eMedicine Specialties > Sports Medicine > Foot and Ankle

Achilles Tendonitis

Laura M Gottschlich, DO, Assistant Professor of Family and Community Medicine, Medical College of Wisconsin; Consulting Staff, St. Joseph Family Medicine Residency Program
Kevin J Eerkes, MD, Clinical Assistant Professor, Department of Medicine, New York University School of Medicine; Medical team physician, New York University athletic teams; David Y Lin, MD, Fellow, Department of Orthopedic Surgery, Section of Pediatrics, University of Tennessee Campbell Clinic; Evan Schwartz, MD, Director of Orthopedic Surgery, New York Medical College; Assistant Professor, St John's Queens Hospital, Department of Surgery, Albert Einstein School of Medicine
Contributor Information and Disclosures

Updated: Aug 5, 2008

Introduction

Background

The Achilles tendon, named after the seemingly indestructible mythologic Greek warrior, is the largest and strongest tendon in the human body. Achilles tendinitis was the term originally used to describe the spectrum of tendon injuries ranging from inflammation to tendon rupture. Despite this spectrum, through extensive study of the histopathology of Achilles tendinitis, it has been determined that there is no evidence to support primary prostaglandin-mediated inflammation. There are, however, signs of “neurogenic inflammation with presence of neuropeptides like substance P and calcitonin gene related peptide.”
 
Tendon histopathology has been divided into 4 categories^{1, 2, 3, 4}: (1) Cellular activation and increase in cell numbers, (2) increase in ground substance, (3) collagen disarray, and (4) neovascularization. Using this as a guide, a histopathologically determined nomenclature has evolved to classify this range of Achilles tendon pathology into 3 stages: (1) paratenonitis, (2), tendinosis, and (3) paratenonitis with tendinosis.

Partial or full tendon ruptures may result from end-stage paratenonitis. Causes of tendon ruptures are associated with multiple factors including overuse, with both extrinsic and intrinsic factors playing a role in increasing susceptibility.^{3, 5, 6, 7, 8, 9, 10, 11} Athletes who are poorly conditioned, overtrained, or insufficiently prepared are at the highest risk for this disease process. Repetitive stresses to the tendon, such as prolonged jumping or running, result in chronic pain and tightness along the tendon.

Tendinitis usually develops insidiously after sudden changes in activity or training level, use of inappropriate footwear, or training on poor running surfaces, especially if high-risk factors are present (eg, age, cavus feet, tibia vara, heel and forefoot varus deformities).

For excellent patient education resources, visit eMedicine's Foot, Ankle, Knee, and Hip Center. Also, see eMedicine's patient education articles Tendinitis, Ruptured Tendon, and Achilles Tendon Rupture.

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Frequency

United States

The true incidence of Achilles tendinitis is unknown, although there is a reported incidence of 6.5-18% in runners.

Functional Anatomy

The Achilles tendon (tendo calcaneus) is formed from the tendinous contributions of the gastrocnemius and soleus muscles, coalescing approximately 15 cm proximal to its insertion. Along its course in the posterior aspect of the leg, the tendon spirals 30-150° until it inserts into the calcaneal tuberosity. The tendon's ability to glide is facilitated by the presence of a thin paratenon sheath, which is composed of both a visceral layer and parietal layer, rather than simply a true synovial sheath. The tendon's blood supply arises from the osseous insertion, the musculotendinous junction, and multiple infiltrating mesotenon vessels, which cross the layers of the anterior paratenon.

Various injection and nuclear medicine studies have demonstrated a paucity of mesotenon and intratendinous vessels 2-6 cm proximal to the heel insertion known as the watershed area. Due to the relative lack of blood supply in the watershed area, this region of the tendon is less resilient to repetitive microtrauma and has a higher tendency for irritation, degeneration, and possible rupture than the calcaneal insertion site.¹²

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Sport-Specific Biomechanics

The entire gastrocnemius/soleus musculotendinous unit spans the knee joint, tibiotalar (ankle) joint, and talocalcaneal (subtalar) joint. Contracture of this complex flexes the knee, plantar flexes the ankle, and supinates the subtalar joint. During running, forces equaling 10 times the body weight have been measured within the tendon.

Clinical

History

• Achilles tendon injuries often occur in older recreational athletes (eg, athletes who are usually sedentary and deconditioned) but may also occur in younger well-conditioned athletes.
• Determine any recent changes in activity level, training duration, running surface, or footwear.
• Ask for previous history of calf pain or weakness.
• If there is clinical suspicion of a partial or complete tear, inquire if there has been any history of quinolone use.
• Achilles tendon injuries may be classified as follows:
  • Paratenonitis
    • Localized/burning pain during or following activity occurs.
    • As the disease progresses, onset of pain may occur earlier during activity, with decreased activity level, or even at rest.
    • In this condition, the paratenon itself is inflamed and thickened and is typically adherent to the underlying unaffected tendon. Under the microscope, there is capillary proliferation and infiltration of inflammatory cells within the paratenon.¹³
  • Tendinosis
    • Usually, this injury is an asymptomatic, noninflammatory, degenerative disease process (mucoid degeneration).
    • The patient may complain of a sensation of fullness or a nodule in the back of the leg.
    • With tendinosis, there are thickened and yellowish areas of mucoid degeneration within the tendon itself. The tendon loses its normal coloration and striation patterns.
    • Hypocellularity, collagen disorganization, lack of inflammatory reaction, scattered vascular ingrowth, and intermittent areas of calcification or necrosis are hallmarks of this disease process.^{13, 14}
    • Pathology is usually found within the watershed area of the tendon.
  • Paratenonitis with tendinosis
    • Activity-related pain and diffuse swelling of the tendon sheath with nodularity is present.
    • Histologically and macroscopically, this entity combines findings found in both tendinosis and paratenonitis.^{13, 14}

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Physical

• Palpate the entire gastroc-soleus complex for tenderness, nodules, swelling, warmth, atrophy, and tendon defects with the patient in a prone position with feet off the table. Localization of the tenderness should be differentiated between musculotendinous (tennis leg), intrasubstance (Achilles tendon injury), and insertional (eg, Haglund deformity, pump bump). Nodules should be palpated for tenderness, boundaries, mobility, and size. Calf atrophy, determined by calf circumference as compared with the contralateral side, may provide information as to the chronicity of the disease process (acute vs chronic). "Gaps" or areas of tendon discontinuity are often signs of partial or complete tendon rupture.
• • Patients with paratenonitis typically present with warmth, swelling, and diffuse tenderness localized 2-6 cm proximal to the tendon's insertion. Crepitation may also be felt if peritenonitis presents acutely. As the condition becomes more chronic, symptoms may be provoked by decreased amounts of physical activity.
  • Tendinosis is often pain free. Typically, the only sign may be a palpable intratendinous nodule that accompanies the tendon as the ankle is placed through its range of motion (ROM). Occasionally, a thickening along the entire tendon may develop in chronic conditions.
  • Peritenonitis with tendinosis is diagnosed in patients with activity-related pain and swelling of the tendon sheath and tendon nodularity.
• Perform a Thompson test to check for Achilles tendon rupture.
• • With the patient prone and the knee flexed, the calf is squeezed proximal to the affected area. If passive plantar flexion of the foot is achieved with this maneuver, the test is negative, and the Achilles tendon is at least partially intact. If no motion at the ankle is generated, the Thompson test is positive and a complete rupture of the tendon has occurred.
  • This test is important to perform because incomplete or complete ruptures may occur in patients with a history of paratenonitis, with or without tendinosis. With acute partial or complete tendon ruptures, patients often relate focal pain and swelling at the sight of injury.
• Ascertain active and passive ROM and strength of the knee, ankle, and subtalar joints. Patients with overuse Achilles tendon injuries typically have decreased motion and strength in the ankle and/or subtalar joints.
• Note the resting alignment and motion of the forefoot and ankle. Forefoot and heel varus, pronated feet, cavus feet, and tibia vara are known predisposing risk factors for this disease process.
• Determine if evidence of neurovascular compromise is present.

Causes

• Extrinsic causes of Achilles tendinitis include the following^{1, 2}:
  • Overuse
  • Increased intensity of activity
  • Increased duration of training
  • Stairs
  • Hill climbing
  • Poor conditioning
  • Improper shoes
  • Improper training surfaces
  • Improper stretching exercises
• Intrinsic Achilles tendinitis causes may include the following^{1, 2}:
  • Age
  • Tight Achilles tendon
  • Varus heel
  • Varus forefoot
  • Cavus foot
  • Tibia vara
  • Medical diseases that may affect tendon tissue (eg, diabetes mellitus) and diseases requiring corticosteroid treatment (eg, lupus, asthma, transplants)

References

• Achilles Tendon Rupture
• Ankle Fracture
• Ankle Impingement Syndrome
• Ankle Sprain
• Athletic Foot Injuries
• Calcaneofibular Ligament Injury
• Compartment Syndromes
• Retrocalcaneal Bursitis
• Talofibular Ligament Injury

• Foot, Ankle, Knee, and Hip Center
• Tendinitis Overview
• Tendinitis Causes
• Tendinitis Symptoms
• Tendinitis Treatment
• Achilles Tendon Rupture Overview
• Ruptured Tendon Overview