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Achilles Tendinopathy

Author: Miguel A. Medina Pabón Author: Rachel Bergman Editor: Usker Naqvi Updated: 6/8/2026 5:22:14 AM

Introduction

The Achilles tendon, also known as the triceps surae, ranks as the strongest and largest tendon in the human body.[1] This tendon connects the aponeuroses of the gastrocnemius, soleus, and plantaris muscles to the calcaneus bone.[2] A sheath-like structure composed of a single layer of cells surrounds the tendon; this structure is not a true synovial sheath but is known as the paratenon.[2][3][4] The paratenon supplies a significant portion of the blood supply to the tendon.[4] 

Results from studies identified a hypovascular area susceptible to injury, located approximately 2 to 6 cm proximal to the calcaneal insertion.[5] The Achilles tendon is essential for transmitting force from the calf muscles to the heel during walking and running.[6] Additionally, various factors can contribute to Achilles tendinopathies, with specific locations more commonly affected. This activity explores insertional and noninsertional tendinitis, paratenonitis, and tendon rupture.

Etiology

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Etiology

The causes and mechanisms of Achilles tendinopathy include the following:

  • Intrinsic factors: These include anatomical factors, age, sex, body weight,[7] metabolic dysfunction,[8] pes cavus, dysmetria, muscle weakness, muscle imbalance, gastrocnemius dysfunction,[9] anatomical variation of the plantaris muscle,[10] tendon vascularity,[11] torsion of the Achilles tendons,[12] slippage of the fascicle,[13] and lateral instability of the ankle.
  • Extrinsic factors: These include mechanical overload, constant effort, inadequate equipment,[14] medications (including corticosteroids, anabolic steroids, fluoroquinolones),[15][16] improper footwear, insufficient warming or stretching,[17] hard training surfaces, and direct trauma, among others.[18]

Several factors increase the risk of Achilles tendon rupture, including older age, tendon heterogeneity, fascicle slippage, and excessive exercise in athletes.[19] Athletes tend to present with pathology localized to the Achilles tendon insertion site.[20]

Epidemiology

The Achilles tendon has a cumulative lifetime injury incidence of approximately 24% in athletes. Running-related injuries have a prevalence of 11% to 85% or 2.5 to 59 injuries per 1000 hours of running.[21] Results from one study reported a prevalence of Achilles tendinopathy of 1% to 2% among elite adolescent athletes.[22] Findings from another study reported an injury rate of 9% among recreational athletes.[23] The lifetime injury incidence of 2.35 per 1000 is strongly associated with sporting activities.[24][25][26] This incidence increases in older men.[27] The overall incidence rate of Achilles tendin ruptures is 2.1 per 100,000 person-years, and most Achilles tendon ruptures occur in men, with a 3.5:1 male to female ratio.[28]

Pathophysiology

The etiology of Achilles tendinopathy remains uncertain, and many factors have been implicated, including free radical damage during reperfusion after ischemia, hypoxia, and hyperthermia, as well as impaired tenocyte apoptosis.[29] Macrophages and other phagocytic cells are key regulators of immunobiology, tissue repair, and extracellular matrix remodeling in tendons. Results from current studies have demonstrated heterogeneity among macrophages across tendon compartments, particularly between M1 and M2 macrophages, highlighting the importance of interactions between macrophages and resident tendon cells in specific local niches within this tissue.[30] 

Changes in the expression of genes regulating cell-cell and cell-matrix interactions have been reported, with downregulation of MMP3 messenger RNA in tendinopathic Achilles tendon samples.[31] An imbalance in matrix metalloproteinase activity in response to repeated injury or mechanical strain may result in tendon degeneration. The Achilles tendon consists of 2 tendinous portions. The proximal portion gradually merges with the distal portion to form a single, homogeneous tendon. Additionally, the triceps surae muscle group comprises 3 muscular heads; the soleus is monoarticular, and the plantaris and gastrocnemius are biarticular. The mechanical tension of the tendon is concentrated at 2 sites. The sites include the medial or central portion of the paratenon and the middle segment of the tendon, which is the most common site of injury.[32]

As the Achilles tendon descends from its origin, it twists counterclockwise on the right and clockwise on the left, rotating 90°.[33] Smaller soleus fibers insert anteromedially while larger gastrocnemius fibers insert posterolaterally. This configuration is thought to contribute to alterations in tendon biomechanics and influence the pathophysiologic mechanisms of Achilles tendinopathies.[2][13] Tendon damage may even result from stresses within physiological limits because frequent microtrauma may not allow enough time for repair. Microtrauma can also result from nonuniform stress within tendons, producing abnormal load concentrations and frictional forces between fibrils, leading to localized fiber damage.[34] In cases of insertional Achilles tendinopathy, tendon degeneration is characterized by loss of strong parallel type I collagen fibers, fatty infiltration, and capillary proliferation.[2][35] Advanced imaging findings demonstrate tendon thickening, which will be further discussed in the next sections.

Histopathology

The Achilles tendon comprises 95% type I collagen fibers, which are very strong and flexible. A decrease in type I collagen fibers can occur with normal aging or injury. Tendinopathy, encompassing both tendinosis and tendinitis, is characterized by increased proteoglycan and water content and disorganized type III collagen fibers.[35] 

The tendon is enveloped by a thin layer of connective tissue called the paratenon, which is rich in elastin and extends into the tendon, binding the collagen bundles together while permitting movement among them.[36] Tendinosis and tendinitis have distinct characteristics. Tendinosis involves degenerative changes in the tendon and its sheath, making the tendon more vulnerable to rupture. At the cellular level, no evidence of acute inflammation is observed. In contrast, tendinitis is marked by an acute inflammatory response resulting from acute trauma, overuse, or improper training.[37]

Paratenonitis is an inflammation affecting the outer layers of the tendon and includes conditions such as tenosynovitis.[38] This pathologic condition results in edema and exudate formation accompanied by inflammatory cells. Subsequently, a fibrinous exudate develops, leading to crepitus and restriction of tendon movement within the sheath. Without treatment, paratenonitis can progress to a chronic state through the development of immature connective tissue that expands into an organized fibrin network known as adhesions.[39]

Results from a study conducted in a rat model showed that the microenvironment of the Achilles tendon promoted the differentiation of stem cells toward chondrogenic and osteogenic lineages, predisposing the tendon to rupture (tendinosis). Following tendon rupture, an inflammatory cascade begins, leading to elevated expression of proinflammatory cytokine messenger RNA, including matrix metalloproteinase 3 (MMP3), cyclooxygenase 2, interleukin 6, and tumor necrosis factor α.[40] Conversely, chronic inflammation triggers neovascularization, which increases the risk of tendon rupture, resulting in greater disability and more complex treatment.[41] Results from a study conducted in rats showed that denervated tendons exhibited morphological alterations, including disorganization of the collagen network, increased production of type III collagen, hypercellularity, altered cell morphology, and elevated expression of the neurokinin 1 receptor. These changes resemble those observed in Achilles tendon injuries.[42]

History and Physical

The term Achilles tendinopathy refers to tendinitis (acute inflammation) and tendinosis (chronic degeneration). Achilles tendinopathy is characterized by pain, inflammation, and stiffness of the Achilles tendon.[43][44][45] The condition can occur in athletes and nonathletes, usually due to an imbalance between muscle power and tendon elasticity.[46] Achilles tendinopathies are divided anatomically into insertional and noninsertional tendinopathies.

Insertional Achilles tendinopathy affects the osseous attachment of the tendon to the posterior calcaneus. Patients with this condition may experience pain in the distal third of the tendon, extending to the insertion site, as well as morning stiffness.[47] Conversely, noninsertional Achilles tendinopathy occurs in the middle to proximal third of the tendon (2 to 6 cm proximal to the insertion). Palpation may reveal nodules and tendon enlargement.[47] 

The clinical diagnosis of Achilles tendinopathy is primarily based on the patient history and a detailed physical examination. Characteristic symptoms include Achilles tendon pain that is typically worse in the morning, improves during activity, and often develops after a sudden increase in activity that overloads the tendon. Patients commonly report a gradual onset of pain and stiffness in the posterior heel or lower leg, with chronic recurrent calf or Achilles tendon pain being a hallmark feature. In chronic cases, exercise-induced pain remains the cardinal symptom, whereas crepitations and effusions diminish.

Physical examination begins with inspection of the tendon for bruising, swelling, and visible or palpable tendon enlargement or nodular thickening, particularly 2 to 6 cm proximal to the calcaneal insertion in midportion tendinopathy or directly at the insertion site in insertional tendinopathy. Palpation of the tendon is a key diagnostic component because the technique is simple, reproducible, and reliable for identifying localized tenderness along the affected portion of the Achilles tendon. In some cases, fibrin precipitated from the fibrinogen-rich fluid around the tendon can result in palpable crepitus.

Physical examination should also include a multidimensional assessment of calf muscle capacity with endurance tests such as the standing calf raise test, along with evaluation of the hip and knee to identify biomechanical contributions and muscle imbalances that may predispose patients to tendinopathy. Additional examination findings include pain with active and passive ankle motion, reduced ankle range of motion, and associated conditions, such as retrocalcaneal bursitis or Haglund deformity, in patients with insertional tendinopathy. A complete lower-extremity biomechanical assessment is essential to identify contributing factors, such as pes planus, pes cavus, subtalar joint immobility, or gluteal and foot core muscle weakness, that may require intervention.

Clinical tests include:

  • Arc sign: Swelling or nodules within the tendon are palpated while the ankle joint is moved through plantarflexion and dorsiflexion. A positive arc sign is observed when the swelling or nodules move with range of motion.[46][48][49] In cases of paratendinopathy, the area of maximum thickening remains fixed in one position.[48]
  • Royal London Hospital test: The point of maximum tenderness is palpated when the ankle is in a neutral position. The patient is then instructed to actively dorsiflex and plantarflex the ankle joint. The previous area of maximum tenderness is again palpated when the ankle joint is in maximum plantarflexion and dorsiflexion. Tendinopathy is present when tenderness significantly decreases or disappears under tension.[46][48]

Evaluation

Imaging Studies 

Radiography: Radiography has a limited but specific role in evaluating Achilles tendinopathy because it does not directly visualize soft tissues such as tendons; however, radiography can provide useful complementary information. The primary utility of radiography is to identify bony abnormalities and exclude other conditions that can cause similar symptoms, particularly in insertional Achilles tendinopathy, in which posterior calcaneal exostoses are often present. Lateral ankle radiographs can demonstrate indirect signs of Achilles tendon pathology, including obliteration or alteration of the Kager fat pad (the radiolucent triangle posterior to the ankle and anterior to the Achilles tendon), which becomes obscured by effusion and soft tissue changes associated with tendon injury. In insertional Achilles tendinopathy, radiographs can show multiple parameters, including the calcaneal pitch angle, Fowler-Phillip angle, posterior calcaneal angle, Chauveau-Liet angle, Haglund deformity measurements, and intratendinous calcification length and width, though these parameters have limited diagnostic sensitivity and specificity for the condition. Radiography may also demonstrate increased tendon width when the Achilles tendon is bordered anteriorly by the Kager fat pad and posteriorly by subcutaneous fat, providing an indirect assessment of tendon enlargement. Although radiography can assist in diagnosis by identifying associated bony pathology and excluding differential diagnoses, ultrasonography is considered the first-line imaging modality for Achilles tendinopathy, with MRI reserved for patients who require more detailed soft tissue evaluation.[50][51][52]

Ultrasonography: Ultrasonography is commonly used in the evaluation of tendinopathies because it is readily available, safe, and inexpensive.[53][54] This imaging modality may reveal findings such as increased Achilles tendon thickness, hyperemia associated with hypervascularity, a decreased gastrocnemius-soleus rotation angle, and a reduced Kager fat pad length. Additionally, ultrasonography is useful during interventional treatment.[55] The Achilles tendon's large tissue volume facilitates visualization, and ultrasonography allows dynamic evaluation of the tendon throughout its range of motion.[56]

  • Insertional Achilles tendinopathy: Ultrasonography findings include a hypoechoic area and loss of the fibrillar appearance in the distal third of the tendon.[47]
  • Noninsertional Achilles tendinopathy: Ultrasonography findings include focal or diffuse thickening of the middle to proximal section of the tendon and hypoechoic areas with loss of the compact linear fibrillar appearance.[47]

Magnetic resonance imaging: This imaging modality provides comprehensive information about joint structures, enabling studies in multiple planes and in both static and dynamic views.[57][58] The normal Achilles tendon is less than 7 mm thick from anterior to posterior on sagittal MRI images. Increased measurements suggest chronic intrasubstance tendinopathy and degeneration.[59] Results from one study showed that MRI had lower sensitivity than ultrasonography in detecting early changes of enthesopathy.[60] However, results from another study demonstrated excellent agreement between tendon thickness measurements obtained from MRI and ultrasonography.[61] 

  • Insertional Achilles tendinopathy: MRI findings include distal tendon thickening with an intense signal on fat-suppressed images.[47]
  • Noninsertional Achilles tendinopathy: MRI findings include thickening of the middle to proximal section of the tendon with heterogeneous signal intensity on T1- and T2-weighted images.[47]

Computed tomography: CT is useful for excluding trabecular structural alterations of the calcaneus in insertional Achilles tendon pathology. However, this imaging modality exposes the patient to radiation.[62][63][64]

Victoria Institute of Sports Assessment-Achilles (VISA-A): VISA-A questionnaire remains the gold standard for assessing pain and function, but additional studies are needed to improve its reliability.[65][66] Nevertheless, this questionnaire is an essential tool for monitoring patients after treatment.

Treatment / Management

Management of Achilles tendinopathy can be divided into conservative and surgical approaches, and further based on whether the condition is acute or chronic. In cases of tendon rupture, surgical treatment is often recommended.  

Conservative Management

Conservative treatment strategies are considered first-line in management of Achilles tendinitis and include the following:

  • Activity modification or reduction of activity levels [67]
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) [68][69]
  • Orthotics: Orthotics are particularly beneficial for patients with abnormal foot alignment. Custom orthotics can modify the biomechanics of the foot and ankle, while a 12-15 mm heel lift is typically used as an adjunct for Achilles tendinopathy.
  • Cryotherapy: Cryotherapy has an analgesic effect, reduces the metabolic rate of the tendon, and decreases extravasation of blood and protein from the new capillaries found in tendon injuries.
  • Lower-tendon compression rehabilitation: This therapy modality consists of a progressive 4-stage tendon-loading program that includes isometric, isotonic, energy-storage-and-release, and sport-specific exercises.[70][71]
  • Eccentric stretching exercises: These exercises are an integral component of physical therapy. Moderate-level evidence favors eccentric exercise over concentric exercise for reducing pain.[72][73][74] Eccentric exercises for chronic insertional Achilles tendinopathy are less effective in patients with metabolic syndrome but most effective when combined with extracorporeal shockwave therapy.[75]
  • Extracorporeal shock wave therapy (ESWT):  Results from studies showed that ESWT reduced pain by 60% and achieved 80% patient satisfaction, improving function and quality of life.[76] ESWT provides effective short-term pain relief and tendon healing, making it the preferred treatment for some healthcare professionals.[63][75] Other findings from studies found that combining ESWT with eccentric exercises yielded the best results.[75]
  • Biologic injections:
    • Platelet-rich plasma: Platelet-rich plasma is an autologous treatment containing many growth factors and may offer a promising treatment for chronic Achilles tendinopathy, with evidence of pain relief and functional improvement. However, variability in results emphasizes the need for standardized approaches to its use in clinical practice. Results from meta-analyses and recent studies have demonstrated no greater efficacy of platelet-rich plasma than placebo and no reduction in symptom duration.[56][77][78]
    • Bone marrow aspirate concentrate: This treatment modality controls inflammation, reduces fibrosis, and recruits tenocytes and mesenchymal cells to damaged tissues. Results from one study showed that 92% of patients with Achilles tendon ruptures who underwent bone marrow aspirate concentrate returned to sports within 6 months, with no reruptures noted.[56][77]
    • Peripheral blood mononuclear cells:  Peripheral blood mononuclear cells comprise monocytes, macrophages, and lymphocytes. These cells are considered the new generation of regenerative autologous cell concentrates, but studies are lacking in the literature.[56]
    • Scaffolds: Scaffolds are composed of a combination of natural and synthetic materials. Among these options, an acellular graft comprising human dermal allograft showed the most promising outcomes in studies. Results from these studies showed an increased return to activity without associated complications.[56] 
    • Prolotherapy: Prolotherapy (proliferative therapy) is a technique that induces the proliferation of new cells, promoting the regeneration of healthy tissue. Small amounts of hyperosmolar dextrose are injected into the affected area of the Achilles tendon under ultrasonography guidance. Results from one study showed that this procedure improved pain symptoms by 74.2% within 1 year.[72][73][74][76][74][79][80][81][82][83]
    • Surgical Management:  In 24% to 45.5% of patients with Achilles tendinopathy, conservative treatment is unsuccessful, and a surgical procedure should be considered if symptoms fail to resolve.[84][85] Surgical procedures and approaches can vary and are described in the following sections.
    • (A1)

Midportion (Noninsertional) Achilles Tendinopathy

  • Debridement of diseased tendon: This procedure involves removing the damaged, degenerative portion of the Achilles tendon and repairing the remaining healthy tendon with sutures.
  • Tendon transfer (flexor hallucis longus transfer): When extensive tendon damage exists, the flexor hallucis longus tendon from the big toe is transferred to reinforce or replace the damaged Achilles tendon.
  • Gastrocnemius recession (calf muscle lengthening): This procedure involves surgical lengthening of tight calf muscles to reduce stress on the Achilles tendon.
  • Minimally invasive tendon debridement: This procedure is often performed arthroscopically through smaller incisions, with camera assistance to remove diseased tissue.

Insertional Achilles Tendinopathy

  • Achilles tendon detachment with debridement and reattachment: The tendon is detached from the calcaneus, diseased tissue and calcific deposits are removed, and the tendon is reattached using bone anchors or sutures.
  • Haglund deformity excision (calcaneal exostectomy): This procedure involves removal of the bony prominence (calcaneal exostosis) at the back of the calcaneus using a chisel or saw.
  • Retrocalcaneal bursectomy: This procedure involves removal of the inflamed, fluid-filled bursa between the Achilles tendon and calcaneus.
  • Percutaneous Zadek osteotomy: This minimally invasive procedure involves removing a 5-mm wedge of bone from the calcaneus via 2 small incisions, thereby altering tendon fiber orientation and reducing stress.
  • Traditional open Zadek osteotomy: This procedure requires an incision of up to 6 cm and a longer recovery time (9 to 12 months vs 6 weeks for the minimally invasive approach).

Additional Procedures

  • Tenotomy: Tenotomy involves surgically lengthening a shortened Achilles tendon by making incisions that allow the tendon edges to draw apart and heal in a lengthened position.
  • Tendon grafting: Tendon grafting involves replacing part or all of the Achilles tendon with a tendon graft from elsewhere in the foot when severe damage is present.

In cases of insertional Achilles tendinopathy, a combination of surgical interventions, including debridement, resection of the superior calcaneus and bursa, and reattachment of the Achilles tendon, has a success rate of more than 95%. On average, patients can return to activity within approximately 7 months following the surgical procedure.[86] Although calcinosis may be present, it does not interfere with the results. Furthermore, recurrent calcification is common but not associated with inferior surgical outcomes.[86][87]

In patients with noninsertional Achilles tendinopathy, satisfaction rates after surgical treatment range from 69% to 100%.[77] Complication rates are higher in patients with noninsertional tendinopathy. When more than 50% of the tendon is ruptured, reattachment of the Achilles tendon should be considered.[77]

Differential Diagnosis

Posterior heel and ankle pain are common concerns in primary care settings, and the risk of pain is elevated in individuals with higher body mass index and older age. Further evaluation is necessary when patients do not improve with initial treatment approaches.[65] The most common musculoskeletal soft tissue disorders associated with posterior ankle pain include the following:

  • Retrocalcaneal bursitis: This condition is easily identified on ultrasonography or MRI.[47]
  • Kager fat pad inflammation: Findings include pain on palpation bilaterally at the level of the ankle, anterior to the Achilles tendon.
  • Achilles tendon rupture:  Thompson test results are positive.[47]
  • Achilles paratenonitis: Ultrasonography findings demonstrate fluid and adhesions around the tendon.[47]
  • Posterior impingement (os trigonum syndrome):  Findings include posterior ankle pain with forced dorsiflexion. Radiography findings demonstrate the presence of an os trigonum.
  • Calcaneal stress fracture: Squeeze test results are positive.[47]
  • Flexor hallucis longus tendinopathy: Findings include pain during the toe-off phase of gait and increased fluid around the flexor hallucis longus tendon on short tau inversion recovery MRI images.[47]
  • Plantar fasciitis: Findings include pain with palpation of the plantar-medial calcaneal tubercle.[66][67]
  • Nerve entrapment or neuroma: Findings include pain accompanied by burning, tingling, or numbness. Tinel sign results are positive along the course of the sural nerve.[47]
  • Heel pad syndrome: Findings include deep, bruise-like pain in the midheel.[66][67]
  • Haglund deformity: This condition causes acute or chronic posterolateral heel pain due to prominence of the calcaneus; the deformity may lead to retrocalcaneal bursitis and often requires surgical resection of the calcaneus.[88]
  • Sever disease: This condition is a clinical diagnosis of calcaneal apophysitis in children and adolescents with immature growth plates.[66][67]
  • Insertional calcific tendinosis: Mucoid degeneration of the tendon causes gradually worsening pain in middle-aged patients with a high body mass index and often requires surgical detachment and reattachment of the tendon.[88]
  • Lumbar S1 radiculopathy: Findings include pain with decreased sensation over the posterolateral ankle.[47]

Erdheim-Chester disease is a rare non–Langerhans cell histiocytosis reported in a 36-year-old man who presented with bilateral xanthogranulomas of the Achilles tendon. Although rare, Erdheim-Chester disease should be considered in the differential diagnosis of intratendinous masses.[68] Additionally, clinicians should evaluate for serious nonmusculoskeletal causes of pain and systemic disease.[69]

Prognosis

The prognosis for patients with Achilles tendinopathy varies significantly between conservative and surgical treatment, with most patients responding well to nonsurgical treatment. Conservative treatment has a favorable long-term prognosis, particularly for acute-to-subacute cases, with eccentric exercise protocols achieving approximately 89% success rates for midportion (noninsertional) Achilles tendinopathy. Most patients with Achilles tendinopathy can recover with nonsurgical treatments, including activity modification, physical therapy, eccentric exercises, and tendon-loading programs, though recovery timelines can be lengthy and require patient commitment to rehabilitation protocols. Achilles tendinopathy has a better prognosis with early, adequate treatment because degenerative tendinopathy represents the final stage of the tendon pathology continuum and carries a poor prognosis due to irreversible changes. However, a small percentage of patients experience persistent symptoms despite conservative treatments lasting several months to more than 1 year, at which point a surgical procedure may be considered.[89][90][91][92]

Results from studies showed good to excellent outcomes after surgical treatment of Achilles tendinopathy in appropriately selected patients, with overall success rates of 80% to 90%. Surgical procedures for insertional Achilles tendinopathy yield good functional outcomes and a satisfactory return to sports when surgical care is tailored to the individual patient. Recovery from a surgical procedure is protracted, typically requiring 9 months to 1 year for full return to all activities, with patients remaining nonweight-bearing for 3 to 4 weeks postoperatively, followed by extensive physical therapy. Results from studies of minimally invasive surgical techniques, such as percutaneous Zadek osteotomy, were promising, with 95% of patients reporting they would choose the procedure again and significantly faster recovery timelines than those associated with traditional open surgical procedures. Final surgical outcomes vary based on the patient's baseline function, degree of tendon degeneration, and adherence to postoperative rehabilitation, with some patients experiencing residual pain or calf weakness despite technically successful procedures. Surgical treatment for Achilles tendinosis carries risks, including infection, nerve damage, wound-healing complications, blood clots, and ongoing pain, which must be weighed against potential benefits when conservative treatment is unsuccessful.[93][94][95][96]

Complications

When considering major and minor complications, the incidence ranges from 3% to 41% after surgical treatment for Achilles tendinopathy.[77] In addition, results from a study by Lohrer et al showed that the success rates of open and minimally invasive surgical procedures were comparable (83.4%), and patient satisfaction rates were comparable.[97] However, complication rates were lower after minimally invasive procedures. Baltes et al classified complications associated with surgical treatment as follows:

  • Major complications: Tendon avulsion or rupture, any reoperation, deep vein thrombosis, reflex dystrophy, persistent neuralgia, deep infections, deep suture reactions, and deep wound infections.[77][86]
  • Minor complications: Persistent pain, superficial infections, delayed wound healing, scar sensitivity, hypertrophy, mild paresthesia, and prolonged hospitalization.[77][96]

Complication rates also vary depending on whether the surgical procedure is performed for insertional or noninsertional Achilles tendinopathy. For insertional Achilles tendinopathy, the complication rate has been reported as high as 41%; for noninsertional Achilles tendinopathy, it has been reported as high as 85% after surgical procedures.[77][96]

Postoperative and Rehabilitation Care

Following surgical treatment for Achilles tendinopathy, a period of immobilization is required and may involve a cast, walking boot, or posterior splint. The duration of immobilization ranges from 3 to 8 weeks. However, recent articles increasingly advocate accelerated postoperative weight-bearing rehabilitation protocols.

In 2021, Arunakul et al prospectively analyzed conventional and accelerated rehabilitation protocols following surgical treatment for insertional Achilles tendinopathy. Results from the study showed that an accelerated protocol improved short-term functional outcome scores. Templates for both protocols are provided in the following sections.[98]

Conventional Postoperative Protocol

  • Weeks 0-2: Nonweight-bearing with immobilization in a cast or splint in the equinus position
  • Weeks 2 to 4: Transition to partial weight bearing (25%) with axillary crutches in a controlled ankle motion boot with a 3-layer heel lift (2.4 cm).
  • Weeks 4 to 6: Increase partial weight bearing to 50% with axillary crutches and a 1.6-cm heel lift.
  • Weeks 6 to 8: Increase partial weight bearing to 75% with axillary crutches in the controlled ankle movement (CAM) boot with a 0.8-cm heel lift.
  • Weeks 8 to 10: Full weight bearing with axillary crutches in the CAM boot without a heel lift.
  • Week 10: Transition to regular shoes, as tolerated.[98] 

Accelerated Postoperative Weight-Bearing Protocol

  • Weeks 0 to 2: Nonweight-bearing with immobilization in a cast or splint in equinus position
  • Weeks 2 to 3: Transition to full weight bearing as tolerated in a CAM boot with a 3-layer (2.4-cm) step heel lift.
  • Weeks 3 to 4: Continue full weight bearing as tolerated in the CAM boot, with the heel lift decreased to 1.6 cm.
  • Weeks 4 to 5: Continue full weight bearing as tolerated in the CAM boot, with the heel lift decreased to 0.8 cm.
  • Weeks 5 to 6: Full weight bearing in the CAM boot without a heel lift.
  • Week 6: Transition to regular shoes, as tolerated.[98]

Consultations

Collaborative care involving multiple specialty groups is necessary to treat Achilles tendinopathy comprehensively. The involvement of various healthcare professionals ensures an interdisciplinary approach, leading to more effective treatment and improved patient outcomes. The 3 specialty groups commonly involved in the treatment of Achilles tendinopathy are as follows:

Podiatry: Podiatrists are crucial in treating Achilles tendinopathy, providing expertise in foot biomechanics, gait analysis, and prescribing orthotics or custom footwear. Podiatrists may also perform corticosteroid injections or extracorporeal shockwave therapy to alleviate pain and promote healing.

Physical therapy: Physical therapists are instrumental in the rehabilitation process for Achilles tendinopathy. They design individualized exercise programs focusing on strengthening the affected tendon, improving flexibility, and addressing any associated biomechanical issues. Physical therapists may use various modalities, such as therapeutic exercises, manual therapy, ultrasonography, and electrical stimulation, to facilitate recovery and restore optimal function.

Orthopedic surgical treatment: Orthopedic surgeons specialize in treating patients for whom conservative treatments do not provide adequate relief, or those with severe tendon damage or rupture; an orthopedic consultation may be necessary. Orthopedic surgeons can assess the need for surgery, perform tendon repairs or reconstructions, and provide postoperative care to facilitate recovery.

Deterrence and Patient Education

Patient education and a more conservative approach can prevent Achilles tendinopathy.[99][100][101][102] Evidence-based strategies include:

  • Sport modification: Switching to low-impact activities (eg, swimming, weight training, rowing, and cycling) allows the Achilles tendon time to rest.[102]
  • Eccentric exercise therapy: Incorporating eccentric exercises, which involve controlled lengthening of the muscle-tendon unit, has decreased pain and prevented progression to chronic tendinopathy.[57][58][60]
  • Nonsteroidal anti-inflammatory drugs: Prior literature supports their use to reduce inflammation and treat pain.[54][55][77]
  • Proper footwear: Shoes that provide adequate cushioning and support during heel strike can reduce stress on the Achilles tendon.[84]
  • Warm-up and stretching: Stretching the calf muscles before engaging in sports or exercise may be beneficial.[84]
  • Gradual progression: Distance and speed should be increased gradually by no more than 10% per week. Avoiding sudden increases in intensity, running on uneven slopes, and performing an appropriate cool-down after exercise are important for preventing overload of the Achilles tendon.[84][85]
  • Extracorporeal shock wave therapy: ESWT is a noninvasive treatment that uses shock waves to stimulate healing in the Achilles tendon. This treatment may be beneficial if other interventions have not provided satisfactory results.[63]

Enhancing Healthcare Team Outcomes

Effective treatment of Achilles tendinopathy requires coordinated interprofessional collaboration among orthopedic surgeons, sports medicine clinicians, physical therapists, podiatrists, and nursing staff to optimize patient outcomes and ensure comprehensive care from diagnosis through rehabilitation. Clinicians must clearly communicate diagnostic findings and treatment plans to physical therapists who design and implement evidence-based exercise protocols, particularly the Alfredson eccentric training program, while radiologists provide critical imaging interpretation to guide clinical decision-making and monitor treatment response. Nurses play a vital role in patient education regarding activity modification, proper footwear selection, medication adherence for pain treatment, and monitoring for potential complications, while pharmacists counsel patients on appropriate nonsteroidal anti-inflammatory drug use, potential drug interactions, and the risks associated with fluoroquinolone antibiotics and corticosteroids that can predispose patients to tendinopathy or rupture.

Ethical responsibilities include placing the patient's interests at the center of care, respecting patient autonomy in shared decision-making between conservative and surgical treatment options, and maintaining transparent communication about realistic recovery timelines, treatment risks, and expected functional outcomes. The interprofessional team must use structured communication strategies to facilitate handoffs between clinicians, particularly when transitioning athletes from acute treatment to rehabilitation phases or from unsuccessful conservative treatment to surgical consultation, ensuring continuity of care across treatment modalities. Care coordination is enhanced when team members recognize their professional limitations, actively engage complementary expertise from other disciplines, including podiatry for biomechanical assessment and orthotics, and share accountability for patient outcomes, ensuring that active individuals receive timely diagnosis, appropriate conservative treatment with validated outcome measures, and seamless progression to surgical treatment when indicated after adequate trials of nonsurgical treatment.

Media


(Click Image to Enlarge)
<p>Dorsal Radiograph,&nbsp;Achilles Tendon

Dorsal Radiograph, Achilles Tendon. Radiograph showing the Achilles tendon, calcaneus, talus, heel pad, and tibia.

Contributed by S Bhimji, MD

(Click Image to Enlarge)
Achilles Tendonitis T1 MRI demonstrating bulbous appearing Achilles tendon with homogenous signal.
Achilles Tendonitis T1 MRI demonstrating bulbous appearing Achilles tendon with homogenous signal. Contributed by Mark A. Dreyer, DPM, FACFAS

(Click Image to Enlarge)
Achilles Tendonitis - MRI demonstrating classic fusiform thickening of the Achilles tendon in the "watershed" area
Achilles Tendonitis - MRI demonstrating classic fusiform thickening of the Achilles tendon in the "watershed" area Contributed by Mark A. Dreyer, DPM, FACFAS

(Click Image to Enlarge)
Achilles Tendonitis - lateral weight-bearing radiograph demonstrating a retro-calcaneal bone spur along with intra-tendinous
Achilles Tendonitis - lateral weight-bearing radiograph demonstrating a retro-calcaneal bone spur along with intra-tendinous calcification Contributed by Mark A. Dreyer, DPM, FACFAS

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