Achilles tendinopathy appears to cause difficulties with physical activities in the active
population, but exactly how it affects the lower leg muscle-tendon functions is not fully
understood69. Muscular strength, power, muscular endurance, flexibility and motor control
are important in physical performance. The improvements of these factors are therefore
often prescribed in rehabilitation and injury prevention programs for tendon injuries 14,73.
StrengthStrength measurements with dynamometry have been performed in patients with Achilles
tendinopathy, in both etiological and prospective treatment studies1,2,21,42,45,50,76.
Isokinetic dynamometry has been used to test ankle plantarflexion and dorsiflexion
strength both concentrically and eccentrically at various angular velocities such as 30o/s,
50o/s, 60o/s, 120o/s, 180o/s, and 225o/s1,2,21,42,45. Paavola and co-workers50, on the other
hand, measured the isometric strength of the lower limb in an isometric leg press dyna-
mometer. Testa and co-workers76 measured maximum isometric muscle activation, as well as
isometric muscular endurance, in patients with Achilles tendinopathy.
The various body positions described in the literature and used in the clinical setting to
measure plantarflexion and dorsiflexion strength are supine with the knee and hip extended,
sitting with the hip in 100-110 degrees of flexion and the knee in either 40 degrees or 90
degrees of flexion and a closed-chain position in which the measurement pad was placed
on the knee1,2,21,42,43,45. The reliability of isokinetic and isometric dynamometry is generally
high, and the various testing positions for plantarflexion and dorsiflexion have good test-
retest reliability2,43. A test for measuring muscular strength and power of the ankle plan-
tarflexion in a regular weight-training machine has also been shown to be reliable and valid
for patients with Achilles tendinopathy69. In this test, muscle power development, i.e. the
ability to produce a high force quickly, was evaluated both concentrically and eccentrically-
concentrically. The reason for evaluating muscle power was because power is considered to
be more important for both sports performance and injury protection, than the ability to
produce a high force31. Patients with Achilles tendinopathy had a significant deficit on their
injured side (or most symptomatic side) compared with their uninjured (or least symptomatic
side) in both concentric and eccentric-concentric plantarflexion while standing69.
It is, however, important to remember that strength tests are valid for measuring improve-
ments in strength, but they are only moderately correlated to functional performance and
need to be complemented with other types of functional assessment4.
Endurance testMuscular endurance testing is another type of muscle function measurement. In a heel-rise
test (also called heel-raise, heel-drop or toe-raise), repetitive plantarflexion of the ankle is
Ch
apter 2
Ou
tcom
e measu
res and
assessmen
t too
ls
45
performed on standing until fatigued. It is the most commonly used test for measuring the
muscular endurance of the calf musculature. The normal number of heel-rise repetitions
on one healthy leg is regarded to be approximately 25, but it can range from six to 70
in healthy individuals 35. The testing position for the subject is standing on one leg while
maintaining a straight knee, support with the fingertips for balance and avoiding body sway
forward. This test has been used in several research studies and has shown good reliability
(ICC 0.78-0.84) 43,74. The heel-rise test has been used in evaluations of patients with Achilles
tendon ruptures, as part of a scoring scale used for patients with Achilles tendinopathy
and in prospective studies of Achilles tendinopathy44,49,50. Even though heel-rises are often
prescribed during the rehabilitation of Achilles tendinopathy, they are not commonly used to
evaluate the effect of treatment. One study found no significant deficit on their injured side
(or most symptomatic side) compared with their uninjured (or least symptomatic side) on
the toe-raise test69. Since the treatment for Achilles tendinopathy include toe-raises, the test
is useful to evaluate the effect of treatment and improvements in heel-rise endurance with
treatment has been found in patients with Achilles tendinopathy70.
Jump testsVarious jump tests are often used to evaluate function in patients with lower extremity
injuries, as well as to evaluate functional performance in athletes18,47,83. High loads occur on
the Achilles tendon during activities during which the so-called stretch-shortening cycle (SSC)
is utilized20,30. The SSC is a combination of an eccentric muscle action (with lengthening of
the muscle and tendon) immediately followed by a concentric muscle action (shortening
of the muscle-tendon complex)8,29. The concentric force production will be higher when
preceded by an eccentric muscle action compared with a pure concentric muscle action8,29.
The efficiency of utilizing the SSC in various types of jumps reportedly ranges from 17-34% 5,20. Achilles tendon elasticity is important to store and release energy during the SSC, and
thereby improves the economy and performance of motion20,29. Changes in lower leg
functions such as muscle-tendon strength, endurance, flexibility and motor control could all
affect the various mechanisms in the SSC, and these changes might be etiological factors for
the development of Achilles tendinopathy21,74.
Jump tests such as counter-movement jumps (CMJ), squat jump (SJ) and hopping have
been used to evaluate the loading of the Achilles tendon30. CMJ and SJ are vertical jumps
where the jump height is used for evaluation. In the CMJ, the starting position is upright
whereas for the SJ the starting position is with the knees bent. Hopping is a continuous
rhythmical jump, similar to jumping rope and here the contact times and flight times are
usually evaluated 20,30. A drop counter-movement jump (Drop CMJ) is performed jumping
down from a box/step and directly on landing performing maximal vertical jump. This type
of jump is often used in training to improve jumping ability in athletes and it also places high
46
demands on the ability to utilize the SSC. One study on patients with Achilles tendinopathy
found significant deficit in hopping and Drop CMJ on their injured side (or most symptomatic
side) compared to their uninjured (or least symptomatic side) but this was not found on the
CMJ69,70. Another often used jump test is the one-legged hop for distance and it has also
been used in a prospective study to identify intrinsic risk factors for Achilles tendon overuse
injury42. Even though Achilles tendinopathy is thought to be related to running and jumping,
there are only a few prospective treatment studies that have evaluated the patient’s recovery
in terms of jumping ability.
coNcLUsioN
Thorough history taking and clinical examination are essential in diagnosing Achilles tendi-
nopathy. Although our findings suggest that imaging adds little information of use for expert
sports medicine clinicians in diagnosing tendinopathy, it is useful in preoperative planning
and possibly for less experienced clinicians, who are unsure of their diagnoses and unfamiliar
with subjective outcome measures.
Achilles tendinopathy causes not only pain, symptoms and difficulty with physical activity
but also impairments in various aspects of lower leg function. It is therefore important to
continuously evaluate the patients’ progress with both validated subjective scoring systems,
such as the VISA-A questionnaire, and with various validated functional tests. Also the
patients’ reported subjective pain and ability to return to previous physical activity and sports
are important outcome measures. Proper evaluations with validated tests are not only for
scientific purposes, but also of importance to the practitioner and the patient to follow the
progress with treatment and rehabilitation.
Ch
apter 2
Ou
tcom
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assessmen
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ls
47
refereNces
1. Alfredson H, Pietilä T, Jonsson P, Lorentzon R.
Heavy-load eccentric calf muscle training for
the treatment of chronic Achilles tendinosis.
Am J Sports Med 1998; 26(3): 360-366.
2. Alfredson H, Pietilä T, Öhberg L, Lorentzon R.
Achilles tendinosis and calf muscle strength.
The effect of short-term immobilization
after surgical treatment. Am J Sports Med
1998; 26(2): 166-171.
3. Archambault JM, Wiley JP, Bray RC, Verhoef
M, Wiseman DA, Elliott PD. Can sonogra-
phy predict the outcome in patients with
achillodynia? J Clin Ultrasound 1998; 26(7):
335-339.
4. Augustsson J, Thomeé R. Ability of closed
and open kinetic chain tests of muscular
strength to assess functional performance.
Scand J Med Sci Sports 2000; 10(3): 164-168.
5. Belli A, Bosco C. Influence of stretch-
shortening cycle on mechanical behaviour
of triceps surae during hopping. Acta Physiol
Scand 1992; 144(4): 401-408.
6. Bleakney RR, White LM. Imaging of the
Achilles tendon. Foot Ankle Clin 2005; 10(2):
239-254.
7. Boone DC, Azen SP, Lin CM, Spence C,
Baron C, Lee L. Reliability of goniometric
measurements. Phys Ther 1978; 58(11):
1355-1390.
8. Bosco C, Tarkka I, Komi PV. Effect of elastic
energy and myoelectrical potentiation of
triceps surae during stretch-shortening cycle
exercise. Int J Sports Med 1982; 3(3): 137-
140.
9. Brown R, Orchard J, Kinchington M, Hooper
A, Nalder G. Aprotinin in the management
of Achilles tendinopathy: a randomised
controlled trial. Br J Sports Med 2006; 40(3):
275-279.
10. Chan O, O’Dowd D, Padhiar N, et al. High
volume image guided injections in chronic
Achilles tendinopathy. Disabil Rehabil. 2008;
30(20-22): 1697-1708.
11. Christenson RE. Effectiveness of specific soft
tissue mobilizations for the management
of Achilles tendinosis: single case study--
experimental design. Man Ther 2007; 12(1):
63-71.
12. Coleman BD, Khan KM, Maffulli N, Cook JL,
Wark JD. Studies of surgical outcome after
patellar tendinopathy: clinical significance of
methodological deficiencies and guidelines
for future studies. Victorian Institute of
Sport Tendon Study Group. Scand J Med Sci
Sports 2000; 10(1): 2-11.
13. Cook JL, Khan KM, Kiss ZS, Purdam CR,
Griffiths L. Reproducibility and clinical util-
ity of tendon palpation to detect patellar
tendinopathy in young basketball players.
Victorian Institute of Sport tendon study
group. Br J Sports Med 2001; 35(1): 65-69.
14. Cook JL, Purdam CR. Rehabilitation of lower
limb tendinopathies. Clin Sports Med 2003;
22(4): 777-789.
15. de Jonge S, de Vos RJ, van Schie HT, Verhaar
JA, Weir A, Tol JL. One-year follow-up of a
randomised controlled trial on added splint-
ing to eccentric exercises in chronic midpor-
tion Achilles tendinopathy. Br J Sports Med
2010; 44(9): 673-7
16. de Vos RJ, Weir A, Cobben LP, Tol JL. The
value of power Doppler ultrasonography in
Achilles tendinopathy: a prospective study.
Am J Sports Med 2007; 35(10): 1696-1701.
17. de Vos RJ, Weir A, Visser RJ, de Winter T,
Tol JL. The additional value of a night splint
to eccentric exercises in chronic midportion
Achilles tendinopathy: a randomised con-
trolled trial. Br J Sports Med 2007; 41(7): e5.
18. Eastlack ME, Axe MJ, Snyder-Mackler L. Lax-
ity, instability, and functional outcome after
ACL injury: copers versus noncopers. Med
Sci Sports Exerc 1999; 31(2): 210-215.
19. Fredberg U, Bolvig L. Significance of ultraso-
nographically detected asymptomatic tendi-
nosis in the patellar and achilles tendons of
48
elite soccer players: a longitudinal study. Am
J Sports Med 2002; 30(4): 488-491.
20. Fukashiro S, Komi PV, Järvinen M, Miyashita
M. In vivo Achilles tendon loading during
jumping in humans. Eur J Appl Physiol
Occup Physiol 1995; 71(5): 453-458.
21. Haglund-Åkerlind Y, Eriksson E. Range of
motion, muscle torque and training habits
in runners with and without Achilles tendon
problems. Knee Surg Sports Traumatol
Arthrosc 1993; 1(3-4): 195-199.
22. Järvinen TA, Kannus P, Maffulli N, Khan
KM. Achilles tendon disorders: etiology and
epidemiology. Foot Ankle Clin 2005; 10(2):
255-266.
23. Järvinen TA, Kannus P, Paavola M, Järvinen
TL, Jozsa L, Järvinen M. Achilles tendon
injuries. Curr Opin Rheumatol 2001; 13(2):
150-155.
24. Kader D, Saxena A, Movin T, Maffulli N.
Achilles tendinopathy: some aspects of basic
science and clinical management. Br J Sports
Med 2002; 36(4): 239-249.
25. Kaikkonen A, Kannus P, Järvinen M. A per-
formance test protocol and scoring scale for
the evaluation of ankle injuries. Am J Sports
Med 1994; 22(4): 462-469.
26. Kaufman KR, Brodine SK, Shaffer RA,
Johnson CW, Cullison TR. The effect of foot
structure and range of motion on musculo-
skeletal overuse injuries. Am J Sports Med
1999; 27(5): 585-593.
27. Khan KM, Forster BB, Robinson J, et al. Are
ultrasound and magnetic resonance imag-
ing of value in assessment of Achilles tendon
disorders? A two year prospective study. Br J
Sports Med 2003; 37(2): 149-153.
28. Knobloch K, Schreibmueller L, Longo
UG, Vogt PM. Eccentric exercises for the
management of tendinopathy of the main
body of the Achilles tendon with or without
the AirHeel Brace. A randomized controlled
trial. A: effects on pain and microcirculation.
Disabil Rehabil 2008; 30(20-22): 1685-1691.
29. Komi PV. Stretch-shortening cycle: a power-
ful model to study normal and fatigued
muscle. J Biomech. Oct 2000; 33(10): 1197-
1206.
30. Komi PV, Fukashiro S, Järvinen M. Biome-
chanical loading of Achilles tendon during
normal locomotion. Clin Sports Med 1992;
11(3): 521-531.
31. Kraemer WJ, Adams K, Cafarelli E, et al.
American College of Sports Medicine posi-
tion stand. Progression models in resistance
training for healthy adults. Med Sci Sports
Exerc 2002; 34(2): 364-380.
32. Kvist M. Achilles tendon injuries in athletes.
Ann Chir Gynaecol. 1991; 80(2): 188-201.
33. Kvist M. Achilles tendon injuries in athletes.
Sports Med 1994; 18(3): 173-201.
34. Lowdon A, Bader DL, Mowat AG. The effect
of heel pads on the treatment of Achilles
tendinitis: a double blind trial. Am J Sports
Med 1984; 12(6): 431-435.
35. Lunsford BR, Perry J. The standing heel-rise
test for ankle plantar flexion: criterion for
normal. Phys Ther. Aug 1995; 75(8): 694-
698.
36. Maffulli N, Kenward MG, Testa V, Capasso
G, Regine R, King JB. Clinical diagnosis of
Achilles tendinopathy with tendinosis. Clin J
Sport Med 2003; 13(1): 11-15.
37. Maffulli N, Khan KM, Puddu G. Overuse
tendon conditions: time to change a confus-
ing terminology. Arthroscopy 1998; 14(8):
840-843.
38. Maffulli N, Longo UG, Testa V, Oliva F,
Capasso G, Denaro V. Italian translation of
the VISA-A score for tendinopathy of the
main body of the Achilles tendon. Disabil
Rehabil 2008; 30(20-22): 1635-1639.
39. Maffulli N, Testa V, Capasso G, Sullo A.
Calcific insertional Achilles tendinopathy:
reattachment with bone anchors. Am J
Sports Med. Jan-Feb 2004; 32(1): 174-182.
40. Maffulli N, Walley G, Sayana MK, Longo UG,
Denaro V. Eccentric calf muscle training in
athletic patients with Achilles tendinopathy.
Disabil Rehabil 2008; 30(20-22): 1677-1684.
41. Mafi N, Lorentzon R, Alfredson H. Superior
short-term results with eccentric calf muscle
Ch
apter 2
Ou
tcom
e measu
res and
assessmen
t too
ls
49
training compared to concentric training in
a randomized prospective multicenter study
on patients with chronic Achilles tendinosis.
Knee Surg Sports Traumatol Arthrosc. 2001;
9(1): 42-47.
42. Mahieu NN, Witvrouw E, Stevens V, Van Tig-
gelen D, Roget P. Intrinsic Risk Factors for the
Development of Achilles Tendon Overuse
Injury: A Prospective Study. Am J Sports Med
2006; 34(2): 226-35
43. Möller M, Lind K, Styf J, Karlsson J. The reli-
ability of isokinetic testing of the ankle joint
and a heel-raise test for endurance. Knee
Surg Sports Traumatol Arthrosc. Jan 2005;
13(1): 60-71.
44. Möller M, Movin T, Granhed H, Lind K,
Faxen E, Karlsson J. Acute rupture of
tendon Achillis. A prospective randomised
study of comparison between surgical and
non-surgical treatment. J Bone Joint Surg Br
2001; 83(6): 843-848.
45. Niesen-Vertommen S, Taunton J, Clement
D, Mosher R. The effect of eccentric versus
concentric exercise in the management of
Achilles tendonitis. Clin J Sport Med 1992;
2: 109-113.
46. Norkin CC, White DJ. Measurement of joint
motion : a guide to goniometry. Philadel-
phia: Davis; 1985.
47. Noyes FR, Barber SD, Mangine RE. Abnor-
mal lower limb symmetry determined by
function hop tests after anterior cruciate
ligament rupture. Am J Sports Med 1991;
19(5): 513-518.
48. Paavola M, Kannus P, Järvinen TA, Khan K,
Jozsa L, Järvinen M. Achilles tendinopathy.
J Bone Joint Surg Am 2002; 84-A(11): 2062-
2076.
49. Paavola M, Kannus P, Orava S, Pasanen M,
Järvinen M. Surgical treatment for chronic
Achilles tendinopathy: a prospective seven
month follow up study. Br J Sports Med
2002; 36(3): 178-182.
50. Paavola M, Kannus P, Paakkala T, Pasanen M,
Järvinen M. Long-term prognosis of patients
with achilles tendinopathy. An observational
8-year follow-up study. Am J Sports Med
2000; 28(5): 634-642.
51. Paavola M, Orava S, Leppilahti J, Kannus
P, Järvinen M. Chronic Achilles tendon
overuse injury: complications after surgical
treatment. An analysis of 432 consecutive
patients. Am J Sports Med 2000; 28(1):
77-82.
52. Paavola M, Paakkala T, Kannus P, Järvinen M.
Ultrasonography in the differential diagnosis
of Achilles tendon injuries and related disor-
ders. A comparison between pre-operative
ultrasonography and surgical findings. Acta
Radiol 1998; 39(6): 612-619.
53. Paoloni JA, Murrell GA. Three-year fol-
lowup study of topical glyceryl trinitrate
treatment of chronic noninsertional Achilles
tendinopathy. Foot Ankle Int 2007; 28(10):
1064-1068.
54. Peers KH, Brys PP, Lysens RJ. Correlation
between power Doppler ultrasonography
and clinical severity in Achilles tendinopathy.
Int Orthop 2003; 27(3): 180-183.
55. Robinson JM, Cook JL, Purdam C, et al. The
VISA-A questionnaire: a valid and reliable
index of the clinical severity of Achilles
tendinopathy. Br J Sports Med 2001; 35(5):
335-341.
56. Rolf C, Movin T. Etiology, histopathology,
and outcome of surgery in achillodynia. Foot
Ankle Int 1997; 18(9): 565-569.
57. Rompe JD, Furia J, Maffulli N. Eccentric load-
ing compared with shock wave treatment
for chronic insertional achilles tendinopathy.
A randomized, controlled trial. J Bone Joint
Surg Am 2008; 90(1): 52-61.
58. Rompe JD, Furia J, Maffulli N. Eccentric
loading versus eccentric loading plus shock-
wave treatment for midportion achilles
tendinopathy: a randomized controlled trial.
Am J Sports Med 2009; 37(3): 463-470.
59. Rompe JD, Nafe B, Furia JP, Maffulli N.
Eccentric loading, shock-wave treatment,
or a wait-and-see policy for tendinopathy of
the main body of tendo Achillis: a random-
50
ized controlled trial. Am J Sports Med 2007;
35(3): 374-383.
60. Roos EM, Brandsson S, Karlsson J. Validation
of the foot and ankle outcome score for
ankle ligament reconstruction. Foot Ankle
Int 2001; 22(10): 788-794.
61. Roos EM, Engström M, Lagerquist A,
Söderberg B. Clinical improvement after 6
weeks of eccentric exercise in patients with
mid-portion Achilles tendinopathy -- a ran-
domized trial with 1-year follow-up. Scand J
Med Sci Sports 2004; 14(5): 286-295.
62. Rothstein JM, Miller PJ, Roettger RF. Gonio-
metric reliability in a clinical setting. Elbow
and knee measurements. Phys Ther 1983;
63(10): 1611-1615.
63. Sandmeier R, Renström PA. Diagnosis and
treatment of chronic tendon disorders in
sports. Scand J Med Sci Sports 1997; 7(2):
96-106.
64. Saxena A. Surgery for chronic Achilles
tendon problems. J Foot Ankle Surg 1995;
34(3): 294-300.
65. Sayana MK, Maffulli N. Eccentric calf muscle
training in non-athletic patients with Achil-
les tendinopathy. J Sci Med Sport. Feb 2007;
10(1): 52-58.
66. Schunck J, Jerosch J. Operative treatment
of Haglund’s syndrome. Basic, indications,
procedure, surgical techniques, results and
problems. Foot and Ankle Surgery. 2005; 11:
123-130.
67. Shalabi A, Kristoffersen-Wiberg M, Aspelin
P, Movin T. MR evaluation of chronic
Achilles tendinosis. A longitudinal study of
15 patients preoperatively and two years
postoperatively. Acta Radiol 2001; 42(3):
269-276.
68. Shalabi A, Kristoffersen-Wilberg M, Svens-
son L, Aspelin P, Movin T. Eccentric training
of the gastrocnemius-soleus complex in
chronic Achilles tendinopathy results in
decreased tendon volume and intratendi-
nous signal as evaluated by MRI. Am J Sports
Med 2004; 32(5): 1286-1296.
69. Silbernagel KG, Gustavsson A, Thomee R,
Karlsson J. Evaluation of lower leg func-
tion in patients with Achilles tendinopathy.
Knee Surg Sports Traumatol Arthrosc 2006;
14(11): 1207-1217.
70. Silbernagel KG, Thomee R, Eriksson BI,
Karlsson J. Continued Sports Activity, Using
a Pain-Monitoring Model, During Rehabilita-
tion in Patients With Achilles Tendinopathy:
A Randomized Controlled Study. Am J
Sports Med 2007; 35(6): 897-906.
71. Silbernagel KG, Thomee R, Eriksson BI,
Karlsson J. Full symptomatic recovery does
not ensure full recovery of muscle-tendon
function in patients with Achilles tendinopa-
thy. Br J Sports Med 2007; 41(4): 276-80
72. Silbernagel KG, Thomeé R, Karlsson J.
Cross-cultural adaptation of the VISA-A
questionnaire, an index of clinical severity
for patients with Achilles tendinopathy, with
reliability, validity and structure evaluations.
BMC Musculoskelet Disord 2005; 6(1): 12.
73. Stanish WD, Curwin S, Mandell S. Tendinitis:
its etiology and treatment. New York: Oxford
University Press; 2000.
74. Svantesson U, Carlsson U, Takahashi H,
Thomeé R, Grimby G. Comparison of muscle
and tendon stiffness, jumping ability, muscle
strength and fatigue in the plantar flexors.
Scand J Med Sci Sports 1998; 8(5 Pt 1): 252-
256.
75. Tallon C, Coleman BD, Khan KM, Maffulli
N. Outcome of surgery for chronic Achilles
tendinopathy. A critical review. Am J Sports
Med 2001; 29(3): 315-320.
76. Testa V, Capasso G, Benazzo F, Maffulli N.
Management of Achilles tendinopathy by
ultrasound-guided percutaneous tenotomy.
Med Sci Sports Exerc 2002; 34(4): 573-580.
77. Tumilty S, Munn J, Abbott JH, McDonough
S, Hurley DA, Baxter GD. Laser therapy in
the treatment of achilles tendinopathy: a
pilot study. Photomed Laser Surg 2008;
26(1): 25-30.
78. van Snellenberg W, Wiley JP, Brunet G.
Achilles tendon pain intensity and level of
Ch
apter 2
Ou
tcom
e measu
res and
assessmen
t too
ls
51
neovascularization in athletes as determined
by color Doppler ultrasound. Scand J Med
Sci Sports 2007; 17(5): 530-534.
79. Visentini PJ, Khan KM, Cook JL, Kiss ZS, Har-
court PR, Wark JD. The VISA score: an index
of severity of symptoms in patients with
jumper’s knee (patellar tendinosis). Victorian
Institute of Sport Tendon Study Group. J Sci
Med Sport 1998; 1(1): 22-28.
80. Visnes H, Hoksrud A, Cook J, Bahr R. No
effect of eccentric training on jumper’s knee
in volleyball players during the competitive
season: a randomized clinical trial. Clin J
Sport Med 2005; 15(4): 227-234.
81. Åström M, Gentz CF, Nilsson P, Rausing A,
Sjöberg S, Westlin N. Imaging in chronic
achilles tendinopathy: a comparison of
ultrasonography, magnetic resonance imag-
ing and surgical findings in 27 histologically
verified cases. Skeletal Radiol 1996; 25(7):
615-620.
82. Öhberg L, Lorentzon R, Alfredson H.
Neovascularisation in Achilles tendons
with painful tendinosis but not in normal
tendons: an ultrasonographic investigation.
Knee Surg Sports Traumatol Arthrosc 2001;
9(4): 233-238.
83. Östenberg A, Roos E, Ekdahl C, Roos H.
Isokinetic knee extensor strength and func-
tional performance in healthy female soccer
players. Scand J Med Sci Sports 1998; 8(5 Pt
1): 257-264.
Chapter 3
Reliability and validity of the Dutch VISA-A questionnaire
for Achilles tendinopathy and applicability to non-athletes
MN van Sterkenburg
IN Sierevelt
JL Tol
IV van Dalen
D Haverkamp
CN van Dijk
Submitted
54
ABstrAct
BackgroundIn 2001, the Victorian Institute of Sports Assessment developed a self-administered question-
naire evaluating symptoms and their effect on physical activity for patients with Achilles
tendinopathy. It has proven to be an effective outcome questionnaire in various languages.
The aim of this project is to translate and validate the VISA-A questionnaire into the Dutch
language (VISA-A-NL) and to assess its applicability to non-athletes.
MethodsAfter translation according to a forward-backward protocol, 101 patients with complaints of
Achilles tendinopathy were asked to fill out the VISA-A-NL at two time points together with
VAS, FAOS and SF-36 questionnaires. Reliability, internal consistency, construct- and content
validity were tested.
ResultsThe VISA-A-NL showed high reliability (0.97 (95% CI 0.95-0.98)). Crohnbach’s alpha (internal
consistency) was 0.80. It increased to 0.88 without activity domain. Correlation with other
questionnaires was moderate or poorer.
ConclusionThe VISA-A-NL proved to be an excellent evaluation instrument for the Dutch physician. If
applied to non-athletes, using a modified score (questions 1-6) should be considered.
Ch
apter 3
Reliab
ility and
validity o
f the D
utch
VISA
-A q
uestio
nn
aire for A
chilles ten
din
op
athy an
d ap
plicab
ility to n
on
-athletes
55
iNtroDUctioN
Achilles tendinopathy is a major cause of chronic pain and disability. This may lead to sub-
optimal overall health as physical inactivity is a risk factor for cardiovascular disease16. Many
studies have been published on a magnitude of treatments for Achilles tendinopathy, but
prospective series on the outcome are lacking. One of the factors limiting the quality of
research may be the absence of standardised outcome measures to evaluate the outcome of
treatment19. A patient’s subjective assessment of treatment outcome such as pain, functional
ability and satisfaction fulfils the criteria of being valid, reliable and sensitive to change if
gathered by a correctly designed and tested patient-centred questionnaire6. The Victorian
Institute of Sports Assessment- Achilles (VISA-A) questionnaire was created in 2001 to assess
clinical severity for patients with Achilles tendinopathy. It is a self- administered question-
naire evaluating symptoms and their effect on physical activity19, and displayed reliability
and construct validity. Subjective scoring systems can be used in countries other than the
ones in which they were developed if translated and validated for a specific language and
population10,11,17. The VISA-A has been translated into Swedish, Italian, and German and
proved to be able to determine the clinical severity and provide information about the effect
of the management of patients with Achilles tendinopathy in these languages15,16,21. The
aim of this project is to translate and validate the VISA-A questionnaire into the Dutch
language (VISA-A-NL) to provide a valid questionnaire for the Dutch population. Moreover,
the questionnaire seems to be designed only for athletes as 40% of the points account for
activity. As approximately 30% of patients with complaints of Achilles tendinopathy have a
sedentary lifestyle2, applicability to non-athletes is also evaluated.
methoDs
Translation procedure A Dutch translation was made using a forward-backward translation protocol according to
the guidelines of Guillemin and co-workers10,11. Three people independently translated the
English version of the VISA-A questionnaire to Dutch. All three were in the medical field, and
had English as a second language. One independent native speaker, not active in the medi-
cal field translated this Dutch version back into English. Discrepancies were discussed and
adjusted for the final Dutch questionnaire (VISA-A-NL, see addendum). It was assumed that
no major cultural differences in lifestyle exist between the Dutch and Canadian population,
and that therefore cultural adaptation of the questionnaire was not required 3,10.
56
Patients104 consecutive patients were included from the outpatient clinic of 3 participating Dutch
hospitals of whom 47% were female. Mean age was 48.5 years (SD 11.6), 79 (76%) patients
were athletes, 25 (24%) were non-athletes.
All patients had complaints of Achilles tendinopathy (including midportion- and inser-
tional tendinopathy, paratendinopathy and retrocalcaneal bursitis)25.
They were clinically assessed and an AOFAS was taken by the consulting physician. All
patients were asked to fill out 2 sets of questionnaires; the first (A= VISA-A-NL, VAS pain,
VAS function, FAOS, SF-36) at the day of consultation, the second (B= VISA-A-NL) they were
to complete 4-5 days later24. Additionally they were asked whether their complaints had
changed since the first assessment.
QuestionnairesThe original English version of the VISA-A questionnaire as designed by Robinson and co-
workers19 contains eight questions that cover three domains; pain (questions 1-3), function
(questions 4-6), and activity (questions 7-8). Scores are summed to yield a total of 100 points
in an asymptomatic subject: questions 1-7 score a maximum of 10 points each; question 8,
on sporting activity, carries a maximum of 30. Pain on undertaking sports will automatically
lead to a loss of 10-20 points.
Since question 7 and 8 refer to sport activities (accounting for 40% of points) and the
study population contained both athletes and non-athletes, we modified the VISA-A score
by deleting both questions and investigated the psychometric properties of both the VISA
and the modified VISA.
The FAOS is a 42-item questionnaire divided into 5 subscales: pain (9 items), other symp-
toms (7 items), activities of daily living (17 items), sport and recreation function (5 items), foot
and ankle related quality of life (4 items). Each question can be scored on a 5-point Likert
scale (0-4) and each of the five subscale scores is calculated as the sum of the items included.
Raw scores are then transformed to a 0-100, worst to best score20.
The SF-36 is a self-administered, generic HRQL (health related quality of life) instru-
ment1,5,23,26. It comprises 36 items across 8 dimensions (physical functioning, role limitation
due to physical problems, bodily pain, perception of general health, energy and vitality, social
functioning, role limitation due to emotional problems, and mental health). The 8 dimen-
sions of the SF-36 score are calculated on a 0-100 worst to best scale13.
The VAS is a 100 mm visual analogue scale and is used to determine the seriousness of
pain and functional problems18.
In 1994 the American Orthopaedic Foot and Ankle Society (AOFAS) developed a question-
naire to provide a standard method for reporting clinical status of the ankle and foot. The
AOFAS- ankle and hindfoot clinical rating system combines both subjective and objective fac-
Ch
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57
tors into numerical scales to describe function, alignment and pain. Since objective aspects
are incorporated, this questionnaire has to be completed by the investigator14.
TestingWhen a questionnaire is developed or translated, the most important consideration is that it
must be able to accurately measure that for which it is designed. To evaluate the psychomet-
ric properties of the VISA-A-NL, both reliability and validity were assessed.
Reliability
Reliability is defined as the extent to which patients can be distinguished from each other,
despite measurement errors22.
Test-retest reliability refers to the repeatability of the test and measures the extent to
which the same results are obtained on repeated administration when no change in physical
functioning has occurred8. To determine the test-retest reliability, a second VISA-A-NL (B)
questionnaire was given to all patients; 67 patients responded. In 15 patients, complaints
had changed at re-test. Test-retest reliability was therefore assessed in 52 patients, using
the intra-class coefficient (ICCagreement, two-way random effects model). An ICC >0.75 was
considered good9. A t-test was performed to determine the presence of a systematic differ-
ence between the first and second assessment. Additionally, Standard Error of Measurement
(SEM) was calculated as the square root of the within subject variance. The Smallest Detect-
able Change (SDC) was calculated as 1.96 x √2 x SEM. The SDC is the smallest measurement
change that can be interpreted as real change4.
Internal consistency of the scale is the extent to which the items are inter-correlated and
cover the same construct (homogeneity of the scale). To evaluate the internal consistency of
the VISA-A Cronbach’s alpha was calculated. A Crohnbach’s alpha of 0.7 was considered to
represent an acceptable degree of internal consistency, 0.8 was considered as good and 0.9
as excellent internal consistency7.
Validity
Validity relates to the ability of a questionnaire to measure to outcome parameter of interest.
Construct validity was tested by determining the association between the VISA-A-NL
questionnaire and the FAOS, SF-36, VAS-scores for pain and function, and the AOFAS, using
Pearson correlation coefficients. We evaluated convergent and divergent validity by hypoth-
esizing that correlation coefficients between the VISA-A-NL (with and without the activity
questions) and VAS pain, FAOS pain, -symptoms, -sport and recreation and SF-36 bodily pain
and physical functioning would be higher than correlations with the other domains.
Content validity examines the extent to which all concepts of interest are adequately
represented by the items in the questionnaire24. It was evaluated by assessing distribution
58
and floor and ceiling effects of the VISA-A-NL. These are considered to be present if more
than 15% of responders achieve the lowest or highest possible score24.
Statistics
Statistical analysis was performed using PASW statistics 18.0 software (SPSS Inc., Chicago,
IL). A p-value of less than 0.05 was considered statistically significant.
resULts
Of 104 participans, 11 questionnaires were filled out incompletely or erroneously and there-
fore excluded from analysis (n=93).
ReliabilityOf 93 patients, 52 (56%) returned the second set of questionnaires. The ICCagreement of
the questionnaire was 0.97 (95% CI: 0.95-0.98) and Crohnbach’s alpha was 0.78 for the
entire study population (table 1). A statistically significant difference between the two assess-
ments was not observed for both versions of the VISA-A-NL in athletes nor in non-athletes
(0.29<p<0.67).
Table 1. Results
Athletes (n=39) Non-athletes (n=13) Total (n=52)
ICC VISA total (95%CI)
0.95 (0.91-0.97) - 0.97 (0.95-0.98)
ICC VISA modified(95%CI)
0.96 (0.92-0.98) 0.98 (0.93-0.99) 0.97 (0.95-0.98)
SEM VISA total 4.41 (4.4%) - 4.07 (4.1%)
SEM VISA modified 2,64 (4.4%) 2,42 (4.0%) 2,68 (4.5%)
SDC VISA total 12,21 (12.2%) - 11,28 (11.3%)
SDC VISA modified 7,32 (12.2%) 6,70 (11.2%) 7,44 (12.4%)
ICC= Intra Class Correlation coefficient, SEM = Standard Error of Measurement, SDC = smallest detect-able change
Athletes (n=71) Non-athletes (n=22) Total (n=93)
Crohbach’s Alpha VISA total 0.72 0.82 0.78
Crohbach’s Alpha VISA
modified
0.83 0.86 0.86
Ch
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ValidityPearson correlation coefficients of the VISA-A-NL with the other questionnaires are shown in
table 2. The subscale ‘SF-36 physical functioning’ correlated well with the VISA-A-NL ques-
tionnaire, both with and without activity domain. Most other physical domains correlated
moderately but, the subscales of FAOS quality of life showed poor correlation with VISA-A.
Poor correlation was also observed for the psychological domains (SF-36 social functioning,
mental health, role emotional, vitality, general health perception).
The mean scores of the VISA-A-NL questionnaire was 52.4 (SD 19.7) and 22.0 (SD 15.7) for
athletes and non-athletes, respectively. The mean scores of the modified VISA-A-NL question-
naire was 36.2 (SD 13.9) and again 22.0 (SD 15.7) for athletes and non-athletes, respectively.
Table 2. Pearson correlation coefficients of the VISA-A-NL with the other questionnaires of subject (with and without activity domain). * p<0.05
VISA-A TotalAthletes (n=71)
VISA-AModifiedAthletes (n=71)
VISA-AModifiedNon-athletes (n=22)
VISA-A Totalentire population (n=93)
VISA-AModifiedentire population (n=93)
VAS Pain -0.54* -0.58* -0.39 -0.54* -0.57*
VAS Function 0.52* 0.51* 0.44* 0.50* 0.52*
AOFAS 0.48* 0.46* 0.31 0.56* 0.50*
FAOS Symptoms 0.45* 0.52* 0.53* 0.58* 0.60*
FAOS Pain 0.53* 0.56* 0.52* 0.58* 0.60*
FAOS ADL 0.56* 0.55* 0.47* 0.59* 0.58*
FAOS Sport 0.56* 0.61* 0.43* 0.55* 0.59*
FAOS QOL 0.29* 0.33* 0.14 0.38* 0.37*
SF -36 Physical functioning
0.55* 0.63* 0.66* 0.70* 0.71*
SF-36 Role physical 0.13 0.12 0.58* 0.31* 0.32*
SF-36 Bodily pain 0.31 0.40* 0.46* 0.49* 0.51*
SF-36 Social functioning 0.01 -0.04 0.29 0.27* 0.21
SF-36 Mental health -0.11 -0.07 0.39 0.21 0.20
SF-36 Role emotional -0.06 0.02 0.65* 0.37* 0.39*
SF-36 Vitality -0.26 -0.25 0.26 -0.05 -0.09
SF-36 General health perception
-0.01 -0.02 0.28 0.25* 0.21
SF-36 Physical component scale
0.43* 0.47* 0.36 0.52* 0.51*
SF-36 Mental component scale
-0.34* -0.32* 0.49* 0.04 0.03
60
Floor and ceiling effects were not observed in both versions of the questionnaire, as only 1
subject (1%) scored 0 points, nobody scored 100 points, and 1 patient scored the maximum
of 60 points in the modified VISA-A score.
DiscUssioN
The aim of this study was to translate the original VISA-A questionnaire on the subjective
complaints of patients with Achilles tendinopathy into the Dutch language, to validate it, and
to assess its applicability to non-athletes.
The translation procedure did not create any problems, since the items are universal and
there is no large cultural difference between Dutch and Canadian patients.
Reliability of the translation was excellent, with a statistically not significant difference
between assessments. This outcome may be explained by the fact that, as the procedure
for the Dutch Oxford 12-item knee questionnaire taught us12, we introduced a question if
complaints had changed between assessments. 15/67 patients (22%) answered this ques-
tion with ‘yes’, and therefore they were excluded from reliability testing.
The smallest detectable change (SDT) in this study indicates that under stable condition,
the VISA-A score can vary up to 12 points. For clinical studies, this implies that clinical changes
can only be detected if they exceed the 12 points.
The study questionnaire showed good internal consistency (Crohnbach’s alpha 0.80), but
there indeed was a negative effect of the activity domain. Subanalysis without these ques-
tions showed an increase of Crohnbach’s alpha to 0.88. However, when measuring the effect
of a treatment in a mixed group of athletes and non-athletes, the effect of treatment could
be underestimated. For example, an athlete can score 0 points with question 7 and 8 before
treatment as complaints withhold him/her from being sports active. After treatment, the
athlete is complaint-free and scores 100 points. The non-athlete also scores 0 points for
questions 7 and 8 before treatment, and is also complaint-free after treatment. However,
he/she will never score higher than 60 points as question 7 and 8 will not be answered
differently between assessments. The effect of treatment, when using the VISA-A score to
measure outcome, is therefore underestimated in non-athletes.
When choosing the VISA-A questionnaire for a mixed population of athletes and non-
athletes, deleting questions 7 and 8 can be considered, since the psychometric properties of
the modified VISA- A were comparable with the original version.
Generally Pearson correlation coefficients were higher for physical than psychological
components. Convergent and divergent validity is confirmed as correlation coefficients were
higher for the physical domains of the questionnaires. However, for non-athletes correlation
with socio- emotional components was also higher. This could imply that physical restrictions
Ch
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61
in this subgroup with chronic Achilles tendinopathy have greater emotional and social conse-
quences than in athletes. Noticeable is the moderate correlation of VISA-A with VAS, which
is a validated subjective outcome measure frequently used for scientific means.
Low correlations can be explained by the fact that none of the questionnaires except for the
VISA-A were validated for Achilles tendinopathy. Initially it was intended to do so, but this
study aim was departed to not further enlarge patient burden as many of these question-
naires are extensive. Given the laborious inclusion of 104 patients in 3.5 years and 56%
response rate to both assessments this was well decided. This was also why responsiveness
was not tested.
coNcLUsioN
The VISA-A-NL questionnaire seems suitable for use in athletes. However, in a combined
population of atletes and non-athletes results will become incomparable as the highest pos-
sible score for non-athetes is 40 points lower than for non-athletes. Psychometric properties
of the VISA-A-NL, without questions 7 and 8, are satisfactory for both athletes and non-
athletes. It is therefore proposed that the modified VISA-A-NL questionnaire is considered in
a mixed population of patients with Achilles tendinopathy.
62
refereNce List
1. Aaronson NK, Muller M, Cohen PD et al.
Translation, validation, and norming of the
Dutch language version of the SF-36 Health
Survey in community and chronic disease
populations. J Clin Epidemiol 1998; 51(11):
1055-1068.
2. Ames PR, Longo UG, Denaro V, Maffulli
N. Achilles tendon problems: not just an
orthopaedic issue. Disabil Rehabil 2008;
30(20-22): 1646-1650.
3. Beaton DE, Bombardier C, Guillemin F, Fer-
raz MB. Guidelines for the process of cross-
cultural adaptation of self-report measures.
Spine 2000; 25(24): 3186-3191.
4. Beckerman H, Roebroeck ME, Lankhorst
GJ, Becher JG, Bezemer PD, Verbeek AL.
Smallest real difference, a link between
reproducibility and responsiveness. Qual Life
Res 2001; 10(7): 571-578.
5. Brazier JE, Harper R, Jones NM et al. Validat-
ing the SF-36 health survey questionnaire:
new outcome measure for primary care.
BMJ 1992; 305(6846): 160-164.
6. Dawson J, Carr A. Outcomes evaluation in
orthopaedics. J Bone Joint Surg Br 2001;
83(3): 313-315.
7. Dunbar MJ, Robertsson O, Ryd L, Lidgren L.
Translation and validation of the Oxford-12
item knee score for use in Sweden. Acta
Orthop Scand 2000; 71: 268-274.
8. Eechaute C, Vaes P, Duquet W, Van GB.
Test-retest reliability of sudden ankle inver-
sion measurements in subjects with healthy
ankle joints. J Athl Train 2007; 42(1): 60-65.
9. Fleiss JL. The design and analysis of clinical
experiments. 1986. New York, Wiley.
10. Guillemin F. Cross-cultural adaptation and
validation of health status measures. Scand J
Rheumatol 1995; 24(2): 61-63.
11. Guillemin F, Bombardier C, Beaton D. Cross-
cultural adaptation of health-related quality
of life measures: literature review and
proposed guidelines. J Clin Epidemiol 1993;
46(12): 1417-1432.
12. Haverkamp D, Breugem SJ, Sierevelt IN,
Blankevoort L, van Dijk CN. Translation and
validation of the Dutch version of the Oxford
12-item knee questionnaire for knee arthro-
plasty. Acta Orthop 2005; 76(3): 347-352.
13. Insall JN, Dorr LD, Scott RD, Scott WN.
Rationale of the Knee Society clinical rating
system. Clin Orthop Relat Res 1989; (248):
13-14.
14. Kitaoka HB, Alexander IJ, Adelaar RS, Nunley
JA, Myerson MS, Sanders M. Clinical rating
systems for the ankle-hindfoot, midfoot,
hallux, and lesser toes. Foot Ankle Int 1994;
15(7): 349-353.
15. Lohrer H, Nauck T. Cross-cultural adaptation
and validation of the VISA-A questionnaire
for German-speaking Achilles tendinopathy
patients. BMC Musculoskelet Disord 2009;
10(1): 134.
16. Maffulli N, Longo UG, Testa V, Oliva F,
Capasso G, Denaro V. Italian translation of
the VISA-A score for tendinopathy of the
main body of the Achilles tendon. Disabil
Rehabil 2008; 30(20-22): 1635-1639.
17. Mathias SD, Fifer SK, Patrick DL. Rapid
translation of quality of life measures for
international clinical trials: avoiding errors
in the minimalist approach. Qual Life Res
1994; 3(6): 403-412.
18. Price DD, McGrath PA, Rafii A, Buckingham
B. The validation of visual analogue scales
as ratio scale measures for chronic and
experimental pain. Pain 1983; 17(1): 45-56.
19. Robinson JM, Cook JL, Purdam C et al. The
VISA-A questionnaire: a valid and reliable
index of the clinical severity of Achilles
tendinopathy. Br J Sports Med 2001; 35(5):
335-341.
20. Roos EM, Brandsson S, Karlsson J. Validation
of the foot and ankle outcome score for
ankle ligament reconstruction. Foot Ankle
Int 2001; 22(10): 788-794.
21. Silbernagel KG, Thomee R, Karlsson J.
Cross-cultural adaptation of the VISA-A
Ch
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questionnaire, an index of clinical severity
for patients with Achilles tendinopathy, with
reliability, validity and structure evaluations.
BMC Musculoskelet Disord 2005; 6: 12.
22. Streiner DL. Starting at the beginning: an
introduction to coefficient alpha and inter-
nal consistency. J Pers Assess 2003; 80(1):
99-103.
23. Sullivan LM, Dukes KA, Harris L, Dittus RS,
Greenfield S, Kaplan SH. A comparison of
various methods of collecting self-reported
health outcomes data among low-income
and minority patients. Med Care 1995; 33(4
Suppl): AS183-AS194.
24. Terwee CB, Bot SD, DE Boer MR et al. Qual-
ity criteria were proposed for measurement
properties of health status questionnaires. J
Clin Epidemiol 2007; 60(1): 34-42.
25. van Dijk CN, van Sterkenburg MN, Wieger-
inck JI, Karlsson J, Maffulli N. Terminology
for Achilles tendon related disorders. Knee
Surg Sports Traumatol Arthrosc 2011; 19(5):
835-41.
26. Ware JE, Jr., Sherbourne CD. The MOS
36-item short-form health survey (SF-36). I.
Conceptual framework and item selection.
Med Care 1992; 30(6): 473-483.
64
Addendum- Dutch translation of VISA-A questionnaire
VISA-A-NL VRAGENLIJST
Geboortedatum: / / Datum:
Naam:
IN DEZE VRAGENLIJST STAAT HET BEGRIP ‘PIJN’ SPECIFIEK VOOR PIJN IN DE OMGEVING VAN UW ACHILLESPEES
1. Hoeveel minuten heeft u stijfheid in de omgeving van uw achillespees nadat u ’s ochtends bent op-gestaan?
100 min of langer
0 min PUNTEN
0 1 2 3 4 5 6 7 8 9 10
2. Heeft u, na het ‘op gang komen’ ’s ochtends, pijn bij het maximaal rekken van de achillespees op de rand van een verhoging (bijvoorbeeld traptrede)? (met de knie gestrekt)
Extreem hevige pijn
geen pijn
PUNTEN
0 1 2 3 4 5 6 7 8 9 10
3. Volgt er pijn in de eerste 2 uur na een 30 minuten durende wandeling op een vlakke ondergrond? (Als u door de pijn geen 30 minuten kúnt lopen op een vlakke ondergrond, vul da ‘0’ in bij deze vraag).
Extreem hevige pijn
geen pijn
PUNTEN
0 1 2 3 4 5 6 7 8 9 10
4. Heeft u pijn wanneer u normaal de trap af zou lopen?
Extreem hevige pijn
geen pijn
PUNTEN
0 1 2 3 4 5 6 7 8 9 10
5. Heeft u pijn tijdens of direct nadat u 10 keer (op één been) op uw tenen gestaan heeft op een vlakke ondergrond?
Extreem hevige pijn
geen pijn
PUNTEN
0 1 2 3 4 5 6 7 8 9 10
6. Hoe vaak kunt u hinkelen zonder pijn?
0 10 of meer
PUNTEN
0 1 2 3 4 5 6 7 8 9 10
7. Doet u op dit moment aan sport of een andere vorm van lichaamsbeweging?
0Helemaal niet
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4Aangepast trainingsschema/ trainingsniveau en aangepaste competitie
7Volledige training en volledige competitie, maar op lager niveau dan voor het ontstaan van de klachten
PUNTEN
10Competitie en training op hetzelfde of hoger niveau dan voor aanvang van de klachten
8. Van de volgende vraag dient u alleen A, B OF C te beantwoorden.
* U vult vraag A in indien: u GEEN pijn ervaart tijdens sportactiviteiten die de achillespees
belasten
* U vult vraag B in indien: u tijdens sportactiviteiten die de achillespees belasten pijn
ervaart waarbij u de sportactiviteit NIET hoeft te staken
* U vult vraag C in indien: u tijdens sportactiviteiten die de achillespees belasten een
zodanige pijn ervaart dat u uw activiteit MOET staken.
A. Indien u geen pijn heeft tijdens sportactiviteiten die de achillespees belasten, hoe lang bent u dan in staat te sporten/ trainen?
NIET 1-10 min
11-20 min
21-30 min
>30 min
PUNTEN
0 7 14 21 30
OF B. Indien u enige pijn heeft tijdens sportactiviteiten die de achillespees belasten maar waarbij u de activiteit wel af kunt maken, hoe lang bent u dan in staat te sporten/trainen?
NIET 1-10 min
11-20 min
21-30 min
>30 min
PUNTEN
0 4 10 14 20
OF C. Indien u tijdens sportactiviteiten die de achillespees belasten een zodanige pijn heeft dat u de activiteit moet stoppen, hoe lang bent u dan toch in staat geweest te sporten/trainen?
NIET 1-10 min
11-20 min
21-30 min
>30 min
PUNTEN
0 2 5 7 10
TOTALE SCORE ( /100)%
PArt iii miDPortioN AchiLLes
teNDiNoPAthY: cAUse of PAiN AND treAtmeNt moDALities
Chapter 4
Less promising results with sclerosing Ethoxysclerol injections for
midportion Achilles tendinopathy
A retrospective study
MN van Sterkenburg
MC de Jonge
IN Sierevelt
CN van Dijk
Am J Sports Med 2010; 38: 2226-2232
70
ABstrAct
BackgroundIn patients with complaints of chronic midportion Achilles tendinopathy, neovascularisation
around the Achilles tendon and structural changes in the area were observed, but not in pain
free normal tendons. Local injections of the sclerosing substance Polidocanol (Ethoxysclerol)
have shown to yield good clinical results in patients with chronic Achilles tendinopathy. After
training by the inventors of the technique, sclerosing Ethoxysclerol injections were applied on
a group of patients in our center.
HypothesisWe hypothesized that sclerosing Ethoxysclerol injections did not yield good results in the
majority of patients.
Study designRetrospective cohort study with 2.7-5.1 year follow-up.
MethodsIn 113 patients (140 tendons) with midportion Achilles tendinopathy, 62 patients (70 tendons)
showing neovascularisation on colour Doppler ultrasound (US) were identified. 53 Achilles
tendons (48 patients) were treated with sclerosing Ethoxysclerol injections, with intervals of
6 weeks and a maximum of 5 sessions. Treatment was completed when neovascularisation
or pain had disappeared, or when there was no positive treatment effect after 3-4 sessions.
ResultsFourty-eight patients (20 females and 28 males) with a median age of 45 (33-68) years, were
treated. Median symptom duration was 23 months (range 3 to 300). Fifty-three tendons
were treated with a median of 3 sessions of Ethoxysclerol injections. Six weeks after the
last injection, 35% had no complaints, 9% minimal, 42% had the same and 14% had
more complaints. Pain correlated positively with neovessels on US (p<0.01). At 2.7-5.1 year
follow-up, 53% had received additional (surgical/ conservative) treatment, and 3 of these
patients (7.5%) still had complaints of midportion Achilles tendinopathy. In 6 complaints
after six weeks had resolved spontaneously.
ConclusionOur study did not confirm the high beneficial value of sclerosing neovascularisation in
patients with midportion Achilles tendinopathy.
Ch
apter 4
Less pro
misin
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sclerosin
g Eth
oxysclero
l injectio
ns fo
r mid
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Ach
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71
Clinical RelevanceIn recent years good results on the injection of sclerosing Ethoxysclerol have been reported,
which we were not able to reproduce. Despite the retrospective design of our study, we
consider it important to stress that injection of Ethoxysclerol may not be as promising as was
thought.
72
iNtroDUctioN
Chronic midportion Achilles tendinopathy is a common painful condition that is generally dif-
ficult to treat. It is defined as a painful thickening of the tendon typically 2-7 cm proximal to
its insertion in the calcaneus, without an inflammatory cellular response inside the tendon2.
Often it is accompanied by paratendinopathy. Complaints consist of long-term pain, tender-
ness and stiffness. The most apparent finding from clinical examination is a painful nodule
on palpation of the Achilles tendon. On ultrasound (US) or Magnetic Resonance Imaging
(MRI) examination thickening of the tendon and structural abnormalities in the painful area
are seen.
Currently, a wide range of conservative treatments is available for midportion Achilles
tendinopathy such as cast immobilisation, night splint, heel-raise, wait-and-see policy,
friction therapy, shock-wave treatment, and eccentric training of the muscle-tendon com-
plex6,32,34,38,45.
Studies on eccentric training have generally showed good outcomes in the majority of
patients6,14,26,31,39,42. Other studies have not been able to replicate these results12,38. When
conservative measures fail surgical treatment is indicated. To reduce the necessity of surgical
interference, new conservative measures have been developed worldwide. In 2002, a new
type of injection therapy was introduced30.
Using colour Doppler ultrasound, neovascularisation on the ventral side of the Achilles
tendon was demonstrated in symptomatic patients21. Normal tendons lack these changes.
It was hypothesized that neovessels and accompanying nerves were responsible for the
pain in Achilles tendinopathy. Local injections of these areas with neovascularisation with
Polidocanol (Ethoxysclerol) gave good clinical results in a double blind randomised controlled
trial on patients with chronic Achilles tendinopathy5,30. At 2-year follow-up, they showed
remaining good clinical results25.
One of our radiologists specialized in musculoskeletal radiology, was trained by the inven-
tors of the procedure to perform it according to the method as originally described30. From
August 2004 until February 2007 48 patients were treated with Ethoxysclerol injections for
chronic midportion Achilles tendinopathy. The purpose of this study was to analyze our
results of this new intervention.
methoDs
Between August 2004 and February 2007, a total of 113 consecutive patients with 140
symptomatic Achilles tendons underwent colour Doppler ultrasonography investigation
(US). Patients with midportion Achilles tendinopathy and neovascularisation were offered
Ch
apter 4
Less pro
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sclerosin
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oxysclero
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ns fo
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po
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Ach
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73
treatment with Ethoxysclerol. Sixty-two patients had 70 symptomatic tendons showing
neovascularisation (50%). In 50% of tendons with Achilles tendinopathy no neovessels were
found. Fourteen patients were excluded from treatment because they refused sclerosing
therapy (Figure 1). Results of these injections were retrospectively analyzed.
Ultrasonography and colour Doppler examination (US)All tendons were examined with high-resolution greyscale ultrasound and with colour
Doppler. A linear 17 MHz transducer was used. Achilles tendons showing midportion ten-
dinopathy with neovascularisation, and accompanying clinical data concerning age, gender,
symptom duration, presence and amount of neovascularisation, frequency of injections, and
complaints after treatment were extracted.
Injection of EthoxysclerolEthoxysclerol has a selective effect in the vascular intimae, causing thrombosis of the vessel,
even if the injection is performed extravasally, which is important when very small vessels are
targeted16. It also has a local anaesthetic effect.
Only patients, who already underwent six months of conservative treatment including
physical therapy involving eccentric training for their current complaints, were offered this
treatment.
If patients had at least a minimal amount of injectable neovascularisation (Figure 1) around
their Achilles tendon on US, they were injected with Ethoxysclerol. Patients were in prone
position, and the skin was washed with chlorohexidin 0.5% in 70% alcohol. For injection, a
23 gauge needle connected to a 3 ml syringe was used.
Figure 1. Number of tendons with neovascularisation and inclusion
74
The injections at the target vessels were performed under US guidance, from the medial
side of the Achilles tendon to minimise the risk of sural nerve injury. Ethoxysclerol (2-4 ml)
was injected until neovessels were no longer visible on US. After injection, a compressive
bandage was applied. Patients were instructed to take the bandage off 24 hours after treat-
ment, and free activity such as walking, bicycling, and light strength training were allowed
the first 2 weeks. After these 2 weeks, free tendon loading activity was allowed.
Six weeks after treatment patients were assessed again by US, and if they still had com-
plaints and neovascularisation injection with Ethoxysclerol was repeated, with a maximum
of 5 treatments. Treatment was completed when no neovascularisation was present on US,
when pain had disappeared, or when there was no positive treatment effect after 3 to 4
sessions. The same radiologist performed all US examinations and treatments.
Follow-upThe primary outcomes were defined as persistent pain and the absence or presence of neo-
vascularisation. Patients were retrospectively questioned about the amount of pain six weeks
after treatment as described on a 4- point scale as being no, minimal, same, or more. The
amount of neovessels present after sclerosing therapy was described likewise as being no,
minimal, same, or more by the radiologist performing the procedure. Information on weight,
sports activity, employment, co- morbidity and medication was taken.
Subjective outcome at midterm follow-up (2.7-5.1 years; mean 3.9 years) was assessed
using the same 4- point scale (no, minimal, same, or more), Visual Analogue Scales (VAS)
for pain and function, and the Victorian Institute of Sports Assessment- Achilles (VISA-A)
questionnaire. This questionnaire was created in 2001 to assess clinical severity for patients
with Achilles tendinopathy. It is a self- administered questionnaire evaluating symptoms and
their effect on physical activity36. Information was gathered on current sporting activity and
interventions in the past years after sclerosing injections.
Statistical analysis All obtained data were entered in a database and statistical analysis was performed using
SPSS 15.0, (SPSS Inc., Chicago, IL, USA). Due to skewed distributions, continuous data (e.g.
age, VAS, VISA-A) were described as medians and ranges and analysed non-parametrically.
Categorical and dichotomous data (e.g. pain after treatment, complaints, amount of neovas-
cularisation) were presented as frequencies and accompanying proportions. Wilcoxon Rank
Sum test was performed to assess the change in sport activities/duration before and during
complaints of the Achilles tendon, and to investigate change in pain level at six weeks and
mid-term follow-up.
Spearman’s correlation coefficient was calculated to determine the association between
pain level and amount of neovessels at six weeks follow-up, and pain level and several demo-
graphic factors (symptom duration, age and BMI) at mid-term follow-up.
Ch
apter 4
Less pro
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75
To assess whether gender significantly influenced complaints, we dichotomised com-
plaints to none/minimal and same/more. Chi-square tests were performed and Odds- ratios
(with 95%CI) were calculated. Mann Whitney U-tests were performed to assess difference in
age between nine/minimal and same/more complaints and to assess a learning curve of the
injection procedure. Therefore, we compared the dichotomised complaints six weeks after
injection from the first and the last 15 patients.
Reported P values were 2-sided and were considered significant if p<.05.
resULts
Patient populationDemographics are summarized in table 1.
Table 1. Demographics
Patients with Achilles tendinopathy
Patients with neovascularisation
Patients treated with sclerosing injections
Age (years)median (min-max) 46 (14-81) 47 (14-79) 45 (33-68)
Gender (m/f) 60 (53%)/53 (47%) 35 (56%)/27 (44%) 28 (70%)/20 (30%)
Side (l/r) 80 (57%)/60 (43%) 38 (54%)/32 (46%) 31 (58%)/22 (42%)
Forty-eight patients (53 tendons) were treated. Eleven patients (12 tendons) were lost to
follow-up and one patient deceased. Thirty six patients (75%) with 40 treated tendons, 19
male and 17 female, with a median age of 50 (range; 38-72) and BMI of 25.9 (range; 21-39),
returned the questionnaires for follow-up.
Median symptom duration before sclerosing was 23 months (range; 3-300). Five patients
had comorbidity: cardiovascular symptoms (n=2), CRPS (n=1), fibromyalgia (n=1) and lipo-
edema of the legs (n=1). Nine patients used prescription drugs; of these 2 used inhalation
glucocorticosteriods and the others used different medication for pain and cardiovascular
disease.
Most subjects (58%) had fulltime employment in a physical or office setting. Prior to
complaints, 30 out of the 36 patients (83%) were sports active. The most common activities
were running (39%), tennis (22%) and soccer (14%). Sport level was recreational for 24
patients (67%), competitive for 11 patients (31%), and professional for 1 patient (2%).
Median hours of sports activity a week was 4 (range; 0-30).
During complaints of midportion Achilles tendinopathy, 7 patients were unable to con-
tinue playing any sports and 1 voluntarily quit. Median number of hours a week playing
sports diminished to 1 (range; 0-30) (p=0,00). Seven patients were still able to continue their
activities on a competitive level.
The type of conservative treatment prior to sclerosing injections is shown in table 2.
76
Fifty-three symptomatic tendons were treated with a median of 3 sessions (range; 1-7) of
Ethoxysclerol injections (Table 3). Fifty-six percent of patients rated the injections as unpleas-
ant.
Short term results (6 weeks after the last injection)All patients, except one, returned to work within 2 days after injection with Ethoxysclerol
(median 0.0, range; 1-7 days). Of the 30 patients who were sports active before complaints,
18 patients (60%) resumed sporting activities, 12 (67%) at the same level, 5 (28%) on a
lower level and 1 (5%) on a higher level. Median time to sports resumption was 2 weeks
(0-104).
At 6 weeks follow-up 40 patients (45 tendons) showed up for US. Decrease of neovascu-
larisation was present in 21 tendons (47%) (Table 4) and patients experienced pain relief in
19 treated tendons (44%): 15 (35%) caused no pain and 4 (9%) still produced minimal pain;
42% still experienced the same pain and 14% even had more pain.
Spearman’s correlation coefficient showed a moderate correlation between the amount
of neovessels observed on Doppler ultrasound and the pain level experienced by the patient
(r=0.48, p=0.001).
Table 2. Most common types of conservative measures prior to injection with Ethoxysclerol
Conservative measures prior to sclerosing injections (n=46)
Physical therapy (eccentric training, friction, stretching) 40 (87%)
Cast immobilization 12 (26%)
Inlays 7 (15%)
Cortisone injection 13 (28%)
Rest 26 (57%)
NSAIDs 3 (7%)
Table 3. Number of injections per tendon
Number of injections per tendon Frequency (%)
1 14 (26%)
2 11 (21%)
3 15 (28%)
4 6 (11%)
5 6 (11%)
6 0 (0%)
7 1 (1.9%)
Ch
apter 4
Less pro
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sclerosin
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Ach
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77Six weeks after treatment, significantly more male patients (58%) had no or minimal com-
plaints than female patients (26%) (p=0.04). The odds ratio for females compared to males
having the same or more complaints after treatment was 3.8 (95% CI 1.1-13.8), which
means they had a 3.8 times higher chance of an unsatisfying outcome than males. Age did
not significantly affect outcome (p=0.09). The median age of patients with no or minimal
complaints after treatment was 43.5 (range; 33-68) years, and for patients with same or
more complaints 49.0 (range; 35-60).
We could not identify a learning curve for performing the treatment. The outcome in
the first 15 patients demonstrated that 56% to experienced no/minimal pain while 44% of
patients demonstrated the same or more pain at follow-up. Results of treatment in the last
15 patients showed that 43% of these patients had none/ minimal pain whilst 57% had the
same or more pain (p= 0.46).
Results at mid-term follow-up: 3.9 (range; 2.7-5.1) yearsMedian VISA-A score was 82 points (range; 20-100), median VAS for pain was 0 mm (range;
0-82) and for function 99 mm (range; 14-100).
Of the 40 tendons (of the 36 patients who had returned the questionnaire), 21 (53%) had
additional treatment in the years following sclerosing injections. Fifteen tendons (71%) were
treated operatively (open surgical debridement or Achilles tendoscopy), sometimes in com-
bination with conservative treatment (2 tendons). The other 6 tendons (29%) were treated
with different conservative measures. Of patients with 21 additionally treated tendons, 18
(86%) had the same or more complaints six weeks after injection and 3 (14%) had minimal
complaints. Of patients with 19 tendons who did not report seeking additional treatment, 6
(32%) had same/more complaints and 13 (69%) had no complaints after six weeks follow-
up. The 6 with same/ more complaints at six weeks had no complaints at mid-term follow-up
without additional treatment.
The level of pain had significantly decreased at mid-term follow-up compared to six-week
follow-up (p<0.01) (Diagram 1).
Of the 40 tendons at mid- term follow-up, 3 (7.5%) still showed the same or more com-
plaints, even after additional surgical or conservative treatment.
Table 4. Information on the quantity of neovascularisation present 6 weeks after the last injection was present in 45 treated tendons. In 8 this outcome was not described
Neovascularisation 6 weeks after treatment Tendons (n= 45)
No 5 (11%)
Less 16 (36%)
Same 20 (44%)
More 4 (9%)
78
No significant correlations were observed between complaints at midterm follow-up and
symptom duration, age, and BMI.
DiscUssioN
We could not demonstrate a beneficial effect of Ethoxysclerol injections in patients with mid-
portion Achilles tendinopathy as opposed to earlier published results of this treatment5,25.
Only 44% of tendons were painless or minimally painful at six weeks after treatment with
Ethoxysclerol.
At 2.7-5.1 year follow-up 53% of all treated tendons had undergone additional treat-
ment (nonoperative or surgical).
The treatment of chronic tendinopathy of the Achilles tendon with Ethoxysclerol as introduced
by Alfredson and Ohberg in 2002 appeared to be a promising method of treatment30. It was
hypothesized that neovessels and accompanying nerves were responsible for the pain in mid-
portion Achilles tendinopathy. After a pilot study in 2002 in which they treated 10 patients,
8 of whom had favourable outcome, they further developed their technique resulting in a
publication in 2005 in which the outcome of a double-blind randomised trial was published.
Patients were injected with either Ethoxysclerol or lidocain combined with adrenalin5. The
study showed that 10 out of 10 patients reported satisfaction with the result of the treatment
with a significant improvement on VAS. Nine out of 10 patients in the control group reported
Diagram 1. Outcome of pain at 6 weeks and 2.7-5.1 years after sclerosing therapy
Ch
apter 4
Less pro
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Ach
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79
satisfaction, but the difference in VAS before and after the treatment in the Ethoxysclerol
group was significantly larger. Also, patients in the sclerosing group showed no remaining
neovascularisation on colour Doppler5. Extending their proposed pathophysiological prin-
ciples of midportion Achilles tendinopathy and the role of neovessels in patellar tendinopathy
they applied the same treatment regime of injecting a sclerosing agent into these patients
in 2005, again with promising results4. In 2006, the group published the results of the first
2-year follow-up which showed remaining good clinical results and a lasting decrease in vol-
ume of the Achilles tendon. The favourable outcome in patients treated with this technique
has also been published by Clementson and co-workers in 2008 in a retrospective study of
25 patients9. The technique has currently been introduced by Alfredson and co-workers for
the treatment of painful tennis elbow and shoulder impingement syndromes1,3,47. All this
suggests a beneficial value of Ethoxysclerol in midportion tendinopathy.
A possible reason for our less favourable outcome is the retrospective design of our study.
We did not use neovascularisation scores or valid subjective outcome measures at six
weeks follow-up. Treatment in our clinic was initially not set up as a clinical trail but we just
implemented it as a new conservative measure for midportion Achilles tendinopathy. The
reason for this was the high percentage of good and excellent results in various publications
by the group of Alfredson indicating injection therapy to be a valuable treatment strategy.
As opposed to a good outcome, patients reported low satisfaction all along the way. We
considered this important to report, irrespective of the retrospective design.
Our success-rate from the injection of Ethoxysclerol is close to placebo-controlled studies
on conservative measures such as corticosteroid injections and external triglyceryltrinitrate
application, as well as the administration of placebo. These treatments also yield positive
results in 33-49% of patients10,32, well below the success percentage of eccentric training
and various surgical approaches. Eccentric loading should be the very first treatment method
for patients with midportion Achilles tendinopathy, since this treatment modality has been
tested in a proper manner and yields good results6,37-39. However, the training programme
is extensive, painful and requires strong perseverance. Eighty- seven percent of our patients
reported to be subjected to an eccentric training program guided by a physiotherapist before
being offered Ethoxysclerol injections, without a beneficial outcome. This may be a subgroup
not responding to eccentric training, or it may be due to inadequate instructions or insuf-
ficient compliance.
Injection with Ethoxysclerol is a conservative treatment method and positive outcome in 44%
of patients might be sufficient to implement this therapy as primary or secondary treatment
option for some patients with symptomatic midportion Achilles tendinopathy. On the other
hand, with an average of 2.7 injections with intervals of six to eight weeks it is an unpleasant
80
and time-consuming conservative treatment. This might particularly be problematic in active
patients and professional athletes demanding a quicker solution to return to sports.
The origin of pain in midportion Achilles tendinopathy, its natural history and the mecha-
nism by which a wide range of treatments generates relief is largely unknown. Sclerosing
treatment is based on the hypothesis that neovessels at the ventral side of the Achilles
tendon accompanied by nerves are the cause of pain. However, of 140 Achilles tendons
with clinically and ultrasonographically demonstrated Achilles tendinopathy, only 70 tendons
showed neovascularisation (50%). De Vos-, Peers-, Reiter- and Zanetti and co-workers found
equal proportions of neovascularisation in 50-88% of symptomatic tendons11,33,35,46.
The focus of treating Achilles tendinopathy is on relieving pain. Most often the intraten-
dinous changes are addressed. However, it is questionable if degeneration of the tendon
itself is the main cause of pain, since intratendinous changes are found in up to 34% of
people without complaints13,15,18,19. Very recently a long-term follow-up study was published
revealing persistent structural abnormalities and thickening of the tendon 13 years after
intra-tendinous surgery for Achilles tendinopathy, whereas all patients were satisfied with
the results and went back to Achilles tendon loading activities without restrictions7. Mid-
portion Achilles tendinopathy and paratendinopathy often co-exist43. Adhesions between
the tendon, peritendineum and crural fascia in the chronic phase are formed, prohibiting a
normal gliding movement of the tendon. The healthy tendon proper is normally aneuronal8,
but chronic painful tendons have been shown to exhibit new ingrowth of sensory nerve
fibers in the tendon proper24,41. We theorize that ‘denervation’ of the tendon is sufficient
to relieve symptoms. With Ethoxysclerol, by addressing neovessels, nerves are probably also
attacked. Injection may not suffice because of low volume and effectiveness of the substance
on nerves, and adhesions are too solid to be adequately released.
In agreement with this theory, surgical release of these adhesions though an open
approach17,20,22,23,29,40 or via endoscopically assisted techniques27,28,43,44, leaving the ten-
don proper untouched has demonstrated to be effective and provides quick rehabilitation.
However, these series are small and follow-up is of short duration. Fundamental research and
larger comparative series on surgical measures need to be done with proper study design
and at least one year follow-up to verify the cause of complaints before optimal treatment
can be developed.
coNcLUsioN
Our study did not confirm a beneficial value of sclerosing Ethoxysclerol injections in patients
with midportion Achilles tendinopathy. On the basis of our results, we decided to discontinue
the implementation of this treatment in our clinic.
Ch
apter 4
Less pro
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Ach
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81
refereNce List
1. Alfredson H, Harstad H, Haugen S, Ohberg
L. Sclerosing polidocanol injections to treat
chronic painful shoulder impingement
syndrome-results of a two-centre collabora-
tive pilot study. Knee Surg Sports Traumatol
Arthrosc 2006; 14: 1321-1326.
2. Alfredson H, Lorentzon R. Intratendinous
glutamate levels and eccentric training in
chronic Achilles tendinosis: a prospective
study using microdialysis technique. Knee
Surg Sports Traumatol Arthrosc 2003; 11:
196-199.
3. Alfredson H, Lorentzon R. Sclerosing polido-
canol injections of small vessels to treat the
chronic painful tendon. Cardiovasc Hematol
Agents Med Chem 2007; 5: 97-100.
4. Alfredson H, Ohberg L. Neovascularisation
in chronic painful patellar tendinosis--
promising results after sclerosing neovessels
outside the tendon challenge the need
for surgery. Knee Surg Sports Traumatol
Arthrosc 2005; 13: 74-80.
5. Alfredson H, Ohberg L. Sclerosing injections
to areas of neo-vascularisation reduce pain
in chronic Achilles tendinopathy: a double-
blind randomised controlled trial. Knee
Surg Sports Traumatol Arthrosc 2005; 13:
338-344.
6. Alfredson H, Pietila T, Jonsson P, Lorentzon
R. Heavy-load eccentric calf muscle training
for the treatment of chronic Achilles tendi-
nosis. Am J Sports Med 1998; 26: 360-366.
7. Alfredson H, Zeisig E, Fahlstrom M. No
normalisation of the tendon structure and
thickness after intratendinous surgery for
chronic painful midportion Achilles tendino-
sis. Br J Sports Med 2009; 43(12): 948-9.
8. Andersson G, Danielson P, Alfredson H,
Forsgren S. Nerve-related characteristics
of ventral paratendinous tissue in chronic
Achilles tendinosis. Knee Surg Sports Trau-
matol Arthrosc 2007; 15: 1272-1279.
9. Clementson M, Loren I, Dahlberg L, Astrom
M. Sclerosing injections in midportion
Achilles tendinopathy: a retrospective study
of 25 patients. Knee Surg Sports Traumatol
Arthrosc 2008; 16: 887-890.
10. DaCruz DJ, Geeson M, Allen MJ, Phair I.
Achilles paratendonitis: an evaluation of
steroid injection. Br J Sports Med 1988; 22:
64-65.
11. de Vos RJ, Weir A, Cobben LP, Tol JL. The
value of power Doppler ultrasonography in
Achilles tendinopathy: a prospective study.
Am J Sports Med 2007; 35: 1696-1701.
12. de Vos RJ, Weir A, Visser RJ, de WT, Tol JL.
The additional value of a night splint to
eccentric exercises in chronic midportion
Achilles tendinopathy: a randomised con-
trolled trial. Br J Sports Med 2007; 41: e5.
13. Emerson C, Morrissey D, Perry M, Jalan
R. Ultrasonographically detected changes
in Achilles tendons and self reported
symptoms in elite gymnasts compared with
controls - An observational study. Man Ther
2010; 15(1): 37-42.
14. Fahlstrom M, Jonsson P, Lorentzon R,
Alfredson H. Chronic Achilles tendon pain
treated with eccentric calf-muscle training.
Knee Surg Sports Traumatol Arthrosc 2003;
11: 327-333.
15. Haims AH, Schweitzer ME, Patel RS, Hecht
P, Wapner KL. MR imaging of the Achilles
tendon: overlap of findings in symptomatic
and asymptomatic individuals. Skeletal
Radiol 2000; 29: 640-645.
16. Hoksrud A, Ohberg L, Alfredson H, Bahr R.
Ultrasound-guided sclerosis of neovessels
in painful chronic patellar tendinopathy:
a randomized controlled trial. Am J Sports
Med 2006; 34: 1738-1746.
17. Jarvinen M. Lower leg overuse injuries
in athletes. Knee Surg Sports Traumatol
Arthrosc 1993; 1: 126-130.
18. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73: 1507-1525.
82
19. Khan KM, Forster BB, Robinson J et al. Are
ultrasound and magnetic resonance imag-
ing of value in assessment of Achilles tendon
disorders? A two year prospective study. Br J
Sports Med 2003; 37: 149-153.
20. Kvist M. Achilles tendon injuries in athletes.
Sports Med 1994; 18: 173-201.
21. Langberg H, Bulow J, Kjaer M. Blood flow
in the peritendinous space of the human
Achilles tendon during exercise. Acta Physiol
Scand 1998; 163: 149-153.
22. Leach RE, Schepsis AA, Takai H. Long-term
results of surgical management of Achilles
tendinitis in runners. Clin Orthop Relat Res
1992; 282: 208-212.
23. Lehto MU, Jarvinen M, Suominen P. Chronic
Achilles peritendinitis and retrocalcanear
bursitis. Long-term follow-up of surgically
treated cases. Knee Surg Sports Traumatol
Arthrosc 1994; 2: 182-185.
24. Lian O, Dahl J, Ackermann PW, Frihagen F,
Engebretsen L, Bahr R. Pronociceptive and
antinociceptive neuromediators in patellar
tendinopathy. Am J Sports Med 2006; 34:
1801-1808.
25. Lind B, Ohberg L, Alfredson H. Scleros-
ing polidocanol injections in mid-portion
Achilles tendinosis: remaining good clinical
results and decreased tendon thickness at
2-year follow-up. Knee Surg Sports Trauma-
tol Arthrosc 2006; 14: 1327-1332.
26. Mafi N, Lorentzon R, Alfredson H. Superior
short-term results with eccentric calf muscle
training compared to concentric training in
a randomized prospective multicenter study
on patients with chronic Achilles tendinosis.
Knee Surg Sports Traumatol Arthrosc 2001;
9: 42-47.
27. Maquirriain J, Ayerza M, Costa-Paz M,
Muscolo DL. Endoscopic surgery in chronic
achilles tendinopathies: A preliminary
report. Arthroscopy 2002; 18: 298-303.
28. Morag G, Maman E, Arbel R. Endoscopic
treatment of hindfoot pathology. Arthros-
copy 2003; 19: E13.
29. Nelen G, Martens M, Burssens A. Surgical
treatment of chronic Achilles tendinitis. Am
J Sports Med 1989; 17: 754-759.
30. Ohberg L, Alfredson H. Ultrasound guided
sclerosis of neovessels in painful chronic
Achilles tendinosis: pilot study of a new
treatment. Br J Sports Med 2002; 36: 173-
175.
31. Ohberg L, Lorentzon R, Alfredson H. Eccen-
tric training in patients with chronic Achilles
tendinosis: normalised tendon structure and
decreased thickness at follow up. Br J Sports
Med 2004; 38: 8-11.
32. Paoloni JA, Appleyard RC, Nelson J, Murrell
GA. Topical glyceryl trinitrate treatment of
chronic noninsertional achilles tendinopathy.
A randomized, double-blind, placebo-
controlled trial. J Bone Joint Surg Am 2004;
86-A: 916-922.
33. Peers KH, Brys PP, Lysens RJ. Correlation
between power Doppler ultrasonography
and clinical severity in Achilles tendinopathy.
Int Orthop 2003; 27: 180-183.
34. Perlick L, Schiffmann R, Kraft CN, Wallny T,
Diedrich O. [Extracorporal shock wave treat-
ment of the achilles tendinitis: Experimental
and preliminary clinical results]. Z Orthop
Ihre Grenzgeb 2002; 140: 275-280.
35. Reiter M, Ulreich N, Dirisamer A, Tschola-
koff D, Bucek RA. [Extended field-of-view
sonography in Achilles tendon disease: a
comparison with MR imaging]. Rofo 2004;
176: 704-708.
36. Robinson JM, Cook JL, Purdam C et al. The
VISA-A questionnaire: a valid and reliable
index of the clinical severity of Achilles tendi-
nopathy. Br J Sports Med 2001; 35: 335-341.
37. Rompe JD, Furia J, Maffulli N. Eccentric
loading versus eccentric loading plus shock-
wave treatment for midportion achilles
tendinopathy: a randomized controlled trial.
Am J Sports Med 2009; 37: 463-470.
38. Rompe JD, Nafe B, Furia JP, Maffulli N.
Eccentric loading, shock-wave treatment, or
a wait-and-see policy for tendinopathy of the
main body of tendo Achillis: a randomized
Ch
apter 4
Less pro
misin
g resu
lts with
sclerosin
g Eth
oxysclero
l injectio
ns fo
r mid
po
rtion
Ach
illes tend
ino
path
y
83
controlled trial. Am J Sports Med 2007; 35:
374-383.
39. Roos EM, Engstrom M, Lagerquist A,
Soderberg B. Clinical improvement after 6
weeks of eccentric exercise in patients with
mid-portion Achilles tendinopathy -- a ran-
domized trial with 1-year follow-up. Scand J
Med Sci Sports 2004; 14: 286-295.
40. Schepsis AA, Leach RE. Surgical manage-
ment of Achilles tendinitis. Am J Sports Med
1987; 15: 308-315.
41. Schubert TE, Weidler C, Lerch K, Hofstadter
F, Straub RH. Achilles tendinosis is associated
with sprouting of substance P positive nerve
fibres. Ann Rheum Dis 2005; 64: 1083-1086.
42. Silbernagel KG, Thomee R, Thomee P,
Karlsson J. Eccentric overload training for
patients with chronic Achilles tendon pain--a
randomised controlled study with reliability
testing of the evaluation methods. Scand J
Med Sci Sports 2001; 11: 197-206.
43. Steenstra F, van Dijk CN. Achilles tendos-
copy. Foot Ankle Clin 2006; 11: 429-38, viii.
44. van Dijk CN, Scholten PE, Kort N. Tendos-
copy (tendon sheath endoscopy) for overuse
tendon injuries. Oper Techn Sports Med
1997; 5: 170-178.
45. van LR, den Hoed PT, de Jongh AC.
[Guideline ‘Chronic Achilles tendinopathy,
in particular tendinosis, in sportsmen/sports-
women’]. Ned Tijdschr Geneeskd 2007; 151:
2319-2324.
46. Zanetti M, Metzdorf A, Kundert HP et
al. Achilles tendons: clinical relevance of
neovascularization diagnosed with power
Doppler US. Radiology 2003; 227: 556-560.
47. Zeisig E, Ohberg L, Alfredson H. Sclerosing
polidocanol injections in chronic painful ten-
nis elbow-promising results in a pilot study.
Knee Surg Sports Traumatol Arthrosc 2006;
14: 1218-1224.
Chapter 5
Endoscopy of tendons around the ankle
Officially translated to German
Tendoskopie am Sprunggelenk und Fuß
MN van Sterkenburg
PAJ de Leeuw
CN van Dijk
Artroskopie 2009; 22: 132-140
86
ABstrAct
Ankle arthroscopy is increasingly used as a technique for dealing with a wide range of ankle
pathologies. In contrast, extra-articular problems of the ankle still most often demand open
surgery. In the recent years, endoscopic procedures for treating various tendon pathologies
have been developed. Like arthroscopic surgery, tendoscopy offers the advantages related
to any minimally invasive procedure such as fewer wound infections, less blood loss, smaller
wounds and less morbidity. This article defines the major indications in which tendoscopy is
appropriate and presents current techniques for treatment.
Ch
apter 5
End
osco
py o
f tend
on
s arou
nd
the an
kle
87
iNtroDUctioN
In contrast to arthroscopy, which has become the preferred technique to treat intra-articular
ankle pathology, extra-articular problems of the ankle have traditionally demanded open sur-
gery. Open ankle surgery has been associated with complications such as injury to the sural
nerve or superficial peroneal nerve, infection, scarring, and stiffness of the ankle joint1,12,29.
The percentage of complications reported with open surgery for posterior ankle impinge-
ment (removal of os trigonum, scar tissue, hypertrophic posterior talar process, or ossicles)
varies between 15 and 24%1,12,29,50. The incidence of these complications has stimulated
the development of extra- articular endoscopic techniques. Endoscopic surgery offers the
advantages related to any minimally invasive procedure, such as fewer wound infections, less
blood loss, smaller wounds and less morbidity. Aftertreatment is functional, and surgery is
performed on an outpatient basis46.
Tendoscopy can be performed for the treatment and diagnosis of various pathologic
conditions of the peroneal tendons, the posterior tibial tendon, and the Achilles tendon. In
this manuscript, we describe these procedures and their indications.
1. teNDoscoPY of the PeroNeAL teNDoNs
IntroductionPathology of the peroneal tendons is most often seen with, and secondary to chronic lat-
eral ankle instability. These disorders frequently cause chronic ankle pain in runners and
ballet dancers6. Post-traumatic lateral ankle pain is seen frequently, but peroneal tendon
pathology is not always recognized as a cause of these symptoms. In a study by Dombek
and co-workers, only 60% of peroneal tendon disorders were accurately diagnosed at the
first clinical evaluation11. Because the peroneal tendons act as lateral ankle stabilizers, in
chronic instability of the ankle more strain is put on these tendons, resulting in hypertrophic
tendinopathy, tenosynovitis, and ultimately in tendon tears39.
Anatomically, the peroneus brevis tendon is situated dorsomedially to the peroneus longus
tendon from its proximal aspect up to the fibular tip, where it is relatively flat. Just distally
to this tip, the peroneus brevis tendon becomes rounder, and crosses the round peroneus
longus tendon. The distal posterolateral part of the fibula forms a sliding channel for the two
peroneal tendons. This malleolar groove is formed by a periosteal cushion of fibrocartilage
that covers the bony groove. The tendons are held into position by the superior peroneal
retinaculum39,47,49.
Pathology of the peroneal tendons consists of tenosynovitis, tendon dislocation or sublux-
ation, and (subtotal) rupture or snapping of one or both of the peroneal tendons. It accounts
for the majority of symptoms at the posterolateral aspect of the ankle37, 40. Other causes
of posterolateral ankle pain are rheumatoid synovitis, bony spurs, calcifications or ossicles,
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pathology to the posterior talofibular ligament (PTFL), or disorders of the posterior compart-
ment of the subtalar joint. Posterior ankle impingement can present as posterolateral ankle
pain. On clinical examination, there is recognizable tenderness over the tendons on palpa-
tion. Swelling, tendon dislocation and signs of tenosynovitis can be found.
The diagnosis of peroneal tendon pathology can be difficult in a patient with lateral
ankle pain. A detailed history should include the presence of associated conditions such as
rheumatoid arthritis, psoriasis, hyperparathyroidism, diabetic neuropathy, calcaneal fracture,
fluoroquinolone use, and local steroid injections. These can all increase the prevalence of
peroneal tendon dysfunction13. A diagnostic differentiation must be made with fatigue
fractures or fractures of the fibula, posterior impingement of the ankle, and lesions of the
lateral ligament complex.
Additional investigations such as MRI and ultrasonography may be helpful in confirming
the diagnosis in (partial) tears of the tendon of peroneus brevis or longus54. Post-traumatic
or post-surgical adhesions and irregularities of the posterior aspect of the fibula (peroneal
groove) can also be responsible for symptoms in this region.
The primary indication of treating pathology of the peroneal tendons is pain. Conserva-
tive management should be attempted first. This includes activity modification, footwear
changes, temporary immobilization, and corticosteroid injections. Also, lateral heel wedges
can take the strain off the peroneal tendons which may allow healing. Failure of these
conservative measures may be an indication for surgery. We therefore developed a safe and
reliable endoscopic technique which we describe in detail here39,47.
Surgical techniqueThe patient is placed in the lateral decubitus position, with the operative side up. Before
anaesthesia is administered, the patient is asked to actively evert the affected foot. In this
way, the tendon can be palpated, and the location of the portals is drawn onto the skin. The
surgery can be performed under local, regional, epidural or general anaesthesia. A support is
placed under the affected leg making it possible to move the ankle freely. After exsanguina-
tion a tourniquet is inflated around the thigh of the affected leg.
A distal portal is made first, 2-2.5 cm distal to the posterior edge of the lateral mal-
leolus. An incision is made through the skin, and the tendon sheath is penetrated with an
arthroscopic shaft with a blunt trocar. After this, a 2.7 mm 30° arthroscope is introduced.
The inspection starts approximately 6 cm proximal from the posterior tip of the fibula, where
a thin membrane splints the tendon compartment into two separate tendon chambers. More
distally, the tendons lie in one compartment. A second portal is made 2-2.5 cm proximal to
the posterior edge of the lateral malleolus under direct vision by placing a spinal needle,
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producing a portal directly over the tendons (Figure 1). Through the distal portal, a complete
overview of both tendons can be obtained.
By rotating the arthroscope over and in between both tendons, the whole compartment
can be inspected. When a total synovectomy of the tendon sheath is to be performed, it is
advisable to produce a third portal more distal or more proximal than the portals described
previously.
When a rupture of one of the tendons is seen (Figure 2), endoscopic synovectomy is
performed, and the rupture is repaired through a mini-open approach.
In patients with recurrent dislocation of the peroneal tendon, endoscopic fibular groove
deepening can be performed through this approach. This is a time consuming proce-
dure, because of the limited working area. Groove deepening is performed from within the
Figure 1. Peroneal tendoscopy of the right ankle: (A) marking the anatomy of the peroneal tendons. (B) Arthroscopic view at introduction of the arthroscope looking from distal to proximal. An arrow indicates a thin membrane separating the two tendons proximally. (C) Placement of spinal needle under direct vi-sion for preparation of the second portal. (D) Endoscopic view of needle inside the tendon sheath. (PB= peroneus brevis, PL= peroneus longus)
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tendon sheath with the risk of iatrogenic damage to the tendons. We therefore prefer an
approach by the 2 hindfoot portal technique47,50.
At the end of the procedure, the portals are sutured to prevent sinus formation, and a
compressive dressing is applied. Full weight bearing is allowed as tolerated and active range
of motion exercises are advised starting immediately post surgery.
ResultsWe reported the results of peroneal tendoscopy in 23 patients operated on between 1995
and 2000, with a minimum follow up of 2 years47. Eleven patients were diagnosed with
a longitudinal rupture of the peroneus brevis tendon; 8 of these presented with pain and
swelling over the posterior aspect of the lateral malleolus and 3 presented with a snapping
sensation at the level of the lateral malleolus.
Ten patients had persisting symptoms after surgery for a fracture of the fibula, lateral
ankle ligament reconstruction, or after operative repair of recurrent tendon dislocation.
Surgery consisted of endoscopic tenosynovectomy, adhesiolysis, removal of an exostosis,
and suturing a longitudinal rupture via a mini-open procedure. The two remaining patients
underwent endoscopic groove deepening of the fibular groove for complaints of recurrent
tendon dislocation.
No complications occurred, and complaints disappeared after surgery. Since then, we
performed another 28 procedures mainly for adhesiolysis, and diagnosis and management
of longitudinal ruptures. For recurrent peroneal tendon dislocation we treated another 12
patients by means of endoscopic groove deepening with good results at one year follow-up.
Figure 2. Peroneal tendoscopy in a 39-year-old male patient with a longitudinal tear of the right pero-neus brevis tendon. The arthroscope is introduced through the distal portal looking into a proximal direc-tion. Hypervascularisation (HV) of the peroneus brevis tendon as an expression of chronic irritation. (PB= peroneus brevis tendon, PL= peroneus longus tendon. The arrow indicates the tear.)
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The technique uses the 2 traditional hindfoot portals and one additional superoposterolateral
working portal50,10.
Lui and co-workers21 described an endoscopic technique to reconstruct the superior
peroneal retinaculum keeping the peroneal tendons in place when intact. In addition to
the two portals described earlier, retinacular openings are made slightly larger than the skin
openings of the portals. The lateral surface of the lateral malleolus where the retinaculum is
stripped off is roughened with an arthroscopic burr or curette. Three holes are drilled through
the portals with an interval of 1 cm, and three suture anchors are inserted into the fibular
ridge. A needle is inserted through the portal and the retinaculum pierced in an “inside-out”
manner. The sutures are pulled out and then retrieved at the surface of the retinaculum
through the skin wounds. When the sutures are tightened the retinaculum can be pushed
onto the fibular ridge. The authors describe 2 cases with good outcome, and a possible
great advantage could be that patients with endoscopic reconstruction seem to have less
subjective tightness as compared to those undergoing open procedures.
2. teNDoscoPY of the Posterior tiBiAL teNDoN
IntroductionIn the absence of intra-articular ankle pathology, posteromedial ankle pain is most often
caused by disorders of the posterior tibial tendon.
Inactivity of the posterior tibial tendon gives midtarsal instability and is the commonest
cause of adult onset flatfoot deformity. The relative strength of this tendon is more than
twice that of its primary antagonist, the peroneus brevis tendon. Without the activity of the
posterior tibial tendon, there is no stability at the midtarsal joint, and the forward propulsive
force of the gastrocnemius/soleus complex acts at the midfoot instead of at the midtarsal
heads. Total dysfunction eventually leads to a flatfoot deformity.
These disorders can be divided in two groups: the younger group of patients with dysfunc-
tion of the tendon, caused by some form of systemic inflammatory disease (e.g. rheumatoid
arthritis); and an older group of patients whose tendon dysfunction is mostly caused by
chronic overuse32.
Following trauma, surgery, and fractures, adhesions and irregularity of the posterior aspect
of the tibia can be responsible for symptoms in this region. Also, the vincula can become
symptomatic in these circumstances7,48. The vincula connect the posterior tibial tendon to its
tendon sheath49. Damage to the vincula can cause thickening, shortening and scarring of the
distal free edge. In these patients, a painful local thickening can be palpated posterior and
just proximal of the tip of the medial malleolus.
Mostly a dysfunctioning posterior tibial tendon evolves in a painful tenosynovitis. Tenosy-
novitis is also a common extra-articular manifestation of rheumatoid arthritis, where hindfoot
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problems are a significant cause of disability. Tenosynovitis in rheumatoid patients eventually
leads to a ruptured tendon30.
Although the precise aetiology is unknown, the condition is classified on the basis of clinical
and radiographic findings. In the early stage of dysfunction, patients complain of persisting
ankle pain medially along the course of the tendon, in addition to fatigue and aching on the
plantar medial aspect of the ankle. When a tenosynovitis is present, swelling is common. On
clinical examination, valgus angulation of the hindfoot is frequently seen, with accompanying
abduction of the forefoot, the “too-many-toes” sign45. This sign is positive when inspecting
the patient’s foot from behind: in case of significant forefoot abduction, 3 or more toes are
visible lateral to the calcaneus, where normally only 1 or 2 toes are seen.
Intra-articular lesions such as a posteromedial impingement syndrome, subtalar pathology,
calcifications in the dorsal capsule of the ankle joint, loose bodies or osteochondral defects
should be excluded. Entrapment of the posterior tibial nerve in the tarsal canal is commonly
known as a tarsal tunnel syndrome. Clinical examination is normally sufficient to adequately
differentiate these disorders from an isolated posterior tibia tendon disorder.
For additional investigation, magnetic resonance imaging (MRI) is the best method to
assess a tendon rupture18. Also, ultrasound imaging is known as a cost-effective and accu-
rate to evaluate disorders of the tendon31.
Initially, conservative management is indicated, with rest, combined with nonsteroidal anti-
inflammatory drugs (NSAIDS), and immobilization using a plaster cast or tape. There is no
consensus whether to use corticosteroid injections; some cases of tendon rupture following
corticosteroid injections have recently been described36.
After failure of 3-6 months of conservative management, surgery can be indicated22.
This can be performed open or endoscopically. An open synovectomy is performed by sharp
dissection of the inflamed synovium, while preserving blood supply to the tendon. Post-
operative management consists of plaster cast immobilization for 3 weeks with the possible
disadvantage of new formation of adhesions, followed by wearing a functional brace with
controlled ankle movement for another 3 weeks, and physical therapy5.
Endoscopic synovectomy is our surgical modality of choice when access allows radical
removal of inflamed synovium35. Several studies have been described previously in which
endoscopic synovectomy was successfully performed, offering the advantages that are
related to minimally invasive surgery47,48,49.
Surgical techniqueThe procedure can be performed on an outpatient basis under local, regional or general
anaesthesia. Patients are placed in the supine position. A tourniquet is placed around the
upper leg. Before anaesthesia, the patient is asked to actively invert the foot, so that the
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posterior tibial tendon can be palpated and the portals can be marked. Access to the tendon
can be obtained anywhere along the course of it.
We prefer to make the two main portals directly over the tendon 2-3 cm distal and 2-3
cm proximal to the posterior edge of the medial malleolus. The distal portal is made first: the
incision is made through the skin, and the tendon sheath is penetrated by the arthroscopic
shaft with a blunt trocar. A 2.7 mm 30° arthroscope is introduced, and the tendon sheath is
filled with saline Irrigation is performed using gravity flow.
Under direct vision, the proximal portal is made by introducing a spinal needle, and subse-
quently an incision is made into the tendon sheath (Figure 3). Instruments as a retrograde
knife, a shaver system, blunt probes, and scissors can be used. For synovectomy in patients
with rheumatoid arthritis, a 3.5 mm shaver can be used. The complete tendon sheath can be
inspected by rotating the arthroscope around the tendon.
Figure 3. (A) Marked anatomy of posterior tibial tendon of the right foot. (B) Introduction of a 2.7mm 30° arthroscope. (C) Endoscopic view of the posterior tibial tendon at introduction of the arthroscope. (D) Blunt dissection with mosquito clamp under direct vision creating a second proximal portal
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Synovectomy can be performed with a complete overview of the tendon from the distal
portal, over the insertion of the navicular bone to approximately 6 cm above the tip of the
medial malleolus.
Special attention should be given to inspecting the tendon sheath, the posterior aspect
of the medial malleolar surface, and the posterior ankle joint capsule. The tendon sheath
between the posterior tibial tendon and the flexor digitorum longus is relatively thin: inspec-
tion of the correct tendon should always be checked. This can be accomplished by passively
flexing and extending the toes; if the tendon sheath of the flexor digitorum longus tendon is
entered, the tendon will move up and down.
When remaining in the posterior tibial tendon sheath, the neurovascular bundle is not in
danger.
When a rupture of the posterior tibial tendon is seen (Figure 4), endoscopic synovectomy
is performed and the rupture is repaired through a mini-open approach. The advantage to
start this procedure endoscopically over the standard open procedure is that localization
of the problem is made easier by exploration of the endoscopically magnified tendon, and
consequently the size of the incision for repair of the rupture can be minimized.
At the end of the procedure, the portals are sutured to prevent sinus formation.
Post-operative management consists of a pressure bandage and partial weight-bearing
for 2-3 days. Active range of motion exercises are encouraged from the first day.
ResultsIn 1997, the senior author first described tendoscopy of the posterior tibial tendon to man-
age pathology of this tendon in an anatomic study48. From 1994 to 1997, 16 procedures
were performed on 16 patients with a mean follow up of 1.1 years7. All had a history of
Figure 4. Posterior tibial tendoscopy of the right foot in a 46- year- old female patient with pain over the posterior tibial tendon. The arthroscope is in the anterolateral portal looking proximally. (A) Superficial tear of the posterior tibial tendon (asterisk). (B) Rupture demonstrated with the arthroscopic probe. (C) Repair of the rupture through a mini open repair. (P= probe; PTT= posterior tibial tendon; TS= tendon sheath)
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persistent posteromedial ankle pain for at least 6 months, with pain on palpation of the
posterior tibial tendon, positive resistance test results, and often local swelling. Five patients
underwent a diagnostic procedure after surgery, in 5 a diagnostic procedure after a fracture
was performed, a diagnostic procedure after trauma in 1, chronic tenosynovitis in 2, screw
removal from the medial malleolus in 1, and posterior ankle arthrotomy in 2 patients. No
complications were observed.
Between 1997 and 2004, we described 19 procedures in 17 patients7. Ten endoscopic
synovectomies were performed in 8 patients who had chronic tenosynovitis due to rheuma-
toid arthritis. All had a history of persistent posteromedial ankle pain, with pain on palpation
of the posterior tibial tendon, positive resistance test results, and local swelling. All patients
were first managed conservatively, and experienced temporary pain relief. All 8 patients were
diagnosed with synovitis without a tendon rupture by MRI or ultrasound. In 3 of these 8
patients, the endoscopy was combined with an arthroscopic synovectomy of the ankle or a
hallux valgus correction. In the other nine patients, tendoscopy of the posterior tibial tendon
was performed for miscellaneous reasons. Patients were allowed full weight bearing after
the operation, except for the patient who had hallux valgus correction. All were able to
actively move the ankle post-operatively.
Johnson and Strom classified tenosynovitis of the posterior tibial tendon into three stages14:
stage one tenosynovitis, where the tendon length is normal; stage two, elongated tendon
with mobile hindfoot deformity; and stage three, elongated tendon with fixed hindfoot
deformity. Myerson modified the classification by adding stage four: a valgus angulation
of the talus and early degeneration of the ankle joint32. Chow8 reported a case series of 6
patients with posterior tibial tendon synovitis who underwent an endoscopic synovectomy
for stage 1 posterior tibial tendon insufficiency. All patients reported good results.
Lui and co-workers22 described an endoscopic assisted posterior tibial tendon reconstruc-
tion for stage 2 posterior tibial tendon insufficiency, when the posterior tibial tendon has
become permanently elongated but the flatfoot deformity still is flexible. The endoscopic
technique used is similar to the one described above. Additionally, a portal is made close to
the insertion of the anterior tibial tendon, of which the medial half is cut and stripped to
the insertion with a tendon stripper. The tendon is then retrieved through the distal portal,
and the graft is transferred to the posterior tibial tendon. The construction is augmented by
side-to-side anastomosis with the flexor digitorum longus tendon, which is supplemented by
a subtalar arthroereisis with a bioabsorbable implant. Thus far only one case was described,
with a good clinical outcome.
96
3. AchiLLes teNDoscoPY
IntroductionPathology of the Achilles tendon can be divided into non-insertional and insertional prob-
lems9,38. The first type can present as local degeneration of the tendon that can be combined
with paratendinopathy. Insertional problems are related to abnormalities at the insertion of
the Achilles tendon, including the posterior aspect of the calcaneus and the retrocalcaneal
bursa. This chapter will describe the management of non-insertional tendinopathy. These can
be divided into three entities: tendinopathy, paratendinopathy, and a combination of both.
General symptoms include painful swelling typically 2-7 cm proximal to the insertion, and
stiffness especially when getting up after a period of rest.
Patients with tendinopathy can present with three patterns: diffuse thickening of the
tendon, local degeneration of the tendon which is mechanically intact, or insufficiency of the
tendon with a partial tear. In paratendinopathy, there is local thickening of the paratenon.
Clinically, a differentiation between tendinopathy and paratendinopathy can be made. Maf-
fulli and co-workers describe the Royal London Hospital test, which is found to be positive
in patients with isolated tendinopathy of the main body of the tendon: the portion of the
tendon originally found to be tender on palpation shows little or no pain with the ankle in
maximum dorsiflexion24,26. In paratendinopathy, the area of swelling does not move with
dorsiflexion and plantarflexion of the ankle, where it does in tendinopathy26,42,53. Paratendi-
nopathy can be acute or chronic.
Differential diagnoses include pathology of the tendons of the peroneus longus and brevis,
intra-articular pathology of the ankle joint and subtalar joint, degenerative changes of the
posterior tibial tendon, and tendinopathy of the flexor hallucis longus muscle must be ruled
out. MRI and ultrasound can be used to differentiate between the various forms of tendi-
nopathy17.
We normally initiate conservative management first. Modification of the activity level of the
patient is advised together with avoidance of strenuous activities in case of paratendinopathy.
Shoe modifications and inlays can be given. Physical therapy includes an extensive eccentric
exercise program, which can be combined with icing and NSAIDs27,33,34,41. Shockwave treat-
ment, a night splint, and cast immobilization are alternative conservative methods. Sclerosing
injections of neovascularisation and accompanying nerves around the Achilles tendon have
initially shown promising results. This treatment is based on the theory that neovascularisa-
tion is seen in the vast majority of patients with Achilles tendinopathy but not in pain free
normal tendons2-4,20.
If these conservative measures fail, surgery must be considered. The percentage of patients
requiring surgery is around 25%19,23,26. The technique used for operative management of
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tendinopathy depends on the stage of the disease. Local degeneration and thickening are
usually treated by excision and curettage. An insufficient Achilles tendon due to extensive
degeneration can be reconstructed. Isolated paratendinopathy can be treated by excision of
the diseased paratenon.
Open surgery has a guarded prognosis, and is associated with a higher risk of complications
than endoscopy 1,12,29. Open techniques are also associated with an extensive rehabilitation
period of 4-12 months. Therefore, recently minimally invasive techniques were developed.
Percutaneous needling of the tendon has been described, but until now no results have
been published. Testa and co-workers described a minimally invasive technique consisting of
percutaneous longitudinal tenotomies25,44, which was later optimized by adding ultrasound
control. Eighty-three percent of patients reported symptomatic benefit at the time of their
best outcome; however, the median time to return to sports was 6.5 months43.
In combined tendinopathy and paratendinopathy, the question is whether both patholo-
gies contribute to the complaints. An anatomic cadaver study described degenerative
changes of the Achilles tendon in as much as 34% of subjects with no complaints15. Khan
and co-workers only found abnormal morphology in 65% (37 of 57) of symptomatic ten-
dons, but also in 32% (9 of 28) of asymptomatic Achilles tendons assessed by ultrasound16.
Therefore, it is questionable whether degeneration of the tendon itself is the main cause of
the pain. The authors therefore focus mainly on management of the paratendinopathy leav-
ing the tendinopathy untouched. The current approach is an endoscopic release or resection
of the plantaris tendon at the level of the nodule and removal of the local paratendinopathy
tissue at the level of the painful nodule.
Surgical techniqueLocal, epidural, spinal and general anaesthesia can be used for this procedure, which can be
performed on an outpatient basis. The patient is in prone position. A tourniquet is placed
around the thigh of the affected leg, and a bolster is placed under the foot. Because the
surgeon needs to be able to obtain full plantar and dorsiflexion, the foot is placed right over
the end of the table (Figure 5).
The authors mostly use a 2.7 mm arthroscope for endoscopy of a combined tendinopathy
and paratendinopathy. This small- diameter short arthroscope yields an excellent picture
comparable to the standard 4 mm arthroscope; however, it cannot deliver the same amount
of irrigation fluid per time as the 4 mm sheath. This is important in procedures in which a
large diameter shaver is used (e.g. in endoscopic calcaneoplasty). When a 4 mm arthroscope
is used, gravity inflow of irrigation fluid is usually sufficient. A pressurized bag or pump
device sometimes is used with the 2.7 mm arthroscope.
The distal portal is located on the lateral border of the Achilles tendon, 2-3 cm distal to the
pathologic nodule. The proximal portal is located medial to the border of the Achilles tendon,
98 Figure 5. Positioning of a patient for endoscopy of the left Achilles tendon. (A) The patient is placed prone. (B, C) The affected leg is placed on a bolster and right over the end of the table. (C) The other foot is positioned so that the surgeon has sufficient working area
Figure 6. Posterior aspect of the right foot and ankle. Anatomy and portals for Achilles tendosopy are marked. (DP= distal portal, N= nodule, PP= proximal portal)
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2-4 cm above the nodule. When the portals are placed this way, it is usually possible to visual-
ize and work around the complete surface of the tendon, over a length of approximately 10
cm (Figure 6).
The distal portal is made first. After making the skin incision, the mosquito clamp is intro-
duced, followed by the blunt 2.7 mm trocar in a craniomedial direction. With this blunt
trocar the paratenon is approached, and is blindly released from the tendon by moving
around it. Subsequently, the 2.7 mm 30° arthroscope is introduced. To minimize the risk of
iatrogenic damage, the arthroscope should be kept on the tendon. At this moment, it can
be confirmed whether the surgeon is in the right layer between the deepest layer of the
paratenon and Achilles tendon. If not, now it can be identified and a further release can be
performed (Figure 7A-C).
The proximal portal is made by introducing a spinal needle, followed by a mosquito clamp
and probe. The plantaris tendon can be identified at the anteromedial border of the Achilles
tendon (Figure 7D). In a typical case of local paratendinopathy, the plantaris tendon, the
Achilles tendon, and the paratenon are tight together in the process. Removal of the local
Figure 7. Tendoscopy of the left Achilles tendon in a 52- year old female patient with combined tendi-nopathy and paratendinopathy. The 2.7 mm arthroscope is introduced through the distal portal looking proximally. (A) Adhesions of the paratenon (PAR) to the subcutaneous tissue (ST) overlying the Achilles tendon. (B) Removal of adhesions (AD) of the paratenon to the Achilles tendon (AT), looking from distal to proximal. (C) Paratenon released from the Achilles tendon. (D) Plantaris tendon (PT) running medial to the Achilles tendon (AT). (E) Release of the plantaris tendon. (F) Neovascularisation (arrows) before removal by bonecutter shaver
100
thickened paratenon on the anteromedial side of the Achilles tendon at the level of the
nodule, and release of the plantaris tendon which is often involved in the process (Figure 7E)
are the goals of this procedure. In cases where the fibrotic paratenon is firmly attached to the
lateral or posterior border of the tendon, a release in these areas is performed. Neovessels
(Figure 7F) accompanied by small nerve fibres can be found in this area and are removed with
a 2.7 mm full radius resector.
Changing portals can be helpful. At the end of the procedure it must be possible to move the
arthroscope over the complete symptomatic area of the Achilles tendon. After the procedure,
the portals are sutured.
Aftercare consists of a compressive dressing for 2-3 days. Patients are encouraged to
actively perform range of motion exercises. Full weight-bearing is allowed as tolerated.
Initially, the foot must be elevated when not walking.
ResultsThe senior author earlier described the results of 20 patients treated with an endoscopic
release for non-insertional tendinopathy combined with a paratendinopathy42. All patients
had had complaints for more than 2 years, and underwent conservative treatment for their
complaints before the indication for surgery was set. The results were analyzed with a follow
up of 2-7 years with a mean of 6 years. Sixteen patients were assessed at follow up, which
included completing of subjective outcome scores. The Foot and Ankle Outcome Score
(FAOS) and the Short Form general health survey with 36 questions (SF-36) were utilized.
There were no complications. Most patients were able to resume their sporting activities after
4 to 8 weeks. All patients had significant pain relief. The results of the subjective outcome
scores used were comparable to a cohort of people without Achilles tendon complaints.
Maquirriain and co-workers reported the outcome of 7 patients who underwent an
endoscopic release for chronic Achilles tendinopathy, with similar results. The mean score
of this group improved from 39 preoperatively to 89 post-operatively (on a scale of 0-100),
and there were no complications28. Most recently, Vega and co-workers published a modi-
fied endoscopic technique for the treatment of Achilles tendinopathy51. Pathological tissue
was endoscopically removed, and multiple longitudinal tenotomies were performed using a
retrograde knife blade. They reported a series of 8 patients with an excellent outcome, return
to their previous sports activities and no complications.
Patellar tendinopathy has a histological picture similar to that of Achilles tendinopathy.
Recently, Wilberg and co-workers have developed an arthroscopic technique for patellar
tendinopathy53. Part of their technique is comparable to Achilles tendoscopy; the main goal
is to shave the area with neovessels and accompanying nerves on the posterior aspect of the
patellar tendon, whereas this is one of the goals for endoscopic management of Achilles
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tendinopathy. A pilot study showed good clinical results in 13/15 tendons (6/8 elite athletes);
all satisfied patients were back to their previous sport activity level.
coNcLUsioNs
The results of endoscopic surgery of tendons around the ankle seem promising. More experi-
ence must be acquired by different orthopaedic surgeons. Also, accurately designed studies
need to be performed, to optimize techniques and ultimately be able to offer patients these
minimally invasive treatments with its great advantages.
102
refereNce List
1. Abramowitz Y, Wollstein R, Barzilay Y et
al. Outcome of resection of a symptomatic
os trigonum. J Bone Joint Surg Am 2003;
85-A(6): 1051-1057.
2. Alfredson H, Lorentzon R. Sclerosing polido-
canol injections of small vessels to treat the
chronic painful tendon. Cardiovasc Hematol
Agents Med Chem 2007; 5(2): 97-100.
3. Alfredson H, Ohberg L, Zeisig E, Lorentzon
R. Treatment of midportion Achilles ten-
dinosis: similar clinical results with US and
CD-guided surgery outside the tendon and
sclerosing polidocanol injections. Knee Surg
Sports Traumatol Arthrosc 2007; 15(12):
1504-1509.
4. Andersson G, Danielson P, Alfredson H,
Forsgren S. Nerve-related characteristics
of ventral paratendinous tissue in chronic
Achilles tendinosis. Knee Surg Sports Trau-
matol Arthrosc 2007; 15(10): 1272-1279.
5. Bare AA, Haddad SL. Tenosynovitis of the
posterior tibial tendon. Foot Ankle Clin
2001; 6(1): 37-66.
6. Bassett FH, III, Billys JB, Gates HS, III. A
simple surgical approach to the postero-
medial ankle. Am J Sports Med 1993; 21(1):
144-146.
7. Bulstra GH, Olsthoorn PG, Niek van DC.
Tendoscopy of the posterior tibial tendon.
Foot Ankle Clin 2006; 11(2): 421-7.
8. Chow HT, Chan KB, Lui TH. Tendoscopic
debridement for stage I posterior tibial
tendon dysfunction. Knee Surg Sports Trau-
matol Arthrosc 2005; 13(8): 695-698.
9. Clain MR, Baxter DE. Achilles tendinitis. Foot
Ankle 1992; 13(8): 482-487.
10. de Leeuw PAJ, Golano P, van Dijk CN. A
3- portal endoscopic groove deepening
technique for recurrent peroneal tendon
dislocation. Techniques in Foot and Ankle
Surgery 2008; 7 (4): 250-256.
11. Dombek MF, Lamm BM, Saltrick K, Men-
dicino RW, Catanzariti AR. Peroneal tendon
tears: a retrospective review. J Foot Ankle
Surg 2003; 42(5): 250-258.
12. Hamilton WG, Geppert MJ, Thompson FM.
Pain in the posterior aspect of the ankle in
dancers. Differential diagnosis and operative
treatment. J Bone Joint Surg Am 1996;
78(10): 1491-1500.
13. Heckman DS, Reddy S, Pedowitz D, Wapner
KL, Parekh SG. Operative treatment for
peroneal tendon disorders. J Bone Joint Surg
Am 2008; 90(2): 404-418.
14. Johnson KA, Strom DE. Tibialis posterior
tendon dysfunction. Clin Orthop Relat Res
1989; (239): 196-206.
15. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73(10): 1507-1525.
16. Khan KM, Forster BB, Robinson J et al. Are
ultrasound and magnetic resonance imag-
ing of value in assessment of Achilles tendon
disorders? A two year prospective study. Br J
Sports Med 2003; 37(2): 149-153.
17. Ko R., Porter M. Interactive foot and ankle 2.
London: Primal Pictures 2000.
18. Kong A, Van D, V. Imaging of tibialis poste-
rior dysfunction. Br J Radiol 2008; 81(970):
826-836.
19. Kvist M. Achilles tendon injuries in athletes.
Ann Chir Gynaecol 1991; 80(2): 188-201.
20. Lind B, Ohberg L, Alfredson H. Scleros-
ing polidocanol injections in mid-portion
Achilles tendinosis: remaining good clinical
results and decreased tendon thickness at
2-year follow-up. Knee Surg Sports Trauma-
tol Arthrosc 2006; 14(12): 1327-1332.
21. Lui TH. Endoscopic peroneal retinaculum
reconstruction. Knee Surg Sports Traumatol
Arthrosc 2006; 14(5): 478-481.
22. Lui TH. Endoscopic assisted posterior tibial
tendon reconstruction for stage 2 posterior
tibial tendon insufficiency. Knee Surg Sports
Traumatol Arthrosc 2007; 15(10): 1228-
1234.
Ch
apter 5
End
osco
py o
f tend
on
s arou
nd
the an
kle
103
23. Maffulli N. Augmented repair of acute Achil-
les tendon ruptures using gastrocnemius-
soleus fascia. Int Orthop 2005; 29(2): 134.
24. Maffulli N, Kenward MG, Testa V, Capasso
G, Regine R, King JB. Clinical diagnosis of
Achilles tendinopathy with tendinosis. Clin J
Sport Med 2003; 13(1): 11-15.
25. Maffulli N, Testa V, Capasso G, Bifulco G,
Binfield PM. Results of percutaneous longi-
tudinal tenotomy for Achilles tendinopathy
in middle- and long-distance runners. Am J
Sports Med 1997; 25(6): 835-840.
26. Maffulli N, Walley G, Sayana MK, Longo UG,
Denaro V. Eccentric calf muscle training in
athletic patients with Achilles tendinopathy.
Disabil Rehabil 2008; 1-8.
27. Mafi N, Lorentzon R, Alfredson H. Superior
short-term results with eccentric calf muscle
training compared to concentric training in
a randomized prospective multicenter study
on patients with chronic Achilles tendinosis.
Knee Surg Sports Traumatol Arthrosc 2001;
9(1): 42-47.
28. Maquirriain J, Ayerza M, Costa-Paz M,
Muscolo DL. Endoscopic surgery in chronic
achilles tendinopathies: A preliminary
report. Arthroscopy 2002; 18(3): 298-303.
29. Marotta JJ, Micheli LJ. Os trigonum impinge-
ment in dancers. Am J Sports Med 1992;
20(5): 533-536.
30. Michelson J, Easley M, Wigley FM, Hellmann
D. Posterior tibial tendon dysfunction in
rheumatoid arthritis. Foot Ankle Int 1995;
16(3): 156-161.
31. Miller SD, Van HM, Boruta PM, Wu KK,
Katcherian DA. Ultrasound in the diagnosis
of posterior tibial tendon pathology. Foot
Ankle Int 1996; 17(9): 555-558.
32. Myerson MS. Adult acquired flatfoot
deformity: treatment of dysfunction of the
posterior tibial tendon. Instr Course Lect
1997; 46: 393-405.
33. Norregaard J, Larsen CC, Bieler T, Langberg
H. Eccentric exercise in treatment of Achilles
tendinopathy. Scand J Med Sci Sports 2007;
17(2): 133-138.
34. Ohberg L, Lorentzon R, Alfredson H. Eccen-
tric training in patients with chronic Achilles
tendinosis: normalised tendon structure and
decreased thickness at follow up. Br J Sports
Med 2004; 38(1): 8-11.
35. Paus AC. Arthroscopic synovectomy. When,
which diseases and which joints. Z Rheuma-
tol 1996; 55(6): 394-400.
36. Porter DA, Baxter DE, Clanton TO, Klootwyk
TE. Posterior tibial tendon tears in young
competitive athletes: two case reports. Foot
Ankle Int 1998; 19(9): 627-630.
37. Roggatz J, Urban A. The calcareous periten-
dinitis of the long peroneal tendon. Arch
Orthop Trauma Surg 1980; 96(3): 161-164.
38. Saltzman CL, Tearse DS. Achilles tendon
injuries. J Am Acad Orthop Surg 1998; 6(5):
316-325.
39. Scholten PE, van Dijk CN. Tendoscopy of the
peroneal tendons. Foot Ankle Clin 2006;
11(2): 415-20.
40. Schweitzer GJ. Stenosing peroneal tenovagi-
nitis. Case reports. S Afr Med J 1982; 61(14):
521-523.
41. Silbernagel KG, Thomee R, Thomee P,
Karlsson J. Eccentric overload training for
patients with chronic Achilles tendon pain--a
randomised controlled study with reliability
testing of the evaluation methods. Scand J
Med Sci Sports 2001; 11(4): 197-206.
42. Steenstra F, van Dijk CN. Achilles tendos-
copy. Foot Ankle Clin 2006; 11(2): 429-38.
43. Testa V, Capasso G, Benazzo F, Maffulli N.
Management of Achilles tendinopathy by
ultrasound-guided percutaneous tenotomy.
Med Sci Sports Exerc 2002; 34(4): 573-580.
44. Testa V, Maffulli N, Capasso G, Bifulco G.
Percutaneous longitudinal tenotomy in
chronic Achilles tendonitis. Bull Hosp Jt Dis
1996; 54(4): 241-244.
104
45. Trnka HJ. Dysfunction of the tendon of
tibialis posterior. J Bone Joint Surg Br 2004;
86(7): 939-946.
46. van Dijk CN. Hindfoot Endoscopy. Sports
Med Arthrosc Rev 2000; 8: 365-371.
47. van Dijk CN, Kort N. Tendoscopy of the
peroneal tendons. Arthroscopy 1998; 14(5):
471-478.
48. van Dijk CN, Kort N, Scholten PE. Tendoscopy
of the posterior tibial tendon. Arthroscopy
1997; 13(6): 692-698.
49. van Dijk CN, Scholten PE, Kort N. Tendos-
copy (tendon sheath endoscopy) for overuse
tendon injuries. Oper Techn Sports Med
1997; 5: 170-178.
50. van Dijk CN, Scholten PE, Krips R. A 2-portal
endoscopic approach for diagnosis and
treatment of posterior ankle pathology.
Arthroscopy 2000; 16(8): 871-876.
51. Vega J, Cabestany JM, Golano P, Perez-Carro
L. Endoscopic treatment for chronic Achilles
tendinopathy. Foot Ankle Surg 2008; 14(4):
204-210.
52. Willberg L, Sunding K, Ohberg L, Forssblad
M, Alfredson H. Treatment of Jumper’s knee:
promising short-term results in a pilot study
using a new arthroscopic approach based
on imaging findings. Knee Surg Sports
Traumatol Arthrosc 2007; 15(5): 676-681.
53. Williams JG. Achilles tendon lesions in sport.
Sports Med 1993; 16(3): 216-220.
54. Yao L, Tong DJ, Cracchiolo A, Seeger LL.
MR findings in peroneal tendonopathy. J
Comput Assist Tomogr 1995; 19(3): 460-464.
Chapter 6
The plantaris tendon and a potential role in midportion
Achilles tendinopathy: an observational anatomical study
MN van Sterkenburg
GMMJ Kerkhoffs
RP Kleipool
CN van Dijk
J Anat 2011; 218: 336-341
108
ABstrAct
The source of pain and the background to the pain mechanisms associated with midportion
Achilles tendinopathy have not yet been clarified. Intratendinous degenerative changes are
most often addressed when present. However, it is questionable if degeneration of the ten-
don itself is the main cause of pain. Pain is often most prominent on the medial side, 2-7 cm
from the insertion onto the calcaneus. The medial location of the pain has been explained to
be caused by enhanced stress on the calcaneal tendon due to hyperpronation. However, on
this medial side the plantaris tendon is also located. It has been postulated that the plantaris
tendon might play a role in these medially located symptoms. To our knowledge, the exact
anatomy and relationship between plantaris- and calcaneal tendon at the level of complaints
have not been anatomically assessed. This was the purpose of our study. One-hundred and
seven lower extremities were dissected. After opening the superficial fascia and paraten-
don, the plantaris tendon was bluntly released from the calcaneal tendon moving distally.
Incidence of the plantaris tendon, its course, site of insertion and possible connections were
documented. When with manual force the plantaris tendon could not be released, it was
defined as a ‘connection’ with the calcaneal tendon. In all specimens a plantaris tendon
was identified. Nine different sites of insertion were found, mostly medial and fan-shaped
onto the calcaneus. In 11 specimens (10%) firm connections were found at the level of the
calcaneal tendon midportion. Clinical and histological studies are needed to confirm the role
of the plantaris tendon in midportion Achilles tendinopathy.
Ch
apter 6
The p
lantaris ten
do
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d a p
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mid
po
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Ach
illes tend
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109
iNtroDUctioN
Midportion Achilles tendinopathy is an entity that is generally difficult to treat. Peritendinous
and intratendinous changes seem to co-exist in the majority of patients29. The source of
pain and the background to the pain mechanisms associated with midportion Achilles tendi-
nopathy have not yet been clarified17. Therefore, a wide range of conservative and surgical
treatments is available, addressing different possible contributing properties of the tendon
and its surrounding tissues. Why surgery promotes healing of the Achilles tendon is still not
understood22. Intratendinous degenerative changes are most often addressed when present.
However, it is questionable if degeneration of the tendon itself is the main cause of pain,
since intratendinous changes are found in up to 34% of people without complaints8,12,14,15.
Recently a long-term follow-up study was published revealing persistent structural abnor-
malities and thickening of the tendon 13 years after intra-tendon surgery for midportion
Achilles tendinopathy, whereas all patients were satisfied with the results and went back to
calcaneal tendon loading activities without restrictions1.
Pain is the main symptom that leads a patient to seek medical help. It is often most
prominent at 2-7 cm from the insertion onto the calcaneus on the medial side26. Most
ultrasonographic midportion disorders (91-100%) are found in this medial segment of the
tendon7,10. It has been proposed that the medial pain is caused by enhanced stress on the
calcaneal tendon due to hyperpronation. However, on this medial side the plantaris tendon
is also located. It is enclosed in a paratendon collectively with the calcaneal tendon. Steenstra
and co-workers described that during Achilles tendoscopy for patients with symptomatic
Achilles tendinopathy, the plantaris tendon was fixed to the Achilles tendon at the level of
complaints. Where in a normal situation the plantaris tendon can glide in relation to the
Achilles tendon, it was postulated that the plantaris tendon plays a role in these medially
located symptoms28.
To our knowledge, the exact anatomy and relationship between the anatomical structures
at the level of midportion calcaneal tendon complaints have not been assessed. This was the
purpose of our study.
methoDs
SpecimensOne hundred and seven lower extremities were obtained from donors. During their lives
the donors signed informed consent for the use of their bodies for scientific or educational
purposes. Twenty six were fresh-frozen (– 200) and thawed at room temperature for dissec-
tion. Eighty-one had been fixated in formalin. Sixty-two were male legs, 37 female and of 8
this information was not available. History was unknown. Mean age was 84 years (SD±9.3).
110
Fifty-three left (49.5%)-, and 54 (50.5%) right lower legs were dissected. Of 22 specimens
both legs were available (n=44), 63 were unilateral.
Anatomical dissectionDissection was done by two observers. A longitudinal incision though the skin and subcu-
taneous tissue was made from the condylus medialis femoris to the medial distal 1/3 of the
calcaneus, after which it was lengthened perpendicularly to the lateral side of the calcaneus.
After opening the superficial fascia and paratendon, the midportion of the calcaneal tendon
was inspected. Distally the plantaris tendon was not always visible; when searched for proxi-
mally after bluntly releasing the fascia between the medial belly of the gastrocnemius muscle
and the soleus muscle, it could always be identified. After this it was released by hand from
the calcaneal tendon moving distally (Figure 1).
When with maximum manual pulling force the plantaris tendon could not be released
from the calcaneal tendon, it was defined as an attachment to the calcaneal tendon. Loca-
tion of the attachment in relation to the insertion of the calcaneal tendon was measured with
a millimetre precise ruler.
Figure 1. Technique of identification of plantaris tendon (A) The skin, subcutaneous layers, superficial fascia and paratendon are dissected. (B) The plantaris tendon is identified proximally between the medial head of the gastrocnemius muscle and the soleus muscle. (C,D,E,F) With the index finger, the tendon is released to its distal insertion. Then the insertion is carefully exposed
Ch
apter 6
The p
lantaris ten
do
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d a p
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tial role in
mid
po
rtion
Ach
illes tend
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111
The calcaneal tendon, incidence of the plantaris tendon, their relationships and the site
of the midportion calcaneal tendon and of the insertion of the plantaris tendon onto the
calcaneus were documented.
resULts
One- hundred and seven lower legs were dissected.
In 96 specimens the calcaneal tendon and plantaris tendon run separately and can glide
in relation with each other. In the other 11 specimens we found a firm attachment of the
plantaris tendon to the calcaneal tendon; in 6 of 26 fresh frozen specimens (23%), and in 5
of 81 formalin fixated specimens. In 3 specimens the plantaris- and calcaneal tendon were
held together by a retinaculum- like structure, transversally constricting the calcaneal and
plantaris tendon 32-88 millimetres (mm) proximal to the insertion (Figure 2); in 3 specimens
the plantaris tendon inserted on the midportion of the calcaneal tendon at 20- 65 mm
proximal to the calcaneal insertion of the calcaneal tendon; two inserted into the deep
fascia; 2 adhered onto the anteromedial- and one onto the anterior side of the calcaneal
tendon by cords of solid tissue but inserted into the calcaneus. The macroscopic image of a
retinaculum-like structure made us consider this as being prone to pathology (Figure 2). Four
of 11 attachments were in legs of which the other side was also available; however, none of
the connections were bilateral.
In all specimens a plantaris tendon was identified (100%).
We found 9 different sites of insertion of the plantaris tendon, which are described and
depicted in figure 3. In only 14% of 22 paired legs (3 pairs) site of insertion on the left leg
was identical to that of the right.
Figure 2. A firm attachment between the calcaneal - and plantaris tendons at the midportion level of the Achilles tendon. This type was named ‘retinaculum-like’
112
DiscUssioN
In 11 specimens a firm connection between calcaneal - and plantaris tendon was found, at
the level of the midportion of the calcaneal tendon. This corresponds to the level at which
complaints in patients with midportion Achilles tendinopathy are present. In 3 other speci-
mens (2.8%) the plantaris tendon inserted into the calcaneal tendon. This variance has been
described before6. On the contrary, the firm connections (10%) between the plantaris- and
calcaneal tendon have not been described before. We however found connections in 10% of
our specimens. How then can we explain these findings? One way could be that these con-
nections are congenital or an anatomical variation. Another explanation could be that these
connections have developed later in life. We do not have a history of our specimens and
thus we do not know whether they were symptomatic or not. Degenerative changes in the
calcaneal tendon have been found in up to 34% of subjects without complaints1,8,12,14,15.
If peritendinous adhesions occur secondary to intratendinous changes, this can offer an
explanation for the connections and adhesions that we found. Development later on in life
Figure 3. Sites of insertion of the plantaris tendon
Ch
apter 6
The p
lantaris ten
do
n an
d a p
oten
tial role in
mid
po
rtion
Ach
illes tend
ino
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113
Figure 4. Degree of rotation and position of the gastrocnemius-soleus complex at the midportion of the calcaneal tendon. (GC= gastrocnemius; S= soleus.) The most common (52%) position is depicted in (A), (B) occurs in 35%, and (C) in 13%. In all situations, the soleus fibres are positioned medially. The location of the plantaris tendon is shown (PT) (Illustration as adapted from Cummins and co-workers4)
seems to be the most likely explanation of this high percentage of a firm connection between
the plantaris- and calcaneal tendon at the midportion level.
Now could these connections between calcaneal-and plantaris tendon explain the medial
pain in midportion Achilles tendinopathy? We aimed to theorize this by applying anatomical
and pathophysiological evidence.
The calcaneal tendon consists of the fibers of two muscle units in the superficial compart-
ment of the posterior leg: the gastrocnemius muscle (medial and lateral head) and the soleus
muscle. The gastrocnemius muscle crosses the knee and ankle joints (ankle and subtalar);
originating from the posterior surface of condylus medialis and -lateralis femoris and insert-
ing onto the calcaneus. The soleus muscle lies anterior to the gastrocnemius muscle and
originates from each side of the anterior aponeurosis attached to the tibia and fibula, and
from the posterior surfaces of the head of the fibula and its proximal quarter, as well as the
middle third of the medial border of the tibia. The soleus muscle only crosses the 2 ankle
joints. Distally, both the gastrocnemius and soleus muscles form an aponeurosis, from each
of which a tendon originates. At about the level where the soleus contributes fibers to the
calcaneal tendon, rotation of the tendon begins and becomes more marked in the distal 5-6
cm. The gastrocnemius fibers rotate to lateral and the soleus fibers are positioned medial to
the insertion20. This anatomical observation means that the medial portion of the calcaneal
tendon, where pain is often most prominent, is bi-articular since it consists of fibers originat-
ing from the soleus muscle (Figure 4). The calcaneal tendon is involved in plantarflexion,
whereas according to its anatomical course, the tri-articular plantaris tendon also contributes
114
to ankle inversion. These opposite forces result in an intermittent small change of position
between calcaneal - and plantaris tendon which occurs with every step.
Unlike other tendons in the leg, the Achilles tendon lacks a synovial sheath. Instead, it has a
paratendon, which is an array of thin, fibrous tissue containing blood vessels23. In patients
with symptomatic Achilles tendinopathy, enhanced neurovascular growth from the para-
tendon into the calcaneal tendon in an attempt to repair the tendon proper is seen. Also
myofibroblasts responsible for the formation of permanent scarring and the shrinkage of
peritendinous tissue have been shown. The plantaris tendon runs with the calcaneal tendon
inside a collective paratendon. With the development of scarring and shrinkage of periten-
dinous tissue, the calcaneal - and plantaris tendon will adhere. The opposite movements
between plantaris- and calcaneal tendon will result in traction to the firm peritendinous tissue
that connects both tendons and the level of the tendinopathy. This tissue has recently been
described to be richly innervated by neonerves which may be involved in causing pain2,24.
Pain then aggravates with movement, given the fact that the traction forces occur with every
step with an average of 5,000 - 12,500 steps/ day30,31.
There are 2 drawbacks to our study. Histological examination would have provided us with
more information on the nature of the connections, and is necessary to gain more relevant
data for conclusions concerning a potential role in midportion Achilles tendinopathy. Another
drawback is the fact that age and former lifestyle of our specimens did not match with the
group of active 30 to 50 year-olds in which midportion Achilles tendinopathy most often
occurs.
The consequences of formalin fixation are yet unknown. It may alter the properties of
soft tissue structures, making blunt division of calcaneal- and plantaris tendons easier, con-
sequently missing possible connections. We found 23% of connections in fresh-frozen but
only 6% in formalin- fixated specimens. Larger numbers of specimens may be needed to
substantiate this finding. Dissection of exclusively fresh frozen specimens might have been
beneficial since this may be the closest we can get to in vivo tissue texture.
A strinking finding was that, as opposed to the widely accepted rule that in a large sample of
patients a number of plantaris muscles/tendons is missing, in all our 107 specimens a plan-
taris tendon was identified. According to previous anatomical studies with large numbers of
specimens, the plantaris tendon is absent in a number of cases (7-20%)5,6,9,11,19,25. Daseler
found in 542 pairs of legs that in 9 the right plantaris tendon was absent, and in 21 the left.
Moreover, in 31 pairs the plantaris muscle could not be identified. Harvey and co-workers
noted the absence of plantaris in 18.2% of 658 lower limb dissections13.
These earlier findings of absence in anatomical studies could be attributable to the tech-
nique of dissection. In our 5 cases where the tendon inserted into the calcaneal tendon,
Ch
apter 6
The p
lantaris ten
do
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d a p
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mid
po
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Ach
illes tend
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115
Figure 5. (A) Anatomical course of the plantaris tendon according to Sobotta Anatomy; (B) course found during 107 dissections
anterior to the tendon on the calcaneus and in the crural fascia (4.6%), the plantaris
tendon could not be identified distally (Figure 3). We started our dissection between the
gastrocnemius and soleus muscles (Figure 1), and identified a plantaris tendon in all our
specimens. Unfortunately only two studies specified their dissection techniques. Freeman
and co-workers (13% absence) specifically aim for the muscle belly dissecting the proximal
dorsal compartment of the lower leg; Harvey (18.2% absence) mentions not dissecting the
lower legs all the way to proximal13. With our relatively large group of specimens, we not
only contradict earlier findings of its absence, but also raise implications for daily practise.
The plantaris tendon is often used for grafting because it can be sacrificed without markable
deficit, and is of adequate length and thickness for most applications3,16,18,27. It is often
excised from distally. In this case it will be missed in a substantial number of cases. We advise
to retrieve it more proximally (e.g. with a tendon stripper). Using ultrasound- or MR- imaging
prior to surgery to pre-assess its course may be helpful.
Another discrepancy with the existing knowledge was the mid-course of the plantaris tendon
in the posterior compartment of the lower leg.
According to Sobotta Anatomy21, the plantaris tendon instantly crosses the posterior side
of the calf, to run medial with the calcaneal tendon until its insertion (Figure 5). In our
observations the plantaris tendon along its course gradually crosses the calf between the
gastrocnemius and the soleus muscle.
116
With this study we can theorize but not confirm that the plantaris tendon plays a role in
complaints in patients with midportion Achilles tendinopathy. However, we do know more
about the course and insertion of the plantaris tendon. Interesting and unexpected find-
ings were the firm connections between plantaris- and calcaneal tendon at the level of in
midportion of the calcaneal tendon in 10% of specimens. Clinical studies on the outcome
of surgically removing plantaris tendons and thereby severing adhesions and accompanying
enhanced neurovascular growth from the paratendon at the medial side of the calcaneal
tendon may provide us with more evidence on the relation between the plantaris tendon and
symptomatic midportion Achilles tendinopathy.
AckNowLeDGemeNts
The authors would like to thank the Department of Anatomy & Embryology, particularly Mrs.
C.G.J. Cleypool, and the Department of Pathology for facilitating the dissections.
Ch
apter 6
The p
lantaris ten
do
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mid
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Ach
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117
refereNce List
1. Alfredson H, Zeisig E, Fahlstrom M. No
normalisation of the tendon structure and
thickness after intratendinous surgery for
chronic painful midportion Achilles tendino-
sis. Br J Sports Med 2009; 43(12): 948-949.
2. Andersson G, Danielson P, Alfredson H,
Forsgren S. Nerve-related characteristics
of ventral paratendinous tissue in chronic
Achilles tendinosis. Knee Surg Sports Trau-
matol Arthrosc 2007; 15(10): 1272-1279.
3. Bertelli JA, Santos MA, Kechele PR, Rost
JR, Tacca CP. Flexor tendon grafting using
a plantaris tendon with a fragment of
attached bone for fixation to the distal
phalanx: a preliminary cohort study. J Hand
Surg Am 2007; 32(10): 1543-1548.
4. Cummins EJ, Anson JB, Carr WB. The struc-
ture of the calcaneal tendon [of Achilles] in
relation to orthopedic surgery with addi-
tional observations on the plantaris muscle.
Surg Gynecol Obstet 1946; 83: 107-110.
5. Danforth CH. The Heredity of Unilateral
Variations in Man. Genetics 1923; 9: 199-
210.
6. Daseler EH. The Plantaris Muscle: An Ana-
tomical Study of 750 Specimens. J Bone
Joint Surg 1943; 25: 822-827.
7. de Vos RJ, Heijboer MP, Weinans H, Verhaar
JA, van Schie H.T. Tendon Structure is Not
Related to Clinical Outcome Following
Eccentric Exercises in Chronic Mid-Portion
Achilles Tendinopathy. Unpublished results.
8. Emerson C, Morrissey D, Perry M, Jalan
R. Ultrasonographically detected changes
in Achilles tendons and self reported
symptoms in elite gymnasts compared with
controls - An observational study. Man Ther
2010; 15(1): 37-42.
9. Freeman AJ, Jacobson NA, Fogg QA. Ana-
tomical variations of the plantaris muscle
and a potential role in patellofemoral pain
syndrome. Clin Anat 2008; 21(2): 178-181.
10. Gibbon WW, Cooper JR, Radcliffe GS.
Sonographic incidence of tendon microtears
in athletes with chronic Achilles tendinosis.
Br J Sports Med 1999; 33(2): 129-130.
11. Gruber W. Beobachtungen aus der Men-
schlichen und Vergleichenden Anatomie.
1879. Berlin, A. Hirschwald.
12. Haims AH, Schweitzer ME, Patel RS, Hecht
P, Wapner KL. MR imaging of the Achilles
tendon: overlap of findings in symptomatic
and asymptomatic individuals. Skeletal
Radiol 2000; 29(11): 640-645.
13. Harvey FJ, Chu G, Harvey PM. Surgical avail-
ability of the plantaris tendon. J Hand Surg
[Am ] 1983; 8(3): 243-247.
14. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73(10): 1507-1525.
15. Khan KM, Forster BB, Robinson J et al. Are
ultrasound and magnetic resonance imag-
ing of value in assessment of Achilles tendon
disorders? A two year prospective study. Br J
Sports Med 2003; 37(2): 149-153.
16. Lynn TA. Repair of the torn achilles tendon,
using the plantaris tendon as a reinforcing
membrane. J Bone Joint Surg Am 1966;
48(2): 268-272.
17. Maffulli N, Sharma P, Luscombe KL. Achilles
tendinopathy: aetiology and management. J
R Soc Med 2004; 97(10): 472-476.
18. Morrison WA, Schlicht SM. The plantaris
tendon as a tendo-osseous graft. Part II.
Clinical studies. J Hand Surg Br 1992; 17(4):
471-475.
19. Moss ALH. Is There an Association Between
an Absence of Palmaris Longus Tendon and
an Absence of Plantaris Tendon? Eur J Plast
Surg 1988; 11: 32-34.
20. O’Brien M. The anatomy of the Achilles ten-
don. Foot Ankle Clin 2005; 10(2): 225-238.
21. Putz R, Pabst R. Sobotta Atlas of Human
Anatomy. 12 (English) ed. Urban and
Schwarzenberg; 1994.
22. Sandmeier R, Renstrom PA. Diagnosis and
treatment of chronic tendon disorders in
118
sports. Scand J Med Sci Sports 1997; 7(2):
96-106.
23. Saxena A, Bareither D. Magnetic resonance
and cadaveric findings of the “watershed
band” of the achilles tendon. J Foot Ankle
Surg 2001; 40(3): 132-136.
24. Schubert TE, Weidler C, Lerch K, Hofstadter
F, Straub RH. Achilles tendinosis is associated
with sprouting of substance P positive nerve
fibres. Ann Rheum Dis 2005; 64(7): 1083-
1086.
25. Schwalbe, Pfitzner. Varietäten-Statistik und
Anthropologie. Deutsche Med Wchnschr
1894; XXV(3): 459.
26. Segesser B, Goesele A, Renggli P. [The
Achilles tendon in sports]. Orthopade 1995;
24(3): 252-267.
27. Shuhaiber JH, Shuhaiber HH. Plantaris ten-
don graft for atrioventricular valve repair: a
novel hypothetical technique. Tex Heart Inst
J 2003; 30(1): 42-44.
28. Steenstra F, van Dijk CN. Achilles tendos-
copy. Foot Ankle Clin 2006; 11(2): 429-38.
29. Tan SC, Chan O. Achilles and patellar
tendinopathy: current understanding of
pathophysiology and management. Disabil
Rehabil 2008; 30(20-22): 1608-1615.
30. Tudor-Locke C, Bassett DR, Jr. How many
steps/day are enough? Preliminary pedom-
eter indices for public health. Sports Med
2004; 34(1): 1-8.
31. Tudor-Locke C, Hatano Y, Pangrazi RP,
Kang M. Revisiting “how many steps are
enough?”. Med Sci Sports Exerc 2008; 40(7
Suppl): S537-S543.
Chapter 7
Good outcome after stripping the plantaris tendon in patients
with chronic midportion Achilles tendinopathy
MN van Sterkenburg
GMMJ Kerkhoffs
CN van Dijk
Knee Surg Sports Traumatol Arthrosc 2011;19:1362-1366
122
ABstrAct
PurposeAchilles tendinopathy is a problem that is generally difficult to treat. The pain is frequently
most prominent on the medial side of the midportion of the tendon, where the plantaris
tendon is running parallel to the Achilles tendon. The purpose of this study was to assess if
excision of the plantaris tendon would relieve symptoms.
MethodsThree patients with pain and stiffness at the midportion of the Achilles tendon were treated
by excision of the plantaris tendon. Pre-operatively these patients experienced recognisable
tenderness on palpation of the medial side of the midportion of the Achilles tendon with
localized nodular thickening at 4-7 cm proximal to the insertion. MRI indicated Achilles
tendinopathy with involvement of the plantaris tendon.
ResultsThe plantaris tendon was bluntly retrieved and excised with a tendon stripper through a 3 cm
incision in the proximal calf. We report a good to excellent outcome of this novel procedure
in 3 patients with chronic midportion Achilles tendinopathy.
ConclusionThe medial pain might be based on involvement of the plantaris tendon in the process.
Ch
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iNtroDUctioN
Midportion Achilles tendinopathy is generally difficult to treat. The source of pain and the
background to the pain mechanisms associated with it have not been scientifically clarified15.
Isolated symptomatic tendinopathy is rare, most often the paratenon is involved28. A wide
range of conservative and surgical treatments is available. The role of surgery is still not
fully understood22. Most operative procedures are directed at the Achilles tendon itself. The
intratendinous degenerative changes are incised or excised. It is questionable however if
degeneration of the tendon itself is the main cause of the pain in midportion tendinopathy.
Morphologic and degenerative changes in the Achilles tendon seem to be a part of aging
and in many cases there is no correlation with symptoms25,29. Several studies have reported
intratendinous changes in up to 34% of cadaver specimens, ultrasound- and MRI images of
patients without complaints6,7,9,10,30. Recently a long-term follow-up study was published by
Alfredson et al. revealing persistent structural abnormalities and thickening of the tendon 13
years after intratendinous surgery for Achilles tendinopathy, whereas all patients were satis-
fied with the results and went back to Achilles tendon loading activities without restrictions1.
In patients with a painful nodular thickening in the Achilles tendon, the pain is often most
prominent on the medial side of the midportion Achilles tendon24. At this level the plantaris
tendon runs closely with- and parallel to the Achilles tendon. An inflammatory response of
the paratenon (located around the Achilles- and plantaris tendon) at the level of the painful
nodule may result in adhesions between plantaris- and Achilles tendon. We hypothesize that
the medial pain may be caused by these adhesions. If this hypothesis were to be correct,
isolated stripping or release of the plantaris tendon would be sufficient to relieve complaints.
This paper reports on a novel technique of isolated stripping of the plantaris tendon in 3
patients with chronic midportion Achilles tendinopathy.
methoDs
Three consecutive patients with midportion tendinopathy of the Achilles tendon were
included (2 female, 1 male). Mean age was 47 years (43, 48, and 50). Patients had complaints
of pain and stiffness of the Achilles tendon for a mean of 32 months (11, 37 and 48), with
a palpable painful nodule 4, 6, and 7 centimetres proximal of the insertion of the Achilles
tendon onto the calcaneus. In all 3 patients pain on palpation was predominantly on the
medial side. Conservative treatment had failed and none had had previous hindfoot surgery.
Magnetic Resonance Imaging (MRI) confirmed the clinical diagnosis of Achilles tendinopathy
with involvement of the plantaris tendon in this process.
Visual Analogue Scales (VAS) for pain and function19 and Victorian Institute of Sports Assess-
ment –Achilles (VISA-A) questionnaires20 were filled out by all three patients pre-operatively,
124
6 weeks and 1 year postoperatively. Additionally time to- and level of sport resumption, as
well as 4 point scales for satisfaction (bad, poor, good, excellent) and complaints (more,
same, less, none) were documented.
Surgical procedure The procedure was performed under general or spinal anaesthesia. The patients were placed
in the prone position. A tourniquet was applied. A 4 cm posteromedial incision was made in
the proximal third of the calf. The plane dividing the medial belly of the gastrocnemius muscle
and the soleus muscle was retrieved by blunt dissection. This is where the plantaris tendon
runs in this plane from the posterolateral femoral condyle to the medial calcaneus. The
plantaris tendon was identified, released, and pulled medially for visualization through the
incision. After placing holding sutures, the tendon was transsected and threaded through a
tendon stripper. The stripper was advanced slowly with the leg fully extended, until it passed
the palpable nodule (Figure 1). Then the plantaris tendon was cut distally and removed
Figure 1. Surgical technique. (A) A 4-5 cm incision is made. The plantaris tendon is bluntly identified.and pulled medially for visualization through the incision. (B) A holding suture is placed. (C) The tendon is transsected and threaded through a tendon stripper. (D) The stripper is advanced slowly with the leg fully extended. When the calcaneus is reached the tendon is cut
Ch
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Figure 2. Result; right is the distal portion of the Achilles tendon removed past the adhesions, left (with holding suture) the proximal portion
through the proximal incision (Figure 2). The superficial fascia, subcutaneous tissues and skin
were closed. Aftertreatment consisted of a compression bandage for 2 days. Weight- bearing
was allowed as tolerated.
resULts
All three patients were scheduled for the surgical procedure as explained above. Pre-
operatively VAS for pain was 69, 58 and 59 (mm) respectively. VAS for function was only
taken from case 2 and 3, being 16 and 24 (mm). Pre-operative VISA-A-NL scores were 19,
25 and 45 points.
The first case had a large lower leg for which the stripper was too short, so it was decided
to convert. At the level of the nodule a 3 cm medial longitudinal incision was made and
the superficial fascia was opened. The paratenon was longitudinally dissected. The plantaris
tendon could not be identified at this level because of extensive adhesions. After lengthening
the incision 3 cm to proximal the plantaris tendon came into view. It was cut proximally,
bluntly released distal from the process and resected. Six weeks after the procedure VAS for
pain was 13 (mm), - for function 64 (mm), the VISA-A-NL score measured 64 points. There
were less complaints and a good outcome. After 4 weeks he had resumed sporting activities,
but still on a lower level. At one year follow-up, VAS for pain was 3 (mm), VAS for function
92 (mm) and VISA-A-NL 97. There were no complaints and excellent outcome playing sports
after 6 weeks at a higher level than pre-operatively.
The second case went without technical problems. The plantaris tendon was histologically
examined and showed signs of chronic inflammation. Six weeks postoperatively she had less
complaints and an excellent subjective outcome. VAS for pain was 17 (mm), - for function 78
(mm) and VISA-A-NL measured 55 points. After one year she reported less complaints and
excellent outcome, with VAS for pain of 4 (mm), for function 95 (mm) and VISA-A-NL 55. As
the VISA-A accredits 45 out of 100 points to sports, this patient could not score higher than
55 points as she was not sports active.
In the third case, the connection between Achilles- and plantaris tendon was so tight
that the stripper could not pass the process and the plantaris tendon ruptured proximal to
this process. It was decided to end the procedure. Histology obviously showed no signs of
pathology. On 6 weeks follow- up she had less complaints and was moderately satisfied with
126
the surgery. VAS for pain measured 0 (mm), for function 98 (mm), and VISA-A-NL scored
77 points. She resumed her sporting activities after 6 weeks at the same level as before
complaints. After one year she reported no complaints and a good outcome with VAS for
pain of 0 points (mm), - for function 100 (mm) and VISA-A-NL outcome of 91 points.
DiscUssioN
The most important finding of our study was that all patients had a good outcome with strip-
ping of the plantaris tendon only. A new surgical technique to relieve symptoms in patients
with midportion Achilles tendinopathy with pain predominantly located on the medial side
of the Achilles tendon is reported. Involvement of the plantaris tendon in the pathological
process was confirmed on MRI.
How can removal of this possibly rudimentary plantaris tendon relieve the often recalci-
trant complaints? The plantaris tendon lies posterior to the knee joint, originating from the
inferior part of the lateral supracondylar line of the femur. Its tendon travels inferomedially,
posterior to the soleus muscle and anterior to the medial gastrocnemius muscle. The tendon
crosses the calf relatively proximal, running medial from, and parallel with the Achilles tendon
from the midportion of the calf; in the majority of cases ultimately inserting medially onto
the calcaneus5, 8. The plantaris muscle-tendon complex is a weak ankle- and knee flexor and
ankle invertor. Additionally, the medial portion of the Achilles tendon consists solely of the
soleus tendon since at about the level where the soleus contributes fibers to the Achilles
tendon, rotation of the tendon begins. Gastrocnemius fibers are therefore positioned lateral-
and soleus fibers medial of the insertion. The soleus is biarticular (ankle- and subtalar joints).
The plantaris tendon runs medial to it.
In a healthy situation the plantaris tendon can move freely in relation to the Achilles
tendon, however an inflammatory response of the paratenon may cause adhesions between
plantaris- and Achilles tendon. Adhesions cause the mechanical problem of obstruction as
the plantaris muscle-tendon complex not only causes flexion but also inversion, whereas the
triceps surae is a flexor only. Although the movement between the two is limited, traction
onto the surrounding paratenon will take place with every step. Chronic painful tendons
have been shown to exhibit new ingrowth of sensory nerve fibers from the paratenon12,23.
Repetitive traction onto this richly innervated area might explain the pain and stiffness during
and after walking. On the basis of this theory, symptom relief in our 3 cases is probably
caused by discontinuing the proximally directed drawing forces of the plantaris tendon from
its distal adhesion onto the Achilles tendon.
Another explanation for the pain relief might be ‘denervation’. As seen in studies on various
species, it is shown that the nerves to the Achilles tendon have in part a cutaneous origin,
including the sural nerve, and an origin from the associated muscles2,3,27. The healthy Achilles
Ch
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127
tendon proper is superficially innervated by the paratenon, but does not seem to have a rich
nervous supply itself2. The healthy tendon proper is normally aneuronal; conversely chronic
painful tendons have been shown to exhibit new ingrowth of sensory nerve fibers from the
paratenon into the tendon proper12,23. Can pain yet originate from the Achilles tendon itself
or is it caused by this nerve ingrowth from the paratenon2?
With many surgical procedures for recalcitrant Achilles tendinopathy of the tendon proper
the paratenon is released or removed. In open surgical debridement of the tendon proper the
paratenon has to be opened11,14,21, and during minimally invasive tenotomy the paratenon is
also addressed. Paratendinopathy and tendinopathy often co-exist, but in some procedures
only the peritendinous structures are addressed, such as in open or minimally invasive parate-
nectomy13,18 and Achilles tendoscopy17,26. These procedures all render good to excellent
results in 75-100% of patients. The pain relief can probably be explained by destruction of
these sensory nerves running from the paratenon into the Achilles tendon proper. When
stripping the plantaris tendon, the paratenon is also being released since plantaris- and
Achilles tendon run together within one paratenon. If pain can be relieved which isolated
release of the paratenon, surgery of the tendon proper and consequently major tendon
reconstruction becomes redundant. The advantages of a minimal invasive approach are clear
and consist of decreased peri- operative morbidity, decreased duration of hospital stay, and
reduced costs4,13,16.
There are two major limitations to our study. To advocate this technique for everyday
practise more patients are needed. The technique also needs to be optimized, e.g. the plan-
taris tendon should be identified more distally (but still proximal from the nodular thickening
in the Achilles tendon) or a longer tendon stripper is needed to avoid conversion of the
technique as in case 1.
coNcLUsioN
A good to excellent outcome of stripping tendon in 3 patients with chronic midportion Achil-
les tendinopathy is reported. The medial location of pain at physical examination might be
based on involvement of the plantaris tendon in the process. More patients and optimization
of the surgical procedure are needed to advocate this technique for everyday practise and to
support this novel approach to the pathogenesis of chronic midportion Achilles tendinopathy.
128
refereNce List
1. Alfredson H, Zeisig E, Fahlstrom M. No
normalisation of the tendon structure and
thickness after intratendinous surgery for
chronic painful midportion Achilles tendino-
sis. Br J Sports Med 2009; 43: 948-949.
2. Andersson G, Danielson P, Alfredson H,
Forsgren S. Nerve-related characteristics
of ventral paratendinous tissue in chronic
Achilles tendinosis. Knee Surg Sports Trau-
matol Arthrosc 2007; 15(10): 1272-1279.
3. Andres KH, von DM, Schmidt RF. Sensory
innervation of the Achilles tendon by group
III and IV afferent fibers. Anat Embryol (Berl)
1985; 172(2): 145-156.
4. Carmont MR, Maffulli N. Less invasive Achil-
les tendon reconstruction. BMC Musculosk-
elet Disord 2007; 8: 100.
5. Daseler EH. The Plantaris Muscle: An Ana-
tomical Study of 750 Specimens. J Bone
Joint Surg 1943; 25: 822-827.
6. Emerson C, Morrissey D, Perry M, Jalan
R. Ultrasonographically detected changes
in Achilles tendons and self reported
symptoms in elite gymnasts compared with
controls - An observational study. Man Ther
2010; 15: 37-42.
7. Haims AH, Schweitzer ME, Patel RS, Hecht
P, Wapner KL. MR imaging of the Achilles
tendon: overlap of findings in symptomatic
and asymptomatic individuals. Skeletal
Radiol 2000; 29(11): 640-645.
8. Harvey FJ, Chu G, Harvey PM. Surgical avail-
ability of the plantaris tendon. J Hand Surg
[Am ] 1983; 8(3): 243-247.
9. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73(10): 1507-1525.
10. Khan KM, Forster BB, Robinson J et al. Are
ultrasound and magnetic resonance imag-
ing of value in assessment of Achilles tendon
disorders? A two year prospective study. Br J
Sports Med 2003; 37(2): 149-153.
11. Kvist H, Kvist M. The operative treatment of
chronic calcaneal paratenonitis. J Bone Joint
Surg Br 1980; 62(3): 353-357.
12. Lian O, Dahl J, Ackermann PW, Frihagen F,
Engebretsen L, Bahr R. Pronociceptive and
antinociceptive neuromediators in patellar
tendinopathy. Am J Sports Med 2006;
34(11): 1801-1808.
13. Longo UG, Ramamurthy C, Denaro V,
Maffulli N. Minimally invasive stripping for
chronic Achilles tendinopathy. Disabil Reha-
bil 2008; 30(20-22): 1709-1713.
14. Maffulli N, Binfield PM, Moore D, King JB.
Surgical decompression of chronic central
core lesions of the Achilles tendon. Am J
Sports Med 1999; 27(6): 747-752.
15. Maffulli N, Sharma P, Luscombe KL. Achilles
tendinopathy: aetiology and management. J
R Soc Med 2004; 97(10): 472-476.
16. Maffulli N, Testa V, Capasso G, Bifulco G,
Binfield PM. Results of percutaneous longi-
tudinal tenotomy for Achilles tendinopathy
in middle- and long-distance runners. Am J
Sports Med 1997; 25(6): 835-840.
17. Maquirriain J, Ayerza M, Costa-Paz M,
Muscolo DL. Endoscopic surgery in chronic
achilles tendinopathies: A preliminary
report. Arthroscopy 2002; 18(3): 298-303.
18. Nelen G, Martens M, Burssens A. Surgical
treatment of chronic Achilles tendinitis. Am
J Sports Med 1989; 17(6): 754-759.
19. Price DD, McGrath PA, Rafii A, Buckingham
B. The validation of visual analogue scales
as ratio scale measures for chronic and
experimental pain. Pain 1983; 17(1): 45-56.
20. Robinson JM, Cook JL, Purdam C et al. The
VISA-A questionnaire: a valid and reliable
index of the clinical severity of Achilles
tendinopathy. Br J Sports Med 2001; 35(5):
335-341.
21. Rolf C, Movin T. Etiology, histopathology,
and outcome of surgery in achillodynia. Foot
Ankle Int 1997; 18(9): 565-569.
Ch
apter 7
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od
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tcom
e after stripp
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the p
lantaris ten
do
n in
patien
ts with
chro
nic m
idp
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n A
chilles ten
din
op
athy
129
22. Sandmeier R, Renström PA. Diagnosis and
treatment of chronic tendon disorders in
sports. Scand J Med Sci Sports 1997; 7(2):
96-106.
23. Schubert TE, Weidler C, Lerch K, Hofstadter
F, Straub RH. Achilles tendinosis is associated
with sprouting of substance P positive nerve
fibres. Ann Rheum Dis 2005; 64(7): 1083-
1086.
24. Segesser B, Goesele A, Renggli P. The Achil-
les tendon in sports. Orthopade 1995; 24(3):
252-267.
25. Smith RK, Birch HL, Goodman S, Heinegard
D, Goodship AE. The influence of age-
ing and exercise on tendon growth and
degeneration--hypotheses for the initiation
and prevention of strain-induced tendinopa-
thies. Comp Biochem Physiol A Mol Integr
Physiol 2002; 133(4): 1039-1050.
26. Steenstra F, van Dijk CN. Achilles tendos-
copy. Foot Ankle Clin 2006; 11(2): 429-38.
27. STILWELL DL, Jr. The innervation of tendons
and aponeuroses. Am J Anat 1957; 100(3):
289-317.
28. Tan SC, Chan O. Achilles and patellar
tendinopathy: current understanding of
pathophysiology and management. Disabil
Rehabil 2008; 30(20-22): 1608-1615.
29. Tuite DJ, Renstrom PA, O’Brien M. The aging
tendon. Scand J Med Sci Sports 1997; 7(2):
72-77.
30. van Schie HT, de Vos RJ, de JS et al. Ultraso-
nographic tissue characterisation of human
Achilles tendons: quantification of tendon
structure through a novel non-invasive
approach. Br.J.Sports Med Br J Sports Med
2010; 44(16): 1153-1159.
Chapter 8
Midportion Achilles tendinopathy: why painful?
An Evidence-based philosophy
MN van Sterkenburg
CN van Dijk
Knee Surg Sports Traumatol Arthrosc 2011;19:1367-1375
132
ABstrAct
Chronic midportion Achilles tendinopathy is generally difficult to treat as the background to
the pain mechanisms has not yet been clarified. A wide range of conservative and surgical
treatment options are available. Most address intratendinous degenerative changes when
present, as it is believed that these changes are found responsible for the symptoms. Since
up to 34% of asymptomatic tendons show histopathological changes, we believe that the
tendon proper is not the cause of pain in the majority of patients. Chronic painful tendons
show ingrowth of sensory- and sympathetic nerves from the paratenon with release of noci-
ceptive substances. Denervating the Achilles tendon by release of the paratenon, is sufficient
to cause pain relief in the majority of patients. This type of treatment has the additional
advantage that it is associated with a shorter recovery time when compared to treatment
options that address the tendon itself. An evidence- based philosophy on the cause of pain
in chronic midportion Achilles tendinopathy is presented.
Ch
apter 8
Mid
po
rtion
Ach
illes tend
ino
path
y: wh
y pain
ful?
133
iNtroDUctioN
Chronic Achilles tendon pathology is one of the most frequent injuries in sports involving
running and jumping. In elite long-distance runners there is a lifetime risk of 52% for sustain-
ing an Achilles tendon injury39. Thirty percent of patients have a sedentary lifestyle7.
Chronic midportion Achilles tendinopathy78 is characterized by impaired performance due
to Achilles tendon pain and swelling located typically at 2-7 cm from the insertion onto the
calcaneus48. The source of pain and the background to the pain mechanisms associated with
midportion Achilles tendinopathy have not yet been clarified49. Many different explanations
have been raised. Consequently, a wide range of conservative and surgical treatment options
are available. Most of them address the intratendinous degenerative changes when pres-
ent. Surgical measures include open excision of degenerative tendon. This means that the
intratendinous changes are found responsible for the symptoms. But does the origin of the
pain in these patients indeed rise from the Achilles tendon itself? It is known that the tendon
itself is relatively aneuronal. It is also recognized that intratendinous degenerative changes
often occur without symptoms.
It is hypothesized that the main cause of the pain in patients with symptomatic midpor-
tion Achilles tendinopathy does not arise from the tendon proper but is generated by its sur-
rounding tissues. In this paper, a premise on the cause of pain based on existing knowledge
and personal research is presented.
ANAtomY
The Achilles tendon is the combination of tendons of soleus and gastrocnemius muscles,
inserting approximately halfway the calcaneus. The gastrocnemius muscle crosses the knee,
subtalar and ankle joints; originating from the posterior medial and lateral femoral condyles
and inserting onto the calcaneus. The soleus muscle lies anterior to the gastrocnemius
muscle and originates from the proximal tibia, fibula and interosseous membrane and crosses
the ankle and subtalar joints. Distally, both the gastrocnemius and soleus muscles form an
aponeurosis, from each of which a tendon originates. At about the level where the soleus
contributes fibres to the Achilles tendon, rotation of the tendon begins and becomes more
marked 2-7 cm proximal to the insertion onto the calcaneus. The gastrocnemius fibres rotate
to lateral and the soleus fibres are positioned medial to the insertion9,21,57. Medial to the
Achilles tendon the plantaris tendon is located, originating from the lateral femoral condyle
and inserting onto the medial calcaneus. The Achilles tendon is involved in plantarflexion,
whereas according to its anatomical course, the tri-articular plantaris tendon also contributes
to ankle inversion.
134
The Achilles and plantaris tendon are collectively surrounded by a paratenon, which lies
on an inner layer of endotenon, and exists of a layer of mesotenon and an outer layer of
epitenon.
Tendon consists predominantly of extracellular tissue with low metabolic requirements,
and therefore appears white on macroscopic inspection. This relatively bradytrophic char-
acter enables the tendon to remain under tension for a long period, without the risk of
necrosis or ischemia. The Achilles tendon has 3 sources of vascular supply, which are (1) the
perimyseal vessels at the musculotendinous junction; (2) periosteal vessels at the osteotendi-
nous junction; and (3) vessels around the tendon within the paratenon, forming a capillary
loop system. This last system is the main vascular supply for the Achilles tendon. The neural
supply to the Achilles tendon and the surrounding paratenon is provided by nerves from
the attaching muscles and by small fasciculi from cutaneous nerves, in particular the sural
nerve9,71. The number of nerves and nerve endings is relatively low, and the tendon proper
is relatively aneuronal43,65.
AetioLoGY
A distinction is made between the aetiology of intratendinous degenerative changes and
the aetiology of complaints in patients with midportion Achilles tendinopathy. Causes of
intratendinous changes can be divided into extrinsic and intrinsic factors, but most com-
monly will be a combination of both. Malalignment of the foot, hyperpronation63,68, age45
and chronic disease like diabetes mellitus, obesity and hypertension28 have been described.
Malalignment and hyperpronation impose excessive strain on the Achilles tendon. The aging
tendon loses its elastic properties causing the muscle to work more, resulting in a local rise in
temperature with subsequent tendon changes68.
Inappropriate physical training may also be an important issue37,46 causing degenerative
Achilles tendon changes. Tendons transmit muscle forces to bone, allowing locomotion and
enhancing joint stability. They respond to mechanical forces by changing their metabolism
and their structural and mechanical properties. Appropriate training increases the diameter
and tensile strength of tendons, with tendon fibroblasts increasing the production of collagen
type I42,53,72,75. Training also induces biochemical changes in tendons. Strenuous endurance
training increases collagen turnover and decreases collagen maturation in tendons; exces-
sive mechanical loading is considered a major concern. Repetitive strains below the failure
threshold of the tendon cause tendon micro- injuries38,61. Quality of foot gear and training
surface influencing the alignment and statics of the ankle are also often mentioned as a
cause of intratendinous pathology.
The aetiology of the pain in a patient with midportion Achilles tendinopathy has not
yet been entirely clarified. Pain was believed to be caused by expansion of the Achilles
tendon proper due to increased ground substance and an increased concentration of
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glucosaminoglycans (GAGs). A few years ago the presence of neovascularisation around
symptomatic tendons was raised as the cause of pain; now accompanying nerves with high
concentrations of nociceptive substances (glutamate, substance P, calcitonin gene related
peptide (CGRP)) are also supposed to play a role5,8.
cLiNicAL PreseNtAtioN
Symptoms of a patient with midportion Achilles tendinopathy include painful swelling
typically 2-7 cm proximal to the insertion, and stiffness especially when getting up after a
period of rest. Pain is the main symptom in Achilles tendinopathy that leads a patient to seek
medical help. It is often most prominent 2-7 cm from the insertion onto the calcaneus on the
medial side67. Tendinopathy and paratendinopathy often co-exist64. Intratendinous changes
most often remain asymptomatic35. In these cases a painless swelling at 2-7 cm proximal
to the insertion is the only finding58. In isolated paratendinopathy, there is local thickening
of the paratenon. The area of swelling does not move with dorsiflexion and plantarflexion
of the ankle, where it does in isolated tendinopathy50,69,82. Paratendinopathy can be acute
or chronic. Acute isolated paratendinopathy manifests itself as painful peritendinous crepi-
tus as the tendon glides within the inflamed covering. Areas of increased erythema, local
heat, and asymptomatic palpable tendon nodules or defects may also be present at clinical
examination. In chronic paratendinopathy, exercise-induced pain is the main symptom while
crepitation and swelling diminish.
histoPAthoLoGY
Normal situationMorphologically, healthy tendon is a complex composite material consisting of collagen fibrils
embedded in a matrix of proteoglycans, with a relative small number of cells. Between the
parallel collagen bundles, fibroblasts are arranged, which are the predominant cells within
tendons10. The matrix has tight bundles of long strands of type I collagen, which give the
tendon its inherent strength. Between the collagen is the ground substance, made up of
mainly small proteoglycans and glycosaminoglycan (GAG) chains. In normal tendon, there is
minimal ground substance14.
The paratenon consists of straight bundles of type I and type III collagen fibrils with
straight microfibrillar arrangement and variable diameter23,41. This peritendinous tissue is
lined on its inner surface by synovial cells31,82 and acts as an elastic sleeve permitting the
movement of tendon against the surrounding tissues34. The paratenon serves to carry blood
vessels, lymphatics and nerves.
136
Pathological situationIn contrast with the white appearance of healthy tendon, in tendinopathy they macroscopi-
cally appear grey or yellow-brown and amorphous. Microscopically the tendon shows dis-
rupted collagen, a decrease in the amount of type I collagen and an increase of the amount
of the weak type III collagen which is produced in response to injury and is less able to
bundle. The classical hierarchical structure is lost, there is increased ground substance with a
high concentration of GAGs, more prominent and numerous tenocytes without their normal
fine spindle shape and with more rounded nuclei14,24. Some areas of tendinopathy become
acellular36 or have decreased cell numbers and function14,33.
In the peritendinous tissue in the chronic phase of Achilles tendinopathy 2 types of cells
have been identified: fibroblasts and myofibroblasts41. During biological processes that include
extensive tissue remodelling, fibroblasts may acquire morphological and biochemical features
of contractile cells which have been named myofibroblasts20. The myofibroblasts have stress
fibers composed of α–smooth muscle actin in their cytoplasm and thus are capable of creat-
ing forces required for wound contraction20. In chronic Achilles tendinopathy, these cells are
especially well established at the sites of scar formation, and it is estimated that about 20%
of peritendinous cells are myofibroblasts41. The myofibroblasts synthesize abundant amounts
of collagen and are believed to be responsible for the formation of permanent scarring and
the shrinkage of peritendinous tissue around the tendon30,41. They can induce and maintain
a prolonged contracted state in the peritendinous adhesions around the tendon and thus
influence the development of a contracture30,41. This, in turn may lead to constriction of
vascular channels and to impaired circulation and further contribute to the pathogenesis of
Achilles tendinopathy. The proliferating connective tissue around the Achilles tendon causes
increased intratendinous tension and pressure resulting in increased friction between the
tendon, paratenon, crural fascia, and the skin30.
Vascularity seems increased in tendinopathy, as neovascularisation with thick walls, a
tortuous appearance and small lumen ventral from the Achilles tendon and in the paratenon
is found in 50-88% of symptomatic tendons but not in pain- free tendons18,59,60,80,83.
The healthy Achilles tendon proper is superficially innervated by the paratenon, but
does not have a rich nervous supply itself8. It is normally aneuronal; conversely chronic
painful tendons have been shown to exhibit new ingrowth of nerve fibers accompanying
the peritendinous neovascularisation from the paratenon into the tendon proper43,65. Sen-
sory nerve ingrowth has been observed as a reaction to repetitive loading52 and also as a
response to injury2,4. With this nerve ingrowth, levels of glutamate, calcitonin gene-related
peptide (CGRP) and substance P rise4,8,43,65. These substances are all linked with increased
nociception. Substance P is also associated with vasodilation and stimulates proliferation of
fibroblasts70, possibly causing some of the morphologic changes in Achilles tendinopathy.
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Figure 1A-C. (A) Schematic depiction of normal tendon. (B) Pathological tendon proper. (C) Vasculoneuronal ingrowth from the paratenon into the tendon proper
cAUse of PAiN
Several factors play a role in the cause of pain in a patient with Achilles tendinopathy.
The process starts with localized tendon micro- injury and degeneration which are caused
by ageing and repetitive strain below the failure threshold of the tendon. The most hypovas-
cular region is in the midportion area (2-7 cm from the insertion), where the tendon makes
a marked twist. This is the location where the degeneration and micro-injury most often
occur. Blood flow further declines with ageing and mechanical loading. When the demands
of the tendon are higher than can be managed, micro-injuries develop1. The body reacts
with a repair process, which is adequate in most cases, but inadequate in patients developing
tendinopathy. This inadequate repair causes a repetitive cycle of inadequate collagen and
matrix production, tenocyte disruption, a further decrease of collagen and matrix and an
increased vulnerability to further micro-injuries. Due to the lack of bloodvessels within the
tendon, instead of a chemical- a neurogenic inflammatory process is activated to repair these
microruptures. This neurogenic inflammation occurs in the tissue surrounding the Achilles
tendon. Matrix metalloproteinases (MMPs) responsible for the degradation of extracellular
matrix, cytokines (vascular endothelial growth- factor (VEGF), epidermal growth factor (EGF),
and platelet- derived growth factor (PDGF)) are over- expressed. VEGF promotes angiogen-
esis, upregulates the expression of MMPs and down-regulates tissue inhibitors of metal-
loproteinases (TIMP-3), altering the properties of tendon. Invasion of vessels derived from the
paratenon into a normally hypovascular intratendinous region weakens the normal tendon
structure. When the repair of tendon is inadequate, e.g. due to submission to further loads
without adequate recovery time or a declined blood flow due to ageing, the healing process
fails and the pathogenic cascade leading to symptomatic tendinopathy occurs. The transition
to symptomatic tendinopathy is marked by nerve proliferation accompanying the neovessels.
Vascular ingrowth to repair the defect arises from the paratenon. These bloodvessels are
accompanied by sensory neonerves11,22 (Figure 1), causing an increase in pain signalling by
138
producing nociceptive substances (glutamate, substance P, calcitonin gene related peptide
(CGRP)) past the critical threshold5,8. Neovascularisation has indeed been found to correlate
with the location of pain in patients with symptomatic tendinopathy19. The upregulated
nociceptive substances further damage the tendon by inducing vasodilation, tendon cell
apoptosis and the vicious circle of neurogenic inflammation1,5,8,22,54.
Myofibroblasts proliferate and are transported by the peritendinous blood vessels and neo-
vascularisation into the peritendineum and the tendon proper. Myofibroblasts synthesize
abundant amounts of collagen to repair the tendon proper, but also cause the formation
of scar tissue around the tendon and consequently adhesions of the paratenon onto the
Achilles tendon at the location of the neurovascular ingrowth. Scarring in turn may lead
to constriction of vascular channels and to impaired circulation and further contribute to
the pathogenesis of Achilles tendinopathy, meaning that there is no further action towards
repair.
Vasoconstriction and scarring with mechanical constriction will lead to obliteration of
neovessels. In 20-50% of long lasting tendinopathy patients no neovascularisation is
Figure 2A-D. (A) Adhesion of the paratenon onto the Achilles tendon due to myofibroblast prolif-eration and consequently formation of scar tissue. (B) Continuing ingrowth of vessels and nerves and augmented adhesion (C) Obliteration of neovessels due to constriction. (D) The painful end situation in which neovascularisation has been mostly obliterated but nerve endings persist
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Figure 3. The most common position (52%) of the gastrocnemius-soleus complex at the midportion of the Achilles tendon 15 (PT= plantaris tendon, S= Soleus, GC= Gastrocnemius)
found18,59,60,80,83. Nerves however will survive (Figure 2), secreting glutamate and substance
P causing pain on activity as described earlier.
Reduction of blood flow may also be explained by the fact that pathological tendons exhibit
a decreased occurrence of sympathetic nerve fibres. This reduction in vasoregulatory nor-
adrenalin causes vasoconstriction3.
It has been described that the location of the pain in patients with Achilles tendinopathy is
most often located on the medial side67,69. During Achilles tendoscopy in patients with Achil-
les tendinopathy, it has been observed that at the level of complaints the plantaris tendon
is affixed onto the Achilles tendon on the medial side69 (Figure 3). Some authors describe a
higher medial stress onto the Achilles tendon due to hyperpronation. This is supported by the
finding that most ultrasonographic midportion disorders (91%) are found in the (postero)-
medial segment of the tendon26,79.
In patients with a painful nodular thickening in the Achilles tendon, the pain is often most
prominent on the medial side of the midportion Achilles tendon. At this level the plantaris
tendon runs closely with- and parallel to the Achilles tendon.
The plantaris tendon originally is a knee -and ankle flexor. In primates it attaches to the
plantar aspect of the proximal interphalangeal joints of the toes in primates, explaining its
functionality for grasping with their feet. Darwinists suggest that through evolution in humans
140
the plantaris tendon is rudimental since human beings do not grasp with feet nor swing from
trees any longer. Absence in 7-20% human lower limbs has been reported16,17,25,55,66.
In humans the plantaris muscle is triangularly shaped and lies posterior to the knee joint,
originating from the inferior part of the lateral supracondylar line of the femur. Its tendon
travels inferomedially, posterior to the soleus muscle and anterior to the medial gastroc-
nemius muscle. The tendon crosses the calf relatively proximal, running medial from, and
parallel with the Achilles tendon from the midportion of the calf; in the majority of cases
ultimately inserting medially onto the calcaneus17,27. The plantaris muscle-tendon complex
nowadays is a weak ankle- and knee flexor and ankle invertor.
The medial portion of the Achilles tendon consists solely of the soleus tendon since at
about the level where the soleus contributes fibers to the Achilles tendon (3-11 cm), rotation
of the tendon begins and becomes more marked in the distal 5-6 cm. Gastrocnemius fibers
are therefore positioned lateral- and the soleus fibers on the medial side of the insertion
(Figure 4). The soleus is biarticular (ankle- and subtalar joints). The plantaris tendon runs
anteromedial to it. It is believed that in a healthy situation the plantaris tendon can move
freely in relation to the Achilles tendon. Adhesions between plantaris- and Achilles tendon
can be the results of an inflammatory response of the paratenon, which is located around
the Achilles- and plantaris tendons.
The plantaris muscle-tendon complex not only causes flexion but also inversion, whereas
the triceps surae is a flexor only. Adhesions between both tendons obstruct the opposite
forces of these two bi- and tri-articular muscle groups. Although the movement between the
two will be limited, traction onto the surrounding paratenon will take place with every step
Figure 4A-B. Endoscopic image of a patient with medial pain of his right Achilles tendon due to mid-portion Achilles tendinopathy. On Achilles tendoscopy the paratenon is released from the Achilles ten-don and in this image the plantaris tendon is identified. (A) The plantaris tendon is attached to the Achilles tendon. (B) With a trocar (in this case) the plantaris tendon is released from the Achilles tendon
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Figure 5A-D. The rationale of Achilles tendoscopy. (A) With a blunt trocar the paratenon is released from the Achilles tendon. (B) Thereby the nerves are destructed. (C) The plantaris tendon is cut at the level of complaints. (D) In the weeks postoperative, remnants of nerves obliterate and the proximal end of the plantaris tendon retracts
with a mean of 5,000 - 12,500 steps/ day in people with a low active to active lifestyle76,77.
Chronic painful tendons have been shown to exhibit new ingrowth of sensory nerve fibers
from the paratenon43,65. Repetitive traction onto this richly innervated area might contribute
to the medially located pain and stiffness during and after walking.
sUrGicAL treAtmeNt
Most surgical procedures aim at debridement or tenotomy of the tendon itself. In all these
procedures the paratenon is incised, released or removed as well. In open surgical debride-
ment of the tendon proper the paratenon has to be opened32,40,47,62, and during minimally
invasive tenotomy the paratenon is also addressed. It is therefore uncertain which part
of the procedure is responsible for a possible favourable outcome of such an approach.
Paratendinopathy and tendinopathy often co-exist. In some procedures only peritendinous
structures are addressed, such as in open or minimally invasive paratenectomy44,56 and
Achilles tendoscopy where the paratenon is released and the plantaris tendon cut to relieve
symptoms (Figure 5)51,69. These procedures render good results not in all, but in 75-100%
of patients. Aftertreatment most often is functional and recovery time, although not often
142
described, is 6 weeks to 6 months44,51,69,74. With surgery of the tendon proper, including
minimally invasive tenotomy, the tendon is temporarily weakened. Recovery time until sport
resumption therefore can be extensive and takes 3-18 months12,73,81.
How can the favourable results of addressing the paratenon only in patients with symptom-
atic Achilles tendinopathy be explained? Pain relief could be explained by destruction of the
sensory nerves running from the paratenon into the Achilles tendon proper in these chronic
patients: denervation of the Achilles tendon by releasing the paratenon may be the most
important part of all these procedures.
Positive results obtained from the more invasive conservative treatments may also be contrib-
utable to the destruction of nerve fibres. For example sclerosing injections with Polidocanol
and High Volume Image Guided Injections (HVIGI) aim at obliterating neovessels and the
accompanying nerve fibres6,13,29.
If pain can be relieved with denervation, extensive surgery of the tendon proper becomes
redundant.
coNcLUsioN
The goal of treatment of patients with chronic complaints of midportion Achilles tendinopa-
thy is to relieve pain. Many surgical procedures focus on the debridement of alterations in the
tendon proper. Since up to 34% of asymptomatic tendons show histopathological changes,
it is now believed that the tendon proper is not the cause of pain in the majority of patients
with symptomatic midportion Achilles tendinopathy. Chronic painful tendons show ingrowth
of sensory- and sympathetic nerves from the paratenon with release of nociceptive sub-
stances. Denervating the Achilles tendon by release of the paratenon, is sufficient to cause
pain relief in the majority of patients. This type of treatment has the additional advantage
that it is associated with a shorter recovery time when compared to treatment options that
address the tendon itself.
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refereNce List
1. Abate M, Gravare SK, Siljeholm C et al.
Pathogenesis of tendinopathies: inflam-
mation or degeneration? Arthritis Res Ther
2009; 11(3): 235.
2. Ackermann PW, Ahmed M, Kreicbergs
A. Early nerve regeneration after achilles
tendon rupture--a prerequisite for healing?
A study in the rat. J Orthop Res 2002; 20(4):
849-856.
3. Ackermann PW, Li J, Finn A, Ahmed M,
Kreicbergs A. Autonomic innervation of
tendons, ligaments and joint capsules. A
morphologic and quantitative study in the
rat. J Orthop Res 2001; 19(3): 372-378.
4. Ackermann PW, Li J, Lundeberg T, Kreicbergs
A. Neuronal plasticity in relation to nocicep-
tion and healing of rat achilles tendon. J
Orthop Res 2003; 21(3): 432-441.
5. Alfredson H, Forsgren S, Thorsen K, Fahl-
strom M, Johansson H, Lorentzon R. Gluta-
mate NMDAR1 receptors localised to nerves
in human Achilles tendons. Implications for
treatment? Knee Surg Sports Traumatol
Arthrosc 2001; 9(2): 123-126.
6. Alfredson H, Ohberg L. Sclerosing injections
to areas of neo-vascularisation reduce pain
in chronic Achilles tendinopathy: a double-
blind randomised controlled trial. Knee Surg
Sports Traumatol Arthrosc 2005; 13(4): 338-
344.
7. Ames PR, Longo UG, Denaro V, Maffulli
N. Achilles tendon problems: not just an
orthopaedic issue. Disabil Rehabil 2008;
30(20-22): 1646-1650.
8. Andersson G, Danielson P, Alfredson H,
Forsgren S. Nerve-related characteristics
of ventral paratendinous tissue in chronic
Achilles tendinosis. Knee Surg Sports Trau-
matol Arthrosc 2007; 15(10): 1272-1279.
9. Andres KH, von DM, Schmidt RF. Sensory
innervation of the Achilles tendon by group
III and IV afferent fibers. Anat Embryol (Berl)
1985; 172(2): 145-156.
10. Beason DP, Soslowsky LJ, Karthikey T,
Huard J. Muscle, Tendon, and Ligament. In:
Fischgrund JS, editor. American Academy
of Orthopaedic Surgeons Orthopaedic
Knowledge Update 9. Boston, MA: Bayer
Healthcare; 2009: 35-48.
11. Bjur D, Alfredson H, Forsgren S. The innerva-
tion pattern of the human Achilles tendon:
studies of the normal and tendinosis tendon
with markers for general and sensory
innervation. Cell Tissue Res 2005; 320(1):
201-206.
12. Bohu Y, Lefevre N, Bauer T et al. Surgical
treatment of Achilles tendinopathies in
athletes. Multicenter retrospective series of
open surgery and endoscopic techniques.
Orthop Traumatol Surg Res 2009; 95(8 Suppl
1): S72-S77.
13. Chan O, O’Dowd D, Padhiar N et al. High
volume image guided injections in chronic
Achilles tendinopathy. Disabil Rehabil 2008;
30(20-22): 1697-1708.
14. Cook JL, Khan KM, Purdam C. Achilles ten-
dinopathy. Man Ther 2002; 7(3): 121-130.
15. Cummins EJ, Anson JB, Carr WB. The struc-
ture of the calcaneal tendon [of Achilles] in
relation to orthopedic surgery with addi-
tional observations on the plantaris muscle.
Surg Gynecol Obstet 1946; 83: 107-110.
16. Danforth CH. The Heredity of Unilateral
Variations in Man. Genetics 1923; 9: 199-
210.
17. Daseler EH. The Plantaris Muscle: An Ana-
tomical Study of 750 Specimens. J Bone
Joint Surg 1943; 25: 822-827.
18. de Vos RJ, Weir A, Cobben LP, Tol JL. The
value of power Doppler ultrasonography in
Achilles tendinopathy: a prospective study.
Am J Sports Med 2007; 35(10): 1696-1701.
19. Divani K, Chan O, Padhiar N et al. Site of
maximum neovascularisation correlates with
the site of pain in recalcitrant mid-tendon
Achilles tendinopathy. Man Ther 2010;
15(5): 463-8.
144
20. Ehrlich HP, Desmouliere A, Diegelmann RF et
al. Morphological and immunochemical dif-
ferences between keloid and hypertrophic
scar. Am J Pathol 1994; 145(1): 105-113.
21. Evans NA, Stanish WD. The basic science of
tendon injuries. Curr Orthop 2000; 14: 403-
412.
22. Forsgren S, Danielson P, Alfredson H. Vas-
cular NK-1 receptor occurrence in normal
and chronic painful Achilles and patellar
tendons: studies on chemically unfixed as
well as fixed specimens. Regul Pept 2005;
126(3): 173-181.
23. Franchi M, Quaranta M, De P, V et al. Tendon
crimps and peritendinous tissues responding
to tensional forces. Eur J Histochem 2007; 51
Suppl 1: 9-14.
24. Fredberg U, Stengaard-Pedersen K. Chronic
tendinopathy tissue pathology, pain mecha-
nisms, and etiology with a special focus on
inflammation. Scand J Med Sci Sports 2008;
18(1): 3-15.
25. Freeman AJ, Jacobson NA, Fogg QA. Ana-
tomical variations of the plantaris muscle
and a potential role in patellofemoral pain
syndrome. Clin Anat 2008; 21(2): 178-181.
26. Gibbon WW, Cooper JR, Radcliffe GS. Distri-
bution of sonographically detected tendon
abnormalities in patients with a clinical
diagnosis of chronic achilles tendinosis. J
Clin Ultrasound 2000; 28(2): 61-66.
27. Harvey FJ, Chu G, Harvey PM. Surgical avail-
ability of the plantaris tendon. J Hand Surg
Am 1983; 8(3): 243-247.
28. Holmes GB, Lin J. Etiologic factors associated
with symptomatic achilles tendinopathy.
Foot Ankle Int 2006; 27(11): 952-959.
29. Humphrey J, Chan O, Crisp T et al. The
short-term effects of high volume image
guided injections in resistant non-insertional
Achilles tendinopathy. J Sci Med Sport 2010;
13(3): 295-298.
30. Jarvinen M, Jozsa L, Kannus P, Jarvinen TL,
Kvist M, Leadbetter W. Histopathological
findings in chronic tendon disorders. Scand J
Med Sci Sports 1997; 7(2): 86-95.
31. Jozsa L, Balint J. [Pathology of the spontane-
ous tendon ruptures (author’s transl)]. Magy
Traumatol Orthop Helyreallito Seb 1978;
21(3): 176-193.
32. Jozsa L, Kannus P. Human Tendons:
Anatomy, Physiology, and Pathology. Human
Kinetics 1997.
33. Jozsa L, Reffy A, Kannus P, Demel S, Elek E.
Pathological alterations in human tendons.
Arch Orthop Trauma Surg 1990; 110(1):
15-21.
34. Kannus P. Structure of the tendon connec-
tive tissue. Scand J Med Sci Sports 2000;
10(6): 312-320.
35. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73(10): 1507-1525.
36. Khan KM, Bonar F, Desmond PM et al.
Patellar tendinosis (jumper’s knee): findings
at histopathologic examination, US, and MR
imaging. Victorian Institute of Sport Tendon
Study Group. Radiology 1996; 200(3): 821-
827.
37. Khan KM, Maffulli N. Tendinopathy: an
Achilles’ heel for athletes and clinicians. Clin
J Sport Med 1998; 8(3): 151-154.
38. Kjaer M. Role of extracellular matrix in
adaptation of tendon and skeletal muscle to
mechanical loading. Physiol Rev 2004; 84(2):
649-698.
39. Kujala UM, Sarna S, Kaprio J. Cumulative
incidence of achilles tendon rupture and
tendinopathy in male former elite athletes.
Clin J Sport Med 2005; 15(3): 133-135.
40. Kvist H, Kvist M. The operative treatment of
chronic calcaneal paratenonitis. J Bone Joint
Surg Br 1980; 62(3): 353-357.
41. Kvist M, Jozsa L, Jarvinen M, Kvist H. Fine
structural alterations in chronic Achilles
paratenonitis in athletes. Pathol Res Pract
1985; 180(4): 416-423.
42. Langberg H, Rosendal L, Kjaer M. Training-
induced changes in peritendinous type I
collagen turnover determined by microdi-
Ch
apter 8
Mid
po
rtion
Ach
illes tend
ino
path
y: wh
y pain
ful?
145
alysis in humans. J Physiol 2001; 534(Pt 1):
297-302.
43. Lian O, Dahl J, Ackermann PW, Frihagen F,
Engebretsen L, Bahr R. Pronociceptive and
antinociceptive neuromediators in patellar
tendinopathy. Am J Sports Med 2006;
34(11): 1801-1808.
44. Longo UG, Ramamurthy C, Denaro V,
Maffulli N. Minimally invasive stripping for
chronic Achilles tendinopathy. Disabil Reha-
bil 2008; 30(20-22): 1709-1713.
45. Macaluso A, De VG. Muscle strength, power
and adaptations to resistance training in
older people. Eur J Appl Physiol 2004; 91(4):
450-472.
46. Maffulli N. Current concepts in the manage-
ment of subcutaneous tears of the Achilles
tendon. Bull Hosp Jt Dis 1998; 57(3): 152-
158.
47. Maffulli N, Binfield PM, Moore D, King JB.
Surgical decompression of chronic central
core lesions of the Achilles tendon. Am J
Sports Med 1999; 27(6): 747-752.
48. Maffulli N, Khan KM, Puddu G. Overuse
tendon conditions: time to change a confus-
ing terminology. Arthroscopy 1998; 14(8):
840-843.
49. Maffulli N, Sharma P, Luscombe KL. Achilles
tendinopathy: aetiology and management. J
R Soc Med 2004; 97(10): 472-476.
50. Maffulli N, Walley G, Sayana MK, Longo UG,
Denaro V. Eccentric calf muscle training in
athletic patients with Achilles tendinopathy.
Disabil Rehabil 2008; 30(20-22): 1677-1684.
51. Maquirriain J, Ayerza M, Costa-Paz M,
Muscolo DL. Endoscopic surgery in chronic
achilles tendinopathies: A preliminary
report. Arthroscopy 2002; 18(3): 298-303.
52. Messner K, Wei Y, Andersson B, Gillquist
J, Rasanen T. Rat model of Achilles tendon
disorder. A pilot study. Cells Tissues Organs
1999; 165(1): 30-39.
53. Michna H, Hartmann G. Adaptation of ten-
don collagen to exercise. Int Orthop 1989;
13(3): 161-165.
54. Molloy TJ, Kemp MW, Wang Y, Murrell GA.
Microarray analysis of the tendinopathic rat
supraspinatus tendon: glutamate signaling
and its potential role in tendon degenera-
tion. J Appl Physiol 2006; 101(6): 1702-1709.
55. Moss ALH. Is There an Association Between
an Absence of Palmaris Longus Tendon and
an Absence of Plantaris Tendon? Eur J Plast
Surg 1988; 11: 32-34.
56. Nelen G, Martens M, Burssens A. Surgical
treatment of chronic Achilles tendinitis. Am
J Sports Med 1989; 17(6): 754-759.
57. O’Brien M. The anatomy of the Achilles ten-
don. Foot Ankle Clin 2005; 10(2): 225-238.
58. Pearce C, Donley B, Calder J. Achilles
Tendinopathy: Non-operative Treatment. In:
Calder J, Karlsson J, Maffulli N, Thermann H,
van Dijk CN, editors. Achilles Tendinopathy:
Current Concepts. 1 ed. London: DJO Publi-
cations; 2010: 79-87.
59. Peers KH, Brys PP, Lysens RJ. Correlation
between power Doppler ultrasonography
and clinical severity in Achilles tendinopathy.
Int Orthop 2003; 27(3): 180-183.
60. Reiter M, Ulreich N, Dirisamer A, Tschola-
koff D, Bucek RA. [Extended field-of-view
sonography in Achilles tendon disease: a
comparison with MR imaging]. Rofo 2004;
176(5): 704-708.
61. Riley G. Tendinopathy--from basic science to
treatment. Nat Clin Pract Rheumatol 2008;
4(2): 82-89.
62. Rolf C, Movin T. Etiology, histopathology,
and outcome of surgery in achillodynia. Foot
Ankle Int 1997; 18(9): 565-569.
63. Ryan M, Grau S, Krauss I, Maiwald C,
Taunton J, Horstmann T. Kinematic analysis
of runners with achilles mid-portion tendi-
nopathy. Foot Ankle Int 2009; 30(12): 1190-
1195.
64. Saxena A. Surgery for chronic Achilles
tendon problems. J Foot Ankle Surg 1995;
34(3): 294-300.
65. Schubert TE, Weidler C, Lerch K, Hofstadter
F, Straub RH. Achilles tendinosis is associated
with sprouting of substance P positive nerve
146
fibres. Ann Rheum Dis 2005; 64(7): 1083-
1086.
66. Schwalbe, Pfitzner. Varietäten-Statistik und
Anthropologie. Deutsche Med Wchnschr
1894; 25(3): 459.
67. Segesser B, Goesele A, Renggli P. [The
Achilles tendon in sports]. Orthopade 1995;
24(3): 252-267.
68. Sharma P, Maffulli N. Tendon injury and
tendinopathy: healing and repair. J Bone
Joint Surg Am 2005; 87(1): 187-202.
69. Steenstra F, van Dijk CN. Achilles tendos-
copy. Foot Ankle Clin 2006; 11(2): 429-438.
70. Steyaert AE, Burssens PJ, Vercruysse CW,
Vanderstraeten GG, Verbeeck RM. The
effects of substance P on the biomechanic
properties of ruptured rat Achilles’ tendon.
Arch Phys Med Rehabil 2006; 87(2): 254-
258.
71. Stilwell DL, Jr. The innervation of tendons
and aponeuroses. Am J Anat 1957; 100(3):
289-317.
72. Suominen H, Kiiskinen A, Heikkinen E.
Effects of physical training on metabolism
of connective tissues in young mice. Acta
Physiol Scand 1980; 108(1): 17-22.
73. Testa V, Capasso G, Benazzo F, Maffulli N.
Management of Achilles tendinopathy by
ultrasound-guided percutaneous tenotomy.
Med Sci Sports Exerc 2002; 34(4): 573-580.
74. Thermann H, Benetos IS, Panelli C, Gavriilidis
I, Feil S. Endoscopic treatment of chronic
mid-portion Achilles tendinopathy: novel
technique with short-term results. Knee
Surg Sports Traumatol Arthrosc 2009;
17(10): 1264-1269.
75. Tipton CM, Matthes RD, Maynard JA,
Carey RA. The influence of physical activity
on ligaments and tendons. Med Sci Sports
1975; 7(3): 165-175.
76. Tudor-Locke C, Bassett DR, Jr. How many
steps/day are enough? Preliminary pedom-
eter indices for public health. Sports Med
2004; 34(1): 1-8.
77. Tudor-Locke C, Hatano Y, Pangrazi RP,
Kang M. Revisiting “how many steps are
enough?”. Med Sci Sports Exerc 2008; 40(7
Suppl): S537-S543.
78. van Dijk CN, van Sterkenburg MN, Wieger-
inck JI, Karlsson J, Maffulli N. Terminology
for Achilles tendon related disorders. Knee
Surg Sports Traumatol Arthrosc 2011; 19(5):
835-841
79. van Schie HT, de Vos RJ, de JS et al. Ultraso-
nographic tissue characterisation of human
Achilles tendons: quantification of tendon
structure through a novel non-invasive
approach. Br J Sports Med 2010; 2010;
44(16): 1153-1159.
80. van Sterkenburg MN, de Jonge MC, Sierev-
elt IN, van Dijk CN. Less promising results
with sclerosing ethoxysclerol injections
for midportion achilles tendinopathy: a
retrospective study. Am J Sports Med 2010;
38(11): 2226-2232.
81. Vega J, Cabestany JM, Golano P, Perez-Carro
L. Endoscopic treatment for chronic Achilles
tendinopathy. Foot Ankle Surg 2008; 14(4):
204-210.
82. Williams JG. Achilles tendon lesions in sport.
Sports Med 1986; 3(2): 114-135.
83. Zanetti M, Metzdorf A, Kundert HP et al.
Achilles tendons: clinical relevance of neo-
vascularization diagnosed with power Dop-
pler US. Radiology 2003; 227(2): 556-560.
PArt iv retrocALcANeAL BUrsitis: DiAGNosis AND treAtmeNt
Chapter 9
Appearance of the weight- bearing lateral radiograph
in retrocalcaneal bursitis
MN van Sterkenburg
B Muller
M Maas
IN Sierevelt
CN van Dijk
Acta Orthop 2010; 81: 387-390
152
ABstrAct
Background and purposeA retrocalcaneal bursitis is caused by repetitive impingement of the bursa between the Achil-
les tendon and the posterosuperior calcaneus. The bursa is situated in the posteroinferior
corner of Kager’s triangle (retrocalcaneal recess), which is a radiolucency with sharp borders
on the lateral radiograph of the ankle. In case of inflammation, the fluid-filled bursa is less
radiolucent, making it difficult to delineate the retrocalcaneal recess. We assessed if the
radiographic appearance of the retrocalcaneal recess on plain digital (film-less) radiographs
could be used in the diagnosis of a retrocalcaneal bursitis.
MethodsObliteration of the retrocalcaneal recess (yes/no) on 74 digital weight- bearing lateral radio-
graphs of the ankle was independently assessed by 2 observers. Radiographs were of 24
patients (25 heels) with retrocalcaneal bursitis (confirmed on endoscopic calcaneoplasty); the
control group consisted of 50 patients (59 heels).
ResultsThe sensitivity of the test was was 83% for observer 1 and 79% for observer 2. Specificity
was 100% and 98% for observer 1 and 2. The interobserver reliability test calculated a
kappa-value of 0.86. For observer 1 intraobserver reliability was 0.96 and 0.92 for observer 2.
InterpretationThere is a typical appearance of the retrocalcaneal recess on digital weight-bearing lateral
radiographs of a retrocalcaneal bursitis.
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iNtroDUctioN
A symptomatic inflammation of the retrocalcaneal bursa is caused by repetitive impingement
of the bursa between the anterior aspect of the Achilles tendon and a bony posterosuperior
calcaneal prominence1,9,10.
Most publications focus on this protrusion, some describe a loss of radiolucency in Kager’s
triangle on lateral radiographs. Ultrasonography or MRI can be used to confirm the diagnosis.
Kager’s fat pad, also known as the pre-Achilles fat pad, occupies Kager’s triangle11. Normally
this fat pad, as seen on a weight-bearing lateral radiograph of the ankle, is a triangular
radio-lucency with sharp, gently curving borders4 (Figure 1).
The retrocalcaneal bursa is situated in the posteroinferior corner of the pad. In bursitis, the
normally sharply outlined radiolucent retrocalcaneal recess is obliterated (Figure 2).
There are few reports on the appearance of the retrocalcaneal recess on radiography and the
series are small5-7. These authors did not yet have the benefit of digital (film-less) examina-
tions with its advances of allowing images to be captured, viewed and reproduced digitally.
This offers several advantages, since contrast, brightness and magnification can be digitally
adjusted, and therefore a more sharp and detailed view is obtained.
We determined the reliability of the radiographical appearance of the retrocalcaneal
recess of Kager’s triangle in diagnosing a retrocalcaneal bursitis.
methoDs
24 patients (25 heels, 13 men) who had digital radiographs and had underwent endoscopic
calcaneoplasty for chronic retrocalcaneal bursitis from 2000-2008 were included (Figure 3). 1
patient underwent surgery on both ankles on different occasions. Mean age was 42 (15-73)
years. Patients with previous hindfoot surgery were excluded.
A control group matched for age and sex of 50 patients (59 heels, 30 men) with ankle prob-
lems not related to the hindfoot, was retrieved from our hospital’s archives from the same
period. From the 10 subjects with bilateral radiographs we randomly selected 1 heel, thus the
study comprised 74 heels (24 patients, 50 controls). Their mean age was 42 (15-72) years.
All heels had been examined with lateral weight-bearing radiographs in 20 degrees
endorotation, as is standard procedure in our hospital.
ObserversTo test interobserver reliability, all radiographs were independently evaluated by 2 experienced
observers: an orthopedic surgeon, and a radiologist. They rated the radiographs positive or
154
negative for the appearance of the retrocalcaneal recess (measurement 1). On a positive
radiograph the retrocalcaneal recess of Kager’s triangle was less radiolucent, meaning that it
was obliterated and had a whiter appearance; on a negative radiograph the retrocalcaneal
recess was radiolucent, meaning that it had a black appearance and its borders were sharp.
Both observers were blinded to the patient’s history. For intraobserver reliability testing, both
observers evaluated the radiographs 2 weeks later, which were now arranged in a different
order (measurement 2).
StatisticsDescriptive statistics on the patient’s demographics were performed. Sensitivity and specific-
ity were calculated to determine the validity of the test in predicting abnormality of the
retrocalcaneal recess of Kager’s triangle in retrocalcaneal bursitis.
Additionally, positive (PPV) and negative predictive values (NPV) were calculated.
For testing inter- and intraobserver reliability the Cohen’s kappa value was used. Kappa
values greater than 0.81 indicate high association. 95% confidence intervals were calculated
for each outcome.
SPSS for Windows version 15.0 was used to perform the analyses.
Figure 1. (A) Kager’s triangle with a normal appearance. (B) This triangular lucency with sharp, smooth-ly curving borders is indicated with the dotted line. (C) The arrowhead indicates the retrocalcaneal recess: the ‘bursal wedge’ of Kager’s fat pad, which normally forms a radiolucent corner posterosuperior to the calcaneus
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Figure 2. A patient with a chronic retrocalcaneal bursitis: the retrocalcaneal recess has disappeared because of the less radiolucent fluid in the distended retrocalcaneal bursa
Figure 3. (A) Clinical image, (B) Radiograph of a patient with a retrocalcaneal bursitis. The retrocalca-neal recess is obliterated by a chronic inflamed bursa (arrow). (C) Endoscopic view of a patient with a retrocalcaneal bursitis
156
resULts
We found a high sensitivity and specificity in both measurements for both observers as well
as high positive- and negative predictive values (PPV respectively NPV) (Table 1).
The interobserver reliability test for measurement 1 and 2 showed a high association
(Table 2). Intraobserver reliability also showed a high association in both observers (Table 3).
DiscUssioN
The terminology is confused when describing a retrocalcaneal bursitis, a syndrome of
combined bony and soft tissue pathology. Often, Haglund’s syndrome, Haglund’s disease,
Haglund’s deformity, pump-bump and retrocalcaneal bursitis are used interchangeably. To
avoid confusion, we chose to use the term ‘retrocalcaneal bursitis’, which is part of Haglund’s
syndrome and can be part of Haglund’s deformity. The bursal inflammation is the cause of
pain and the main reason for treatment.
We have found 2 studies on the appearance of the retrocalcaneal recess on conventional
radiographs. Pavlov et al. (1982)7 described 10 symptomatic heels and a control group of 78
heels. The goal of their study was to evaluate and describe all available clinical and radiologi-
cal findings in patients with Haglund’s syndrome. The appearance of the retrocalcaneal recess
was part of this evaluation. In 1 patient the retrocalcaneal recess was sharp, and in 9 it was
Table 1. Validity
Observer 1 2
Sensitivity (95%CI) 0.83 (0.58-0.96) 0.79 (0.54-0.93)
Specificity (95%CI) 1 (0.90-1) 0.98 (0.87-1)
PPV (95%CI) 1 (0.75-1) 0.94 (0.68-1)
NPV (95%CI) 0.93 (0.81-0.98) 0.92 (0.79-0.97)
Table 2. Interobserver reliability
Radiographs Kappa (95% CI)
Measurement 1 0.86 (0.71-1)
Measurement 2 0.87 (0.73-1)
Table 3. Intraobserver reliability
Radiographs Kappa (95% CI)
Observer 1 0.96 (0.87-1)
Observer 2 0.92 (0.80-1)
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ill-defined. Heneghan and Wallace (1985)6 described the appearance of the retrocalcaneal
recess in children.
6 heels were symptomatic, and the control group consisted of 24 heels. The purpose of
that study was to describe the osseous and soft tissue findings of retrocalcaneal bursitis and
to introduce roentgen criteria to substantiate the diagnosis. The retrocalcaneal recess was
one of these criteria. That study also found consistent loss of the sharp definition of the
retrocalcaneal recess in symptomatic patients.
What should be noted is that our lateral ankle radiographs are made weight-bearing and
in 20 degrees of endorotation, for parallel alignment of the lateral and medial malleolus and
to make sure the lateral and medial aspects of the talus overlap to be able to see the ankle
joint. This is not standard procedure everywhere, and if any, we are unaware of the effect on
the appearance of the retrocalcaneal recess.
When digital techniques are not available, conventional radiography may still suffice. It
is known that lowering the photon energy can be used to clarify details of soft tissues. The
results are essentially similar to increasing contrast in the evaluation of a digital radiograph,
which has been used in the past to assess patients with Achilles tendon problems2,3,8.
In conclusion, the radiographic appearance of the retrocalcaneal recess confirms the
clinical diagnosis of a retrocalcaneal bursitis. Further diagnostic evaluation is not necessary,
resulting in a higher cost-effectiveness and quicker treatment.
158
refereNce List
1. DeVries JG, Summerhays B, Guehlstorf DW.
Surgical correction of Haglund’s triad using
complete detachment and reattachment of
the Achilles tendon. J Foot Ankle Surg 2009;
48(4): 447-451.
2. Fischer E. Soft tissue diagnosis on the
extremities using soft tissue radiography.
Part I. Indications and some technical
aspects of low KeV radiography (author’s
transl). Radiologe 1974; 14(10): 454-456.
3. Fischer E. Soft tissue diagnosis on the
extremities using soft tissue radiography.
Part II. Diseases of the Achilles tendon and
the surrounding tissues (author’s transl).
Radiologe 1974; 14(10): 457-467.
4. Goodman LR, Shanser J.D. The pre-Achilles
fat pad: An aid to early diagnosis of local
or systemic disease. Skeletal Radiol 1997; 2:
81-86.
5. Heneghan MA, Pavlov H. The Haglund pain-
ful heel syndrome. Experimental investiga-
tion of cause and therapeutic implications.
Clin Orthop Relat Res 1984; (187): 228-234.
6. Heneghan MA, Wallace T. Heel pain due
to retrocalcaneal bursitis-radiographic
diagnosis (with an historical footnote on
Sever’s disease). Pediatr Radiol 1985; 15(2):
119-122.
7. Pavlov H, Heneghan MA, Hersh A, Goldman
AB, Vigorita V. The Haglund syndrome:
initial and differential diagnosis. Radiology
1982; 144(1): 83-88.
8. Scotti DM, Sadhu VK, Heimberg F, O’Hara
AE. Osgood-Schlatter’s disease, an emphasis
on soft tissue changes in roentgen diagno-
sis. Skeletal Radiol 1979; 4(1): 21-25.
9. Sofka CM, Adler RS, Positano R, Pavlov H,
Luchs JS. Haglund’s Syndrome: Diagnosis
and Treatment Using Sonography. Humanity
Soc Science J 2006; (2): 27-29.
10. Stephens MM. Haglund’s deformity and
retrocalcaneal bursitis. Orthop Clin North
Am 1994; 25(1): 41-46.
11. Theobald P, Bydder G, Dent C, Nokes L, Pugh
N, Benjamin M. The functional anatomy of
Kager’s fat pad in relation to retrocalcaneal
problems and other hindfoot disorders. J
Anat 2006; 208(1): 91-97.
Chapter 10
Endoscopic calcaneoplasty
MN van Sterkenburg
PAJ de Leeuw
CN van Dijk
Accepted in Minimally Invasive Foot & Ankle Surgery, editor Maffulli, 2010
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iNtroDUctioN
In 1928, the Swedish orthopedic surgeon Patrick Haglund described a patient with a painful
hindfoot caused by a prominent posterosuperior aspect of the calcaneus in conjunction with
a sharp rigid heel counter8. The term Haglund’s disease, deformity and syndrome have been
used interchangeably, but have also been described as different entities by others.
Nowadays, the term ‘Haglund’s deformity’ is used to describe tenderness and pain on the
posterolateral aspect of the calcaneus. On physical examination, a bony prominence can
be palpated at this location. This entity is described by a variety of different names such as
‘pump-bump’5, ‘cucumber heel’6, ‘high-prow heels’31 and ‘winter heel’6.
There is more uncertainty on the definition of Haglund’s disease. It is described to be a
synonym for deformity or syndrome, but has also been referred to as an osteochondrosis of
the accessory navicular bone1,30,35. For this reason, it will not be considered in this chapter.
In Haglund’s syndrome, the retrocalcaneal bursa is inflamed with concomitant swelling. The
swelling is present on both sides of the Achilles tendon at the level of the posterosuperior
calcaneal prominence, sometimes in combination with insertional tendinopathy of the Achil-
les tendon. The syndrome is caused by repetitive impingement of the retrocalcaneal bursa
between the anterior aspect of the Achilles tendon and the enlarged posterosuperior aspect
of the calcaneus. It occurs most often at the end of the 2nd or the 3rd decade, mainly in
females, and is often bilateral. However, it may occur in both sexes and at any age.
In this chapter, the diagnosis and endoscopic treatment for patients with complaints of
a chronic retrocalcaneal bursitis is described, which can be part of Haglund’s deformity and
Haglund’s syndrome.
DiAGNosis
Patients typically describe the onset of pain when starting to walk after a period of rest.
The distinction between Haglund’s deformity, Haglund’s syndrome, and other pathologic
conditions of the posterior aspect of the heel, most importantly Achilles tendinopathy,
should be made.
Insertional tendinopathy is defined as a tendinopathy of the tendon at its insertion. The pain
is most frequently located in the midline at the insertion into the calcaneus. Co-existence
with retrocalcaneal bursitis is known.
In Haglund’s deformity, a bony prominence can be seen at the posterosuperolateral aspect of
the heel, which is painful on palpation. The superficial bursa may be swollen, and the overly-
ing skin can be thickened and dyschromic. A retrocalcaneal bursitis occasionally develops as
a result of this deformity.
In Haglund’s syndrome, on physical examination swelling can be seen on both sides of the
tendon at the level of the posterosuperior calcaneal prominence, and pain can be reproduced
162
by palpation of the lateral and medial side of the Achilles tendon at this level. With dorsi-
flexion of the ankle, the anterior part of the tendon impinges against the posterosuperior
rim of the calcaneus, leading to retrocalcaneal bursitis. A hindfoot varus and a pes cavus
are both predisposing factors for heel pain. In the cavus foot, the calcaneus is not only in
varus malalignment, but it is also more vertical, which results in a more prominent projection
posteriorly7.
mANAGemeNt
Multiple options have been described to manage chronic retrocalcaneal bursitis, including
avoidance of tight shoe heel counters, cast immobilization, NSAIDs, activity modification,
padding, shock wave treatment, physical therapy and a single injection of corticosteroids
into the retrocalcaneal space. If conservative management fails, there are essentially two
distinct operative methods, and one endoscopic surgical technique. The open operative
alternatives include resection of the posterosuperior part of the calcaneus or a calcaneal
wedge osteotomy. Complications include skin breakdown, tenderness in the region of the
operative scar, esthetically non-appealing operative scars and altered sensation around the
heel2,9,15,19,25. More serious complications include Achilles tendon avulsions and calcaneal
(stress) fractures14,15,19. Recurrent persistent pain secondary to an inadequate amount of
bone resected, and stiffness of the Achilles tendon resulting in decreased dorsiflexion have
also been reported22. Wound healing problems have been described in 30% of patients
treated with open procedures29.
eNDoscoPic treAtmeNt
Endoscopic treatment offers advantages that are related to any minimal invasive surgi-
cal procedure, such as a low morbidity, excellent scar healing, functional aftertreatment,
Figure 1. (A) A patient with Haglund’s syndrome in the right hindfoot. (B) The typical swelling (S) on both sides of the Achilles tendon (AT) at the level of the posterosuperior calcaneal prominence is indi-cated
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A B
C D
Figure 2. (A) Schematic lateral view of a hindfoot showing Kager’s triangle (black). (B) Plain conven-tional lateral standing radiograph of an ankle with a normal aspect of the bony and soft tissues in the hindfoot. Kager’s triangle is indicated (dotted line). The arrow points at the retrocalcaneal recess. (C) Kager’s triangle is schematically drawn (black). Indicated in red is the fluid-filled retrocalcaneal bursa. (D) Lateral standing radiograph of a patient’s right ankle showing hypertrophy of the posterosuperior aspect of the calcaneus with infiltration of the retrocalcaneal recess of Kager’s triangle by the fluid-filled retrocalcaneal bursa
short recovery time and a shorter time to sport resumption as compared to open surgical
approaches. Here we describe the technique of endoscopic calcaneoplasty, and compare
the results of this minimal invasive technique34 with those reported for the open surgical
techniques.
IndicationPatient complaints include pain at rest, when standing, walking (uphill), running and walking
on hard surfaces. Conventional lateral radiographs show hypertrophy of the posterosuperior
164 Figure 3. The patient is placed in prone position (A). The affected right leg is placed on a bolster and right over the end of the table (B). The other foot is positioned in a way that the surgeon has sufficient working area (C)
Figure 4. (A) Schematic drawing of lateral view of the foot. The ankle is placed in plantigrade position. A line is drawn through the tip of the fibula parallel to the sole of the foot. The incision for the lateral portal in conventional posterior arthroscopy is placed directly above this line; the center of the incision in pa-tients undergoing endoscopic calcaneoplasty is placed 1.5-2.5 cm below this line (red). (B) Preoperatively this can be verified by drawing these same lines on a lateral standing radiograph of the foot. (C) Location of lateral and medial (D) portal as indicated by the probe (red line)
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aspect of the calcaneus and deep retrocalcaneal bursitis, identified by diminished radiolu-
cency of the retrocalcaneal recess and the lower portion of Kager’s triangle (Figure 2).
If conservative treatment fails, we undertake endoscopic surgery.
Surgical techniqueSurgery is performed with the patient in prone position under general or regional anesthesia.
The involved leg is marked with an arrow by the patient, to avoid wrong side surgery. The
feet are positioned just over the edge of the operation table. The involved leg is slightly
elevated by placing a bolster under the lower leg (Figure 3).
The position of the foot is in plantarflexion through gravity. Prior to surgery important ana-
tomical structures are marked. These include the medial and lateral border of the Achilles
tendon and the calcaneus (Figure 4).
The lateral portal is made first, just lateral of the Achilles tendon at the level of the superior
aspect of the calcaneus. This portal is produced as a small vertical incision through the skin
only. The retrocalcaneal space is penetrated with a blunt trocar. A 4.5 mm arthroscopic shaft
with an inclination angle of 30o is introduced (Figure 5).
Irrigation is performed by gravity flow. A 70o arthroscope can also be used but is seldom
necessary. Under direct vision, a spinal needle is introduced just medial to the Achilles ten-
don, again at the level of the superior aspect of the calcaneus, to locate the medial portal
(Figure 6).
After having prepared the medial portal by a vertical stab incision, a 5.5 mm bonecutter
shaver (Dyonics Bonecutter, Smith & Nephew, Andover, USA) is introduced and visualized
by the arthroscope. The inflamed retrocalcaneal bursa is removed first (Figure 7) to provide
a better view. Now the superior surface of the calcaneus is visualized and its fibrous layer
Figure 5. (A) incision for lateral portal in a left ankle. (B) Penetration of retrocalcaneal space with blunt trocar followed by blunt dissection. (C) Introduction of arthroscope with 30 o inclination angle
166 Figure 6. (A) Introduction of spinal needle (left ankle) under direct vision (B) for placement of medial portal
Figure 7. Endoscopic calcaneoplasty of the right hindfoot of a 38-year-old female patient with Haglund’s syndrome. (A) The retrocalcaneal recess. AT= Achilles tendon; INF= inflamed retrocalcaneal bursa; CA= calcaneus. (B) Retrocalcaneal bursa is removed with bonecutter shaver. BS= bonecutter shaver
Figure 8. (A) Removal of bone at the posteromedial border of the calcaneus with arthroscope in the lateral portal. (B) Removal of bone at the lateral border of the calcaneus after change of portals. AT= Achilles tendon; BS= bonecutter shaver; PM= posteromedial border of calcaneus; LB= posterolateral border of calcaneus; CA= calcaneus
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and periosteum are stripped off. During resection of the bursa and the fibrous layer and
periosteum of the superior aspect of the calcaneus, the full radius resector is facing the bone
to avoid damage to the Achilles tendon.
When the foot is brought into full dorsiflexion, impingement between the posterosuperior
calcaneal edge and the Achilles tendon can be perceived. The foot is subsequently brought
into plantarflexion and now the posterosuperior calcaneal rim is removed. This bone is quite
soft and can be removed by the aggressive synovial full radius resector or bone cutter. A burr
is not needed at this point. The portals are used interchangeably for both the arthroscope
and the resector, so as to remove the entire bony prominence. It is important to remove a
sufficient amount of bone at the posteromedial and lateral corner (Figure 8). These edges
have to be rounded off by moving the synovial resector beyond the posterior edge onto the
lateral respectively medial wall of the calcaneus.
The Achilles tendon is protected throughout the entire procedure by keeping the closed
end of the resector against the tendon. With the foot in full plantarflexion, the insertion of
the Achilles tendon can be visualized.
The bonecutter is placed on the insertion against the calcaneus to smoothen this part of the
calcaneus. Finally, the resector is introduced to clean up loose debris and to smooth pos-
sible rough edges. In the first several patients, fluoroscopic control can be used to ascertain
whether sufficient bone has been resected. With some experience, this will no longer be
necessary. Figure 9 shows an endoscopic view of the end result.
To prevent sinus formation, at the end of the procedure the skin incisions are closed with
3.0 Ethilon sutures. The incisions and surrounding skin are injected with 10 ml of a 0.5%
bupivacain/morphine solution. A sterile compressive dressing is applied.
Post-operative managementPostoperatively, the patient is allowed weight -bearing as tolerated and is instructed to elevate
the foot when not walking. The dressing is removed 3 days postoperatively, after which the
patient is allowed to shower. Patients are encouraged to perform active range of motion
exercises for at least 3 times a day for 10 minutes each. The patient is allowed to return
to wearing regular shoes as soon as tolerated. The sutures are removed after two weeks.
A conventional lateral radiograph is made to ensure that sufficient bone has been excised
(Figure 10). With satisfaction of the surgeon and patient, no further outpatient department
contact is necessary. Patients with limited range of motion are directed to a physiotherapist.
Patient outcomeBetween 1995 and 2000 in the Academic Medical Center in Amsterdam we performed 39
procedures in 36 patients28. The average age was 35 years (range 16-50). Patients had a
168
Figure 9. Result at the end of procedure. CA= calcaneus, BS= bonecutter shaver, AT= Achilles tendon
Figure 10. (A) Preoperative X-ray, with retrocalcaneal bursitis and prominence of the posterosuperior part of the calcaneus (arrow). (B) postoperative X-ray. The posterosuperior part of the calcaneus is suf-ficiently excised (arrow)
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painful swelling of the soft tissue of the posterior heel, medial and lateral of the Achilles
tendon on physical examination, without pain on palpation of the tendon itself. Conservative
management for at least 6 months did not relieve symptoms. The conventional lateral radio-
graph showed a superior calcaneal angle (subtended by lines drawn from the bursal projec-
tion to the posterior calcaneal tuberosity and from the medial calcaneal tuberosity to the
anterior calcaneal tuberosity) of more than 75°. An angle larger than 75° has been deemed
pathologic6,31. The mean follow up after endoscopic calcaneoplasty was 4.5 years (range
2 - 7.5). There were no surgical complications except from one 1 patient who experienced
an area of hypoesthesia over the heel pad. Postoperatively there were no infections, tender
or esthetically non-appealing scars and all patients were content with their small incisions.
Except for two patients, all patients improved. The Ogilvie-Harris score23 was rated fair by 4
patients, 6 rated good and 24 had excellent results. Work and sport resumption took place
at an average of 5 weeks (range 10 days-6 months) and 11 weeks (range 6 weeks-6 months)
respectively28,34.
DiscUssioN
Conservative management for retrocalcaneal bursitis includes a single cortisone injection in
the retrocalcaneal bursa21,22,32. Repeated injections are not advised since these can weaken
the tendon with the potential danger of rupture.
The aim of surgery for retrocalcaneal bursitis, after failure of the conservative treatment,
is preventing impingement between the Achilles tendon and the calcaneus. This can be
accomplished by means of removing the inflamed retrocalcaneal bursa followed by either
resection of the posterosuperior calcaneal rim or by a closing wedge osteotomy. Postero-
superior calcaneal resection can be performed through a posterolateral or posteromedial
incision or via a combination of both2,13,25.
A widely used technique, especially in North America, is the midline-posterior skin incision
combined with a central tendon splitting approach for debridement, retrocalcaneal bursec-
tomy, and removal of the calcaneal bursal projection as necessary18. Another approach is
the Cincinnati-type incision, a transverse skin incision at the level of the insertion of the
Achilles tendon. With this technique, a wide exposure of the insertion of the Achilles tendon
is possible, to debride the peritendinous and tendon tissue and if necessary bursectomy. The
transverse skin incision at the level of the Achilles insertion also allows osteotomy of the
posterosuperior corner of the calcaneus4, and, being in the direction of the skin creases, it
has a lesser potential for healing problems than the longitudinal approaches.
Endoscopic calcaneoplasty offers a good, minimally invasive alternative to open surgery.
Surgeons familiar with the endoscopic approach tend to favor this procedure, because of its
better visualization as compared to the open procedure. Due to inappropriate visualization
of the Achilles tendon during the open procedure, weakening or even rupture of this tendon
170
has been reported14,19. Full recovery time after the open resection can take as long as 2
years. Our patient series shows a high percentage of good to excellent results based on the
Ogilvie- Harris score.
Our results are comparable with other recently published reports on endoscopic treat-
ment.
Jerosh and co-workers published a prospective study in which they described the results of
endoscopic calcaneoplasty in 81 patients with an average follow-up of 35.3 months (range
12 to 72). Using the Ogilvie-Harris score, 41 patients presented excellent results, 34 pre-
sented good results, 3 had fair, and 3 patients showed poor results. These 3 patients showed
an ossified area of the Achilles tendon insertion, and were revised in an open procedure. Only
one patient experienced a superficial inflammation of the skin was found10,11. Ortmann and
co-workers operated on 30 patients (32 heels) with retrocalcaneal bursitis with the endo-
scopic technique. The means follow-up was 35 months, and the AOFAS score averaged 62
preoperatively and 97 postoperatively. There were 26 excellent results, three good results and
one poor result. One patient ruptured an Achilles tendon, one had residual pain and swelling
that required reoperation through an open procedure. There were no other complications.
Patients returned to work after on average of 8 weeks, and all athletes resumed their sport-
ing activities in an average of 12 weeks24.
Morag and co-workers treated 4 patients with endoscopic calcaneoplasty, and after an
average follow-up of 2 years (range 1 to 3.5 years), no complications, pain, disability, or
range of motion deficits were reported20.
The advantages of the endoscopic over the open procedure are the small incisions, avoiding
complications such a wound dehiscence, painful and/or ugly scars and nerve entrapment
within the scar, as described for the open procedure9. He found a considerable amount
of residual complaints in 32 clinically and radiographically examined patients treated by
surgical resection of the posterosuperior calcaneal prominence for Haglund’s syndrome at a
mean follow-up of 18.6 years (range 2-41). 14 of these 32 patients had soft tissue problems
including excessive scar formation and persistent swelling. In 8 patients not enough bone
was excised and 2 had new bone formation, both resulting in persistent painful swelling. The
function of the Achilles tendon was disturbed in 8 patients9.
There is no consensus regarding the ideal open surgical approach: medial, lateral, or
both2,12,25. Jones and James performed 10 partial calcaneal osteotomies for retrocalcaneal
bursitis, followed by a short leg walking cast for 8 weeks, progressively increasing weight-
bearing. Rehabilitation consisted of wearing an elevated heel of 1 inch until the foot came
easily to the neutral position. All patients were back to their desired level of activity within 6
months12. Angermann operated on 40 heels for the same indication using the posterolateral
approach in 32 patients. Postoperatively 29 patients were allowed immediate weight-
bearing. Complications consisted of one superficial heel infection, one haematoma and two
patients with delayed skin healing. At an average follow-up of 6 years (range 1-12) 50%
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of the patients were cured, 20% improved, 20% remained unchanged and in 10% the
pre-operative symptoms worsened2. The rate of poor results in this study corresponds to the
results of Taylor, who reported 36% poor results after the same type of surgery33. Pauker
and co-workers operated on 28 heels in 22 patients with Haglund’s syndrome. 18 heels
were approached laterally, and 10 medially, depending on the direction of the prominent
bone. All patients received a short leg walking cast for 4 weeks followed by mobilization
exercises for aftertreatment. At a mean follow up of 13 years in 19 patients (range 3-20), 15
had good results, 2 fair and 2 poor. No difference in outcome between the two approaches
was reported. The authors advocate using one incision, as many patients have complaints of
tenderness over the operative scar up to one year postoperatively which might be exagger-
ated by a more extensive approach25.
Schepsis and co-workers used the medial approach in 24 patients with retrocalcaneal
bursitis: 6 (25%) had a fair result requiring re-operation. In 49 heels (36 patients) operated
through a lateral approach with a mean follow-up of 4.7 years (range 1 to 11 years), early
complications were reported in 4 cases (3 haematomas and a superficial infection), and
late complications in 3 cases resulting in revision surgery. 7 patients noted some improve-
ment, 1 patient described no change and 7 patients reported worsening of their symptoms
after surgery27. Brunner and co-workers performed calcaneal osteotomies on 39 heels (36
patients), and reported at an average follow-up of 51 months, an average improvement of
the AOFAS score of 32 points as compared to the mean pre-operative score. Recovery time
ranged from 6 months up to 2 years. 6 of the 36 patients reported persisting posterior heel
pain after surgery3.
There are two comparative studies in which both endoscopic and open procedures were
performed. Leitze and co-workers compared the endoscopic approach (n=30, 22 months
follow-up) with the open surgical technique (n=17, 42 months follow-up). The endoscopic
approach revealed 19 excellent, 5 good, 3 fair and 3 poor results, which was numerically
but not significantly better than the open surgical procedure. Recovery time was identical,
but operation time, the amount of complications and scar tissue formation favoured the
endoscopic approach16. In a recent study by Lohrer and co-workers, a comparison was made
between the endoscopic and open resection for Haglund’s syndrome. In this anatomic study,
9 cadaver feet were operated by means of open surgery and 6 were operated through
endoscopic calcaneoplasty. After the procedure the ankles were dissected to determine the
amount of damage following the surgery. Comparable amounts of damage were found for
the sural nerve, the plantaris tendon and the medial column of the Achilles tendon17. Since
this was an anatomic study, no data could be gathered regarding recovery time and scar
healing, which seem to be the advantageous points of the endoscopic procedure. Also,
cadaveric ankles could have been stiffer as compared to patients, which made the endo-
scopic approach more difficult to perform.
172
Overall, looking at the available results of open surgery, studies reported 61-83% good
results and 17-36% complications or poor results requiring re-operation3,12,16,25,26,33.
Endoscopic surgery leads up to an estimated rate of 83-93% good results, and 0.6- 5%
complications or poor results requiring re-operation9,11,24,28.
coNcLUsioN
In summary, whether the operation is performed by endoscopic or open surgery, enough
bone has to be removed to prevent impingement between the calcaneus and Achilles tendon.
The endoscopic calcaneoplasty has demonstrated to show several advantages including low
morbidity, functional aftertreatment, outpatient treatment, excellent scar healing, a short
recovery time and quick sport resumption as compared to the results for the open technique.
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refereNce List
1. Alm A, Lamke LO, Liljedahl SO. Surgical
treatment of dislocation of the peroneal
tendons. Injury 1975; 7(1): 14-19.
2. Angermann P. Chronic retrocalcaneal bur-
sitis treated by resection of the calcaneus.
Foot Ankle 1990; 10(5): 285-287.
3. Brunner J, Anderson J, O’Malley M, Bohne
W, Deland J, Kennedy J. Physician and
patient based outcomes following surgical
resection of Haglund’s deformity. Acta
Orthop Belg 2005; 71(6): 718-723.
4. Carmont MR, Maffulli N. Management of
insertional Achilles tendinopathy through
a Cincinnati incision. BMC Musculoskelet
Disord 2007; 8: 82.
5. Dickinson PH, Coutts MB, Woodward EP,
Handler D. Tendo Achillis bursitis. Report
of twenty-one cases. J Bone Joint Surg Am
1966; 48(1): 77-81.
6. Fowler A. Abnormalities of the calcaneus
as a cause of painful heel: its diagnosis and
operative treatment. Br J Surg 1945; 32: 494-
498.
7. Fuglsang F, Torup D. Bursitis retrocalcanearis.
Acta Orthop Scand 1961; 30: 315-323.
8. Haglund P. Beitrag zur Klinik der Achil-
lessehne. Zeitschr Orthop Chir 1928; 49:
49-58.
9. Huber HM, Waldis M. [The Haglund
exostosis--a surgical indication and a minor
intervention?]. Z Orthop Ihre Grenzgeb
1989; 127(3): 286-290.
10. Jerosch J, Nasef NM. Endoscopic calcane-
oplasty--rationale, surgical technique, and
early results: a preliminary report. Knee Surg
Sports Traumatol Arthrosc 2003; 11(3): 190-
195.
11. Jerosch J, Schunck J, Sokkar SH. Endoscopic
calcaneoplasty (ECP) as a surgical treatment
of Haglund’s syndrome. Knee Surg Sports
Traumatol Arthrosc 2007; 15(7): 927-934.
12. Jones DC, James SL. Partial calcaneal ostec-
tomy for retrocalcaneal bursitis. Am J Sports
Med 1984; 12(1): 72-73.
13. Kolodziej P, Glisson RR, Nunley JA. Risk
of avulsion of the Achilles tendon after
partial excision for treatment of insertional
tendonitis and Haglund’s deformity: a
biomechanical study. Foot Ankle Int 1999;
20(7): 433-437.
14. Le TA, Joseph PM. Common exostectomies
of the rearfoot. Clin Podiatr Med Surg 1991;
8(3): 601-623.
15. Leach RE, DiIorio E, Harney RA. Pathologic
hindfoot conditions in the athlete. Clin
Orthop Relat Res 1983; (177): 116-121.
16. Leitze Z, Sella EJ, Aversa JM. Endoscopic
decompression of the retrocalcaneal space.
J Bone Joint Surg Am 2003; 85-A(8): 1488-
1496.
17. Lohrer H, Nauck T, Dorn NV, Konerding MA.
Comparison of endoscopic and open resec-
tion for Haglund tuberosity in a cadaver
study. Foot Ankle Int 2006; 27(6): 445-450.
18. McGarvey WC, Palumbo RC, Baxter DE,
Leibman BD. Insertional Achilles tendinosis:
surgical treatment through a central tendon
splitting approach. Foot Ankle Int 2002;
23(1): 19-25.
19. Miller AE, Vogel TA. Haglund’s deformity
and the Keck and Kelly osteotomy: a ret-
rospective analysis. J Foot Surg 1989; 28(1):
23-29.
20. Morag G, Maman E, Arbel R. Endoscopic
treatment of hindfoot pathology. Arthros-
copy 2003; 19(2): E13.
21. Myerson MS, McGarvey W. Disorders of the
Achilles tendon insertion and Achilles tendi-
nitis. Instr Course Lect 1999; 48: 211-218.
22. Nesse E, Finsen V. Poor results after resection
for Haglund’s heel. Analysis of 35 heels in
23 patients after 3 years. Acta Orthop Scand
1994; 65(1): 107-109.
23. Ogilvie-Harris DJ, Mahomed N, Demaziere A.
Anterior impingement of the ankle treated
by arthroscopic removal of bony spurs. J
Bone Joint Surg Br 1993; 75(3): 437-440.
174
24. Ortmann FW, McBryde AM. Endoscopic
bony and soft-tissue decompression of
the retrocalcaneal space for the treatment
of Haglund deformity and retrocalcaneal
bursitis. Foot Ankle Int 2007; 28(2): 149-153.
25. Pauker M, Katz K, Yosipovitch Z. Calcaneal
ostectomy for Haglund disease. J Foot Surg
1992; 31(6): 588-589.
26. Schepsis AA, Wagner C, Leach RE. Surgical
management of Achilles tendon overuse
injuries. A long-term follow-up study. Am J
Sports Med 1994; 22(5): 611-619.
27. Schneider W, Niehus W, Knahr K. Haglund’s
syndrome: disappointing results following
surgery -- a clinical and radiographic analy-
sis. Foot Ankle Int 2000; 21(1): 26-30.
28. Scholten PE, van Dijk CN. Endoscopic
calcaneoplasty. Foot Ankle Clin 2006; 11(2):
439-46.
29. Segesser B, Goesele A, Renggli P. [The
Achilles tendon in sports]. Orthopade 1995;
24(3): 252-267.
30. Sella EJ, Caminear DS, McLarney EA.
Haglund’s Syndrome. J Foot Ankle Surg
1997; 37(2): 110-114.
31. Stephens MM. Haglund’s deformity and
retrocalcaneal bursitis. Orthop Clin North
Am 1994; 25(1): 41-46.
32. Subotnick SI, Block AJ. Retrocalcaneal
problems. Clin Podiatr Med Surg 1990; 7(2):
323-332.
33. Taylor GJ. Prominence of the calcaneus:
is operation justified? J Bone Joint Surg Br
1986; 68(3): 467-470.
34. van Dijk CN, van Dyk GE, Scholten PE, Kort
NP. Endoscopic calcaneoplasty. Am J Sports
Med 2001; 29(2): 185-189.
35. Vega MR, Cavolo DJ, Green RM, Cohen RS.
Haglund’s deformity. J Am Podiatry Assoc
1984; 74(3): 129-135.
Chapter 11
Optimization of portal placement for endoscopic calcaneoplasty
MN van Sterkenburg
M Groot
IN Sierevelt
GMMJ Kerkhoffs
CN van Dijk
Arthroscopy 2011; 27: 1110-1117
176
ABstrAct
Purpose The purpose of our study was to determine an anatomical landmark to help locate portals in
endoscopic calcaneoplasty (EC).
MethodsThe DOPP (Device for Optimal Portal Placement) was developed to measure the distance
from the distal fibula tip to the calcaneus (DFC) in 28 volunteers to determine the location of
the posterosuperior calcaneal border in relation to this line.
ResultsThe DOPP demonstrated an inter-observer reliability of 0.99 (95%CI 0.97-0.99). We found
that in patients with flat feet, portals should be placed at a mean of 15 mm (SD 4.5) distal to
the tip of the fibula, in normal feet at 20 mm (SD 4.8) and in cavus feet at a mean of 22 mm
(SD 5.4). The difference of the DFC within the 3 different foot type groups was significant
(p<0.05).
ConclusionsThe DOPP demonstrated to be highly reliable in measuring the DFC (ICC= 0.99). A numeric
distance scale for use in all different foot morphologies could not be constructed. There is a
direct relation between portal location and foot morphology (p<0.05), as in flat feet portal
location is significantly more proximal (15 mm) to the tip of the fibula when compared to
cavus feet (22 mm).
Clinical relevanceThese results may help with portal placement in endoscopic calcaneoplasty for all different
foot morphologies.
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iNtroDUctioN
Endoscopic calcaneoplasty (EC) has demonstrated to be an effective surgical procedure
for treatment of patients with complaints of a retrocalcaneal bursitis not responding to
conservative treatment5,6,14,19. Two portals are used, just lateral and medial to the Achilles
tendon, at the level of the posterosuperior tuberosity of the calcaneus (Figure 1). During the
procedure, the inflamed retrocalcaneal bursal tissue and posterosuperior tuberosity of the
calcaneus are resected. However, due to the local anatomy, bulky subcutaneous tissue and
swelling of the retrocalcaneal bursal tissue, palpation of the posterosuperior calcaneal rim
is difficult and portals can easily be placed too far proximal. This will result in a suboptimal
procedure. Fluoroscopy is sometimes used to make portals, but can be time-consuming and
the surgeon has to depend on availability and personnel. Additionally, retrocalcaneal bursitis
often occurs in young patients in whom especially radiation has to be limited to a minimum.
For this reason there is need for standardization of these portals. Portals in the area that have
been standardised are those for hindfoot endoscopy18.
In the standard 2-portal hindfoot technique, the distal tip of the fibula is used as an ana-
tomical landmark for placement of the posteromedial and -lateral portal16-18. A probe is
hooked under the tip and is held parallel to the foot sole which in turn is placed in a 90
degree position with the lower leg. A (imaginary) line is drawn from the tip to the Achilles
tendon and the portals are made just above this line (Figure 2). The aim of this study was to
determine the optimal location for the portals in EC in relation to this line and to determine
if this distance is reproducible in all individuals.
Figure 1. (A) Medial and lateral portal for endoscopic calcaneoplasty (red marks). Portals are placed at the posterosuperior calcaneal tuberosity. (B) Arthroscope is placed in the lateral- and a bonecutter shaver in the medial portal
178
The hypotheses were that the DOPP is a valid tool for standardizing portal placement, and
that using the distance from the distal tip of the fibula to the posterosuperior calcaneus (DFC)
on a radiograph would help us determine the ultimate position of portals, and provide us
with a numeric distance- scale to be used in all different foot morphologies.
methoDs
PopulationThis study was approved by our local Medical Ethical Committee.
It was decided to use healthy volunteers, as the goal of the procedure is to correct the
posterosuperior calcaneus to a normal situation with some overcorrection. Portals should
not be placed above a possible posterosuperior calcaneal prominence, as the shaver may
consequently not be able to reach the level of insertion.
28 volunteers with a mean age of 25 (SD 3.7) without a history of foot surgery or
trauma were recruited. Informed consent was signed, patient history was taken and physical
examination was performed to assess foot morphology. Of each volunteer one foot was
used for measurements and analysis2. Age, weight, length and Body Mass Index (BMI) were
recorded. Of all volunteers 3 lateral radiographs were made.
Foot morphologyWe considered foot morphology important since as the calcaneus tilts the DFC probably
increases with cavus- and decreases with flat feet (Figure 3). It was decided to group mor-
phology into three generally used types: cavus, normal, and flat feet.
Figure 2. (A) The tip of the fibula, used as a landmark in the standard 2-portal hindfoot procedure. The lateral incision in standard posterior arthroscopy is made just lateral to the Achilles tendon. The portal for endoscopic calcaneoplasty is located at the level of the posterosuperior calcaneal tuberosity (white mark in B)
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Figure 4. (A) The TMT1- angle measures the alignment of the forefoot with respect to the hindfoot, which is useful for interpretation of cavus and planus deformities. The intersection of the talar and the first metatarsal longitudinal axes creates this angle. Normal is 0°, whereas angles are increasingly nega-tive for cavus deformities (forefoot plantar flexion on the hindfoot) and increasingly positive for flat foot malformations (forefoot dorsiflexion on the hindfoot)1,3,7,9,10,15,20. The TMT1-angle is the intersection of the talar and the first metatarsal longitudinal axes. (B) The CI-angle is measured by a line passing parallel to the floor and a second line passing along the inferior border of the calcaneus (Figure 4B). A normal angle is 30°, in cavus feet it is more than 30°, and in flatfeet it is decreased 1,9,13,15
Physical examination as well as radiography was used to determine foot morphology. A foot
was defined as ‘flat’ when there was flattening of the medial longitudinal arch in weight-
bearing and apparent bowing of the Achilles tendon to medial (Helbing sign) as viewed from
posterior. A foot was defined as cavus when there was hindfoot varus and an increase in
height of the medial longitudinal arch of the foot that did not flatten on weight-bearing.
Talo 1st metatarsal (TMT1) - and calcaneal inclination (CI) angles11,12 as measured on a
standard lateral weight-bearing radiograph of the foot were used (Figure 4).
The DOPP, ‘Device for Optimal Portal Placement’It was aimed to measure the DFC on a lateral radiograph. This appeared impracticable since
overlying structures make the tip of the fibula difficult to identify. Also, when measuring the
DFC per-operatively on a patients foot, there is soft tissue interposition between probe and
180
fibula. Therefore we constructed a device prior to study initiation with which a metal probe
can be hooked underneath the tip of the fibula, hereby mimicking the setting in standard
2-portal hindfoot endoscopy (Figure 5A).
Radiographs with the DOPP were made in a sitting position with the ankle in 90° (Figure 5B).
We chose this position to reproduce the conditions of the surgical procedure as accurate
as possible. The surgeon positions the ankle in 90° when creating the portals in standard
2-portal hindfoot endoscopy. We consider the force used by the surgeon best comparable
to the axial force sitting-down. The device was handled by 1 observer throughout the study
and repositioned with each radiograph.
RadiographsAll radiographs were made by a radiology technician. Per volunteer 1 standard lateral
weight-bearing radiograph with the foot in 20 degrees endorotation and 2 radiographs with
the DOPP (alternative radiographs) were made. Radiographs with the DOPP were made in a
neutral position to mimic the surgical setting. Next to measuring the DFC, the 2 radiographs
with the DOPP were also used to assess intra-observer reliability of placement of the DOPP.
All measurements were performed digitally using PACS (Picture Archiving and Communica-
tion System) Viewer by Agfa Health Care, Mortsel, Belgium.
Measurement of the DFC on radiographs was performed according to the methods explained
in figure 6. The acceptable variation of the DFC between two measurements per volunteer
was set to a maximum of 5 mm. This is the diameter of the bonecutter shaver used, chosen
as the radius in which the shaver can be moved without having to lengthen or change portal
location. We use this shaver to reduce the tuberosity in EC. If variation remained within a
limit of 5 mm, the retrocalcaneal space would still be accessible for the surgeon.
Figure 5. (A) Portal placement in standard posterior arthroscopy, using the distal tip of the fibula as a landmark. (B) Mimicking this surgical setting with the DOPP
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Figure 6. Digitally measured distance between the posterosuperior part of the calcaneus and the distal tip of the fibula (DFC, red arrow). Line A: foot sole; Line B: probe of the DOPP hooked under the tip of the fibula (which seems separate from the bone due to soft tissue interposition); Line C: continuation of a line through the vertical aspect of the posterior calcaneal tuberosity; Line D: prolongation of a hori-zontal line from the anterior to the posterior aspect of the calcaneal tuberosity; Line E: helpline parallel to line B (and A) through the junction of lines C and D
For all measurements intra- and interobserver reliability were calculated.
StatisticsResults were analyzed with SPSS (Statistical Package for the Social Sciences) 15.0 for Win-
dows. Volunteer characteristics are described as means and standard deviations or propor-
tions.
For intra- and interobserver reliability for the measurements of the CI- and TMT1- angles,
Intra Class Coefficients (ICC) with 95% confidence intervals (CI) were calculated; an ICC
of 0 - 0.2 indicates a poor reliability, 0.21 - 0.4 is fair, 0.41 – 0.6 is moderate, 0.61 – 0.8 is
substantial, and values between 0.81- 1.0 indicate high reliability8.
Intra-observer reliability for handling the DOPP was tested by calculating ICCs with a 95%
CI. To illustrate the variation for repeated measurements, we presented a Bland and Altmann
plot. This shows the limits of agreement and the 95% confidence interval with an acceptable
variation of 0 ± 5 mm.
182
The clinical validity of the DOPP was assessed through determination of the differences in dis-
tance measured on radiographs between the three foot types by means of an ANOVA-test,
and if necessary, an additional post hoc Bonferroni multiple comparisons test was applied.
Pearson correlation coefficients were calculated to assess association between DFC and
TMT1- and CI- angles, length and shoe size.
Spearman r correlation coefficients were calculated between the DFC and the categorized
variable (foot type according to physical examination).
Pearson- and Spearman correlation coefficients were interpreted as 0.0-0.2 being no; 0.2-
0.4 low; 0.4-0.7 moderate; 0.7-0.9 high; and above 0.9 very high4. A p-value < 0.05 was
considered statistically significant.
Figure 7. Bland and Altmann plot
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resULts
Demographic StatisticsDemographics of the volunteers are shown in Table 1. Twenty-four (85.7%) participants
actively participated in different sports. A ‘too many toes-sign’ was observed in 7 volunteers
(25%).
According to physical examination, we included 10 volunteers with normal feet (a normal
arch), 11 with flat feet (flat arch) and 7 volunteers with cavus feet (high arch).
Table 1. Demographics of the subjects, in means and standard deviations (in brackets)
Volunteers (n=28)
Age (years) 24.5 (±3.7)
Male/Female 8/20
Weight (kg) 69.3 (±13.3)
Length (m) 1.75 (±0.1)
BMI (in kg/m²) 22.5 (±3.5)
Left/right foot 15/13
Talo 1st metatarsal (TMT1) and calcaneal inclination (CI) angleThe forefoot of the first five consecutive volunteers was not properly visible on radiographs
because of technical difficulties, making it impossible to measure the TMT1-angle. We did
not make an additional radiograph to prevent them from exposition to more radiation than
agreed upon with the Medical Ethical Committee. The mean TMT1- angle was 0.1o (SD 9.8).
According to the classification described earlier, 9 had a flat arch, 6 had a normal arch and 8
volunteers had a high arch. Intra-observer reliability for the TMT1-angle showed ICC values
of 0.98 for both observers. Inter-observer reliability for the TMT1-angle was high with an ICC
of 0.91 (Figure 7).
The mean CI- angle was 21o (SD 6.1). According to the classification, 13 volunteers had a
flat arch, 12 a normal arch, and 3 a high arch. Intra-observer reliability for the CI-angle was
0.99 for both observers. The inter-observer reliability showed an ICC-value of 0.98.
No significant correlation was found between BMI, and TMT1- and CI- angle (p>0.1).
The DOPPThe intra-observer reliability for handling the DOPP, demonstrated an ICC of 0.96. The inter-
observer reliability for radiographic measurements of the DFC showed an ICC of 0.99 (95%
CI 0.97-0.99). Figure 7 shows the variation for repeated measurements. The red dotted lines
indicate the acceptable variation of 0 ±5 mm. 95% of our measurements lie within 3.4 and
-3.7 mm. This is within limits. In one volunteer the difference in DFC between two measure-
ments was more than 5 mm due to an error positioning the DOPP for the first radiograph.
184
Correlation between the radiological measurements and physical examination showed that
the TMT1-angle had the best correlation (Table 2).
DFC in different foot morphologiesCorrelation between the DFC and different variables are shown in Table 3.
The Spearman r correlation analysis revealed moderate correlations (r = 0.54 and 0.60, p
< 0.05) between foot morphology on physical examination and DFC and TMT1- angle and
DFC respectively.
The mean DFC for all feet was 18 mm (SD±5.6), with a range of 7.4 - 28 mm. Classifying the
various foot types according to physical examination, mean DFC for the group with flatfeet
was 15 mm (SD 4.5). The mean DFC for the group with normal feet was 20 mm (SD 4.8) and
for the group with cavus feet the mean DFC was 22 mm (SD 5.4) (Figure 8).
Table 2. Descriptive and reliability numbers for the footprint measurements and radiographic angles (for all correlations p< 0.05)
TMT-angle (n=23) CI-angle (n=28)
Mean (SD) 0.1 (±9.8) 21 (±6.1)
Min -17 12
Max 20 33
Classification 9 flat arch6 normal arch8 high arch
13 flat arch12 normal arch3 high arch
Intra-observer reliability observer 1
0.98 (95%CI: 9.94-0.99) 0.99 (95%CI: 0.97-0.99)
Intra-observer reliability observer 2
0.98 (95%CI: 0.96-0.99) 0.99 (95%CI: 0.98-1)
Inter-observer reliability
0.91 (95%CI: 0.74-0.97) 0.98 (95%CI: 0.96-0.99)
Correlation with physical examination
0.77 0.72
Table 3. Pearson’s correlations between DFC and different variables. (*statistically significant with p <0.05)
Correlations (n=28) DFC (Distance Fibula-Calcaneus)
Physical examination 0.54*
TMT-angle 0.60*
CI-angle 0.59*
Shoe size of volunteers 0.39*
Length of volunteers 0.09
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The ANOVA-test showed a significant difference of the DFC within the three different foot
type groups (p<0.05). Additionally, the Bonferroni multiple comparisons test revealed a
significant difference for the DFC between the group with flat feet and the group with cavus
feet (p=0.01). However, the same test did not reveal a significant difference for the DFC
between the group with flat feet and normal feet (p=0.07). Also, no significant difference
for the DFC was found between the group with normal feet and the group with cavus feet
(p=1.0).
DiscUssioN
The DOPP demonstrated to be a reliable instrument and radiological measurements for DFC
were highly reliable. The most important findings were that portal location in patients with
a flat foot should be placed at a mean of 15 mm from the tip of the fibula, in normal feet at
20 mm, and in cavus feet at a mean of 22 mm distal to the tip of the fibula.
Because ultimately most orthopaedists will determine foot type through physical examina-
tion, the most important correlation of the DFC is with foot morphology according to the
physical examination and not the TMT-1 angle. The loss of 5 patients for measuring the TMT
angle is a limitation of our study.
Our presumption that as the calcaneus inclines, the DFC gets larger seems evident. However,
correlation between the DFC and the CI-angle was moderate. Furthermore, not all volunteers
Figure 8. Mean distance for foot type according to physical examination. The distance shows marked overlap all three foot morphologies; there was no significant difference between the distance in flat- and normal or normal- and cavus feet. The Bonferroni multiple comparisons test did reveal a significant dif-ference for the DFC between the group with flat feet and the group with cavus feet (p=0.01)
186
with cavus feet showed a high CI- angle. This may be due to the fact that cavus is not always
associated with a large CI-angle13. As a result of that, the distance of the posterosuperior
calcaneus to the tip of the fibula is smaller than we expected in several cases. Also reported
is that some volunteers with a normal foot shape showed a rather high CI-angle. Due to
hyperpronation, some feet appeared to be flat feet, where hyperpronation and flat feet are
two different morphologies that can co-exist. In these cases, on physical examination foot
shape was normal with a radiographic high CI-angle, rendering a larger than expected DFC.
This could explain why there is marked overlap of DFCs between the group with normal feet
and the group with cavus feet.
Correlation between physical examination and DFC was also moderate so that a numeric
scale for portal placement based on foot morphology (angles) could not be constructed
from our study. Apparently, the various foot types show a marked overlap between the
distances from calcaneus to fibula. We can conclude however that in flat feet portal location
is significantly more proximal to the tip of the fibula, when compared to cavus feet. We real-
ize that we included a limited amount of volunteers; with a larger population we might also
find a significant difference between the DFC in flat and normal- and normal- and cavus feet.
The DOPP demonstrated to be highly reliable; with the limitation that only one observer
handled the DOPP throughout the whole study. Future research is still needed to determine
the inter-observer reliability for using the DOPP, and thereby its validity. The next step could
be testing the correlation of the DFC as measured pre-operatively with measurements of the
distance of the fibula tip to the incision as placed by an experienced orthopaedist. When
correlation is high, the DOPP might eventually be implemented in the daily clinic on individual
patients with a retrocalcaneal bursitis scheduled for EC. Until then, when uncertain about
portal placement, using fluoroscopy can be considered.
coNcLUsioN
The DOPP demonstrated to be highly reliable in measuring the DFC (ICC= 0.99). A numeric
distance scale for use in all different foot morphologies could not be constructed. There is a
direct relation between portal location and foot morphology (p<0.05), as in flat feet portal
location is significantly more proximal (15 mm) to the tip of the fibula when compared to
cavus feet (22 mm).
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refereNce List
1. Aminian A, Sangeorzan BJ. The anatomy of
cavus foot deformity. Foot Ankle Clin 2008;
13(2): 191-8.
2. Bryant D, Havey TC, Roberts R, Guyatt G.
How many patients? How many limbs?
Analysis of patients or limbs in the ortho-
paedic literature: a systematic review. J Bone
Joint Surg Am 2006; 88(1): 41-45.
3. Gould N. Evaluation of hyperpronation and
pes planus in adults. Clin Orthop Relat Res
1983; (181): 37-45.
4. Guilford JP. Fundamental Statistics in Psy-
chology and Education. 4th ed. New York:
McGraw-Hill; 1965.
5. Jerosch J, Nasef NM. Endoscopic calcane-
oplasty--rationale, surgical technique, and
early results: a preliminary report. Knee Surg
Sports Traumatol Arthrosc 2003; 11(3): 190-
195.
6. Jerosch J, Schunck J, Sokkar SH. Endoscopic
calcaneoplasty (ECP) as a surgical treatment
of Haglund’s syndrome. Knee Surg Sports
Traumatol Arthrosc 2007; 15(7): 927-934.
7. Karasick D, Schweitzer ME. Tear of the
posterior tibial tendon causing asymmetric
flatfoot: radiologic findings. AJR Am J
Roentgenol 1993; 161(6): 1237-1240.
8. Landis JR, Koch G.G. The measurement of
observer agreement for categorical data.
Biometrics. 1977: 159-173.
9. Lee MS, Vanore JV, Thomas JL et al. Diag-
nosis and treatment of adult flatfoot. J Foot
Ankle Surg 2005; 44(2): 78-113.
10. Meehan RE, Brage M. Adult acquired flat
foot deformity: clinical and radiographic
examination. Foot Ankle Clin 2003; 8(3):
431-452.
11. Menz HB, Munteanu SE. Validity of 3 clinical
techniques for the measurement of static
foot posture in older people. J Orthop Sports
Phys Ther 2005; 35(8): 479-486.
12. Murley GS, Menz HB, Landorf KB. A proto-
col for classifying normal- and flat-arched
foot posture for research studies using clini-
cal and radiographic measurements. J Foot
Ankle Res 2009; 2: 22.
13. Samilson RL, Dillin W. Cavus, cavovarus,
and calcaneocavus. An update. Clin Orthop
Relat Res 1983; (177): 125-132.
14. Scholten PE, van Dijk CN. Endoscopic
calcaneoplasty. Foot Ankle Clin 2006; 11(2):
439-46.
15. Solis G, Hennessy MS, Saxby TS. Pes cavus: a
review. Foot Ankle Surg 2000; 6: 145-153.
16. van Dijk CN. Hindfoot endoscopy. Foot
Ankle Clin 2006; 11(2): 391-414.
17. van Dijk CN, de Leeuw PA, Scholten PE.
Hindfoot endoscopy for posterior ankle
impingement. Surgical technique. J Bone
Joint Surg Am 2009; 91 Suppl 2: 287-298.
18. van Dijk CN, Scholten PE, Krips R. A 2-portal
endoscopic approach for diagnosis and
treatment of posterior ankle pathology.
Arthroscopy 2000; 16(8): 871-876.
19. van Dijk CN, van Dyk GE, Scholten PE, Kort
NP. Endoscopic calcaneoplasty. Am J Sports
Med 2001; 29(2): 185-189.
20. Younger AS, Sawatzky B, Dryden P. Radio-
graphic assessment of adult flatfoot. Foot
Ankle Int 2005; 26(10): 820-825.
PArt v GeNerAL DiscUssioN
General discussion
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termiNoLoGY
The best possible management of different pathologies begins with universal language in
science and daily clinical practice. Uniform terminology is believed to provide us with higher
consistency and understandability of a problem and therefore ensures that information can
be shared and compared seamlessly amongst clinicians. In chapter 1 a new terminology
for Achilles tendon related disorders was proposed, including the combination of anatomic
location, symptoms, clinical findings and pathological changes for each entity. Examining
the evolution of terminology over the last century, the ways to describe a clinical problem
became endless and eponyms received pole position. The reasoning behind a change in
terminology is unclear; it may for example be caused by different interpretation of pathology.
However, constructing terminology in which Haglund’s deformity, - syndrome and -disease
are all dissimilar entities is not desirable. The use of improper terms however is acquired over
centuries and may be complex to cure. Restrain is advocated regarding the adoption of new
terms or modify a pre-existent terminology solely on personal preference or interpretation.
oUtcome meAsUres AND AssessmeNt tooLs
In 2001 Tallon et al published a review on the outcome after surgery in patients with chronic
Achilles tendinopathy74. They pointed at the deficiencies in outcome assessment and criteria,
and subsequently recommended the use of outcome measures that were condition-specific,
reliable, sensitive, and correlated with clinical severity. Outcome assessment tools provide
the opportunity for universal outcome reporting. Data collected at widespread points can
then be fairly compared, and common goals of therapy can be determined. In chapter 2 a
summary is given of the available outcome measures and assessment tools. Assessment tools
described are strength measurements with dynamometry, endurance- and jump testing.
Strength measurements have shown to be reliable and valid for measuring improvement in
strength, but are curiously not useful in a clinical setting as they do not correlate sufficiently
with (subjective) functional performance13. The normal number of heel rise repetitions in
muscular endurance testing ranges from 25-7048. Therefore only a difference over time can
be measured and again there is no correlation with initial functional performance. This also
accounts for jump tests used to evaluate loading of the Achilles tendon. Assessment tools do
not correlate with initial functional performance, but are useful in measuring the effective-
ness of a treatment modality. The subjective VISA-A score is recommended for scientific
purposes as it has good reliability and validity, and has now been used in at least 19 different
studies16,18,20.
In chapter 3, after the German, Swedish and Italian, the VISA-A questionnaire was trans-
lated to the Dutch language (VISA-A-NL) and tested for reliability, internal consistency, con-
struct- and content validity. Application to non- athletes was also evaluated. The VISA-A-NL
194
showed high reliability (0.97 (95% CI 0.95-0.98)). Reliability of the translation was excellent,
with a statistically not significant difference between assessments. Crohnbach’s alpha for
internal consistency was good at 0.80. It even increased to 0.88 without the activity domain
of the questionnaire, accounting for 40% of points. As approximately 30% of patients do
not participate in sporting activities10 we concluded that patients with a non-athletic history
should receive a modified VISA-A score from which questions 7 and 8 are deleted, especially
as the effect of treatment in non-athletes otherwise can be underestimated.
Correlation of the VISA-A-NL with other subjective questionnaires (VAS, FAOS, SF-36) and
the AOFAS only was good compared with the functional subscale of the SF-36. Correlation
with other questionnaires was moderate or poorer. Noticeable is the moderate correlation
with VAS, with is a validated subjective outcome measure frequently used for scientific
means63. Although the FAOS has shown to be responsive to changes over time65, it has not
been validated for Achilles tendinopathy. To constructively discuss this matter these question-
naires first need to be validated for Achilles tendinopathy. We decided not to, as filling out
larger amounts of paperwork would be a burden for patients, with a lower response rate as
a consequence.
miDPortioN AchiLLes teNDiNoPAthY: cAUse of PAiN AND treAtmeNt moDALities
Numerous treatment modalities for midportion Achilles tendinopathy have been reported
over the last decades. However, only few (e.g. eccentric training) render a good outcome.
Unsatisfactory treatment results can be caused by the reality that the mechanisms by which
these diverse treatments attack pathology are unclear. Moreover, the mechanism by which
the problem originates is even unidentified. In other words: should we not first identify the
problem before coming up with a solution?
When work on this thesis started, one of the newest treatment modalities for midportion
Achilles tendinopathy was Ethoxysclerol as introduced by Alfredson et al.5-8,36,79. Etoxysclerol
damages the intima of bloodvessels after which they obliterate. The theory on which the
injection of this substance was built, neovascularisation and accompanying neo-innervation
in and around the tendon as the cause of complaints, also broke new ground and formed
the basis of current new insights. The godfathers of Etoxysclerol treatment instructed our
team and from 2004-2007 a total of 113 consecutive patients with 140 symptomatic Achilles
tendons underwent colour Doppler ultrasonography investigation (US) in our clinic. Sixty-two
patients had 70 symptomatic tendons showing neovascularisation (50%). In 50% of tendons
with Achilles tendinopathy no neovessels were found. Others found neovascularisation in
50-88% of symptomatic tendons23,62,64,78.
If only present in 50% of tendons, can neovessels yet be the cause of complaints? Or do
they obliterate in the progress of pathology or healing?
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Furthermore, of these patients only 44% of tendons were painless or minimally painful
at six weeks after treatment. At 2.7-5.1 year follow-up 53% of all treated tendons had
undergone various forms of additional treatment (conservative or surgical). Three patients
still had complaints. Can we conclude from this study, combined with Paavola et al.59 that
whatever treatment is commenced, that on the long term the natural history is benign?
The main focus of treatment of Achilles tendinopathy is on relieving pain. It is question-
able if degeneration of the tendon itself is the main cause of pain, since intratendinous
changes are found in up to 34% of people without complaints27,33,40, 42. Persistent structural
abnormalities and thickening of the tendon 13 years after intra-tendinous surgery for Achil-
les tendinopathy was seen, whereas all patients were satisfied with the results and went back
to Achilles tendon loading activities without restrictions9. Degeneration had not completely
resolved, and although ruptured tendons show degenerative changes on histology41, there
is no evidence that pathological tendons are more prone to rupture. On the contrary, most
often intratendinous changes are addressed in surgical treatment. But are these changes
responsible for the pain?
Chapter 8 comprises a philosophy of the cause of pain in midportion Achilles tendinopa-
thy. It is postulated that the process of tendinopathy does start with localized tendon micro-
injury and degeneration, caused by ageing and repetitive strain. The pain is often prominent
at 2-7 cm proximal to the calcaneus, where the tendon makes a twist; it is described that
at this site blood flow even declines10,58. When the demands of the tendon exceed fiber
strength, micro-injuries can develop1. An inadequate repair process causes a repetitive cycle
of inadequate collagen and matrix production, tenocyte disruption, a further decrease of
collagen and matrix and consequently increased vulnerability to further micro-injuries. Due
to the lack of vascularisation, instead of a chemical-, a neurogenic inflammatory process is
activated to repair these microruptures.
This neurogenic inflammatory response comprised of a new ingrowth of nerve fibers15,28
accompanying the peritendinous vascular ingrowth from the paratenon into the tendon
proper46,67. With this nerve ingrowth, levels of glutamate, calcitonin gene-related peptide
(CGRP) and substance P rise2,11. Sensory neonerves cause an increase in pain signalling by
producing these nociceptive substances past the critical threshold4,11. Transition to symp-
tomatic tendinopathy now occurs. Also, myofibroblasts proliferate and synthesize abundant
amounts of collagen to repair the tendon proper, but also cause the formation of scar tissue
around the tendon and consequently the paratenon adheres onto the Achilles tendon at
the location of the neurovascular ingrowth. Scarring in turn may lead to impaired circulation
and further contribute to the pathogenesis of Achilles tendinopathy. In the earlier described
20-50% of patients without neovascularisation, vasoconstriction and scarring with mechani-
cal constriction may already have lead to obliteration of neovessels. Nerves however will
survive.
196
Involvement of the plantaris tendon in the process of tendinopathy is considered, as it runs
with the Achilles tendon on its medial side within a shared paratenon. When constriction
of the paratenon develops, the plantaris tendon gets involved. As described, it is tri-articular
and the medial side of the midportion of the Achilles tendon is bi-articular, hypothetically
causing altered mechanics and pain as a consequence. Recently Lintz et al. performed a
biomechanical study indicating that the Achilles tendon elongates a greater distance than
the plantaris tendon under similar tensile stresses. As a consequence the two surfaces could
trap peritendinous tissues between them, which could be subject to shear stresses and cause
pain47.
In chapter 5 Achilles tendoscopy as invented by van Dijk et al. in 1997 is described75. The
paratenon is endoscopically released from the Achilles- and plantaris tendon is cut with good
clinical results. Alfredson et al. recently described a series of 73 Achilles tendons in which
during treatment with ultrasound and Doppler-guided scraping an invaginated, or close by
located, enlarged plantaris tendon was found in 58 of cases3. In these patients, the plantaris
tendon was surgically removed with good clinical results and the authors confirm that the
plantaris tendon might be of interest in the aetiology and treatment of midportion Achilles
tendinopathy.
However, large comparative studies are lacking as the population in the academical
setting is small, and patients demanding surgery even less. Ideal would be a randomized
clinical trial comparing open surgery with endoscopic release of the paratenon and a group
undergoing the endoscopic approach as well as transsecting the plantaris tendon. Currently
a prospective study on Achilles tendoscopy is being carried out. However, involvement of
the plantaris tendon in the pathological process had not yet been studied anatomically nor
clinically in an isolated procedure.
In chapter 6 it is hypothesized that constriction of the paratenon onto the Achilles
tendon consequently causes adhesion of the plantaris tendon to the surrounding tissues.
After formation of adhesions, the different mechanical properties of both the Achilles- and
plantaris musculotendinous complex may be the cause of complaints. However, absence
of the plantaris tendon in 7-20% of human cadavers has been described21,22,30,32,54,68. An
observational study of 107 lower extremities on the anatomy at the level of the Achilles
tendon was conducted. In all a plantaris tendon was identified, which was occasionally
difficult due to a mixture of 9 different insertion sites, especially the variant with insertion
into the medial side of the Achilles tendon proper. However, when dissecting from proximal
to distal it was identified in all specimens. This could be an explanation for the tentative
absence in the earlier mentioned 7-20% of legs. Another explanation could be absence due
to isolated rupture25,35. With our relatively large group of specimens, we not only contradict
earlier findings of its absence, but also raise implications for daily practise. The plantaris
tendon is often used for grafting because it can be sacrificed without discernible deficit, and
is of adequate length and thickness for many applications14,49,53,69. We advise to retrieve the
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tendon proximally (e.g. with a tendon stripper). The use of ultrasound- or MR- imaging prior
to surgery to pre-assess its course may be helpful.
In 11 specimens (10%) firm connections were found at the level of the Achilles tendon
midportion. It was not possible to perform histology of these findings, or of the involved
Achilles tendons, a flaw of this study.
Chapter 7 illustrates a pilot study of a new surgical technique in which the plantaris
tendon is excised with a hamstring stripper through a small incision on the medial side of the
proximal calf. Three patients with complaints of midportion tendinopathy were treated in this
pilot. Although the tendon stripper appeared too short in one patient, the plantaris tendon
ruptured above the adhesions in the other, and in one the procedure went as planned, all
were satisfied with the result and reported no complaints at 1 year follow-up. This outcome
may well be attributable to coincidence as only 3 patients were treated. Although the pro-
cedure went with varying success, different pull of adhered tendons was eliminated in all by
excising the tendon. Another explanation for pain relief could be indirect stripping of the
paratenon with introduction of the tendon stripper.
Now where should the treatment of Achilles tendinopathy commence? Should the plan-
taris tendon be (surgically) addressed, or should the sympathetic nerves coming from the
paratenon be denervated? What is effective in pain relief in the majority of patients?
Of course direct referral to surgical measures is undesirable. Conservative management
should always be considered first. Injection with Etoxysclerol, saline and PRP could theoreti-
cally yield similar results as surgical denervation. With Etoxysclerol, nerves are probably also
attacked. On the contrary, injection may not suffice because of low volume and effectiveness
of the substance on nerves, and adhesions may be too solid to be adequately released. High-
volume injection has been successfully performed, thereby obliterating neovascularisation
and accompanying neonerves18. Brisement, first described in 199739, was initially meant to
interrupt the degenerative cycle of the tendon proper by initiating a healing cascade, but in
essence seems equivalent to current high-volume injections.
Moreover, small volume injections also seem to generate a response. Injection of PRP
was compared with saline, producing an equivalent outcome24. Corticosteroid injections for
lateral epicondylitis and aprotinin for Achilles tendinopathy were comparable with placebo,
showing no statistically significant difference in outcome70. Could this mean that no matter
what we introduce, an inflammatory response will be generated?
Surgical treatment should be reserved for patients that do not respond to primary con-
servative measures. When sufficiently researched in well-designed clinical trials early surgical
management can be considered for professional athletes or patients depending on their
fitness in daily life for a quicker return to normal activities.
198
retrocALcANeAL BUrsitis: DiAGNosis AND treAtmeNt
A symptomatic inflammation of the retrocalcaneal bursa is caused by repetitive impingement
of the bursa between the anterior aspect of the Achilles tendon and a bony posterosuperior
calcaneal prominence26,71,72. Most publications focus on this prominence, which however
has not shown to be very reliable17,29,61. In retrocalcaneal bursitis, the normally sharply
outlined radiolucent retrocalcaneal recess of Kager’s triangle is obliterated. In chapter 9
we determined the usefulness and reliability of the radiographic appearance of this recess
in diagnosing a retrocalcaneal bursitis on digital radiographs. The sensitivity was 83% for
observer 1 and 79% for observer 2. Specificity was 100% and 98% for observer 1 and 2. The
interobserver reliability test calculated a kappa-value of 0.86. For observer 1 intraobserver
reliability was 0.96 and 0.92 for observer 2. This means further diagnostic evaluation is not
necessary, resulting in a higher cost-effectiveness and quicker treatment. MRI can still be per-
formed in case of doubt. However, does Kager triangle normalize when complaints diminish?
If yes, is the retrocalcaneal recess useful for diagnosis when complaints unhoped-for recur?
Kager’s triangle is distorted due to the inflammatory response after surgical treatment; in
endoscopic surgery the flow of saline also causes distortion. Scar tissue develops which also
causes a change in radiolucency, one that over time might diminish. Research on the useful-
ness of Kager’s triangle after surgery is currently executed.
An optimal treatment algorithm for retrocalcaneal bursitis, as for midportion tendinopathy,
has not been found yet. Conservative management includes inlays, adaptation of shoe wear,
rest, NSAIDs and a single cortisone injection in the retrocalcaneal bursa56,57,73. Cortisone
injections are not advised since these can weaken the tendon with the potential danger of
rupture. The best level of evidence for this potential danger nevertheless is derived from case
reports19,34,43,50,77.
The aim of surgery for retrocalcaneal bursitis is to prevent impingement of the bursa
between the Achilles tendon and the calcaneus. This can be accomplished by removing the
inflamed retrocalcaneal bursa, followed by either resection of the posterosuperior tuberosity
or by a closing wedge osteotomy to prevent recurrence. Posterosuperior calcaneal resection
can be performed through a posterolateral or posteromedial incision or through a combina-
tion of both12,44,60.
Due to inappropriate visualization of the Achilles tendon during open procedures, weaken-
ing or even rupture has been reported45,52. Full recovery time after open resection can take
up to 2 years.
Endoscopic calcaneoplasty offers a minimally invasive alternative to open surgery. Sur-
geons familiar with the endoscopic approach favor this procedure, because of its better
visualization. Our results of endoscopic calcaneoplasty are comparable with other reports
on endoscopic treatment31,37,38,66,76. Two portals are used, just lateral and medial to the
Achilles tendon, at the level of the posterosuperior tuberosity of the calcaneus. During the
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procedure, the inflamed retrocalcaneal bursal tissue and posterosuperior prominence of the
calcaneus are resected using a Bonecutter shaver. However, due to the local anatomy, bulky
subcutaneous tissue and swelling of the bursal tissue, palpation of the posterosuperior tuber-
osity is difficult and portals can easily be placed too proximal. This will result in a suboptimal
procedure. Fluoroscopy is sometimes used to make portals, but can be time-consuming as
the surgeon has to rely on availability and personnel. We therefore aimed to standardize
portal placement using a self-developed ‘Device for Optimal Portal Placement’ (DOPP), using
the distance from the distal tip of the fibula to the posterosuperior calcaneus (DFC) on a
radiograph in volunteers as described in chapter 11. This tip has not been validated but is
already used as a landmark for portal placement in standard 2-portal hindfoot endoscopy
with good visualization. It was decided to use healthy volunteers, as the goals of this study
were to 1) validate the DOPP for portal placement, 2) see if the distance DFC would help us
determine the ultimate position of portals and 3) to recover a direct relationship between
foot morphology and portal location. If standardization was performed in retrocalcaneal
cases, many patients would have been needed as there is a large between- patient variance
in calcaneal contour in retrocalcaneal bursitis.
However, from this study a numeric distance- scale to be used in all different foot mor-
phologies could not be constructed. Although TMT1, -CI-angles and physical examination
were found to be the best available objective measures to determine foot morphology51,55,
disappointing correlations were found. Apparently, the various foot morphologies show a
marked overlap between the distances from posterosuperior calcaneus to fibula. We can
conclude however that in flat feet portal location is significantly more proximal to the tip of
the fibula, when compared to cavus feet. Still a limited amount of volunteers was included;
with a larger population we might also find a significant difference between the DFC in flat
and normal- and normal- and cavus feet and construction of a numeric scale may be possible.
The DOPP demonstrated to be highly reliable; with the limitation that inter-observer reli-
ability was not tested. Future research is still needed to determine its validity. The project
could be extended with a larger amount of volunteers. The next step could be testing the
correlation of the DFC as measured pre-operatively with measurements of the distance of
the fibula tip to the incision as placed by an experienced orthopaedist. When correlation is
high, the DOPP might eventually be implemented in the daily clinic on individual patients
with a retrocalcaneal bursitis scheduled for EC; or a gliding scale for portal placement may
be constructed. Until then, when uncertain about portal placement, fluoroscopy should still
be considered.
fUtUre reseArch
Research on Achilles tendon-related problems is ongoing. The first step to optimal manage-
ment is to speak the same scientific language. This not only accounts for the Achilles tendon,
200
and therefore it is advocated to construct a standard terminology for all medical problems.
Implementation however will be complex. Further research on chronic midportion Achilles
tendinopathy should focus on the cause of pain instead of formulating more substances for
injection in or around the tendon as currently seems to be the tendency. Recognizing the
cause of complaints will help to further define therapeutic strategies. Undoubtedly, caution
should be taken when considering surgical treatment, although endoscopic and minimally
invasive procedures generate considerably less complications and shorter rehabilitation when
compared to open surgery. Treatment in my opinion therefore needs to be individualized.
Currently patients spend months to even years in the medical circuit. This also accounts for
patients with retrocalcaneal bursitis. Surgery is less often considered in non-athletes with low
demands in daily life and minor complaints, but endlessly applying conservative measures in
athletes and patients with high daily physical demands requiring a quick return to normal
activities may be unwanted. In minimally invasive and endoscopic surgery for midportion
tendinopathy the degenerative lesion is often left untouched, of which it would be interest-
ing to research the long-term consequences.
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refereNce List
1. Abate M, Gravare SK, Siljeholm C et al.
Pathogenesis of tendinopathies: inflam-
mation or degeneration? Arthritis Res Ther
2009; 11(3): 235.
2. Ackermann PW, Li J, Lundeberg T, Kreicbergs
A. Neuronal plasticity in relation to nocicep-
tion and healing of rat achilles tendon. J
Orthop Res 2003; 21(3): 432-441.
3. Alfredson H. Midportion Achilles tendinosis
and the plantaris tendon. Br J Sports Med
2011; 45(13): 1023-1025.
4. Alfredson H, Forsgren S, Thorsen K, Fahl-
strom M, Johansson H, Lorentzon R. Gluta-
mate NMDAR1 receptors localised to nerves
in human Achilles tendons. Implications for
treatment? Knee Surg Sports Traumatol
Arthrosc 2001; 9(2): 123-126.
5. Alfredson H, Harstad H, Haugen S, Ohberg
L. Sclerosing polidocanol injections to treat
chronic painful shoulder impingement
syndrome-results of a two-centre collabora-
tive pilot study. Knee Surg Sports Traumatol
Arthrosc 2006; 14(12): 1321-1326.
6. Alfredson H, Lorentzon R. Sclerosing polido-
canol injections of small vessels to treat the
chronic painful tendon. Cardiovasc Hematol
Agents Med Chem 2007; 5(2): 97-100.
7. Alfredson H, Ohberg L. Neovascularisation
in chronic painful patellar tendinosis--
promising results after sclerosing neovessels
outside the tendon challenge the need
for surgery. Knee Surg Sports Traumatol
Arthrosc 2005; 13(2): 74-80.
8. Alfredson H, Ohberg L, Zeisig E, Lorentzon
R. Treatment of midportion Achilles ten-
dinosis: similar clinical results with US and
CD-guided surgery outside the tendon and
sclerosing polidocanol injections. Knee Surg
Sports Traumatol Arthrosc 2007; 15(12):
1504-1509.
9. Alfredson H, Zeisig E, Fahlstrom M. No nor-
malisation of the tendon structure and thick-
ness after intratendinous surgery for chronic
painful midportion Achilles tendinosis. Br J
Sports Med 2009; 43: 948-949.
10. Ames PR, Longo UG, Denaro V, Maffulli
N. Achilles tendon problems: not just an
orthopaedic issue. Disabil Rehabil 2008;
30(20-22): 1646-1650.
11. Andersson G, Danielson P, Alfredson H,
Forsgren S. Nerve-related characteristics
of ventral paratendinous tissue in chronic
Achilles tendinosis. Knee Surg Sports Trau-
matol Arthrosc 2007; 15(10): 1272-1279.
12. Angermann P. Chronic retrocalcaneal bur-
sitis treated by resection of the calcaneus.
Foot Ankle 1990; 10(5): 285-287.
13. Augustsson J, Thomee R. Ability of closed
and open kinetic chain tests of muscular
strength to assess functional performance.
Scand J Med Sci Sports 2000; 10(3): 164-168.
14. Bertelli JA, Santos MA, Kechele PR, Rost
JR, Tacca CP. Flexor tendon grafting using
a plantaris tendon with a fragment of
attached bone for fixation to the distal
phalanx: a preliminary cohort study. J Hand
Surg Am 2007; 32(10): 1543-1548.
15. Bjur D, Alfredson H, Forsgren S. The innerva-
tion pattern of the human Achilles tendon:
studies of the normal and tendinosis tendon
with markers for general and sensory
innervation. Cell Tissue Res 2005; 320(1):
201-206.
16. Brown R, Orchard J, Kinchington M, Hooper
A, Nalder G. Aprotinin in the management
of Achilles tendinopathy: a randomised
controlled trial. Br J Sports Med 2006; 40(3):
275-279.
17. Burhenne LJ, Connell DG. Xeroradiography
in the diagnosis of the Haglund syndrome.
Can Assoc Radiol J 1986; 37(3): 157-160.
18. Chan O, O’Dowd D, Padhiar N et al. High
volume image guided injections in chronic
Achilles tendinopathy. Disabil Rehabil 2008;
30(20-22): 1697-1708.
19. Chechick A, Amit Y, Israeli A, Horoszowski
H. Recurrent rupture of the achilles tendon
202
induced by corticosteroid injection. Br J
Sports Med 1982; 16(2): 89-90.
20. Christenson RE. Effectiveness of specific soft
tissue mobilizations for the management
of Achilles tendinosis: single case study--
experimental design. Man Ther 2007; 12(1):
63-71.
21. Danforth CH. The Heredity of Unilateral
Variations in Man. Genetics 1923; 9: 199-
210.
22. Daseler EH. The Plantaris Muscle: An Ana-
tomical Study of 750 Specimens. J Bone
Joint Surg 1943; 25: 822-827.
23. de Vos RJ, Weir A, Cobben LP, Tol JL. The
value of power Doppler ultrasonography in
Achilles tendinopathy: a prospective study.
Am J Sports Med 2007; 35(10): 1696-1701.
24. de Vos RJ, Weir A, van Schie HT et al. Plate-
let-rich plasma injection for chronic Achilles
tendinopathy: a randomized controlled trial.
JAMA 2010; 303(2): 144-149.
25. Delgado GJ, Chung CB, Lektrakul N et al.
Tennis leg: clinical US study of 141 patients
and anatomic investigation of four cadavers
with MR imaging and US. Radiology 2002;
224(1): 112-119.
26. DeVries JG, Summerhays B, Guehlstorf DW.
Surgical correction of Haglund’s triad using
complete detachment and reattachment of
the Achilles tendon. J Foot Ankle Surg 2009;
48(4): 447-451.
27. Emerson C, Morrissey D, Perry M, Jalan
R. Ultrasonographically detected changes
in Achilles tendons and self reported
symptoms in elite gymnasts compared with
controls - An observational study. Man Ther
2010; 15(1): 37-42.
28. Forsgren S, Danielson P, Alfredson H. Vas-
cular NK-1 receptor occurrence in normal
and chronic painful Achilles and patellar
tendons: studies on chemically unfixed as
well as fixed specimens. Regul Pept 2005;
126(3): 173-181.
29. Fowler A. Abnormalities of the calcaneus
as a cause of painful heel: its diagnosis and
operative treatment. Br J Surg 1945; 32:
494-498.
30. Freeman AJ, Jacobson NA, Fogg QA. Ana-
tomical variations of the plantaris muscle
and a potential role in patellofemoral pain
syndrome. Clin Anat 2008; 21(2): 178-181.
31. Frey C. Surgical advancements: arthroscopic
alternatives to open procedures: great toe,
subtalar joint, Haglund’s deformity, and
tendoscopy. Foot Ankle Clin 2009; 14(2):
313-339.
32. Gruber W. Beobachtungen aus der Men-
schlichen und Vergleichenden Anatomie.
1879. Berlin, A. Hirschwald.
33. Haims AH, Schweitzer ME, Patel RS, Hecht
P, Wapner KL. MR imaging of the Achilles
tendon: overlap of findings in symptomatic
and asymptomatic individuals. Skeletal
Radiol 2000; 29(11): 640-645.
34. Halpern AA, Horowitz BG, Nagel DA. Ten-
don ruptures associated with corticosteroid
therapy. West J Med 1977; 127(5): 378-382.
35. Helms CA, Fritz RC, Garvin GJ. Plantaris
muscle injury: evaluation with MR imaging.
Radiology 1995; 195(1): 201-203.
36. Hoksrud A, Ohberg L, Alfredson H, Bahr R.
Ultrasound-guided sclerosis of neovessels
in painful chronic patellar tendinopathy:
a randomized controlled trial. Am J Sports
Med 2006; 34(11): 1738-1746.
37. Jerosch J, Nasef NM. Endoscopic calcane-
oplasty--rationale, surgical technique, and
early results: a preliminary report. Knee Surg
Sports Traumatol Arthrosc 2003; 11(3): 190-
195.
38. Jerosch J, Schunck J, Sokkar SH. Endoscopic
calcaneoplasty (ECP) as a surgical treatment
of Haglund’s syndrome. Knee Surg Sports
Traumatol Arthrosc 2007; 15(7): 927-934.
39. Johnston E, Scranton P, Jr., Pfeffer GB.
Chronic disorders of the Achilles tendon:
results of conservative and surgical treat-
ments. Foot Ankle Int 1997; 18(9): 570-574.
40. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
Part VG
eneral d
iscussio
n
203
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73(10): 1507-1525.
41. Kannus P, Jozsa L. Histopathological changes
preceding spontaneous rupture of a tendon.
A controlled study of 891 patients. J Bone
Joint Surg Am 1991; 73(10): 1507-1525.
42. Khan KM, Forster BB, Robinson J et al. Are
ultrasound and magnetic resonance imag-
ing of value in assessment of Achilles tendon
disorders? A two year prospective study. Br J
Sports Med 2003; 37(2): 149-153.
43. Kleinman M, Gross AE. Achilles tendon
rupture following steroid injection. Report
of three cases. J Bone Joint Surg Am 1983;
65(9): 1345-1347.
44. Kolodziej P, Glisson RR, Nunley JA. Risk
of avulsion of the Achilles tendon after
partial excision for treatment of insertional
tendonitis and Haglund’s deformity: a
biomechanical study. Foot Ankle Int 1999;
20(7): 433-437.
45. Le TA, Joseph PM. Common exostectomies
of the rearfoot. Clin Podiatr Med Surg 1991;
8(3): 601-623.
46. Lian O, Dahl J, Ackermann PW, Frihagen F,
Engebretsen L, Bahr R. Pronociceptive and
antinociceptive neuromediators in patellar
tendinopathy. Am J Sports Med 2006;
34(11): 1801-1808.
47. Lintz F, Higgs A, Millett M et al. The role of
Plantaris Longus in Achilles tendinopathy: A
biomechanical study. Foot Ankle Surg 2011;
17(4): 252-255.
48. Lunsford BR, Perry J. The standing heel-rise
test for ankle plantar flexion: criterion for
normal. Phys Ther 1995; 75(8): 694-698.
49. Lynn TA. Repair of the torn achilles tendon,
using the plantaris tendon as a reinforcing
membrane. J Bone Joint Surg Am 1966;
48(2): 268-272.
50. Mahler F, Fritschy D. Partial and complete
ruptures of the Achilles tendon and local
corticosteroid injections. Br J Sports Med
1992; 26(1): 7-14.
51. Menz HB, Munteanu SE. Validity of 3 clinical
techniques for the measurement of static
foot posture in older people. J Orthop Sports
Phys Ther 2005; 35(8): 479-486.
52. Miller AE, Vogel TA. Haglund’s deformity
and the Keck and Kelly osteotomy: a ret-
rospective analysis. J Foot Surg 1989; 28(1):
23-29.
53. Morrison WA, Schlicht SM. The plantaris
tendon as a tendo-osseous graft. Part II.
Clinical studies. J Hand Surg Br 1992; 17(4):
471-475.
54. Moss ALH. Is There an Association Between
an Absence of Palmaris Longus Tendon and
an Absence of Plantaris Tendon? Eur J Plast
Surg 1988; 11: 32-34.
55. Murley GS, Menz HB, Landorf KB. A proto-
col for classifying normal- and flat-arched
foot posture for research studies using clini-
cal and radiographic measurements. J Foot
Ankle Res 2009; 2: 22.
56. Myerson MS, McGarvey W. Disorders of the
Achilles tendon insertion and Achilles tendi-
nitis. Instr Course Lect 1999; 48: 211-218.
57. Nesse E, Finsen V. Poor results after resection
for Haglund’s heel. Analysis of 35 heels in
23 patients after 3 years. Acta Orthop Scand
1994; 65(1): 107-109.
58. O’Brien M. The anatomy of the Achilles ten-
don. Foot Ankle Clin 2005; 10(2): 225-238.
59. Paavola M, Kannus P, Paakkala T, Pasanen M,
Järvinen M. Long-term prognosis of patients
with achilles tendinopathy. An observational
8-year follow-up study. Am J Sports Med
2000; 28(5): 634-642.
60. Pauker M, Katz K, Yosipovitch Z. Calcaneal
ostectomy for Haglund disease. J Foot Surg
1992; 31(6): 588-589.
61. Pavlov H, Heneghan MA, Hersh A, Goldman
AB, Vigorita V. The Haglund syndrome:
initial and differential diagnosis. Radiology
1982; 144(1): 83-88.
62. Peers KH, Brys PP, Lysens RJ. Correlation
between power Doppler ultrasonography
and clinical severity in Achilles tendinopathy.
Int Orthop 2003; 27(3): 180-183.
63. Price DD, McGrath PA, Rafii A, Buckingham
B. The validation of visual analogue scales
204
as ratio scale measures for chronic and
experimental pain. Pain 1983; 17(1): 45-56.
64. Reiter M, Ulreich N, Dirisamer A, Tschola-
koff D, Bucek RA. [Extended field-of-view
sonography in Achilles tendon disease: a
comparison with MR imaging]. Rofo 2004;
176(5): 704-708.
65. Roos EM, Brandsson S, Karlsson J. Validation
of the foot and ankle outcome score for
ankle ligament reconstruction. Foot Ankle
Int 2001; 22(10): 788-794.
66. Scholten PE, van Dijk CN. Endoscopic
calcaneoplasty. Foot Ankle Clin 2006; 11(2):
439-46.
67. Schubert TE, Weidler C, Lerch K, Hofstadter
F, Straub RH. Achilles tendinosis is associated
with sprouting of substance P positive nerve
fibres. Ann Rheum Dis 2005; 64(7): 1083-
1086.
68. Schwalbe, Pfitzner. Varietäten-Statistik und
Anthropologie. Deutsche Med Wchnschr
1894; 25(3): 459.
69. Shuhaiber JH, Shuhaiber HH. Plantaris ten-
don graft for atrioventricular valve repair: a
novel hypothetical technique. Tex Heart Inst
J 2003; 30(1): 42-44.
70. Smidt N, van der Windt DA, Assendelft WJ,
Deville WL, Korthals-de Bos IB, Bouter LM.
Corticosteroid injections, physiotherapy, or a
wait-and-see policy for lateral epicondylitis:
a randomised controlled trial. Lancet 2002;
359(9307): 657-662.
71. Sofka CM, Adler RS, Positano R, Pavlov H,
Luchs JS. Haglund’s Syndrome: Diagnosis
and Treatment Using Sonography. Humanity
Soc Science J 2006; (2): 27-29.
72. Stephens MM. Haglund’s deformity and
retrocalcaneal bursitis. Orthop Clin North
Am 1994; 25(1): 41-46.
73. Subotnick SI, Block AJ. Retrocalcaneal
problems. Clin Podiatr Med Surg 1990; 7(2):
323-332.
74. Tallon C, Coleman BD, Khan KM, Maffulli
N. Outcome of surgery for chronic Achilles
tendinopathy. A critical review. Am J Sports
Med 2001; 29(3): 315-320.
75. van Dijk CN, Scholten PE, Kort N. Tendos-
copy (tendon sheath endoscopy) for overuse
tendon injuries. Oper Techn Sports Med
1997; 5: 170-178.
76. van Dijk CN, van Dyk GE, Scholten PE, Kort
NP. Endoscopic calcaneoplasty. Am J Sports
Med 2001; 29(2): 185-189.
77. Wiegerinck JI, Reilingh ML, de Jonge MC,
van Dijk CN, Kerkhoffs GM. Injection
techniques of platelet-rich plasma into and
around the achilles tendon: a cadaveric
study. Am J Sports Med 2011; 39(8): 1681-
1686.
78. Zanetti M, Metzdorf A, Kundert HP et al.
Achilles tendons: clinical relevance of neo-
vascularization diagnosed with power Dop-
pler US. Radiology 2003; 227(2): 556-560.
79. Zeisig E, Ohberg L, Alfredson H. Sclerosing
polidocanol injections in chronic painful ten-
nis elbow-promising results in a pilot study.
Knee Surg Sports Traumatol Arthrosc 2006;
14(11): 1218-1224.
PArt vi
Summary
Part VI
Sum
mary
211
GeNerAL iNtroDUctioN
The prevalence of obesity in the Western World is rising, and therefore getting- and keep-
ing fit has been increasingly important in the recent years. Endurance sports like triathlons
and long distance running have gained popularity. Overuse injuries have become prominent
in daily practice. General inactivity during the week followed by extreme exercise in the
weekend allow for these types of injury to occur. 30-50% of all sports injuries are overuse
injuries. Chronic Achilles tendon pathology is one of the biggest problems in sports involving
running and jumping. In elite long-distance runners there is a lifetime risk of 52% of sustain-
ing an Achilles tendon injury. However, it is not always related to excessive physical activity.
Thirty percent of patients have a sedentary lifestyle. Recalcitrant Achilles tendons may cause
pain for years and are often resistant to any form of treatment. In the end, chronic Achilles
tendon complaints may be self-limiting. Especially athletes will not consent with this possible
prospect. The cause of pain has not yet been clarified, and therefore its treatment is chal-
lenging and often unsatisfactory. The aim of this thesis was to elucidate the cause of pain,
to develop appropriate assessment tools, to invent minimally invasive treatment methods,
and to optimize diagnostic and endoscopic methods for chronic Achilles tendon problems.
chAPter 1
Terminology for Achilles tendon related disordersThe terminology of Achilles tendon pathology has become inconsistent and confusing
throughout the years. A new terminology is proposed; definitions include the anatomic loca-
tion, symptoms, clinical findings and histopathology.
Midportion Achilles tendinopathy: a clinical syndrome characterized by a combination
of pain, swelling and impaired performance. It includes, but is not limited to, the histo-
pathological diagnosis of tendinosis. Achilles paratendinopathy: an acute or chronic inflam-
mation and/or degeneration of the thin membrane around the Achilles tendon. There are
clear distinctions between acute paratendinopathy and chronic paratendinopathy, both in
symptoms as in histopathology. Insertional Achilles tendinopathy: located at the insertion of
the Achilles tendon onto the calcaneus, bone spurs and calcifications in the tendon proper at
the insertion site may exist. Retrocalcaneal bursitis: an inflammation of the bursa in the recess
between the anterior inferior side of the Achilles tendon and the posterosuperior aspect of
the calcaneus (retrocalcaneal recess). Superficial calcaneal bursitis: inflammation of the bursa
located between a calcaneal prominence or the Achilles tendon and the skin.
Finally, it is suggested that previous terms as Haglund’s disease; Haglund’s syndrome;
Haglund’s deformity; pump bump (calcaneus altus; high prow heels; knobbly heels; cucum-
ber heel), are no longer used.
212
chAPter 2
Outcome measures and assessment toolsThorough history taking and clinical examination are essential in diagnosing Achilles tendi-
nopathy. Moreover, it is important to continuously evaluate the patients’ progress with both
validated subjective scoring systems, such as the VISA-A questionnaire, and with various
validated functional tests. Also, general subjective complaints and ability to return to previ-
ous physical activity and sports are important outcome measures. Proper evaluations with
validated tests are not only of importance for scientific purposes, but also to the practitioner
and the patient to follow the progress with treatment and rehabilitation.
chAPter 3
Translation and validation of the Dutch VISA-A questionnaire for Achilles tendinopathy and applicability to non-athletesIn 2001, the Victorian Institute of Sports Assessment developed a self-administered question-
naire evaluating symptoms and their effect on physical activity for patients with Achilles
tendinopathy. It has proven to be an effective outcome questionnaire in various languages.
The aim of this project is to translate and validate the VISA-A questionnaire into the Dutch
language (VISA-A-NL) and to assess its applicability to non-athletes. After translation accord-
ing to a forward-backward protocol, 101 patients with complaints of Achilles tendinopathy
were asked to fill out the VISA-A-NL at two time points together with VAS, FAOS and SF-36
questionnaires. Reliability, internal consistency, construct- and content validity were tested.
The VISA-A-NL proved to be an excellent evaluation instrument for the Dutch physician. If
applied to non-athletes, using a modified score (questions 1-6) is recommended. Correlation
of VISA-A-NL with other questionnaires was moderate or poorer.
chAPter 4
Less promising results with sclerosing Ethoxysclerol injections for Achilles tendinopathy: a retrospective studyIn patients with complaints of chronic midportion Achilles tendinopathy, neovascularisation
around the Achilles tendon and structural changes in the area were observed, but not in pain
free normal tendons. Local injections of the sclerosing substance Polidocanol (Etoxysclerol)
have shown to yield good clinical results in patients with chronic Achilles tendinopathy. After
training by the inventors of the technique, sclerosing Etoxysclerol injections were applied to
48 patients (53 tendons) in our center. Six weeks after the last injection, only 44% has less
or no complaints. At 2.7-5.1 year follow-up, 53% had received additional treatments, and
3 of these patients (7.5%) still had complaints of Achilles tendinopathy. We were therefore
Part VI
Sum
mary
213
not able confirm the high beneficial value of sclerosing neovascularisation in patients with
Achilles tendinopathy.
chAPter 5
Tendoskopie am Sprunggelenk und FußIn contrast to arthroscopy, which has become the preferred technique to treat intra-articular
ankle pathology, extra-articular problems of the ankle have traditionally demanded open sur-
gery. Open ankle surgery has been associated with complications such as injury to the sural
nerve or superficial peroneal nerve, infection, scarring, and stiffness of the ankle joint. The
percentage of complications reported with open surgery for e.g. posterior ankle impinge-
ment varies between 15 and 24%. The incidence of these complications has stimulated
the development of extra- articular endoscopic techniques. Endoscopic surgery offers the
advantages related to any minimally invasive procedure, such as fewer wound infections,
less blood loss, smaller wounds and less morbidity. Aftertreatment is functional, and surgery
is performed on an outpatient basis.
Tendoscopy can be performed for the treatment and diagnosis of various pathologic con-
ditions, as described in this chapter. In Achilles tendoscopy the paratenon and the plantaris
tendon are released, leaving the tendon proper untouched. This procedure results in a good
outcome on short- and midterm follow-up.
chAPter 6
Relationship between the plantaris tendon and the Achilles tendon: an anatomical study Pain in midportion Achilles tendinopathy is often most prominent on the medial side, where
degenerative changes are also most often found. During Achilles tendoscopy, we find that
the plantaris tendon is fixed to the Achilles tendon at the level of complaints. In chronic
inflammation, adhesions between Achilles- and plantaris tendon, running collectively in the
paratenon, may be formed. The Achilles tendon is involved in plantarflexion, whereas the
plantaris tendon also contributes to ankle inversion. These opposite forces may cause pain
in case of adhesions. The purpose of this study was to assess the anatomical position of the
plantaris tendon and its relationship with the Achilles tendon. In all specimens a plantaris
tendon was identified. 9 different sites of insertion were found, mostly medial and fan-
shaped onto the calcaneus. In 11 specimens attachments between Achilles- and plantaris
tendon were found at the level of complaints which may contribute to pain.
214
chAPter 7
Good outcome after stripping the plantaris tendon in patients with chronic midportion Achilles tendinopathyAchilles tendinopathy is a problem that is generally difficult to treat. The pain is frequently
most prominent on the medial side of the midportion of the tendon, where the plantaris
tendon is running parallel to the Achilles tendon. The purpose of this study was to assess if
excision of the plantaris tendon would relieve symptoms. Three patients with pain and stiff-
ness at the midportion level of the Achilles tendon were treated by excision of the plantaris
tendon. Pre-operatively these patients experienced recognisable tenderness on palpation of
the medial side of the midportion of the Achilles tendon with localized nodular thickening
at 4-7 cm proximal to the insertion. MRI indicated Achilles tendinopathy with involvement of
the plantaris tendon. The plantaris tendon was bluntly retrieved and excised with a tendon
stripper through a 3 cm incision in the proximal calf. We report a good outcome of this
novel procedure in 3 patients with chronic midportion Achilles tendinopathy. The medial pain
might be based on involvement of the plantaris tendon in the process, but well-designed
studies need to be performed to confirm our hypothesis.
chAPter 8
Midportion Achilles tendinopathy: why painful? An evidence based philosophySeveral factors play a role in the cause of pain in a patient with midportion Achilles tendi-
nopathy. When the demands of the tendon are higher than can be managed, micro-injuries
develop. The body reacts with a repair process, which is inadequate in patients developing
tendinopathy. This inadequate repair causes a repetitive cycle of inadequate collagen and
matrix production, tenocyte disruption, a further decrease of collagen and matrix and an
increased vulnerability to further micro-injuries. Vascular ingrowth to repair the defect arises
from the paratenon. These bloodvessels are accompanied by sensory neonerves, causing an
increase in pain signaling by producing nociceptive substances past the critical threshold.
Myofibroblasts proliferate which synthesize abundant amounts of collagen to repair the ten-
don proper, but also cause the formation of scar tissue around the tendon and consequently
adhesions of the paratenon onto the Achilles tendon at the location of the neurovascular
ingrowth. Scarring in turn may lead to obliteration of neovessels, impaired circulation and
further contribute to the pathogenesis of Achilles tendinopathy, meaning that there is no
further action towards repair. Nerves however will survive. Pain is often most prominent on
the medial side of the midportion Achilles tendon. At this level, the plantaris tendon runs
closely with- and parallel to the Achilles tendon. Adhesions between both tendons obstruct
the opposite forces of these two bi- and tri-articular muscle groups. Repetitive traction onto
Part VI
Sum
mary
215
this richly innervated area might contribute to the medially located pain and stiffness during
and after walking.
chAPter 9
Appearance of the weight-bearing lateral radiograph in retrocalcaneal bursitisA chronic retrocalcaneal bursitis is caused by repetitive impingement of the retrocalcaneal
bursa between the Achilles tendon and posterosuperior calcaneus. On physical examination,
a prominent swelling is palpable lateral and medial from the Achilles tendon just proximal to
the calcaneus. Standard lateral and anteroposterior radiography of the ankle is performed
to assess foot deformities or bony abnormalities. To confirm diagnosis, ultrasound, MRI or
even bone scans are performed. This chapter shows that a visible soft tissue swelling in the
retrocalcaneal recess on standard lateral weight-bearing radiographs of the ankle is useful
in diagnosing a retrocalcaneal bursitis and that expensive and time- consuming additional
imaging is no longer necessary.
chAPter 10
Endoscopic calcaneoplastyWhen a retrocalcaneal bursitis is confirmed and maximum conservative treatment fails,
surgery is considered. Most often open procedures are performed; however, in our clinic the
endoscopic calcaneoplasty was invented. Two portals are used, just lateral and medial to the
Achilles tendon, directly proximal to the superior part of the calcaneus. During the proce-
dure, the retrocalcaneal bursa, posterosuperior tuberosity of the calcaneus and synovitis are
resected. Aftertreatment is functional and patients can resume their normal activities.
chAPter 11
Optimization of portal placement for endoscopic calcaneoplastyDue to the local anatomy and swelling palpation of the superior part of the calcaneus can be
difficult and portals can be placed too far proximal. The calcaneus in these cases cannot be
reached properly resulting in a suboptimal procedure or, when the problem is recognized, a
need to replace or lengthen the incisions. In this chapter, we measured the distance from the
tip of the fibula to the posterosuperior calcaneus in different foot morphologies, as a tool for
accurate portal placement. Portal location in patients with a flat foot should be at a mean of
15 mm from the tip of the fibula, in normal feet at 20 mm, and in cavus feet at a mean of 22
mm distal to the tip of the fibula. The various foot types show a marked overlap between the
216
distances from calcaneus to fibula, however we can conclude that in flat feet portal location
is significantly more proximal to the tip of the fibula, when compared to cavus feet.
GeNerAL DiscUssioN
Before treatment of different types of Achilles tendinopathy can be optimized, some basic
issues need to be taken into account. First, we all need to start speaking the same language,
which is important in both science and daily clinical practice. Worldwide standard terminol-
ogy and validated outcome measures for both athletes- and non-athletes are important first
steps. Secondly, the cause of complaints needs to be found. As is evidently the major concern
in any pathology, it would help us define more accurate and individualized treatment strate-
gies. Sclerosing neovessels did not seem to be the solution. It was tried to get focus off
the intratendinous changes in midportion tendinopathy by formulating an evidence- based
philosophy on the involvement of the paratenon and plantaris tendon. More research is
needed to confirm this hypothesis.
In retrocalcaneal bursitis MRI is no longer indicated if the patient is appropriately assessed
clinically and digital radiographs are available. The value of radiography after previous hind-
foot surgery is currently under investigation. Portal placement in endoscopic calcaneoplasty
needs to be standardized as swelling and local anatomy prevent proper assessment. In
patients with flat feet portals should be placed more proximal than in cavus feet; further
research with a higher number of patients is needed to find significant differences between
all foot morphologies. Until then, for surgeons less familiar with the procedure fluoroscopy
is advocated.
Samenvatting
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ALGemeNe iNtroDUctie
Omdat de prevalentie van obesitas in de Westerse wereld stijgt, is fit worden en –blijven
de afgelopen jaren toenemend belangrijk geworden. Duursport als triatlons en hardlopen,
worden steeds populairder en overbelastingsblessures komen vaker voor in de dagelijkse
praktijk. Dit type blessures wordt veroorzaakt door relatieve inactiviteit op doordeweekse
dagen op kantoor, gevolgd door extreme trainingen in het weekend. 30-50% van alle sport-
letsels zijn overbelastingsblessures. Chronische Achillespees pathologie is één van de meest
voorkomende gevolgen van hardlopen en springsporten. In elite langeafstandslopers is er
tijdens een leven een risico van 52% om een Achillespeesblessure op te lopen. Dit probleem
is niet altijd gerelateerd aan sporten, zelfs 30% van de populatie bestaat uit patiënten die
een voornamelijk zittend leven leiden. Weerspannige Achillespezen kunnen jarenlang pijn
veroorzaken en zijn meestal resistent tegen elke vorm van behandeling. Uiteindelijk gaan
de klachten mogelijk vanzelf weer over, maar zeker atleten zullen niet instemmen met een
afwachtend beleid. Omdat de oorzaak van de pijn tot dusver nog niet opgehelderd is, is de
behandeling een onbevredigende uitdaging. Het doel van dit proefschrift was het ophelderen
van de oorzaak van de pijn, het ontwikkelen van geschikte beoordelingsinstrumenten, het
uitvinden van minimaal invasieve behandelmethoden, en het optimaliseren van diagnostische
en endoscopische werkwijzen voor chronische Achillespeesproblemen.
hoofDstUk 1
Terminologie voor problemen gerelateerd aan de AchillespeesTerminologie voor het omschrijven van Achillespees pathologie is door de jaren heen verand-
erlijk en verwarrend gebleken. Een nieuwe terminologie wordt in dit hoofdstuk voorgesteld:
definities omvatten anatomische locatie, symptomen, klinische bevindingen en histopatholo-
gie.
Midgedeelte Achilles tendinopathie: een klinisch syndroom gekarakteriseerd door een
combinatie van pijn, zwelling en verminderde prestatie. Het omvat, maar is niet beperkt
tot de histopathologische diagnose van tendinose. Achilles paratendinopathie: een acute of
chronische inflammatie en/ of degeneratie van het dunne membraan rond de Achillespees.
Er zijn duidelijke verschillen tussen acute paratendinopathie en chronische paratendinopathie
in symptomatologie en histopathologie. Insertie tendinopathie: gelocaliseerd bij de insertie
van de Achillespees aan de calcaneus, tractiesporen en calcificaties in het peeslichaam ter
plaatste van de insertie kunnen aanwezig zijn. Retrocalcaneaire bursitis: een inflammatoir
proces van de bursa in de recessus tussen het antero-inferieure gedeelte van de Achillespees
en de posterosuperieure gedeelte van de calcaneus (retrocalcaneaire recessus). Superficiele
calcaneaire bursitis: inflammatie van de bursa tussen een calcaneaire prominentie of de
Achillespees en de huid. Er wordt voorgesteld om eerdere termen als Haglund’s ziekte,
222
Haglund’s syndroom, Haglund’s deformiteit, calcaneus altus, komkommerhiel en knobbelhiel
niet meer te gebruiken.
hoofDstUk 2
Uitkomstmaten en onderzoeksinstrumentenEen uitgebreide anamnese en lichamelijk onderzoek zijn essentieel in de diagnose van Achil-
les tendinopathie. Verder is het belangrijk om continu de voortgang van de patiënt te docu-
menteren met gevalideerde functionele tests en uitkomstmaten zoals de VISA-A vragenlijst.
Ook algemene klachten van pijn en functie en de mogelijkheid terug te keren naar eerdere
activiteiten en sport zijn belangrijke maten. Dit geldt niet alleen voor wetenschappelijke
doeleinden, maar ook voor de behandelend therapeut of arts om de voortgang van de
behandeling en revalidatie te kunnen volgen.
hoofDstUk 3
Vertaling en validatie van de Nederlandse VISA-A vragenlijst en zijn toepasbaarheid bij niet-sportersDe VISA-A (Victorian Institute of Sports Assessment- Achilles) vragenlijst is ontworpen in
2001 om de klinische ernst van Achilles tendinopathie te meten. Het is een vragenlijst welke
symptomen en het effect ervan op lichamelijke activiteit evalueert en wordt door patiënten
zelf ingevuld. In dit hoofdstuk hebben we getracht de vragenlijst in het Nederlands te vertalen
en te valideren om hem ook bruikbaar te maken voor onze patiëntenpopulatie. Na vertaling
volgens een voorwaarts- achterwaarts protocol, werden 101 patiënten met klachten van
Achilles tendinopathie geïncludeerd. Zij vulden de VISA-A-NL vragenlijst in op 2 verschil-
lende momenten, tegelijk met VAS, FAOS en SF-36 vragenlijsten. Betrouwbaarheid, interne
consistentie en de validiteit van construct- en inhoud werden getest. De VISA-A-NL bewijst
een uitstekend instrument to zijn voor het evalueren van klachten voor de Nederlandse arts.
Wanneer deze gebruikt gaat worden bij niet-sporters wordt aanbeloven een gemodificeerde
score (vragen 1-6) te gebruiken. Correlatie van VISA-A-NL met andere vragenlijsten was
gematigd of minder.
hoofDstUk 4
Minder gunstige resultaten met scleroserende Etoxysclerol injecties bij patiënten met Achilles tendinopathie: een retrospectief onderzoekBij patiënten met chronische klachten van Achilles tendinopathie wordt neovascularisatie
in de omgeving van de Achillespees gezien, maar niet bij pijnvrije normale pezen. Lokale
injectie van de scleroserende substantie Etoxysclerol hebben goede resultaten laten zien. Na
Part VI
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223
een intensieve training door de bedenkers van de behandeling, werden in ons centrum 48
patiënten (53 pezen) behandeld met Etoxysclerol. Zes weken na de laatste injectie had maar
44% minder of geen klachten meer. Na een follow-up van 2.7-5.1 jaar, heeft 53% aanvul-
lende behandelingen gehad, en 3 van deze patiënten (7.5%) heeft nog steeds klachten.
Gezien deze uitkomst hebben wij de eerder behaalde voordelige resultaten niet kunnen
bevestigen.
hoofDstUk 5
Tendoscopie aan enkel en voetIn tegenstelling tot de arthroscopie, welke de techniek van voorkeur is geworden voor de
behandeling van intra-articulaire enkelproblematiek, worden extra- articulaire problemen van
de enkel traditioneel benaderd middels open chirurgie. Open chirurgie van de enkel is eerder
geassocieerd met complicaties zoals schade aan de nervus suralis en – peroneus superficialis,
infectie, littekenvorming en stijfheid van het enkelgewricht. Het percentage gerapporteerde
complicaties voor bijvoorbeeld posterieure enkel impingement varieert tussen de 15 en 24%.
De incidentie van deze complicaties heeft de ontwikkeling van extra-articulaire scopische
technieken gestimuleerd. Deze technieken hebben voordelen die gerelateerd zijn aan de
meeste minimaal invasieve procedures zoals minder wondinfecten en bloedverlies, kleiner
wondoppervlak en lagere morbiditeit. Nabehandeling is functioneel, en de ingrepen kunnen
in dagbehandeling gedaan worden.
Endoscopie van de pees, tendoscopie, wordt gedaan om verschillende pathologische aan-
doeningen te diagnosticeren en te behandelen. Indicaties voor, en de techniek van Achilles-,
peroneus, - en tibialis posterior tendosocopie, worden beschreven in dit hoofdstuk. Allen
laten op de korte- en langere termijn goede resultaten zien.
hoofDstUk 6
De relatie tussen Achilles- en plantarispees: een anatomische studie De pijnklachten bij midgedeelte Achilles tendinopathie is meest prominent aan de mediale
zijde van de Achillespees, waar ook in de meeste gevallen degeneratieve afwijkingen gezien
worden. Tijdens Achilles tendoscopie zien we dat de plantarispees gefixeerd is aan de Achil-
lespees ter hoogte van de klachten. Bij chronische inflammatie zouden adhesies tussen Achil-
les- en plantarispees, welke collectief in één peritendineum lopen, gevormd kunnen worden.
De Achillespees is betrokken bij plantairflexie, waar de plantarispees ook een klein deel
van de inversie van de enkel verzorgt. Als er adhesies bestaan, kunnen deze tegengestelde
krachten in theorie klachten veroorzaken. Het doel van deze studie was om de anatomische
positie van de plantarispees en de relatie ervan met de Achillespees te bepalen. In tegenstel-
ling tot wat de literatuur beschrijft, werd bij alle preparaten een plantarispees gevonden.
224
Negen verschillende inserties zijn gezien; meestal mediaal en waaiervormig op de calcaneus.
Bij 11 preparaten werden verbindingen gevonden tussen Achilles- en plantarispees, welke
zouden kunnen bijdragen aan het ontstaan van klachten.
hoofDstUk 7
Goede uitkomst na het strippen van de plantarispees als behandeling van patiënten met midgedeelte Achilles tendinopathieMidgedeelte Achilles tendinopathie is doorgaans moeilijk te behandelen. De pijn is meestal
gelokaliseerd aan de mediale zijde van de pees. Hier loopt ook de plantarispees. Onze hypoth-
ese was dat geisoleerd strippen van de plantarispees voldoende is om klachten te behan-
delen. Bij 3 patiënten werd de plantarispees geëxcideerd. Pre-operatief hadden zij klachten
van pijn bij palpatie van de mediale zijde van de Achillespees met nodulaire verdikking ter
plaatse. MRI liet betrokkenheid van de plantarispees in het proces zien. De plantarispees
werd stomp opgezocht en geëxcideerd met een peesstripper door een incisie van 3 cm in
het proximale gedeelte van de kuit. De 3 patiënten in deze publicatie hadden een goede of
uitstekende uitkomst. Mediale pijn zou dus gebaseerd kunnen zijn op betrokkenheid van de
plantarispees in het proces, maar goed uitgevoerde studies zullen moeten plaatshebben om
deze hypothese te bevestigen.
hoofDstUk 8
Midgedeelte Achilles tendinopathie: waarom pijnlijk? Een evidence-based filosofieVerscheidene factoren spelen een rol in de oorzaak van de pijn van patiënten met midgedeelte
Achilles tendinopathie. Als de behoeften van de pees groter zijn dan deze aankan, ontstaat
er microschade. Het lichaam reageert met een reparatieproces welke faalt bij patiënten met
tendinopathie. Dit veroorzaakt inadequate collageen en matrixproductie, tenocyt disruptie,
een verdere vermindering van functioneel collageen en matrix en een verhoogde kwets-
baarheid voor meer microschade. Het paratenon veroorzaakt ingroei van vaten om het
defect te repareren. Deze bloedvaten worden vergezeld door sensibele neo-zenuwen, welke
een verhoging in pijnsignalering door de productie van nociceptieve substanties voorbij de
kritieke drempel induceert. Myofibroblasten prolifereren welke overvloedige hoeveelheden
collageen synthetiseren om het peeslichaam te repareren; maar ook zorgen ook voor het
ontstaan van littekenweefsel waardoor het paratenon aan de Achillespees vast komt te
zitten. Fibrosering veroorzaakt dan weer constrictie van vasculaire kanalen en daarmee
beknelling van de toevoer van nutriënten waardoor bloedvaten oblitereren. Zenuwen zullen
achterblijven.
Part VI
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225
Pijn is meestal aanwezig aan de mediale zijde van de pees. Dit is waar de plantarispees
ook loopt. Adhesies tussen de beide pezen obstrueren de tegengestelde krachten van deze
bi- en triarticulaire spiergroepen. Herhaalde trekkracht aan dit rijk-geïnnerveerde gebied kan
toevoegen aan de mediaal gelokaliseerde pijn en stijfheid tijdens en na het bewegen.
hoofDstUk 9
De belaste laterale röntgenfoto bij een retrocalcaneaire bursitisEen chronische retrocalcaneaire bursitis wordt veroorzaakt door herhaaldelijke beklem-
ming van de retrocalcaneaire bursa tussen Achillespees en posterosuperieure calcaneus. Bij
lichamelijk onderzoek is er lateraal en mediaal van de Achillespees een prominente zwelling
palpabel juist proximaal van de calcaneus. Standaard laterale en anteroposterieure röntgen-
opnamen van de enkel worden doorgaans gemaakt om voetdeformiteiten en benige afwi-
jkingen uit te sluiten. Om de diagnose van een retrocalcaneaire bursitis te bevestigen, wordt
een echo, MRI of zelfs een botscan gemaakt. Dit hoofdstuk beschrijft de hoge bruikbaarheid
van een weke delen- zwelling in de retrocalcaneaire recessus op een standaard belaste
laterale röntgenfoto van de enkel bij patiënten met een retrocalcaneaire bursitis. Kostbaar
en tijdsintensief aanvullend onderzoek is door gebruik van dit diagnostisch hulpmiddel niet
meer nodig.
hoofDstUk 10
Endoscopische calcaneoplastiekAls maximale conservatieve behandeling voor een retrocalcaneaire bursitis faalt, kan chirur-
gisch ingrijpen overwogen worden. Meestal worden open ingrepen gedaan; in onze kliniek is
in 2001 de endoscopische calcaneoplastiek geïntroduceerd. Er worden 2 portals gebruikt net
lateraal en mediaal van de Achillespees, juist proximaal van het posterosuperieure gedeelte
van de calcaneus. Tijdens de procedure worden de retrocalcaneaire bursa, posterosuperieure
tuberositas van de calcaneus en synovitis gereseceerd. De resultaten zijn goed, nabehandel-
ing is functioneel en patiënten kunnen snel hun normale activiteiten hervatten.
hoofDstUk 11
Optimalisatie van portalplaatsing bij endoscopische calcaneoplastiekDoor de lokale anatomie en zwelling is het palperen van het posterosuperieure gedeelte van
de calcaneus bemoeilijkt en kunnen de 2 portals te proximaal geplaatst worden. De calcaneus
kan hierdoor niet behoorlijk bereikt worden, wat resulteert in een suboptimale procedure of,
als het probleem herkend wordt, de noodzaak om de incisies opnieuw te maken of te ver-
lengen. Standaardiseren van de locatie van de portals lijkt essentieel. In dit hoofdstuk hebben
226
we daarom de afstand van de fibulatip tot de posterosuperieure calcaneus bij verschillende
voetvormen gemeten, om als hulpmiddel bij portalplaatsing te dienen. Locatie van portals bij
patiënten met platvoeten zou op gemiddeld 15 mm van de fibulatip moeten zijn, bij normale
voeten op 20 mm, en bij cavus voeten op een gemiddelde van 22 mm, alles distaal van de
tip. De verschillende voetvormen lieten een duidelijke overlap zien tussen de afstanden van
fibulatip tot calcaneus, maar we kunnen concluderen dat in vergelijk met cavus voeten, bij
platvoeten de portals significant meer proximaal van de fibulatip gemaakt moeten worden.
ALGemeNe DiscUssie
Voor de behandeling van de verschillende typen Achilles tendinopathie geoptimaliseerd kan
worden, moeten sommige basale zaken in acht genomen worden. Ten eerste is het van
waarde allemaal dezelfde taal te gaan spreken, wat belangrijk is in de wetenschap maar
ook in de dagelijkse praktijk. Wereldwijde standaard terminologie en gevalideerde uitkomst-
maten voor sporters en niet-sporters zijn de eerste stappen. Voorts moet de oorzaak van de
klachten gevonden worden. Hoewel dit bij elke pathologie de meest belangwekkende zaak
is, zou het ons zo helpen de juiste en zelfs geïndividualiseerde behandelstrategieën te vinden.
Sclerosering van neovascularisatie leek veelbelovend maar is niet de oplossing gebleken.
Een poging is gewaagd het focus van intratendineuze afwijkingen te verleggen naar het
paratenon en de plantarispees door het formuleren van een evidence-based filosofie. Meer
onderzoek is nodig om deze hypothese the bevestigen.
Bij een retrocalcaneaire bursitis is het maken van een MRI niet meer zinvol gebleken; met
adequate anamnese en lichamelijk onderzoek en een digitale röntgenfoto van de voet kan
de diagnose goed gesteld worden. De waarde van deze röntgenfoto na eerdere chirurgische
ingrepen aan de achtervoet wordt momenteel uitgezocht. De endoscopische calcaneoplas-
tiek moet gestandaardiseerd worden omdat zwelling en lokale anatomie portalplaatsing
bemoeilijken. Bij patiënten met platvoeten moeten portals meer proximaal geplaatst worden
dan bij cavus voeten; hoewel de onderzoekspopulatie vergroot moet worden om een sig-
nificant verschil te vinden tussen alle voetmorfologieën. Tot die tijd wordt aanbevolen dat
minder ervaren chirurgen hun portals maken onder beeldversterking.
Addendum
Bibliography
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PUBLicAtioNs AND PreseNtAtioNs reLAteD to this thesis
MN van Sterkenburg, CN van Dijk. Mid- Portion Achilles Tendinopathy: Why Painful? An
evidence based philosophy. Knee Surg Sports Traumatol Arthrosc 2011;19(8):1367-1375
MN van Sterkenburg, GMMJ Kerkhoffs, CN van Dijk. Good outcome after stripping the
plantaris tendon in patients with chronic mid-portion Achilles tendinopathy. Knee Surg
Sports Traumatol Arthrosc 2011;19(8):362-1366
MN van Sterkenburg, M Groot, IN Sierevelt, GMMJ Kerkhoffs, CN van Dijk. Optimization
of Portal Placement for Endoscopic Calcaneoplasty. Arthroscopy 2011;27(8):1110-1117
MN van Sterkenburg, IN Sierevelt, JL Tol, IV van Dalen, D Haverkamp, CN van Dijk.
Translation and validation of the Dutch version of the VISA-A questionnaire and applicability
to non-athletes. Submitted
CN van Dijk, MN van Sterkenburg, JI Wiegerinck, J Karlsson, N Maffulli. Terminology for
Achilles tendon related disorders. Knee Surg Sports Traumatol Arthrosc 2011;19(5):835-41
MN van Sterkenburg, CN van Dijk. Injection treatment for chronic midportion Achilles
tendinopathy: do we need that many alternatives? Knee Surg Sports Traumatol Arthrosc.
2011 Apr;19(4):513-5
MN van Sterkenburg, GMMJ Kerkhoffs, RP Kleipool, CN van Dijk. The plantaris tendon and
a potential role in mid-portion Achilles tendinopathy: an observational anatomical study. J
Anat. 2011; 218(3):336-41
MN van Sterkenburg, MC de Jonge, IN Sierevelt, CN van Dijk. Less Promising Results with
Sclerosing Etoxysclerol Injections for Mid-portion Achilles Tendinopathy: a Retrospective
Study. Am J Sports Med 2010; 38 (11): 2226-32
MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. Appearance of the
weight-bearing lateral radiograph in retrocalcaneal bursitis. Acta Orthopaedica 2010; 81:
387–390
MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Tendoskopie am Sprunggelenk und Fuß.
Arthroskopie 2009;22:132-140
K Gravare Silbernagel, MN van Sterkenburg, J Karlsson. Diagnosis. Achilles Tendinopathy:
Current Concepts 2010:35-40
MN van Sterkenburg, M Paavola, CN van Dijk. Paratendinopathy. Achilles Tendinopathy:
Current Concepts 2010:55-65
MN van Sterkenburg, H Thermann, CN van Dijk. Achilles Tendoscopy. Achilles Tendinopa-
thy: Current Concepts 2010:151-155
MN van Sterkenburg, J Karlsson, CN van Dijk. Sport Specific Issues. Achilles Tendinopathy:
Current Concepts 2010:187-194
K Gravare Silbernagel, MN van Sterkenburg, A Brorsson, J Karlsson. Outcome Measures
and Assessment Tools. Achilles Tendinopathy: Current Concepts. 2010:205-212
232
MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Endoscopic Calcaneoplasty. In press
Minimally Invasive Surgery of the Foot and Ankle, editors Maffulli & Easley
MN van Sterkenburg. Achilles tendinopathy: peritendinous changes [invited lecture].
Scientific Meeting Vereniging voor Sportgeneeskunde 2011, Bilthoven
MN van Sterkenburg, M Groot, IN Sierevelt, GMMJ Kerkhoffs, CN van Dijk. Optimization
of portal placement for endoscopic calcaneoplasty. Biannual ESSKA meeting 2010, Oslo,
Norway
MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. The Aspect of the
Retrocalcaneal Recess of Kager’s triangle: a Reliable Diagnostic Criterion for Retrocalcaneal
Bursitis. Biannual ESSKA meeting 2010, Oslo, Norway
MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. Kager’s Triangle: a Useful
Diagnostic Criterion for Retrocalcaneal Bursitis. Minimally Invasive Surgery of Foot and Ankle
(MISFA) meeting 2009, Murcia, Spain
MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. Kager’s Triangle: a Useful
Diagnostic Criterion for Retrocalcaneal Bursitis. Jaarvergadering Nederlandse
Orthopaedische Vereniging (NOV) 2009, Den Bosch
MN van Sterkenburg, GMMJ Kerkhoffs, RJ Oostra, CN van Dijk. Involvement of the Plan-
taris Tendon in Achilles Tendinopathy: an Anatomical Observational Study. Biannual ESSKA
meeting 2010, Oslo, Norway
MN van Sterkenburg, GMMJ Kerkhoffs, CN van Dijk. Achilles Tendinopathy: Stripping the
Plantaris Tendon Results in a Good to Excellent Outcome. A Report of 3 Cases. Biannual
ESSKA meeting 2010, Oslo, Norway
MN van Sterkenburg, MC de Jonge, IN Sierevelt, CN van Dijk. Sclerosing Polidocanol Injec-
tions in Achilles Tendinopathy: A Retrospective Study. Nordic Orthopaedic Federation (NOF)
meeting 2008, Amsterdam
Additional publications MN van Sterkenburg, CJA van Bergen, GMMJ Kerkhoffs. Juvenile Wakeboarder Locks Ankle
on Shore. Knee Surgery Sports Traumatology and Arthroscopy 2010 Dec;18(12):1661-3.
ML Reilingh, MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Tendoscopy of Posterior
Tibial and Peroneal Tendons. Techn Foot Ankle Surg 2010; 9:43-47
MN van Sterkenburg, D Haverkamp, CN van Dijk, GMMJ Kerkhoffs. A Posterior Tibial
Tendon Skipping Rope. Knee Surg Sports Traumatol Arthrosc 2010; 18(12): 1664-66
PAJ de Leeuw, MN van Sterkenburg, CN van Dijk. Arthroscopy and endoscopy of the Ankle
and Hindfoot. Sports Medicine and Arthroscopy 2009;17:175-184
H Davies, BR Tietjens, MN van Sterkenburg, A Mehgan. Anterior Cruciate Ligament Injuries
in Snowboarders: a Quadriceps induced Injury. Knee Surgery Sports Traumatol Arthrosc
2009;17:1048-51
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ML Reilingh, MN van Sterkenburg, PAJ de Leeuw, IV van Dalen, CN van Dijk. Ankle
Arthroscopy, Indications, Technique and Complications. South African Orthopaedic Journal
2009;8:51-58
GJM Tuijthof, MN van Sterkenburg, IN Sierevelt, GMMJ Kerkhoffs, CN van Dijk. First
Experience with a Physical Simulation Environment for Training of Arthroscopic Skills. Knee
Surg Sports Traumatol Arthrosc 2010;18:218-224
CJA van Bergen, M Zengerink, L Blankevoort, MN van Sterkenburg, J van Oldenrijk, CN van
Dijk. Novel Metallic Implantation Technique for Osteochondral Defects of the Medial Talar
Dome: A Biomechanical Cadaveric Study. Acta Orthop. 2010 Aug;81(4):495-502
CN van Dijk, PAJ de Leeuw, MN van Sterkenburg. Tendoscopy AANA Advanced Arthros-
copy: the Foot and Ankle, editors Amendola, Ryu, Stone
ML Reilingh, PAJ de Leeuw, MN van Sterkenburg, CN van Dijk. Posterior Ankle Arthroscopy
and Tendoscopy. Sports Medicine Volume in the Master Techniques series, editor Fu, 2011
PAJ de Leeuw, MN van Sterkenburg, CJA van Bergen, CN van Dijk. Posterior Ankle Arthros-
copy and Endoscopy. In press International Advances in Foot & Ankle Surgery, editor Saxena
MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Tendoscopy. In press Minimally Invasive
Surgery of the Foot and Ankle, editors Maffulli & Easley
J Karlsson, MN van Sterkenburg, GMMJ Kerkhoffs, CN van Dijk. Open Surgery for Achil-
les Tendon Rupture. Achilles Tendon Rupture: Current Concepts 2008;1st edition:50-56, 2nd
edition:49-56
MN van Sterkenburg, B Donley, CN van Dijk. Guidelines for Sport Resumption Follow-
ing Achilles Tendon Rupture. Achilles Tendon Rupture: Current Concepts 2008;1st edi-
tion:108-117, 2nd edition:107-116
MN van Sterkenburg, CN van Dijk. Overview of Reviews on the Treatment of Acute Achilles
Tendon Ruptures. Achilles Tendon Rupture: Current Concepts 2008;1st edition:34-48, 2nd
edition:33-47
Dankwoord
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Dan
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Prof. dr. C.N. van Dijk, promotor en opleider. Allereerst wil ik u bedanken. De bijna drie
jaar die ik fulltime onderzoek heb gedaan, waren jaren waarin u mij barstensvol energie en
oceanen aan nieuwe ideeën hielp. De vele besprekingen die meestal tegen de deurpost van
mijn ‘kamer’ plaatsvonden, waren aanleiding voor nieuwe inspiratie. Maar ook lastminute
congresbezoeken zorgden er op wonderlijke wijze voor dat de wetenschappelijke moed,
die soms ver in mijn schoenen gezakt was, een extra stimulus kreeg. Alles heeft geresult-
eerd in dit proefschrift en een royaal archief aan digitaal beeldmateriaal. Van uw talent om
gedrevenheid tot het maximum te sturen, hoop ik nog veel gebruik te mogen maken. Ik zie
uit naar de voortzetting van onze samenwerking dit jaar.
Dr. G.M.M.J. Kerkhoffs, co-promotor, Gino. Elke alinea kritisch tegen het licht gehouden,
alle vergeten letters opgespoord, elke referentie bekeken. Toen jij terug kwam naar het
AMC was mijn onderzoek al geruime tijd van start, maar door jouw visie heeft het een
vogelvlucht genomen. Je kunt bij herhaling dezelfde vraag stellen zodat een korte veronder-
stelling verandert in een groot wetenschappelijk project, ofwel in een gedachtewisseling
over persoonlijker levensvragen. Als orthopedisch chirurg maar ook in sociale zin ben je een
inspirator. Dank je wel voor de afgelopen jaren, zin in de komende.
Leden van de promotiecommissie, bestaande uit prof. dr. F.J.G. Backx, prof. dr. R.L.
Diercks, prof. dr. J.C. Goslings, dr. M. Maas, prof. dr. R.J. Oostra en prof. dr. R.J.P.M.
Scholten. U wil ik bedanken voor het beoordelen van het manuscript en ik zie uit naar de
aanstaande academische discussie.
Dr. ir. L. Blankevoort, Leendert. Dank voor je financiële begeleiding en minutieuze weten-
schappelijke kritiek tijdens de algemene onderzoeksbesprekingen.
Drs. I.N. Sierevelt, Inger. Allereerst veel dank voor je hulp bij de methodologie en statistiek
van mijn studies. Je bent van bijzondere waarde voor de ORCA. Daarnaast heb ik goede
herinneringen aan onze vele kilometers hardlopen tijdens lunchpauzes. Je had gewoon mee
moeten gaan naar New York.
Dr. I.V. van Dalen, dr. D. Haverkamp, drs. M.C. de Jonge, drs. R.P. Kleipool, dr. M.
Maas, dr. J.L. Tol. Dank voor jullie waardevolle bijdrage aan dit proefschrift.
Marga en Rosalie. Veel dank voor alle ondersteuning bij administratieve zaken.
Rogier van Sterkenburg en Jan Joost Wiegerinck. Mijn paranimfen. Hoe moet ik jullie
nou in één alinea bedanken? Rogier, vroeger al erg druk met je zusje; van voorlezen via tech-
nisch lego tot wiskundeboek. Van mijn drie broers viel de keuze op jou, omdat ik verwachtte
238
dat jij het meest enthousiast aan de slag zou gaan met je taak als mijn paranimf. En die
gedachte bleek al juist op de dag dat ik je vroeg. Jan Joost, mijn opvolger in de Achillespees-
lijn. Indrukwekkend hoe jij het binnen een aantal maanden presteerde van een bescheiden
opzet genoeg plannen te maken voor 3 proefschriften. Ik denk dat wij naast collega’s goede
vrienden zijn geworden. Bovenal heb je aardig leren photoshoppen.
G4/ De kweekvijver: Jakob, Christiaan, Peter, Job, Sjoerd, Mikel, Bas, Laurens en
Gabriëlle. Wat een mooie avonturen hebben wij beleefd. Een onverstaanbaar congres in
Murcia, AAOS in New Orleans, met Job de marathon van New York, met Chris en Jakob in
de vooropleiding. Er zullen er nog heel veel volgen.
Collega’s Heelkunde Beverwijk. Huib, bedankt voor je positieve wetenschappelijke
beoordelingen ondanks dat er in het RKZ geen enkel onderzoek uit mijn handen kwam.
Is je boekje al af? Dit is hem dan. Wat een ontzettend leuke werksfeer en ik zal de laatste
maanden nog uitgebreid genieten. Vrij van proefschrift.
Vrienden. Bedankt dat jullie er zijn; voor jullie afleiding, interesse, vele glazen bier en wijn
en geweldige kookkunsten.
Broers, schoonzussen, neefjes en nichtjes. Ja heren, als jullie het niet doen, doet jullie
zusje het wel. Of begint het toch te kriebelen? Op nog heel veel mooie momenten samen.
Misschien is het nu tijd jullie te evenaren in de volgende levensfase.
Papa en mama. Vijf jaar geleden hadden jullie deze niet aan zien komen. Vijftién jaar
geleden allerminst. En toch is het gelukt. In de wetenschappelijke voetsporen van vader.
Geniet ervan. Ik hou van jullie.
Part VI
Cu
rriculu
m V
itae
239
cUrricULUm vitAe
Maayke Nadine van Sterkenburg was born on July 11th, 1981 in Leiderdorp, the Netherlands.
After graduating from high school (Gymnasium, Rijnlands Lyceum Oegstgeest), she started
Medical School at the University of Amsterdam. A 5-month internship in Orthopedic Surgery
in Auckland, New Zealand (Prof. Dr. B.R. Tietjens) made her enthousiastic to continue in this
working field. She worked three years as a research fellow at the Department of Orthopedic
Surgery of the Academical Medical Center in Amsterdam (Head: Prof. Dr. C.N. van Dijk)
which resulted in this thesis. In July she will finish a 2-year residency in General Surgery at
the Rode Kruis Ziekenhuis Beverwijk (Head: Dr. H.A. Cense) and return to the Academical
Medical Center Amsterdam for her training in Orthopedic Surgery under supervision of Prof.
Dr. C.N. van Dijk.
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