Achilles Tendinopathy

Contents

Definition and mechanism of injury

Achilles tendinopathy is a common overuse injury caused by repetitive energy storage and release with excessive compression. This can lead to a sudden injury, or in the worst case, can cause a rupture of the Achilles tendon. In both cases, a lack of flexibility or a stiff Achilles tendon can increase the risk of these injuries [1]

The current term that is recommended to describe this cohort of patients is ‘tendinopathy’. Cook and Purdum[2] proposed a new strategy when approaching tendon pain, and this is called the tendon continuum. The continuum model proposed a model for staging tendinopathy based on the changes and distribution of disorganisation within the tendon. The 3 stages are: reactive tendinopathy, tendon disrepair and degenerative tendinopathy. It has been suggested that the tendon can move up and down this continuum and this can be achieved through adding or removing load to the tendon especially in the early stages of a tendinopathy.

Achilles tendinopathy can be described as insertional or mid portion, the difference is in the localisation. The insertional form is situated at the level of transition between the Achilles tendon and the bone, the midportion form is located at the level of the tendon body.

Surgical specimens show a range of degenerative changes of the affected tendon, such as in the tendon fibre structure and arrangement as well as an increase in glycosaminoglycans, which may explain the swelling of the tendon. [3] The precise cause of tendonitis remains unclear. Even though tendonitis of the achilles tendon is often connected to sport activities, the ailment is also often found with people who do not practice sports. The biggest cause is the excessive overburdening of the tendon. A light degeneration of the achilles tendon can be latently present, but pain only appears when the tendon is overburdened. It is also noted that the ailment is usually not preceded by a trauma[4][5].

Clinically Relevant Anatomy

The achilles tendon is the biggest and strongest tendon in the human body.
The tendon has the capacity to resist large tensile forces. It stems from a distal confluence of the gastrocnemius and soleus muscle and inserts at the bottom of the calcaneus.

A typical tendon structure consists of thin, cylindrical cells and an extracellular matrix. The cells of the tendon, respectively tenocytes tenoblasts, are responsible for the synthesis of all of the components of the extracellular matrix. Inside the matrix we find bundles of type I collagen and elastin. This type-I collagen is responsible for the strength of the tendon. Between the collagen there is a ground substance located which is made up of proteoglycans and glycosaminoglycans. [6]

The achilles tendon is surrounded by partenon which works as an elastic sleeve around the tendon which allows the tendon to move freely between surrounding tissue. The partenon consists of a layer of cells and is responsible for blood transportation of the tendon. The layers that are formed under the partenon are in chronological order: the epitenon which is a thin membrane and the endotenon which surrounds the collagen fibers which results in bundles[7]

Etiology

A reactive tendon is the 1st stage on the tendon continuum and is a non-inflammatory proliferative response in the cell matrix. This is as a result of compressive or tensile overload. Straining the tendon during physical exercise has been seen as one of the biggest pathological stimulus and systematic overloading of the Achilles tendon above the physiological limit can cause a micro-trauma.  Repetitive micro-traumas that are linked with a non-uniform tension between the gastrocnemius and soleus, cause frictional forces between the fibers and abnormal concentrations of the loading in the achilles tendon. This has consequences such as the inflammation of the tendon sheath, degeneration, or a combination of both. Without the minimum time for recovery, this can lead to a tendinopathy [8].

Decreased arterial blood flow, local hypoxia, decreased metabolic activity, nutrition, and a persistent inflammatory response have been suggested as possible factors that could lead to chronic tendon overuse injuries and tendon degeneration.

The most common and perhaps the most important malalignment is the one of the ankle caused by hyperpronation of the foot. Increased foot pronation has been proposed to be associated with Achilles tendinopathy.

In acute trauma, the external factors dominate, while injuries caused by overuse generally have a multifactorial origin. The acute phase of Achilles tendinopathy is caused by acute overload, blunt trauma or acute muscle fatigue, and is characterized by an inflammatory reaction and edema formation. If the treatment of the acute phase fails or if they overlooked it, it can cause a fibrin and form adhesions off the tendon.

The progression of the reactive tendinopathy to rendon dysrepair can occur if the tendon is not offloaded and allowed to regress back to the normal state. During this phase there is the continuation of increased protein production which has been shown to result in separation of the collagen and disorgansiation within the cell matrix. This is the attempt of tendon healing as with the 1st phase but with greater involvement and breakdown physiologically.

Degenerative tendinopathy is the final stage on the continuum and it is suggested that at this stage there is a poor prognosis for the tendon and changes are now irreversible.  Often, tendon degeneration is found in combination with peritendinous adhesions, but this does not mean that one condition causes the other one.

In summary the effects of overuse, poor circulation, lack of flexibility, gender, endocrine or metabolic factors can lead to tendinopathies. The structure of the tendon is disturbed by this repetitive strain (often eccentric nature) and collagen fibers go along together, break the crosslinks and the slide denaturation cause tissue, causing inflammation. This cumulative microtrauma is assumed not only weaken collagen cross-linking, but also the collagenous matrix and the vascular elements of influencing the tendon, which ultimately leads to tendinopathy [9]

Clinical Presentation

Morning pain is a hallmark symptom because the achilles tendon must tolerate full range of movement including stretch immediately after getting up in the morning. Symptoms are typically localized to the tendon and the immediate surrounding area.

Swelling and pain are less common. The tendon can appear to have subtle changes in outline, becoming thicker in the A-P and M-L planes. [10]

With people who have a tendinopathy of the achilles tendon that has a sensitive zone, combined with intratendinous swelling, that moves along with the tendon and of which sensitivity increases or decreases when the tendon is put under pressure, there will be a high predictive value that in this situation there is a case of tendinosis. [11] The affected side of the tendon shows a larger diameter, higher stiffness and lower strain in comparison to the non affected side. 

Differential diagnosis

Examination

As alwasy a subjective assessment is important for providing clues related to mechaniasm of injury and history of the condition.

In the objective examination it is important to fully assess the lower limb.  Assessing the hip and knee will give clures to biomechanical contributions and muscle imbalances.  In the foot and ankle we are looking for more local contributory and resulting factors:

  • Observation for muscle atrophy, swelling, asymmetry, joint effusions and erythema. Atrophy is an important clue to the duration of the tendinopathy and it is often present with chronic conditions. Swelling, asymmetry and erythema in pathologic tendons are often observed in the examination. Joint effusions are uncommon with tendinopathy and suggest the possibility of intra-articular pathology.
  • Range of motion testing, strength and flexibility are often limited on the side of the tendinopathy[13][14].
  • Palpation tends to elicit well-localized tenderness that is similar in quality and location to the pain experienced during activity[15] Physical examinations of the Achilles tendon often reveal palpable nodules and thickening.
  • Anatomic deformities such as forefoot, heel varus, excessive pes planus or foot pronation, should receive special attention. These anatomic deformities are often associated with this problem[16][17].

Imaging studies are not necessary to diagnose achilles tendonitis but may be useful for differential diagnosis. Ultrasound is the imaging modality of first choice as it provides a clear indication of the tendons width, changes of water content within the tendon and collagen integrity, as well as bursal swelling.  An MRI may be indicated if the diagnosis is unclear or if symptoms are atypical. The MRI may show an increased signal within the Achilles[18] The use of non-invasive image-forming methods for the assessment of the Achilles tendon (mechanical, structural and biomechanical characteristics) in vivo is relatively young. Ultrasound elastography and ultra-high field magnetic resonance imaging (MRI UHF) have recently emerged as potential powerful techniques to examine the tendon tissues. [19]

Outcome measures 

Patient reported outcome measures such as:

  • A global measure of lower extremity function: e.g., The Lower Extremity Functional Scale (LEFS) ‐ not specific to Achilles tendinopathy
  • Detailed questionnaire, specific to Achilles tendinopathy e.g. the VISA‐A questionnaire[20][21]

Patient specific functional outcome measure such as:

  • How much weight can be applied to the plantar flexed foot on a weighing scale before the onset of pain
  • The number of heel raises before the onset of pain
  • The number of heel drops before the onset of pain
  • The number of heel drops with a specific weight in a backpack before the onset of pain
  • How far can the client walk or run before the onset of pain

Physiotherapy Management

The Achilles Tendinopathy Toolkit is an evidence based clinical decision making aid to assist clinicians in their management of achilles tendinopathy.

Optimise biomechanics

Individuals presenting with achilles tendinopathy should have a full biomechanical assessment. The BC Physical Therapy Tendinopathy Task[22] Force suggest there is a small amount of clinical evidence to support the use of orthotics in the acute stage and a moderate amount of clinical evidence to support the use of orthotics in the chronic stage. Clinically consider using orthotics, perhaps using taping first, in the acute stage; consider using orthotics in the chronic stage.

Controlled tendon loading

Less burdening activities should be encouraged so that the burden on the tendon decreases however complete immobilisation should be avoided, since it can cause atrophy[23][24] The BC Physical Therapy Tendinopathy Task Force[22] suggests that there is a large amount of clinical evidence to support the use of exercise in the chronic stage but the precise parameters to ensure effectiveness are not clear. Eccentric exercise in particular is supported although some protocols use both concentric and eccentric exercise. One RCT showed heavy slow resistance training is equally as effective as eccentric training.

It has been shown that strength training, that is stimulated externally and is linked to a functional tasks, not only helps reduce tendon pain but modulate excitatory and inhibitory control of muscle, and thus potentially tendon load[25].  A popular and effective option is the eccentric strength training[26].  In the past decade eccentric exercises have been shown to have positive effects of Achilles tendopathy and became the main non-surgical choice of treatment for achilles tendinopathy [27][28][29]

There is no convincing evidence that the most effective exercise regimen. A recent systematic review concluded that there is little clinical and mechanistic evidence that supports the use of the eccentric component and compare that well-conducted studies of different load programs are largely lacking[29] New loading based exercise regimes such as isolated concentric exercise, heavy slow resistance training (HSR), and eccentric-concentric have more recently been proposed but lack solid scientific evidence for their effectiveness in achilles tendinopathy[30]. Thorough management guidelines for achilles tendinopathy is covered in detail in the Achilles Tendinopathy Toolkit.

Adjunct therapies

In combination with approaches to optimise biomechanics and prescribe exercise therapy, adjunct therapies may be used.  These forms of therapy usually cannot resolve or prevent injury, they are used more for symptom management.

Manual Therapy

There is no clinical evidence but there is expert level consensus to support the use of joint mobilizations in the acute stage if assessment reveals joint restriction. There is a small amount of clinical evidence and more substantial expert level consensus to support the use of joint mobilizations in the chronic stage if assessment reveals joint restriction[22]. May consider using manual therapy after a comprehensive evaluation of the hip, knee, foot and ankle reveals joint dysfunction.  In the ankle mobilisations can be used for dorsiflexion limitation of the talocrural joint and varus- or valgus limitation of the subtalar joint[31][32]  

The effectiveness of deep cross frictions is not scientifically proven and gives limited results[33][34][35][36] There is a small amount of clinical evidence to support the use of soft tissue techniques, such as frictions, in the chronic stage.  May consider a trial of soft tissue techniques, such as frictions, in the chronic stage[22].

Electrotherapy Modalities[22]

There is conflicting evidence to support the use of Extracorporeal Shock Wave Therapy (ESWT) in the chronic stage. There is evidence suggesting that the outcomes are dependent upon the dosage of the shock wave energy (EFD ‐ energy flux density = mJ/mm²), rather than the type of shock wave generation (focused vs. radial ESWT). There is also evidence that the use of anaesthetic required in high energy protocols decreases the effectiveness of ESWT. Therefore, using low energy ESWT protocols without the need for anaesthetic are recommended as more practical, more tolerable, and less expensive with equivalent results. Low energy ESWT protocols can apply to both focused and radial ESWT.  Consider a trial of ESWT in the chronic stage, especially if other interventions have failed, at the following parameters:

  • Low energy SWT: EFD = 0.18 – 0.3 mJ/mm² (2‐4 Bars)
  • 2000‐3000 shocks
  • 15‐30 Hz
  • 3‐5 sessions, weekly intervals.

There is no clinical evidence to support the use of Ultrasound and Low Level Laser Therapy.  

Iontophoresis

There is a small amount of evidence to support the application of iontophoresis using dexamethasone in the acute stage but not in the chronic stage.  The role of iontophoresis is still investigational. May consider, in the acute stage, a trial of iontophoresis, 0.4% dexamethasone (aqueous), 80 mA‐min; 6 sessions over 3 weeks.  A program of concentric‐eccentric exercises should be continued in combination with iontophoresis, if exercise loading is tolerated.

Taping

Antipronation taping is supported by expert opinion not clinical evidence.  May consider using taping, possibly prior to orthotics in the acute stage[22].

Night splints

There is expert opinion to support the use of night splints and braces in the acute stage and a moderate amount of evidence against the use of night splints and braces in the chronic stage. Consider a trial of night splints and braces in the acute stage but NOT using night splints and braces in the chronic stage in conjunction with exercise[22].

Medical Management

Medication

Inflammation is necessary to start a restoration process in the damaged tissue, but the use of certain medication, such as corticosteroids and quinolones counter the inflammation, and as a result also the restoration process. Even when the patient does not take this medication, tendinopathy is also a consequence of a disrupted restoration process[37]

Corticosteroid injections

Corticosteroid injection (CSI) appears to have short‐term pain‐relieving effects but no effect or detrimental effects in the longer term. The short‐term effect of CSI has been shown in the Achilles tendon with improvement in walking and reduction in tendon diameter as measured by ultrasonography. Intratendinous injection is contraindicated because of the catabolic effects, although a recent study of CSI into intratendinous vessels in six tendons has shown promising results. Peritendinous injection has fewer effects on the tendon and could be a worthwhile adjunct to a considered management programme. CSI may be most beneficial when used to relieve pain while continuing to undertake exercise programmes[38].

Sclerosering injections

The role of the neovascularization in tendon pain has been further examined in a pilot study where a vascular sclerosant (Polidocanol-an aliphatic non‐ionised nitrogen‐free substance with a sclerosing and anaesthetic effect) was injected in the area with neovascularization anterior to the tendon. Short‐term (6 months) evaluation of this treatment showed that the clear majority were pain free after a mean of two treatments. The tendons that were pain free had no neovascularization either on the outside or the inside. A 2‐year follow‐up of these patients showed that the same eight patients remained pain free with no vessels in the tendon. Ultrasonographically, tendon thickness had decreased and the structure looked rather normal [39].

Rehabilitation after a sclerosing injection consists in 1 - 3 days of rest; then tendon-loading activity increases gradually avoiding maximum loading. After 2 weeks tendon loading activity is allowed (jumping, fast runs, heaving strength training). This research suggests a clinical role for sclerosing therapy for those who fail to respond to eccentric exercise[39].

Platelet-rich Plasma injections

Research shows that injections of Platelet-Rich Plasma (PRP) during a period of 3 months in people with chronic Achilles Tendinopathy has no positive effect compared to placebo (saline). The only significant effect of PRP injections compared to placebo was a change in tendon thickness: this difference indicates that a PRP injection could increase tendon thickness compared with saline injection[39]

Operative surgery

The aim of surgical treatment for tendinopathy is to irritate the tendon to initiate a chemically mediated reaction response. Surgery may consist of simple procedures, percutaneous tenotomy, open procedures and removal of the infected tendon part. In 75% of subjects who underwent tenotomy experienced a positive result after 18 months. An open procedure of the achilles tendon resulted in better outcomes of tendons without a focal lesion[39]

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