Contents

1 Achilles tendon injuries / Achillodynia / Achilles tendinitis, tendinosis or tendinopathy

Achilles tendon injuries / Achillodynia / Achilles tendinitis, tendinosis or tendinopathy

ICD: M76.6

Definition

Achillodynia denotes pain in the region of the Achilles tendon, which inserts into the calcaneus and belongs to the triceps surae. The Achilles tendon is among the largest and strongest tendons in the body. Symptoms may occur with regular sporting activity, after an unfamiliar increase in loading, or in relatively inactive people. Load-related tendinopathy is often present. Symptoms in the midportion (midportion tendinopathy) are distinguished from symptoms at the insertion into the calcaneus (insertional tendinopathy). The former is not uncommonly a “weekend warrior” disorder, occurring in people who exercise only at weekends and perhaps not even every weekend. Partial and complete ruptures must be distinguished from these conditions because they require different diagnosis and treatment. Symptoms can occur in both physically active and less active people.

Achilles tendinopathy has a multifactorial origin. Previous tendon symptoms, changes in training volume or intensity, reduced calf muscle performance and individual load tolerance may contribute. Where findings suggest them, systemic conditions, particularly inflammatory rheumatic enthesitis or familial hypercholesterolaemia, also need consideration. Fluoroquinolones and glucocorticoids warrant particular attention in connection with tendon damage. If new tendon pain or swelling develops while taking a fluoroquinolone, the European Medicines Agency recommends stopping the medication, unloading the painful area and contacting a doctor immediately. Further antibiotic treatment should be clarified with a doctor. Other prescribed medicines are not routinely managed in the same way; their use should be reviewed individually by a doctor. Gout, systemic lupus erythematosus (SLE), endocrine disorders such as hyperthyroidism, renal insufficiency also generally predispose to tendon disorders. Other predisposing factors include overloading during training due to muscle fatigue and heavy demands on tendon elasticity. When starting a sporting activity, another predisposition arises because muscle strength increases faster than tendon load tolerance.

Irritation of the Achilles tendon is usually classified as non-insertional tendinopathy (midportion, see below), but may also, or additionally, involve insertional tendinopathies (also see below), and quite regularly represents an overuse syndrome. Symptoms may develop after an increase in loading or after prolonged demands exceeding individual tendon capacity. Common features include start-up pain, morning stiffness and load-related pain. Marked or persistent symptoms may substantially restrict daily life and sport. The course varies between individuals; untreated tendinopathy does not inevitably end in a rupture. A tendinopathy may develop gradually; there is no fixed number of training years before pain develops. It often exists for years without becoming clinically apparent. Onset may also follow a change in loading relatively soon. Initially, pain often occurs only after prolonged loading, but later it may occur during or after moderate loading and may progress to rest pain. Conservative treatment often takes several months. The speed and extent of symptom resolution depend on the course, load management and individual circumstances, among other factors. Initial treatment is generally nonoperative and often takes several months. Symptoms may persist despite consistent treatment; rest alone frequently brings little short-term improvement in chronic cases. Achillodynia may occur together with retrocalcaneal bursitis of the retrocalcaneal bursa, causing additional painful soft-tissue swelling. Superficial bursitis of the subcutaneous calcaneal bursa (pre-Achilles bursa), by contrast, is often caused by pressure from an excessively stiff shoe heel counter. Achillodynia usually involves a thickened tendon with reduced load tolerance: the tendon. Intensive sporting activity over many years, particularly when one-sided, has clear prerequisites if adverse effects are to be avoided. Even small deviations from physiological processes or movement mechanics can, through their cumulative effects, lead to symptomatic disorders after a potentially long asymptomatic period during which suitable methods could already have detected changes. In general, incidence correlates with years of running and training volume.

Tendinopathies usually arise from a mismatch between loading and recovery. Marked degenerative structural changes may regress only to a limited extent; complete restoration of the original tissue cannot always be expected, particularly in Cook stage 3. One reason is that tenocytes lost through apoptosis or necrosis are hardly replaced, so that tendons may fail to achieve complete restoration for this reason alone. Tendons are generally bradytrophic connective tissue with little or no vascularisation. In terms of vascularisation and nutrient supply, the Achilles tendon is relatively well provided for compared with typical tendons: it receives blood from vessels at the muscle–tendon junction, at the insertion and through the paratenon. However, the area approximately 2–5 cm proximal to the insertion has a relatively poor supply and is a site of predilection. Animal and laboratory studies indicate that tendons contain small numbers of tendon stem and progenitor cells (TSPCs) capable of contributing to cellular restoration. Tendons have a relatively slow metabolism and a low tenocyte mitotic rate, which also limit their regenerative response. This does not mean that pain and function cannot improve. Structural findings and imaging alone determine neither individual recovery nor the need for surgery. Damage causes the tendon to swell and lose some of its elasticity, predisposing it to further damage. Whether the perceived pain originates from the damaged or dead tissue itself remains unclear. However, sensory and sympathetic nerve fibres increase in damaged tissue and are thought to mediate pain. A family history may play a role in Achilles tendon symptoms. In a 2012 study, a positive family history was associated with substantially more frequent tendinopathy; the authors reported approximately fivefold greater odds in the statistical comparison (odds ratio 4.8). The estimate was uncertain and identifies neither a single disease-determining genetic finding nor a fixed personal probability of disease. For acute ruptures, the same study found no statistically significant corresponding association. Other predisposing factors include reduced strength of the plantar flexors and an unusual dorsiflexion range.

A distinction is needed between the very common midportion Achilles pain (see below), located 2–7 cm proximal to the insertion into the calcaneus and associated with a notable risk of tears, but not classified as insertional tendinopathy, and insertional tendinopathy (see below, insertional tendinopathy) at the attachment to the calcaneus. The latter not uncommonly accompanies a posterior heel spur and tendon calcification. Stiffness and often a persistent feeling of swelling are reported alongside pain. Degenerative tendon changes can often be demonstrated, as can bony spurs (traction osteophytes). Additional retrocalcaneal bursitis is also located medial and lateral to the Achilles tendon.

Midportion Achilles pain

The midportion tendinopathy affects the middle section of the Achilles tendon above its insertion. Load-adapted conservative treatment remains worthwhile even with chronic or degenerative structural changes, although histological tendon restoration is limited, particularly in Cook stage 3. Changes in Kager’s fat pad may be involved in midportion tendinopathy, the fat pad apparently contributing to tendon nutrition as well as acting as a spacer against tendon buckling. Achilles tendon symptoms occur in both physically active and inactive people. The 2024 JOSPT guideline reports, for midportion tendinopathy, a prevalence of approximately 4–7% in a pooled analysis. For runners, an accumulated lifetime or running-career risk of Achilles tendon injury of approximately 40–52% is described. This lifetime figure is not an annual incidence and is not equivalent to every form of achillodynia. Around one in twenty non-athletes is also affected. Any part of the tendon cross-section can be involved, with thickening and pain. Typical features include start-up pain after rest and, where applicable, persistent load-related pain. Peritendinitis, by contrast, usually causes persistent pain, i.e. Rest pain, warmth (calor) and crepitus. The affected tendon often loses flexibility and is tender to pressure. Examination assesses pain location, local tenderness, possible thickening, and strength and endurance of the plantar flexors, for example through appropriately dosed heel raises. Mobility, gait, functional load capacity and deviations from normal are also assessed. A simple assessment may include single- and double-leg toe standing, heel standing, heel walking, and inspection for hindfoot valgus or hindfoot varus. Thompson and Matles tests (hanging-foot sign) primarily assess possible rupture; the Silfverskiöld test assesses calf muscle shortening. These are not interchangeable standard tests for identifying tendinopathy. Auscultation and palpation assess crepitus, which may also indicate tendinopathy. History-taking, particularly a sporting history, complements testing. Individually structured, progressive calf muscle loading is a central treatment for midportion tendinopathy. Loading is adapted to symptoms, strength and tolerance and progressively developed over at least twelve weeks. Eccentric exercises are one option; slow resistance training (Heavy Slow Repetitions, HSR) with concentric and eccentric phases is also suitable. The gastrocnemius and soleus can be addressed through exercises with the knee straight and bent. Frequency, additional weight and progression depend on the programme and individual response; twice-daily training is not a prerequisite of every effective programme, although regularity is recommended. During rehabilitation, discomfort up to NRS 3 or even 5 may be permitted under two conditions: post-exercise pain must have resolved by the following day at the latest, and pain at the same load must not increase across rehabilitation sessions but gradually decrease. If improvement remains insufficient despite consistent education, load modification and exercise therapy, extracorporeal shockwave therapy may be discussed as an adjunct. It is not a replacement for strengthening therapy. Its possible additional benefit and treatment burden should be weighed individually. Results for midportion and insertional tendinopathy are not directly interchangeable. Heel lifts may be used temporarily to reduce dorsiflexion demands and, where applicable, symptoms. In insertional symptoms, pressure and compression at the attachment need particular consideration. Footwear and, where appropriate, insoles are selected according to findings and tolerance; a general healing advantage of orthopaedic insoles for midportion tendinopathy has not been established. These measures supplement rather than replace active progressive loading. Changes to a heel lift should be adapted to the load response. When a temporary orthopaedic heel lift is used, its removal must be approached cautiously. Measures such as rest alone, purely concentric strengthening or various types of orthoses appear to offer limited prospects of success. Muscular disorders and imbalances should be addressed. Taping may be considered as an adjunct to active treatment for selected symptoms. The benefit of other additional procedures requires separate assessment. A presumed analgesic effect does not make them a substitute for progressive loading. Steroids should not be administered because they increase the risk of rupture. Injection procedures such as PRP, autologous blood or hyaluronic acid are distinct from active core treatment. A reliable additional benefit has not been established for all procedures and patient groups. In a placebo-controlled study of chronic midportion tendinopathy with accompanying eccentric training, PRP offered no additional benefit over saline. Injection is therefore not a general prerequisite for successful conservative treatment. Surgery may be considered for persistently substantial symptoms despite at least six months of consistent active treatment. The decision depends on the clinical course and specific findings, not solely on a Cook stage.

Insertional tendinopathy

For insertional tendinopathy of the Achilles tendon (Insertional Achilles Tendinopathy, IAT) at the calcaneus, various risk factors exist, including non-modifiable factors such as age, modifiable factors such as hypertension, obesity, diabetes mellitus, rheumatic diseases and oral or local steroid use, and biomechanical causes such as axial malalignment, foot deformities, muscular imbalances, leg length discrepancies, etc. Hyperpronation, hindfoot varus, restricted mobility of the hindfoot and shortening of the gastrocnemius appear to present particular risks. Running generally presents a risk, especially with inappropriate training, unsuitable footwear, insufficient warm-up or unsuitable surfaces that are too hard or too soft. Runners have a tenfold greater risk than non-runners.

In insertional symptoms, the tendon attachment, adjacent bursae, bony prominences and mechanical compression may contribute to differing degrees. Primary degeneration of retro-Achilles cartilage may also lead to damage of the Achilles tendon. Specific findings therefore need differentiation rather than assuming a uniform sequence of cartilage and tendon degeneration in every case. The insertional tendinopathy of the Achilles tendon particularly affects young runners developing tendon symptoms after training changes, and older people with chronic problems. Insertional Achilles tendon symptoms may coexist with plantar heel symptoms. Both pain sites and the affected structures should be examined separately, although foot loading may influence both through the connection described above. Morning start-up pain and pain on loading, increasing with duration and intensity of loading, are common. With atypical pain location or accompanying neurological signs, other causes of heel pain should be assessed, including Baxter neuropathy. Absence of burning pain or the presence of start-up pain alone cannot reliably exclude nerve involvement. Precise location, clinical examination and further investigation where needed are decisive. In IAT, the enthesis contains swollen tendon tissue and is also the site of pain. The greater biomechanical demands of barefoot walking exacerbate pain. A Haglund deformity may be present and can be difficult to distinguish from IAT. Sub-Achilles bursitis may also be present above the enthesis and characterised by local tenderness to pressure and increased pain during dorsiflexion. Assessment includes gait, heel walking, and single- and double-leg toe standing. Inspection looks for muscle atrophy or differences in lower-leg contour, malalignment of the calcaneus, including varus alignment and valgus alignment and a steeply inclined position, together with dorsiflexion range and plantar flexion capacity at the ankle joint and supination and pronation of the calcaneus at the subtalar joint. Posterior ankle impingement or an os trigonum are also relevant. A detailed pain history seeks to locate pain as precisely as possible: at the enthesis, insertional tendinopathy should be distinguished from the more proximal bursitis. Imaging assesses intratendinous calcification (Insertional Calcified Achilles Tendinopathy, ICAT), as well as traction osteophytes. ICAT tends towards partial lesions of the deep tendon portions. Tendon neovascularisation is seen particularly on MRI, which is also well suited to demonstrating bone marrow oedema. For insertional tendinopathy, active conservative treatment is initially the first choice. Footwear compressing the Achilles tendon should be avoided. Strength training is adapted to avoid unnecessarily increasing painful compression at the insertion. Initially, exercises on level ground and limiting dorsiflexion may be useful; lowering the heel below a step edge and forced calf stretching are not necessarily suitable starting exercises when the insertion is compression-sensitive. Intensive calf stretching should be avoided unless there is reason to believe that substantial shortening of the triceps surae is a biomechanical component of the aetiopathology. Temporary heel lifts may provide additional unloading. Loading is then built up gradually. A randomised study of physically active adults found better results with an overall low-compression programme than with a higher-compression programme. Whether adjunctive procedures are needed depends on progress and individual findings. If consistent conservative treatment fails after six months, surgical options should be considered. Precise assessment is highly relevant in either case.

Ruptures

An acute Achilles tendon rupture often occurs under a sudden high load, such as pushing off, jumping or unexpectedly decelerating a movement. Degenerative changes usually provide the background, without necessarily causing previous pain. Middle-aged adults participating in sports involving running, jumping or changes of direction are frequently affected. Chronic overuse leads to damage of tendon tissue, including microtears of the collagen fibres and tendon calcification. Recreational ball-sport participants exercising irregularly tend to sustain rupture more often than competitive athletes, possibly also reflecting the latter’s better supervision and monitoring. Ruptures often occur in the midportion a few centimetres above the calcaneal attachment; insertional and musculotendinous tears should be distinguished. The three most important causative scenarios are:

Forced dorsiflexion of the plantar-flexed foot, such as landing from a great height
Unexpected dorsiflexion movements while the triceps surae is contracting forcefully
Pushing off with the foot while extending the knee joint.

A tear of the Achilles tendon, which averages 20–25 cm in length, usually occurs 2–7 cm above the calcaneus, where the arterial supply from above and below is poorest. In general, tendon vascularisation is inadequate relative to its loading (see Anatomical background below). Existing microlesions also compromise vascular supply, further promoting degeneration. Hypervascularisation, presumed to be related to hypoxia, is not uncommon. Surgery usually reveals disrupted fibre structure; microscopy shows abnormal collagen structure that heals poorly. Signs of inflammation are relatively uncommon. Paratendinous tissue is normal or oedematous and often scarred.

Acute Achilles tendon rupture may cause sudden pain, a sensation of being kicked in the calf and an audible snap. Push-off during walking and the single-leg heel raise are substantially impaired. Active plantar flexion may nevertheless remain partially preserved through other muscles, such as the tibialis posterior and fibularis group, and does not rule out rupture. The Thompson test assesses plantar flexion elicited by squeezing the calf; the Matles test may reveal an altered resting foot position compared with the other side. A palpable gap is pathognomonic but may not always be clearly discernible. Suspected rupture requires prompt medical assessment; forced stretching or loading tests should be avoided. Ultrasound can show the extent, location and approximation of tendon ends in a defined foot position. Protected plantar flexion can bring the ends closer together. Measured gap width depends on foot position and examination technique; a single threshold does not alone determine conservative or surgical treatment. Tears are classified by distance from the calcaneal attachment as

Insertional: 0–2 cm
Midportion: 2–8 cm
Proximal: more than 8 cm

The Achilles tendon contains functionally distinguishable components from the soleus and the medial and lateral gastrocnemius heads. Injury can involve one or more of these components. Treatment depends not only on level but also on continuity, tissue quality and the function of the entire muscle–tendon complex. Both operative and nonoperative treatment can provide good functional outcomes after acute Achilles tendon rupture. An appropriate treatment concept and its consistent implementation are decisive. A 2022 randomised study compared nonoperative treatment, open repair and minimally invasive repair. After twelve months, no clear advantage emerged for any group in average reported symptoms and function. Recurrent ruptures occurred in 6.2% without surgery and 0.6% each after open and minimally invasive repair. Nerve injuries were reported in 0.6% without surgery, 2.8% after open repair and 5.2% after minimally invasive repair. These figures describe the study population and do not predict an individual outcome. Rerupture, wound and nerve risks, comorbidities, loading goals and rehabilitation are weighed together when choosing treatment. After Achilles tendon rupture, protective positioning, orthosis use, loading and mobility follow a coordinated protocol. Depending on treatment, controlled early functional rehabilitation can begin during the protective phase; it does not mean immediate unrestricted loading or forced stretching. Progression to unrestricted walking, progressive strengthening, running, jumping and sport is staged according to healing and function. Excessive lengthening of the healing tendon should be avoided, which is why plantar flexion with the knee joint extended is permitted only later. Return-to-play decisions depend not only on elapsed time but particularly on calf strength, heel-raise endurance, movement quality and sport-specific load capacity. This is rarely possible before six months. Return to the previous performance level may take substantially longer than the first resumption of sporting activity. Open and minimally invasive repairs are available, along with reconstructive procedures for specific defects. Selection depends on tear pattern, tissue quality, skin condition, individual risks and the treatment team’s experience. High laboratory tensile strength of a suture model does not automatically prove better clinical outcomes or superiority for all ruptures.

Chronic rupture

Achilles tendon rupture is often described as chronic after approximately four to six weeks, particularly when initially unrecognised or untreated. A complete tear may also be present. Scar bridging and tendon lengthening may impair force transmission. Signs include reduced push-off, difficulty with single-leg heel raises, reduced calf musculature and altered gait; pain or a palpable gap need not be prominent. Partially preserved plantar flexion, due to the available synergists, does not exclude chronic rupture either. Assessment combines history, functional assessment and clinical tests with ultrasound or MRI according to findings. Surgical reconstruction may be appropriate for substantial persistent functional impairment. The procedure depends on defect length, tissue quality and functional goals, among other factors. Comorbidities, operative risks and the feasibility of rehabilitation are considered; nonoperative care may also be chosen with high surgical risk or other individual circumstances.

When selecting treatment for tears, habitual, desired and necessary activities, as well as psychological factors, play a major role.

Anatomical background

The muscles contributing to the Achilles tendon are the gastrocnemius, soleus and usually also the plantaris. Taking the ankle joint and subtalar joint into account, the soleus is
biarticular, whereas the other two are triarticular. The plantaris originates tendinously slightly proximal to the lateral gastrocnemius origin and has only a very short muscle belly; the remainder distally is its tendon, which merges into the Achilles tendon and attaches to the calcaneus. The soleus, with its higher type I fibre content, has a more postural role and can also generate greater force than the gastrocnemius. The soleus also contributes substantially to the venous pump through its deep position. The gastrocnemius, by contrast, is a faster-moving muscle with a higher type II fibre proportion. It atrophies less rapidly than the soleus. The Achilles tendon, usually over 20 cm long, receives fibres from the soleus along almost its entire length. In the gastrocnemius, the medial head is longer and wider and therefore produces greater contractile force than the lateral head. The medial head also has an additional lateral origin. The lateral head additionally originates from the capsule of the knee joint. A particular feature is that the lateral head often contains the fabella, a sesamoid bone found in up to 30% of people and predominantly present bilaterally. If it dislocates or fractures, it causes fabella syndrome. Beneath the medial head there is normally a communicating
bursa, excessive filling of which may appear as a Baker cyst. The lateral head may also have a bursa. Approximately halfway down the lower leg, the aponeurosis, into which both heads of the gastrocnemius insert, joins the fibres of the soleus to form the Achilles tendon. Crossing the knee joint, the gastrocnemius, particularly its medial head, is much more prone to shortening than the soleus. The soleus has a fibular origin on the posterior aspect of the fibular head down to the upper-third point of the fibula. Its tibial origin comprises several parts: the tendinous arch of the tibia, interosseous membrane of the leg and middle third of the posteromedial tibial border. The three-layer crural fascia surrounding the posterior compartments of the lower leg merges with the Achilles tendon. Loose connective tissue separates these three layers to allow gliding. The crural fascia can also be injured. The surrounding fasciae of the Achilles tendon and the paratenon permit gliding and contribute to nutrient supply.

The plantaris tendon is anatomically variable: it may be absent (figures of 6–8% are sometimes quoted), run separately or connect with the Achilles tendon region in different ways. The shape, length and cross-section of the Achilles tendon vary between people and along its course. Measurements of free tendon length also need to be distinguished from measurements including proximal aponeurotic portions. The Achilles tendon tapers distally to its narrowest point approximately 4 cm above the insertion into the calcaneus, within the area considered a site of predilection. Average width is 3.4 cm, with practical measurements of 2–4.8 cm. Distally, the attachment region broadens at the calcaneus. Subtendon arrangement varies between individuals. An anatomical review describes a historical classification into weak, moderate and strong torsion, with frequencies of 52%, 35% and 13% in the respective specimen population. These figures refer to torsion types, not the percentage contribution of soleus or gastrocnemius to the entire tendon. The components do not simply run parallel but twist relative to each other. Direction and extent depend on the subtendon, level examined and individual anatomy. The common description of an approximately right-angle twist is a simplification rather than a constant measurement in everyone. Twisting influences load distribution; its precise contribution to perfusion and disease development is not yet fully clarified. In general, it increases tensile strength but also results in a poorer supply approximately 2–5 cm proximal to the insertion into the calcaneus, also the region where most ruptures and most tendinopathies occur. At the crescent-shaped insertion of the Achilles tendon into the calcaneus, the tendon transitions into a specialised attachment region on the bone, including fibrocartilaginous transition zones. Nearby lie the retrocalcaneal bursa subtendinea tendinis calcanei, whose elasticity cushions tendon gliding against bone, and Kager’s fat pad. These structures may be involved during movement and compression but are not all equivalent components of the tendon itself. Another superficial bursa between tendon and skin can cause symptoms. Between the Achilles region, calcaneus and plantar fascia, there are connective-tissue and functional relationships. They may be mediated through the periosteum and paratenon, vary individually and generally diminish with age. The plantar fascia therefore cannot simply be regarded in all adults as a direct continuation of the Achilles tendon. Symptoms in both structures can coexist, but a finding in one does not establish disease in the other. Weakness of the foot structure may nevertheless directly affect the Achilles tendon–triceps surae structure through this connection. The twisted course changes the subtendons’ spatial relationships down to the calcaneal attachment. Because of the marked twisting of fibres in the Achilles tendon, portions from the lateral head of the gastrocnemius and from the soleus attach to the medial facet of the calcaneal tuberosity and the fibres of the medial head of the gastrocnemius attach inferiorly. However, the precise allocation of attachment surfaces may vary between people and anatomical classifications. Between the Achilles tendon and skin lies a subcutaneous bursa, the subcutaneous calcaneal bursa (pre-Achilles bursa). Instead of a tendon sheath, the Achilles tendon is surrounded by paratenon, a highly vascular connective-tissue structure. Proximally, it merges into muscle fasciae and distally into the periosteum of the calcaneus. Soleus and gastrocnemius make a major contribution to plantar flexion, supported by other muscles. Depending on the author, the triceps surae generates between 73% and 93% of plantar-flexion force; the remaining 7–27% is distributed among the five other relevant muscles: in addition to the toe flexors, the fibularis brevis, fibularis longus and tibialis posterior. Their respective force contributions depend on knee and ankle position and the task, among other factors. Anatomical cross-section, contribution to the Achilles tendon and contribution to the measured joint moment are therefore different quantities. During running, the Achilles tendon is repeatedly exposed to high tensile forces. Their magnitude and rate of increase depend on speed, running technique, muscle strength and the measurement or calculation method used, among other factors. Blood supply to the Achilles tendon comes from vessels around the muscle–tendon junction, the insertion and the vascular paratenon. Anatomical investigations describe contributions particularly from the posterior tibial and fibular arteries; contributions from the anterior tibial artery have also been demonstrated. The midportion is often described as relatively less vascularised. This does not equate to a completely avascular segment, however, and findings also depend on the detection method. In a study of 28 lower-leg specimens, angiography revealed contributions from the anterior tibial artery too small to be recognised by gross dissection. Vascular supply, local mechanical loading and healing capacity should be considered together.

Epidemiology

Achilles tendinopathy and Achilles tendon rupture have different frequency estimates and typical patient populations. Ruptures frequently affect middle-aged men but can occur in other age and activity groups. Tendinopathies occur in physically active and inactive people. For typical midportion achillodynia, different sources report the following: the peak group comprises physically active men aged 30–50. Competitive athletes are often affected from age 24, recreational athletes more often from age 40; the latter also sustain subsequent ruptures more frequently. Around 10% of recreational joggers are affected. The condition is bilateral in almost half of cases, with one side often becoming symptomatic before the other. Athletes with a lowered foot arch are affected one and a half times as often, and those with a high-arched foot almost twice as often. Regular exercisers and professional athletes are also commonly affected: approximately 50% of middle- and long-distance runners are affected during their careers. Non-athletes still account for a prevalence of just under 10%, particularly people who stand for prolonged periods. In a biomechanical study of 20 uninjured high-performing endurance runners at different speeds, average peak forces were estimated at approximately 6.5–7.7 times body weight. Both peak force and its rate of increase rose with speed in that study. Values peak at approximately 10–12 times body weight during sprinting. These model estimates do not represent a universal injury threshold. Training management depends not just on step count but also on load magnitude, duration, progression and recovery.

Causes

Eccentric stretching under high force demands, acute trauma, extreme loading, overuse; often with pre-existing damage or malalignment
Posterior heel spur
Previous fractures in the region of the ankle joint or tibia

Predisposition

The following findings need to be distinguished according to their significance. Some may affect individual tendon loading or load tolerance; others are comorbidities or independent causes of heel and ankle pain. An abnormal foot or joint finding is not automatically an established independent risk factor for Achilles tendinopathy. Stress fractures, osteochondral lesions, other tendon disorders and childhood calcaneal apophysitis in particular also require consideration in the differential diagnosis. Clinical relevance depends on pain location, examination and function.

– Musculoskeletal system

Short calcaneus
Hyperextensible
knee joints (reduce the flexibility required of the triceps surae during walking/running)
Instability of the longitudinal arch of the foot: lowered arch, flat foot
Insufficient flexibility of the triceps surae and the Achilles tendon
Restricted hip extension, restricted internal rotation at the hip joint
Unstable ankle (ligament injuries, e.g. after an inversion injury)
Altered lower-limb alignment, especially knock knees
Leg length discrepancies
Previous Achilles tendon disorders (recurrence)
Knee or hip joint disorders
Deformities or axial deviations
Hyperpronation
Foot deformities such as high-arched foot, flat foot, lowered foot arch, lowered–splay foot,valgus flat foot
In children and adolescents: calcaneal apophysitis
Arthritis of the ankle joint
Pre-existing retrocalcaneal or subcutaneous calcaneal bursitis
Plantar fasciitis or heel spur
Haglund deformity (Haglund heel)
Hallux rigidus, hallux limitus
Insufficiency of the lateral capsular ligament of the ankle joint
Bone disorders
Osteochondritis dissecans
Existing stress fracture
Tendinopathies at the medial malleolus

– Activity and sport

Activities or sports involving sudden loads: running, athletics, dancing, ball sports, racket sports, jumping sports. Indoor participation, asphalt and other hard surfaces are additional contributing factors
Sport without adequate warm-up, and in cold or wet conditions
Inappropriate footwear
Inadequate training status
Poor running technique
Uphill running
Resuming training after a prolonged break
Unfavourable running conditions, e.g. wet, slippery leaves
Overexertion: “too much, too soon”
Unfamiliar surfaces (too hard for trained people, too soft for untrained people)
Predominantly sedentary lifestyle and activities
Mismatch between frequency and duration of loading and training intensity on one hand, and the duration of recovery periods on the other
Running on sand and other loose surfaces
Low heel-to-toe drop in running shoes
Pressure from the running shoe on the Achilles tendon

– Health-related risk factors

Metabolic disorders: hyperuricaemia (Gout), hypertriglyceridaemia, hyperlipoproteinaemias and diabetes mellitus impair microlesion healing
Rheumatic disorders
Older age
Excess weight
Medication history should particularly consider fluoroquinolones and glucocorticoids. The risk associated with fluoroquinolones may increase with concurrent corticosteroid treatment. This warning does not imply that all antibiotics carry the same risk. For other potentially involved medicines, such as statins, individual circumstances and the respective evidence require separate assessment.
Familial hypercholesterolaemia
Smoking

Symptoms

Gradually developing pain on movement (diffuse, dull or even sharply stabbing, often above the attachment to the calcaneus in the region with the poorest supply), particularly during foot roll-over and plantar flexion, more pronounced in the morning and after rest. Pain during roll-over is greatest under eccentric loading when the body moves past the supporting foot. Pain usually radiates clearly along the tendon and is less often diffuse. It may diminish during running, usually without resolving completely.
Marked pain on stretching
Initial irritation causes start-up pain on loading and morning pain; with longer duration, pain also increases during loading and may become stabbing, requiring sport to stop or preventing it altogether. Load-related pain may persist for some time afterwards (post-exercise pain) and progress to rest pain
Tenderness to pressure
Marked thickening of the Achilles tendon
Gliding of the Achilles tendon within surrounding tissue may be restricted or absent
Altered gait to avoid pain
Possibly Signs of inflammation: swelling, warmth and redness
Possible adoption of an equinus position to unload the Achilles tendon
Possible peritendinitis with thickening of the peritendineum and reduced gliding of the Achilles tendon within surrounding tissue, together with auscultated or palpated
crepitus
In rupture: substantially reduced push-off and impaired single-leg heel raise; partially preserved active plantar flexion does not rule out a tear.
In rupture: a whip-crack sound
In rupture: haematoma
Possible altered gait on the affected side: restricted plantar flexion of the ankle joint, early heel rise, reduced hip extension and increased pelvic rotation
Abnormalities when descending stairs backwards: pain during eccentric contraction of the triceps surae to form the dorsiflexion at the ankle leads to observable avoidance behaviour

Diagnosis

Tenderness to pressure of the Achilles tendon (pincer grip)
Palpable gap in partial and complete tears
Typical Achilles tendinopathy is diagnosed predominantly clinically. With an appropriate location, load-related pain and palpation findings, additional imaging is not required in every case.
When findings are unclear, the course is unexpected, associated pathology is suspected or surgery is being planned, ultrasound is often the first additional investigation. Doppler techniques can detect increased vascularity.
For insertional symptoms, a lateral radiograph of the calcaneus may show bony changes or calcifications. MRI can be useful as an additional investigation depending on findings, for example to investigate an unexplained discrepancy or provide further clarification.
Structural findings are not used alone to predict prognosis or as routine proof of training success.
Tests and signs: Thompson test, O’Brien needle test, forefoot-standing test

Complications

Complication of achillodynia: rupture of the Achilles tendon

Treatment

Achilles tendinopathy is generally treated nonoperatively at first. Pain-provoking loading in daily life and sport is temporarily suspended or adapted and, where possible, replaced by tolerable activity; complete rest is generally not the treatment goal in uncomplicated midportion tendinopathy. Subsequent controlled progressive loading is decisive. Analgesics and anti-inflammatory medicines are used according to findings. Taking pain medication to enable pain-free participation in sport is contraindicated. Suspected tears require different protective and treatment measures.
Topical anti-inflammatory ointment
Technique training and optimisation of sports footwear where appropriate
Appropriate running shoes with adequate heel cushioning; consider shoe lifespan, approximately 500–1,000 training kilometres
Heel lifts may be used temporarily to reduce dorsiflexion demands and, where applicable, symptoms. In insertional symptoms, pressure and compression at the attachment need particular consideration. Footwear and, where appropriate, insoles are selected according to findings and tolerance; a general healing advantage of orthopaedic insoles for midportion tendinopathy has not been established. These measures supplement rather than replace active progressive loading. Changes to a heel lift should be adapted to the load response. When a temporary orthopaedic heel lift is used, its removal must be approached cautiously.
For dysfunction of the ankle or forefoot joints: physiotherapy
Identify and address functional deficits in the hip joint (particularly extension, internal rotation)
Weight, general health and individual load capacity may be incorporated into treatment where appropriate. Whether weight reduction is useful and what support it requires are assessed individually; a particular weight relative to height does not by itself determine the Achilles tendinopathy treatment programme.
No training while taking pain medication!
Consider temporarily switching to lower-impact sports such as cycling
Consider nutritional therapy with adequate omega-3 intake
If improvement remains insufficient despite consistent education, load modification and exercise therapy, extracorporeal shockwave therapy may be discussed as an adjunct. It is not a replacement for strengthening therapy. Its possible additional benefit and treatment burden should be weighed individually. Results for midportion and insertional tendinopathy are not directly interchangeable.
Keep the Achilles tendon warm before sport and cool it afterwards
Injection procedures such as PRP, autologous blood or hyaluronic acid are distinct from active core treatment. A reliable additional benefit has not been established for all procedures and patient groups. In a placebo-controlled study of chronic midportion tendinopathy with accompanying eccentric training, PRP offered no additional benefit over saline. Injection is therefore not a general prerequisite for successful conservative treatment.
Strength training, followed later by endurance training
Functional lower-limb alignment training
Physiotherapy
Core treatment consists of understandable education combined with adapted daily and sporting loads and progressive calf strengthening. Mobility deficits can be addressed specifically. Stretching is not necessary in every Achilles tendinopathy, however, and particularly with insertional symptoms must be adapted to compression sensitivity. Sporting activity requires adequate warm-up.
Stretching of the plantar fascia and toe flexors
Heel lifts may be used temporarily to reduce dorsiflexion demands and, where applicable, symptoms. In insertional symptoms, pressure and compression at the attachment need particular consideration. Footwear and, where appropriate, insoles are selected according to findings and tolerance; a general healing advantage of orthopaedic insoles for midportion tendinopathy has not been established. These measures supplement rather than replace active progressive loading. Changes to a heel lift should be adapted to the load response. When a temporary orthopaedic heel lift is used, its removal must be approached cautiously.
Partial and complete tears require separate assessment of tear extent, functional loss, imaging and individual loading demands. Not every partial tear needs surgery. Depending on findings, an acute complete rupture may be treated nonoperatively with early functional rehabilitation or surgically; a chronic defect may require other reconstructive procedures.
Suitable acute ruptures may be treated nonoperatively with a protective orthosis and structured early functional rehabilitation. Assessment considers tendon contact in a documented plantar-flexed position, tear pattern, function, individual risks and the feasibility of rehabilitation. Age alone is not decisive.
Operative and nonoperative approaches to acute complete rupture require individual weighing. Surgery may lower rerupture risk but brings its own complications. Structured early functional rehabilitation is essential with either approach.
When returning to daily and sporting loads, volume, intensity and recovery periods are adapted gradually. A pain scale may help monitor the response during and after loading. A low pain score alone does not guarantee that every load is harmless. Progress, function and the response to the next load are also decisive. After rupture or when weakened tendon structure is suspected, a general pain-monitoring scheme must not replace the prescribed rehabilitation protocol.
Local corticosteroid injections around the Achilles tendon require caution and assessment according to findings because of potential damage and increased rupture risk. Nitrate preparations are not routinely recommended as a better alternative. In the NEAT study, additional GTN ointment did not improve the results of eccentric training more than placebo ointment.
For persistently substantial symptoms despite at least six months of consistent active conservative treatment, specialist assessment for surgery may be appropriate. Findings, previous loading progression, comorbidities, goals and potential risks are weighed together. Timing alone does not justify surgery. The appropriate procedure depends on the specific pathology. General superiority of microinvasive procedures is not assumed, although some evidence suggests a lower complication rate.

Asana practice

If no tear is present, it is important both to maintain good flexibility of the triceps surae and to provide sustained strengthening that increases metabolism in the Achilles tendon and trains it. Sudden loads, as in many sports, are unsuitable for this purpose and, particularly in excess, more likely harmful. Stretching should address both the monoarticular
soleus and especially the biarticular
gastrocnemius, whose tone is likely more relevant in everyday movements and most sports. Exercises therefore need substantial dorsiflexion movements of the ankle with and without an extended knee joint

A stable ankle should also be developed, addressing both muscular performance, particularly explosive strength in sporting movements, and proprioception, for which balance postures or postures with a balance component are well suited. Muscle performance can generally be improved through explosive-strength or maximal-strength training. With a previously damaged tendon, explosive-strength work must be avoided: if muscle performance capacity is exceeded during training, even for milliseconds, tendon elasticity is recruited. This must be avoided in the presence of previous damage.

All muscular imbalances must be investigated and addressed with stretching and strengthening postures to achieve the best possible symmetry.

The supinators of the ankle joint rarely lack flexibility but nevertheless often develop excessive load-related tone, potentially progressing to irritation such as medial tibial stress syndrome. Although the range of movement of the ankle joint in this direction is large, normal foot roll-over generally begins with slight supination, and the gravity-induced reactive pronation must be controlled by the supinators. The pronators, by contrast, are often tense in runners and athletes whose disciplines involve substantial running. This is likely more pronounced the more supinated the foot is at initial contact.

As foot roll-over also depends on the tension-band mechanism of the plantar fascia and the toe flexors as a whole, these also deserve attention. Excessive tension in the plantar fascia tends to overload the Achilles tendon. A small foam roller can be useful here.

Finally, the antagonists of the Achilles tendon–linked triceps surae should not be forgotten: the dorsiflexors should be assessed for excessive tone. Virasana and baddha padasana and hip opener 5 offer useful possibilities.

Among all these tasks, it should not be overlooked that training the flexibility and strength of the triceps surae itself, as the muscle whose force the Achilles tendon transmits, remains most important.

Relevant asanas

Asanas in 851: stretching the foot extensors / plantar flexors / calf muscles
Asanas in 852: strengthening the foot extensors / plantar flexors / calf muscles
Asanas in 861: stretching the supinators
Asanas in 862: strengthening the supinators
Asanas in 871: stretching the pronators
Asanas in 872: strengthening the pronators
Asanas in 971: stretching the toe flexors
Virasana and baddha padasana for relaxed antagonists.

yogabook

pathology: achillodynia