By: 4 December 2015
Treatment options for chronic Achilles tendon disorders

Treatment options for chronic Achilles tendon disorders

Chronic Achilles tendon disorders are a spectrum of disease resulting from a degenerative condition associated with overuse of the Achilles tendon. A Chikate, Yogesh Joshi, Prasad Rao and Asad Syed take a look at some of the options available when treating chronic Achilles tendon disorders

A chronic Achilles tendon disorder is characterised by pain and fusiform swelling along the Achilles tendon within the substance of the tendon or at its insertion. In its severe form it can be incapacitating and sometimes can end an athlete’s career or result in an individual’s loss of independence. Although a common condition, it is a complex and difficult orthopaedic challenge as its pathophysiology is poorly understood. The condition can be either insertional or non-insertional but the microscopic changes essentially are the same. The treatment is largely non-surgical, even though non-surgical management of chronic Achilles tendon disorders has a reported failure rate of 25 per cent. Surgery is reserved for chronic cases not responding to non-operative means. Our understanding of the treatment available keeps evolving and this article serves to highlight some of the treatment options available.


The gastrocnemius and soleus muscle merges to form the Achilles tendon (Figure 1). The Achilles tendon has a round upper part and is relatively flat in its distal 4cm. Fibres of the Achilles tendon spiral 90° as they reach their insertion onto the calcaneus. The Achilles tendon is enveloped by a paratenon, a membrane consisting of a single layer of cells. This anatomic variation contrasts with other tendons that have a synovial sheath. The paratenon originates from the deep fascia of the leg, the fascia cruris, covering the tendon posteriorly. It is highly vascularised and is responsible for blood supply to the tendon. Most of the blood supply is anterior. A microvascular perfusion study in normal Achilles tendons using laser doppler flowmetry has shown that the blood flow is considerably lower – approximately 2–6cm from the calcaneal insertion. In symptomatic Achilles tendon disorder, blood flow is considerably elevated compared with the control tendons [1].




Tendons are stiff and resilient, with high tensile strength. They can stretch up to 4 per cent before damage. Actin and myosin are present in tenocytes and tendons have almost ideal mechanical properties for the transmission of force from muscle to bone. A tendon loses its wavy configuration when it is stretched more than 2 per cent. As collagen fibres deform, they respond linearly to increasing tendon loads. The normal wavy appearance of the tendon is regained if the strain placed on it remains at less than 4 per cent. At strain levels greater than 8 per cent, macroscopic rupture will occur. The loads imposed on the Achilles tendon can reach up to 9kN during running, corresponding to 12.5 times the body weight, 2.6kN during slow walking, and less than 1kN during cycling.



Tendons are subjected to cyclical loads, a major factor in the development of tendon disorders. There is micro-tearing from overuse and proliferation of fibroblasts in response to the tears. The healing response after tendon injury is defined by cell matrix adaptive capability. There are distinct macro-traumatic and micro-traumatic injury patterns and a spectrum of pathologic responses from inflammation to tissue degeneration. Achilles tendon disorders represent a failed healing response. As tendinopathy sets in, there is disruption of collagen fibres and an increase in non-cellular matrix. Macroscopically, the affected portions of the tendon lose their normal glistening white appearance and become grey and amorphous. The thickening that results can be diffuse, fusiform, or nodular.


Risk factors

In athletes, poor technique, sudden increase in exercise or training on hard/ uneven surfaces has been known to increase the risk of developing Achilles tendon disorders. Other intrinsic factors include being middle-aged, male sex, increased body weight, pes cavus deformity and diabetes. Use of fluoroquinolone antibiotics has also been implicated. The interplay between these factors is well known but is yet to be fully elucidated to give a clear causal effect on the development of Achilles tendinopathy.

table 1

Puddu stages:

Stage 1: Pure paratenonitis

Stage 2: Paratenonitis with tendinosis

Stage 3: Tendinosis


Clinical presentation

Achilles tendon disorders typically present with pain along the Achilles tendon or at its insertion. Pain tends to be worse in the morning or after a period of inactivity. Runners may experience pain at the beginning and end of a training session, with a period of diminished discomfort in between. As the condition worsens, pain can interfere with activities of daily living and be continuously present to the extent of disturbing sleep. They may develop a degree of morning stiffness being correlated with the severity of the disease. Patients may present with a painful fusiform lump along the Achilles tendon or with a Haglund’s deformity. Insertional spurs, an adaptive process of formation rather than being due to tendon micro-tears or inflammatory changes, may also be part of the presenting picture. Other clinical presentations include swelling, burning, stiffness, or pressure with footwear on the posterior aspect of the heel.

With both legs exposed above the knees, the patient should be examined in both standing and prone position. Inspection of the foot and the heel is performed to look for any mal-alignment, deformity, obvious asymmetry in tendon size, localised thickening, Haglund’s heel and any previous scars. The Achilles tendon should be palpated to detect tenderness, heat, thickening, nodularity and crepitation. The ‘painful arc’ sign helps to distinguish between tendon and paratenon lesions. In paratendinopathy, the area of maximum thickening and tenderness remains fixed in relation to the malleoli from full dorsiflexion to plantar flexion, whereas lesions within the tendon move with ankle motion. Silfverskiold test can be used to detect the tightness of the gastro-soleus complex.



Clinical presentation

Diffuse discomfort and swelling of the tendon

Tender nodules are often present

Pain is a cardinal symptom.

Clinically tenderness is limited on the sides of the tendon

Ultrasonography and MRI

Fluid surrounding the tendon

A thickened paratenon

High signal seen within the paratenon (Halo sign)


Achilles tendinosis

Clinical presentation

Gradual evolution of symptoms

Includes pain and swelling approximately 2–6cm proximal to the calcaneal insertion

Painful arc sign

Pronated foot

Ultrasonography and MRI

Hypoechoic lesion with or without intratendinous calcification

Tendon thickening on sagittal imaging

Altered signal appearance within the tendon tissue


Paratenonitis with Achilis tendinosis

Clinical presentation

Transient sharp pain or repeated episodes of sharp pain within the tendon while running

Swelling and tenderness are usually found 2–6cm proximal to the insertion of the tendon

Exercise-induced pain is the cardinal symptom

Focal, tender nodules

Ultrasonography and MRI

Features of paratenonitis and tendinosis


Retrocalcaneal bursitis

Clinical presentation

Pain anterior to the Achilles tendon

Often associated with Haglund’s deformity

Athlete who trains uphill

Two-finger squeeze test

Pain is observed on application of pressure medially and laterally anterior to the Achilles tendon insertion

Ultrasonography and MRI

May show secondary changes in tendon

Evidence of inflammation of retrocalcaneal bursa


Insertional tendinosis

Clinical presentation

Often associated with Haglund’s deformity

Aggressive hill running and interval programme

Tenderness at the bone tendon interface

There is also limited dorsiflexion

Ultrasonography and MRI

Prominence of the posterior calcaneal tuberosity, possible calcification, or an intratendinous spur

Associated tendinosis



Reducing pain and returning to activity after tendinopathy is the primary goal of treatment. Often treatment modalities are combined to effect a positive result. Patient counselling on a treatment protocol is paramount if they are to see themselves through the treatment programme. In patients with established early Achilles tendon disorders, seeking medical attention at an early stage may improve outcome, as treatment becomes more complicated and less predictable when the condition becomes chronic [2, 3].


Non-surgical treatment modalities

Preventative measures

Effective coaching and encouraging athletes to follow a sensible training programme with gradual increase in duration and intensity of exercises can theoretically prevent athletes from developing tendinopathy.


Rest, analgesia, compression and elevation

The mainstay of treatment for chronic Achilles tendon disorders is conservative, with initial rest. A rational treatment plan following any immobilisation should involve a gradual integration of reduced load-bearing activities and a monitored physical therapy or stretching regime, modification of training regimes, specific exercises and correction of underlying lower limb malalignment with orthoses. Immobilisation is frequently used in the acute setting to control exacerbating factors, but prolonged immobilisation should be avoided. Using this treatment regimen 71 per cent of patients recovered and only 29 per cent failed to respond adequately to non-operative management after an 8–year follow-up [4].


Eccentric exercises

The patient starts in a single-leg standing position with the weight on the forefoot and the ankle in full plantar flexion (involved leg only tip-toe on a step); the Achilles tendon is then eccentrically loaded by slowly lowering the heel to a dorsi-flexed position (forefoot on step and heel below); the patient then returns to the starting position using the arms and other leg to avoid concentric loading (both feet tip-toe on step). Movements are slow and controlled with moderate but not disabling pain. A 12–week eccentric exercise programme is used with considerable success in non-insertional disorders. In insertional tendinopathy eliminating the ankle dorsi-flexion movement by using floor-level exercises only was found to improve outcomes in 67 per cent of cases, compared with 32 per cent for the original activities. Multiple studies and systematic reviews have found eccentric exercises to be beneficial in the early treatment of non-insertional Achilles tendinopathy, but the mechanism by which these work is poorly understood. It has been shown that they lead to normalisation of tendon structure, observed on ultrasound, with an apparent reduction in neovascularisation [5].


Extracorporeal shock wave therapy (ESWT)

In ESWT, acoustic shockwaves are passed percutaneous to the affected area. The rationale for using ESWT is to stimulate soft-tissue healing and inhibit pain receptors. ESWT is known to cause selective dysfunction of sensory unmyelinated nerve fibres, and changes in the dorsal root ganglia have also been reported. How ESWT works to achieve these effects is still a matter for speculation. Changes in transforming growth factor-beta1 (TGF-β1) and insulin-like growth factor-1 (IGF-1) expression and decrease in some interleukins and matrix metalloproteinases (MMP) have been demonstrated in rats and human cultured tenocytes. Conflicting results have been reported for extracorporeal shockwave therapy (ESWT), usually of low energy, but a recent randomised controlled trial (RCT) demonstrated significant improvement when ESWT was combined with eccentric exercises compared with eccentric exercises alone [6].



Correction with orthotics can alter the biomechanics of the foot and ankle and relieve heel pain. Therefore orthotics is commonly used, especially in runners, with up to 75 per cent success. A heel lift of 12–15mm is classically used as an adjunct to the management of Achilles tendon pain. As morning stiffness is common in Achilles tendinopathy, a night splint might be effective in reducing this problem. Evidence to support the routine use of splints in management on Achilles tendinopathy has however been weak.


Intermittent pulsed laser therapy (IPL)

This treatment uses laser sources at powers too low to cause measurable temperature increases. At the cellular level, it may increase collagen production, down-regulate matrix metalloproteinases and decrease the capillary flow of neovascularisation. In patients with chronic Achilles tendinopathy, treatment with IPL did not result in clinical or measurable improvements after 12 weeks. It remains possible that a positive effect would be found if different parameters of IPL were used [7].


Invasive but non-operative treatment modalities

Hyperosmolar dextrose (prolotherapy)

Prolotherapy essentially irritates the tendon to stimulate a healing response through the release of proinflammatory mediator. A solution of hypertonic glucose and local anaesthetic is injected alongside the painful area of the tendon, with the aim of stimulating inflammation followed by collagen deposition. This is thought to produce a local inflammatory response and increase in tendon strength, but evidence to support its use is lacking. A pilot study by Maxwell and co-workers demonstrated a reduction in tendo-Achilles pain both at rest and with exercise [8]. In a small, randomised study, Yelland and colleagues demonstrated improvements in outcome scores by combining prolotherapy with eccentric exercise [9].


Platelet-rich plasma

Platelet-rich plasma (PRP) has become widely used in various areas of orthopaedics, with some studies demonstrating improved tendon healing using PRP compared with controls. Significant improvement in symptoms has not been found when using PRP to treat Achilles tendinopathy. A randomised double-blind placebo-controlled study evaluating eccentric exercises and PRP or saline injection showed no difference in improvement in pain and activity at six months, and a recent meta-analysis concluded that although there may be benefits in using PRP to increase the healing strength in tendo-Achilles repair following acute rupture, there was no evidence of any benefit in using PRP in the treatment of Achilles tendinopathy [10, 11].


Sclerosing agents

There is a proliferation of small blood vessels in tendinopathy, with nerve fibres alongside the neovascularisation, which may generate the pain associated with the condition. In theory, injecting a sclerosing agent into the areas of neovascularisation could sclerose the vessels and eradicate pain-generating nerve fibres either directly by destruction or indirectly by ischaemia.


Dry needling and autologous blood injections

These are commonly used in combination. Dry needling involves repeatedly introducing a fine needle into the abnormal tendon under ultrasound guidance. Autologous blood injection involves taking a small sample of the patient’s own blood and injecting it in to the abnormal tendon under ultrasound guidance. This procedure can be performed twice, 4–6 weeks apart [12].



Steroids have been used in isolated cases of retrocalcaneal bursitis, but the volume of evidence is lacking. The historic risk of tendon rupture probably explains their infrequent use. In a systematic review by Coombes and co-workers. the corticosteroid injections might be beneficial in the short term in treatment of tendinopathy [13].


Radiofrequency microtenotomy

This is a controlled non-heat-driven process to break molecular bonds within tissues and dissolution. Good results have been documented using this approach. A study by Yeap and colleagues looking at 16 feet treated with this modality demonstrated good short-term outcomes and pain relief [14].



Conventional surgical treatment has consisted of open release of adhesions with or without resection of the paratenon. Macroscopic areas of tendinopathy are excised through a central longitudinal tenotomy, and multiple further tenotomies may be used on the surrounding tissue to initiate vascular ingrowth and a healing response. Newer techniques emphasising on minimal access surgery have emerged.


Open tenotomy

The objective of surgery is to excise fibrotic adhesions, remove degenerated nodules, and make multiple longitudinal incisions in the tendon to detect intra-tendinous lesions, restore vascularity, and possibly stimulate the remaining viable cells to initiate cell matrix response and healing [15]. The reasons why multiple longitudinal tenotomies work are still unclear. Recent investigations show that the procedure triggers neo-angiogenesis at the Achilles tendon, with increased blood flow. This would result in improved nutrition and a more favourable environment for healing. At surgery, the crural fascia is released on both sides of the tendon. Adhesions around the tendon are then trimmed, and the hypertrophied paratenon is excised. In addition, longitudinal splits are made in the tendon to identify the abnormal tendon tissues and excise the areas of degeneration. Reconstruction procedures may be required if large lesions are excised [16, 17].


Gastrocnemius recession

Isolated gastrocnemius recession provides significant and sustained pain relief for chronic Achilles tendinopathy. Good function can be expected for activities of daily living, but power and endurance activities can be more problematic for the Achilles tendinopathy group. Isokinetic strength assessment may not effectively capture patient-reported functional deficit [19].


Debridement with tendon transfer

Debridement of the Achilles tendon followed by augmentation or reconstruction with the flexor hallucis longus tendon is associated with significant improvement in terms of pain intensity and function as demonstrated with a validated measure of global function (SF-36) and tests more directly focused on hindfoot pathology (the visual analogue pain scale and the Ankle Osteoarthritis Score. In a study of 46 patients who had debridement with FHL transfer, significant improvement compared with preoperative baseline was observed at three or six months for all measures except the single-leg heel rise. Improvement in all measures continued through 24 months, with most improvement being achieved by 12 months. These findings support the use of Achilles tendon debridement and tendon augmentation or reconstruction by means of flexor hallucis longus tendon transfer in older, sedentary patients with Achilles tendinosis that is unresponsive to non-operative measures [18].

This procedure includes debridement of the degenerate insertion, decompression of bursal tissue, resection of the bony prominence, reattachment of the insertion as required, and/or augmentation of the tendo-Achilles with a tendon transfer/graft. Biomechanical and clinical data suggest that 50 per cent of the tendon attachment can be safely debrided with minimal risk of re-rupture [20]. Reattachment can be carried out using bone anchors/screws or trans-osseous sutures. As long as proper reattachment is performed the tendon should maintain normal plantar-flexion. For debridement involving more than 50 per cent of the insertion, reattachment has been described using a variety of methods. The most frequently used method of reconstruction method is augmentation using flexor hallucis longus (FHL), as it is in action during the same phase of gait, is in close proximity, has good vascularity with its low-lying muscle belly, and is the second strongest plantar-flexor.

Peroneus brevis transfer has been described, although a major concern is increased ankle instability and the development of foot inversion. Flexor digitorum longus (FDL) transfer can also be used, but is significantly weaker than the FHL (by approximately 50 per cent) and its new course could cross the tibial nerve. Alternative autografts include patellar bone/quadriceps or patellar tendon, but this can cause morbidity of the knee joint or hamstrings.


Reattachment methods

Tendon can be reattached after debriding the tendinous insertion in insertional tendinosis using various techniques. Bone anchors, screws and trans-osseous sutures can be used. Double row theoretically restores the footprint better than a single row repair. Biomechanically, both single and double row repair have similar load to failure [21]. Various methods of reattachment have been described.

Witt et al. concluded in his study of his case series using Arthrex Suture Bridge (Arthrex) and using four suture anchors and Fibrewire (Arthrex) that this suggested a greater area of compression, stability and earlier return to physiological loading. There were no local complications and at two years with good functional outcome [22, 23] (Figure 2).

Fig 2

The Arthrex Speed Bridge uses Fibretape but is very similar in other aspects to the suture bridge technique and it is perceived that they would be more useful where there may be loss of tendon tissue after debridement at the attachment or more robust fixation is required for better stability and compression (Figure 3).

Fig 3


A surgeon’s perspective

In conclusion, Achilles tendon disorders remain an important clinical entity in general orthopaedics as well as sports medicine. The first-line treatment should be physical therapy through an appropriately performed programme of eccentric exercises for at least 12 weeks. If the patient does not respond to this treatment, ESWT and night splints should be considered, although evidence is lacking regarding the efficacy. If the patient is still symptomatic, injections should be considered. Surgical options should be extensively discussed with the patient when non-operative measures fail to respond after three to six months. The chances of local complications and recurrence after any treatment should be made clear.



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Yogesh Joshi

After graduating in India, Yogesh Joshi aspired to be an orthopaedic surgeon. He came to UK, enhanced his skills and completed the FRCS (Orth) in 2011. His interest is in minimally invasive orthopaedic surgeries.

Asad Syed

Asad Syed completed his training in Yorkshire, working at the Leeds Teaching Hospitals. While training he became interested in foot and ankle surgery.

Prasad Rao