Achilles tendon pathologies include rupture and tendonitis. Many experts now believe, however, that tendonitis is a misleading term that should no longer be used, because signs of true inflammation are almost never present on histologic examination. Instead, the following histopathologically determined nomenclature has evolved:
Paratenonitis: Characterized by paratenon inflammation and thickening, as well as fibrin adhesions 
Signs and symptoms
Patients with an Achilles tendon rupture frequently present with complaints of a sudden snap in the lower calf associated with acute, severe pain. The patient reports feeling like he or she has been shot, kicked, or cut in the back of the leg, which may result in an inability to ambulate further. A patient with Achilles tendon rupture will be unable to stand on his or her toes on the affected side.
Tendinosis is often pain free. Typically, the only sign of the condition may be a palpable intratendinous nodule that accompanies the tendon as the ankle is placed through its range of motion (ROM).
Patients with paratenonitis typically present with warmth, swelling, and diffuse tenderness localized 2-6 cm proximal to the tendon's insertion.
Paratenonitis with tendinosis
This is diagnosed in patients with activity-related pain, as well as swelling of the tendon sheath and tendon nodularity.
See Clinical Presentation for more detail.
Laboratory studies usually are not necessary in evaluating and diagnosing an Achilles tendon rupture or injury, although evaluation may help to rule out some of the other possibilities in the differential diagnosis.
Plain radiography: Radiographs are more useful for ruling out other injuries than for ruling in Achilles tendon ruptures
Ultrasonography: Ultrasonography of the leg and thigh can help to evaluate the possibility of deep venous thrombosis and also can be used to rule out a Baker cyst; in experienced hands, ultrasonography can identify a ruptured Achilles tendon or the signs of tendinosis
Magnetic resonance imaging (MRI): MRI can facilitate definitive diagnosis of a disrupted tendon and can be used to distinguish between paratenonitis, tendinosis, and bursitis
See Workup for more detail.
Achilles tendon rupture
Medical therapy for a patient with an Achilles tendon rupture consists of rest, pain control, serial casting, and rehabilitation to maximize function. Ongoing debate surrounds the issue of whether medical or surgical therapy is more appropriate for this injury. [3, 4]
Surgical techniques for rupture repair are varied but usually involve reapproximation of the torn ends of the Achilles tendon, sometimes reinforced by the gastrocsoleus aponeurosis or plantaris tendon. Open reconstruction is undertaken using a medial longitudinal approach.
Studies indicate that patients who undergo percutaneous, rather than an open, Achilles tendon rupture repair have a minimal rate of infection but a high rate of sural nerve entrapment (16.7% of treated cases). 
Achilles tendinosis and paratenonitis
Conservative management of Achilles tendinosis and paratenonitis includes the following:
Orthotics: Orthotic therapy in Achilles tendinosis consists of the use of heel lifts
Nonsteroidal anti-inflammatory drugs (NSAIDs): Tendinosis tends to be less responsive than paratenonitis to NSAIDs
Steroid injections: Although these provide short-term relief of painful symptoms, there is concern that they can weaken the tendon, leading to rupture
Platelet-rich plasma injections
Surgery may also be used in the treatment of Achilles tendinosis and paratenonitis. In paratenonitis, fibrotic adhesions and nodules are excised, freeing up the tendon. Longitudinal tenotomies may be performed to decompress the tendon. Satisfactory results have been obtained in 75-100% of cases.
In tendinosis, in addition to the above procedures, the degenerated portions of the tendon and any osteophytes are excised. Haglund’s deformity, if present, is removed. If the remaining tendon is too thin and weak, the plantaris or flexor hallucis longus tendon can be weaved through the Achilles tendon to provide more strength. The outcome is generally less favorable than it is in paratenonitis surgery.
Achilles tendon pathologies include rupture and tendonitis. Achilles tendon rupture, a complete disruption of the tendon, is observed most commonly in patients aged 30-50 years who have had no previous injury or problem in the affected leg and are typically "weekend warriors" who are active intermittently. (See Etiology and Epidemiology.)
Achilles tendonitis refers to inflammation of the tendon or paratenon, usually resulting from overuse associated with a change in playing surface, footwear, or intensity of an activity. Many experts now believe, however, that tendonitis is a misleading term that should no longer be used, because signs of true inflammation are almost never present on histologic examination. Instead, the following histopathologically determined nomenclature has evolved (See Pathophysiology and Etiology):
Paratenonitis with tendinosis
Educating the patient throughout the physical therapy treatment program and at subsequent follow-up visits is very important. Include information on adequate stretching prior to physical activity, as well as on appropriate technique and appropriate and properly fitting footwear. (See Treatment and Medication.)
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 spiraling of the tendon as it reaches the calcaneus allows for elongation and elastic recoil within the tendon, facilitating storage and release of energy during locomotion. This phenomenon also allows higher shortening velocities and greater instantaneous muscle power than could be generated by the gastrocsoleus complex alone.
Because actin and myosin are present in tenocytes, tendons have almost ideal mechanical properties for the transmission of force from muscle to bone. Tendons are stiff but resilient, possess a high tensile strength, and have the ability to stretch up to 4% before damage occurs.  With stretch greater than 8%, macroscopic rupture occurs.
The tendon's ability to glide is facilitated by the presence of a thin paratenon sheath, which is composed of a visceral layer and a parietal layer, rather than simply a true synovial sheath.
The paratenon can become inflamed and enlarged, this being a form of peritenonitis known specifically as paratenonitis. This condition is often found in runners, with acute crepitus felt over the fusiform swelling (which can originate from the paratenon or from the tendon itself).
Just anterior to the Achilles tendon lies the retrocalcaneal bursa. This can become inflamed, leading to pain anterior to the tendon, especially on dorsiflexion of the foot. It is important to differentiate this type of pain from paratenon inflammation or tendinosis. An enlarged bony prominence at the posterosuperolateral aspect of the calcaneus, called the Haglund process, may be associated with retrocalcaneal bursitis but also with insertional tendonitis as well. This is a reason why plain radiography still has value in diagnosis and management.
On average, Achilles tendons in women have a smaller cross-sectional area than in men. This possibly suggests that less force is generated in a woman’s Achilles tendon, which may account for the lower rate of rupture in women. 
The blood supply to the Achilles tendon is derived mainly from vessels traversing the mesotendon. The main blood supply is derived from the vincula, both long and short, via the paratenon and especially from the ventral mesotendon. Small longitudinal supplies from the muscle bellies and the distal insertion are also present. However, blood supply is also derived directly from the muscle bellies themselves and distally from bone where the tendon inserts into the calcaneus.
Microvascular Doppler flow studies have shown that flow is distributed evenly throughout the tendon, but it is less at the insertion.  Studies have also demonstrated higher resting blood flow rates in individuals with tendinosis than in healthy control subjects. 
Cadaveric studies have shown a relative decrease in the frequency and the total area of vessels in the midportion of the Achilles tendon.  Dynamic studies have refuted the once-popular historical theory that the pathology is related mainly to a hypovascular zone at the midtendon. However, the relative lack of blood vessels in the area that usually ruptures has led to the term watershed area, which is still used today. Although the blood supply is a factor in Achilles tendinosis, whether it is causative or reactive is still under debate.
Achilles tendonitis was the term originally used to describe the spectrum of tendon injuries ranging from inflammation to tendon rupture, but it now is seen as more of a garbage term. Current literature has delineated the terminology further to pinpoint the area of injury in hopes of guiding practitioners to more effective treatment of the patient.
Furthermore, through extensive histopathologic study, it has been determined that there is no evidence to support the presence of primary prostaglandin-mediated inflammation in Achilles tendonitis. There are, however, signs of neurogenic inflammation, with neuropeptides such as substance P and calcitonin gene–related peptide present. 
Cellular activation and increase in cell numbers
Increase in ground substance
Neovascularization: However, some more recent studies comparing the degree of neovascularization and the severity of Achilles tendinosis have failed to link a direct relationship 
Using this as a guide, a histopathologically determined nomenclature has evolved as follows, to classify Achilles complex pathology:
Paratenonitis with tendinosis
Partial or full tendon ruptures may result from end-stage paratenonitis. Causes of tendon pathologies, including ruptures, are associated with multiple intrinsic and extrinsic factors (see Etiology). [19, 1, 17]
Extracellular and intracellular matrices
Histologic changes in the Achilles tendon include changes to the extracellular and intracellular matrices. These include collagen degeneration, fiber disorientation, and increased mucoid ground substance; however, no increase in inflammatory cells occurs. Focal hypercellularity and vascular proliferation are usually present. The number and morphologic variations of tenocytes increases.  Also increased is the number of apoptotic (dead) cells in the degenerate and in the ruptured tendon.  The proportion of type III collagen is also increased in the degenerate tendon.
Pathologically, Achilles degeneration has been described as lipoid or mucoid.  In mucoid degeneration, the tendon becomes more brown or gray, with mucoid patches and vacuoles. Lipoid degeneration involves increased lipid content in the tendon tissue.  Other studies have shown an increase of type I and type III collagen messenger ribonucleic acid (mRNA). Glutamate concentrations also increase in the painful degenerate tendon. 
Neovascularization is often a feature of the degenerate tendon. It is associated with painful tendinosis.  Eccentric training leading to good clinical results is associated with a reduction and/or absence of neovascularization, and conversely, poor results are associated with continuing neovascularization. [25, 26] Tendon rupture is almost always the terminal event in the ongoing degenerative process of the tendon, as confirmed in histologic studies of ruptured tendons. 
Adult tendons are composed of large-diameter type I collagen fibrils. These are 150 nm in diameter, tightly packed with type III collagen, and dispersed in an aqueous gel containing proteoglycan and elastic fibers.  The actin and myosin bundles are arranged helically. In healthy tendons, 95% of the collagen is type I.  Degenerate tendons have less type I collagen and significantly more type III collagen. The same changes are also seen during the natural aging process, although to a lesser extent. This may be why the tendon is less elastic in older individuals and more prone to rupture.
Type III collagen seems to be the major collagen synthesized in the healing tendon after injury. This observation suggests that the tendon degeneration in tendinosis is an incomplete repair process.
Animal testing has shown that tendons can stretch by 4% of their original length before damage occurs. If they are stretched more than 8%, rupture is likely. 
The entire gastrocsoleus 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 runner’s body weight have been measured within the tendon.
When there is dysfunction in the gait cycle secondary to Achilles tightness, excessive pronation, or other factors, compensatory posturing up and down the kinetic chain (eg, hip external rotation), functional genu recurvatum, and midtarsal rotation may occur and add not only to Achilles tendinosis but also, in some cases, to a "whipping effect” of the Achilles tendon. 
A number of intrinsic and extrinsic factors, including excessive, repetitive strain, appear to be linked to the degeneration and rupture of the Achilles tendon.  The exact etiology of such injuries, however, seems to be multifactorial, complicated, and incompletely understood.
Achilles tendinosis is noted more commonly in runners, gymnasts, cyclists, and volleyball players. Hyperpronation may contribute in these cases; moreover, the tendon can be subjected to 8-10 times a person's body weight during strenuous exercise, with Komi having recorded forces of up to 4000 N passing through the Achilles tendon when a person is running on his or her toes. [32, 33]
In cyclists, low saddle height, resulting in extra dorsiflexion of the ankle with pedaling, may be a causative factor in tendinosis.
Systemic diseases that affect the Achilles tendon include the following:
Other intrinsic factors in Achilles tendon injuries include the following  :
Varus alignment with functional hyperpronation
Tibia vara ( Blount disease)
Insufficient gastrocsoleus strength and flexibility
Limited ankle dorsiflexion
As previously mentioned, age is another factor associated with Achilles tendinosis. Increased incidence of Achilles rupture and Achilles tendinosis has also been associated with having blood group O. [36, 37]
Family history is also a possible risk factor for Achilles tendon disorders. According to a study by Kraemer et al, individuals with a positive family history of Achilles tendinosis have a 5-fold greater risk for such injuries. 
Drugs that can play a role in Achilles tendon pathology include the following:
Activities with jumping and running
Participation in a new activity
Increased intensity of activity
Increased duration of training
Improper training surfaces
Improper stretching exercises
Most Achilles tendon tears occur in the left leg in the substance of the tendo-Achilles, approximately 2-6 cm above the calcaneal insertion of the tendon. That the left Achilles tendon is torn more frequently may be related to handedness; right-handed individuals "push off" more frequently with the left foot.
The most common mechanisms of injury include sudden, forced plantar flexion of the foot; unexpected dorsiflexion of the foot; and violent dorsiflexion of a plantar-flexed foot. Other mechanisms include direct trauma and, less frequently, attrition of the tendon as a result of longstanding paratenonitis, with or without tendinosis. [5, 19, 15]
Achilles tendon rupture resulting from forced dorsiflexion during active plantar flexion is commonly seen in basketball, diving, tennis, and other sports that require forceful push off from the foot.
Other risk factors for Achilles tendon rupture, aside from those previously noted (ie, age, systemic illnesses, medications, blood type), include the following  :
Fluoroquinolone antibiotic use
Although a link between smoking and biceps tendon rupture has been proven, no association between smoking and Achilles tendinosis or rupture is reported in the literature.
Persons who have had an Achilles rupture are more likely than others to have tendinosis and repeat rupture on the contralateral side. 
Traditionally, tendinosis is thought to occur with overuse, causing microtrauma to a degree and at a frequency at which the tendon can no longer heal itself. This situation leads to mechanical breakdown of the tendon. 
Several authors have studied factors that may influence the development of tendinosis, such as training mileage, rest periods for military recruits between runs, anatomic alignments of the lower limb, and mechanical factors related to shoes and inserts. As yet, no clear-cut evidence has been found linking these to tendinosis. Further confusion arises because tendinosis also can occur in relatively inactive individuals. [48, 49]
The true incidence of Achilles tendinosis is unknown, although reported incidence rates are 6.5-18% in runners, 9% in dancers, 5% in gymnasts, 2% in tennis players, and less than 1% in American football players. It is estimated that Achilles disorders affect approximately 1 million athletes per year. 
Occurrence in the United States
The incidence of Achilles tendinosis is believed to be rising, in terms of tendinosis and acute ruptures. An estimated 10% of Americans are involved in some form of recreational running or in other jumping or pivoting activities, and often for longer periods than in previous generations. No data describe the incidence or prevalence of Achilles tendinosis, but it is known to affect 7-18% of club runners.
The exact frequency of tendon rupture varies, having been reported at 6 cases per 100,000 persons in Scotland and 37 cases per 100,000 persons in Denmark. 
Sex- and age-related demographics
Compared with females, Achilles tendon injuries are more prevalent in males by a ratio of 6:1, perhaps due to sports-specific involvement.
These injuries usually are observed in recreational athletes aged 30-50 years. Many persons in this age group are active only intermittently but still challenge their bodies with high-force activities, predisposing them to Achilles tendinosis.
Achilles tendon injury has an excellent prognosis, allowing for some degree of morbidity through reduced range of motion (ROM).
With proper treatment (conservative or surgical) and rehabilitation, most athletes with Achilles tendon rupture are able to return to their previous activity levels. However, individuals who undergo surgical treatment have a rerupture rate of just 0-5%, compared with nearly 40% for patients who opt for conservative treatment. 
Surgical repair results following tendon rerupture are poorer than those following the initial operative treatment of an acute tendon rupture.
Achilles tendon contracture and/or scarring may result from excessive immobilization. In addition, permanent weakness has been known to occur with as little as 4 weeks of immobilization.
Operative treatments have several potential complications, including wound complications (eg, infection, skin slough, sinus formation), adhesions, and sural nerve injury (especially if surgery is conducted through a lateral longitudinal approach).
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