Kvarda Peter
ADUS Klinik, Breitestrasse 111, 8157 Dielsdorf
Zusammenfassung
Achillessehnenentzündungen sind eine weit verbreitete Erkrankung des Bewegungsapparates, die sowohl Sportler als auch Nichtsportler betrifft. Dieser Artikel soll einen umfassenden Überblick bieten und sich auf die Ätiologie, das klinische Erscheinungsbild, die Diagnosemethoden, die Behandlungsmodalitäten und die Präventionsstrategien konzentrieren. Durch das Verständnis der Anatomie, Pathophysiologie, des allgemeinen Erscheinungsbildes und der optimalen Behandlungsansätze können behandelnde Ärzte eine Achillessehnenentzündung effektiv diagnostizieren, behandeln und verhindern und so die rechtzeitige Rückkehr zu früheren Aktivitäten erleichtern.
Schlüsselwörter: Achillessehne, Tendinopathie, Haglund
Introduction
Throughout history, the Achilles tendon has posed challenges for both athletes and non-athletes, as well as their medical practitioners. Achilles tendinopathy, marked by inflammation, degenerative alterations, and functional limitations of the Achilles tendon, presents as a common issue in activities involving repetitive motions. Serving as the largest tendon in the human body, the Achilles tendon plays a pivotal role in transmitting forces from the calf muscles to the heel, facilitating propulsion during movement. Nevertheless, the repetitive stress and overuse inherent in certain activities can predispose individuals to inflammatory processes, potentially resulting in pain, functional limitations, and reduced performance. Whether presenting as paratenonitis, midportion tendinopathy, or insertional tendinopathy, the condition compromises the patient’s ability to engage in or resume activities. This article delves into the pathogenesis, clinical manifestations, diagnostic considerations, treatment modalities, and preventive measures pertinent to Achilles tendinopathy.[1–5]
Anatomy
The Achilles tendon, arising from the gastrocnemius, soleus, and possibly the plantaris muscles, is the body’s largest and strongest tendon, crucial for ankle plantar flexion. Situated within the posterior calf compartment, these muscles are separated by fascial septa. The Achilles tendon, approximately 15 cm long, starts at the gastrocnemius-soleus junction and inserts into the calcaneus, its fibers spiraling and undergoing rotational changes. Sensory nerves from superficial and deep sources innervate the tendon, detecting pressure, stretch, and pain stimuli. These receptors monitor tendon health and respond to mechanical stresses. The gastrocnemius-soleus complex is innervated by the tibial nerve. Originating from the femoral condyles and posterior tibia, the gastrocnemius and soleus, respectively, act as effective plantar flexors. The tendon inserts over a broad area on the calcaneal tuberosity and is associated with two bursae: the retrocalcaneal bursa and the Achilles tendon bursa. During activities, the Achilles muscle tendon unit undergoes eccentric lengthening and concentric contracture. Enclosed within a paratenon, it lacks a true synovial sheath, with vascular supply from the calcaneus distally and intramuscular arterial branches proximally. A hypovascular zone 2 to 6 cm proximal to the calcaneal insertion, coupled with the tendon’s twisting 90 degrees, predisposes it to degenerative changes in the distal region. [6–12]

Etiology
- Achilles tendinopathy, both midportion and insertional variants, can arise from a variety of etiological factors.
- Overuse and Repetitive Stress: Prolonged or excessive loading of the Achilles tendon due to repetitive activities such as running, jumping, or sudden changes in activity level can lead to microtrauma, tendon degeneration, and subsequent tendinopathy.
- Biomechanical Factors: Deformities, leg length discrepancies, and poor muscle flexibility or strength imbalance, may contribute to increased strain on the Achilles tendon.
- Poor Training Techniques: Inadequate warm-up routines, improper footwear, rapid increases in training intensity or duration, and insufficient rest intervals can all place stress on the Achilles tendon.
- Age-related Changes: Aging is associated with decreased tendon elasticity and collagen turnover, making older individuals more susceptible to tendon degeneration and development of tendinopathy.
- Systemic Factors: Certain systemic conditions such as obesity, diabetes, metabolic disorders, and inflammatory conditions like rheumatoid arthritis may impair tendon health and contribute to the development of Achilles tendinopathy.
- Anatomical Factors: Anatomical variations such as a prominent calcaneal tuberosity or Haglund’s deformity (insertional tendinopathy) can lead to abnormal mechanical stresses on the Achilles tendon.
- Trauma: Acute trauma or direct injury to the Achilles tendon, such as a sudden forceful impact or laceration, can cause structural damage and inflammation, initiating the pathological process underlying tendinopathy.
- Genetic Predisposition: Genetic factors may influence tendon structure and composition, affecting its susceptibility to degeneration and tendinopathy.
Pathophysiology
Overall, the pathophysiology of Achilles tendinopathy involves a multifaceted cascade of degenerative, inflammatory, and failed healing processes, leading to tendon dysfunction and pain. Understanding these underlying mechanisms is critical for developing targeted therapeutic interventions aimed at promoting tendon healing and restoring function. [1]
Midportion Achilles Tendinopathy
- Degenerative Changes: Chronic overuse and repetitive stress on the Achilles tendon lead to microtrauma, collagen disorganization, and degenerative changes within the tendon matrix. This results in the breakdown of collagen fibers, increased collagen disarray, and disruption of the normal tendon architecture.
- Tendon Hypoxia: Prolonged mechanical loading and repetitive stress reduce blood flow to the tendon, leading to localized hypoxia and ischemia. This impairs tendon cell metabolism, alters matrix homeostasis, and contributes to tissue degeneration.
- Inflammatory Response: While traditionally considered a non-inflammatory condition, recent research suggests that inflammation may play a role in midportion Achilles tendinopathy. Increased expression of inflammatory mediators, such as prostaglandins and cytokines, is observed in the tendon microenvironment, contributing to pain and tissue damage.
- Failed Healing Response: In response to chronic degeneration and microtrauma, the tendon attempts to undergo a reparative process. However, this healing response is often inadequate, characterized by aberrant collagen synthesis, disorganized matrix remodelling, and formation of abnormal neovascularization, leading to further tendon weakening and dysfunction.
Insertional Achilles Tendinopathy
- Tendon-Bone Interface Changes: Insertional Achilles tendinopathy involves pathology at the junction of the Achilles tendon and the calcaneus bone. Chronic mechanical stress and repetitive loading at this insertion site can lead to microtears, fibrocartilaginous metaplasia, and calcification of the tendon-bone interface.
- Enthesopathy: Degenerative changes occur at the enthesis, the interface between tendon and bone, characterized by fibrocartilaginous degeneration, neovascularization, and abnormal bone remodelling. This disrupts the normal biomechanical properties of the insertion site and contributes to pain and functional impairment.
- Bursal Involvement: Inflammation and hypertrophy of the retrocalcaneal bursa, may accompany insertional tendinopathy. Bursal thickening, fibrosis, and calcification can further exacerbate symptoms and hinder tendon healing.

Clinical Presentation and Diagnosis
Individuals affected by Achilles tendinopathy commonly report symptoms indicative of the condition’s progression and impact on daily function. Most commonly swelling of the tendon, stiffness, tenderness along the tendon and posterior heel pain. Increasing discomfort during physical activity, particularly during push-off or dorsiflexion of the ankle. Furthermore, athletes frequently describe morning stiffness or discomfort after prolonged periods of inactivity. Initially, pain may manifest at the beginning and end of training, with intervals of reduced discomfort in between. However, as the condition advances, even minor exertions can induce pain, potentially interfering with routine activities. In severe instances, athletes may experience pain even at rest. Significant variation of methods used to diagnose Achilles tendinopathy exists. [15] Physical examination including palpation of the tendon, assessment of ankle range of motion, and functional tests aid in the diagnosis of Achilles tendonitis. In addition, there are 9 core health domains associated with tendinopathy. This includes the following: patient rating of condition, pain on activity/loading, participation (daily activities, work, sport), function, psychological factors, disability, physical function capacity (including strength), quality of life and pain over a specified timeframe. [16]

Imaging
Radiographs
Lateral weightbearing radiographs serve as a valuable diagnostic tool for detecting any bony irregularities. Typically, they are obtained as part of the initial evaluation in combination of possible further weightbearing images, aiming to exclude underlying bony abnormalities and detect potential intratendinous calcific deposits or ossification.

Ultrasound
Sonography, while dependent on operator, demonstrates strong correlation with histopathological findings and is notably considered the primary imaging modality. Significant advantage of sonography compared to alternative imaging techniques are its interactive nature, quickness, and low cost. Recent advancement of sonography is tissue characterization which allows three-dimensional quantification of tendon structure. [17,18]




MRI
If any other structural changes can’t be clearly evaluated by the clinical examination or ultrasound, MRI investigation is indicated. The most common findings are tendon thickening, high signal alterations in both T1 and T2 sequences, signal inhomogeneity, intrasubstance or surface rupture, mucoid degeneration, calcification, bursitis, bony oedema in posterior heel or Haglund, high signal intensity in the paratenon, swelling around Kager’s fat pad. [21]
Differential diagnosis
A thorough understanding of potential differential diagnoses is crucial in accurately assessing and managing Achilles tendinopathy. While Achilles tendinopathy remains a prevalent musculoskeletal condition various other pathologies can present with similar symptoms. Table 3 provides a comprehensive overview of conditions that may mimic the clinical presentation of Achilles tendinopathy.


Treatment Modalities
Management of Achilles tendinopathy encompasses a multimodal approach aimed at reducing pain, inflammation, and restoring tendon function. Initially, conservative measures are recommended and in recalcitrant cases, surgical treatment offer a viable solution.
Nonoperative methods
Administration of drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs) is widely used, however it has been shown to have only a moderate effect on early symptoms. The side effects of such medication must be incorporated when evaluation risk-benefit ratio of such treatment. It might be useful to relieve pain of concomitant bursitis or paratenonitis. Topical patches containing glyceryl trinitrate might influence collagen production, blood flow and pain relief through release of nitric oxide, however the evidence regarding the beneficial effect is controversial. In addition, topical lidocaine- or NSAID-containing patches might reduce temporarily the pain. Traditionally, resting is advised in acute painful phase, however studies have shown the safety of further physical activity. Certainly, activity/training modification is necessary to consider in painful acute phase. Cryotherapy is also commonly used, although there is a lack of evidence to support it. It might have an effect of tendon metabolism, an analgetic effect and decrease protein and blood extravasation from neocapillars.
Accommodative therapies, such as altering shoe gear (with lower or no heel counter), incorporating heel lifts, and utilizing orthotics, might help by reducing mechanical stress. It’s important to note that these interventions do not address the underlying degenerative disorder.
Physical therapy plays a pivotal role in Achilles tendon rehabilitation, focusing on eccentric strengthening exercises, stretching of the calf musculature, proprioceptive training, and gradual return to sport-specific activities. It is the mainstay not only of the conservative treatment but also the surgical treatment. Six different physical therapy regimen protocols are available for midportion tendinopathy: the Alfredson protocol, low-volume variant of Alfredson protocol, Silbernagel protocol, concentric strength training, heavy slow resistance strength training, and the Stanish protocol. The Alfredson protocol is the most used, which is a 12-week eccentric-progressive tendon loading protocol. It has been shown to achieve great functional improvements.
Instertional tendinopathy poses a more difficult challenge to be improved by physical therapy, since the etiology is often mechanical/structural. The modified Alfredson protocol has been utilized which contains eccentric tendon loading until neutral ankle position and avoid forced dorsiflexion and posterior impingement.


Nonsurgical invasive methods (Injection therapy)
In case of recalcitrant cases or recurrent symptoms where non-invasive physical therapy does not achieve significant improvement, injection therapy might be considered. Under ultrasound guidance placement of injection can be highly accurate. This includes high-volume injectate, prolotherapy, platelet-rich plasma, acupuncture, stromal vascular fraction. The common effect of this injectable therapies is the attempt to jumpstart the body’s own healing ability. Corticosteroid injections are generally not recommended for tendon diseases because of potential adverse effect such as tendon rupture. More recently, injection of microfragmented fat, adipose- or bone marrow-derived signaling cells and bone-marrow aspirate concentrate has been investigated. However, the evidence to support the latter ones is lacking. Multiple studies show positive results of these treatment methods, but the heterogeneity and lack of high-quality evidence doesn’t allow to consider superiority of one treatment over another.
Surgical methods
In about 30% of cases, the conservative treatment doesn’t achieve substantial pain relief and function improvement. In such cases, surgical treatment offers a viable solution. A variety of options are available for the surgeons to treat Achilles tendinopathy including percutaneous to open methods. Most articles report achieving good or excellent results and high success rates. For midportion tendinopathy, the surgeon might opt for percutaneous longitudinal tenotomy, gastrocnemius recession, intratendineous or peritendineous debridement and in case of severely damaged tendon for flexor hallucis longus transfer or allograft augmentation. In case of insertional tendinopathy, the goal of surgical treatment is to unload the posterior heel and insertion area of the tendon. This can be achieved by calcaneal osteotomy, calcaneoplasty, debridement +/- reattachment of the tendon and retrocalcaneal bursectomy. Interestingly, no difference between minimal invasive and open methods could have been shown. [2,3,23–27]
Return to sport
The return-to-sport phase, particularly for athletes, with Achilles tendinopathy aims to safely reintegrate patients into full participation while minimizing the risk of recurrence. A structured program considers factors like pain levels, tissue recovery, strength, and functional deficits. It incorporates a pain-monitoring model to guide activity levels and ensures adequate recovery time between sessions. Activities are categorized as light, medium, or high based on pain ratings and perceived tendon exertion. Progression involves gradually increasing intensity and frequency of activities over approximately 3 weeks, with regular reevaluation and adjustment. Athletes document daily symptoms and exertion levels, facilitating review by clinicians and coaches. Realistic goals are set, considering the potential for slow recovery and recurrence. Monitoring for symptoms during and after activity, along with symptom-free days, guides exercise advancement.[2,28]
Prevention Strategies
Preventing Achilles tendinopathy, particularly in athletes, requires a comprehensive strategy that addresses various risk factors and optimizes training methods. Key elements include implementing proper warm-up routines with dynamic stretching and neuromuscular activation exercises to prepare the lower limbs for activity. Athletes should progressively increase training intensity and volume to avoid sudden workload spikes that can lead to overuse injuries. Footwear selection is critical, with shoes offering adequate support, cushioning, and stability to reduce stress on the Achilles tendon. Regular flexibility exercises targeting the calf complex, Achilles tendon, and plantar fascia can improve tissue flexibility. Coaches and trainers play a vital role in educating athletes on proper biomechanics, training principles, and injury prevention, fostering a collaborative approach to athlete health and performance optimization. Detecting and addressing early signs of Achilles tendinopathy, such as morning stiffness or minor discomfort, is essential to prevent more severe issues. Monitoring training load and performance, along with periodic testing, can help identify potential tendon issues before symptoms arise, enabling prompt intervention and shorter recovery times. [28]
Conclusion
Achilles tendinopathy poses a significant challenge for athletes, non-athletes and physicians, necessitating a comprehensive understanding of its etiology, clinical presentation, diagnosis, and management. By adopting a tailored approach encompassing conservative measures, adjunctive therapies, surgical methods and preventive strategies, physicians can effectively manage this condition.
Corresponding author
Peter Kvarda
Orthopädie
ADUS Klinik
Breitestrasse 111
8157 Dielsdorf
Email: peter.kvarda@adus-klinik.ch
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