Achilles tendinitis, which is either insertional or noninsertional, can occur following trauma, secondary to overuse, or it may by part of a systemic enthesopathy. Tendinitis which is noninsertional may be either limited to the paratenon, and be a paratenonitis, or associated with an underlying degenerative tendinosis. Insertional pathology may be quite varied, and is classified according to the anatomic location and underlying inflammatory condition as either insertional tendinitis, retrocalcaneal bursitis, Haglund deformity, and pre-tendon bursitis. Since each is a different entity, but may overlap with each other, one should identify the specific diagnosis in order to initiate correct treatment.
Incidence and Epidemiology
Distinguishing between these different forms of tendinitis and posterior heel pain is difficult when reviewing the literature, since only recently has a clear distinction been made between these different entities. This is made more complicated since these conditions can occur simultaneously (especially retrocalcaneal bursitis and Haglund’s deformity, or retrocalcaneal bursitis and insertional tendinitis). The majority of patients who develop inflammatory insertional and noninsertional tendinitis do so associated with repetitive or overuse injuries. These are typically associated with running and jumping sports, although may be found in active individuals whose occupations require prolonged standing/walking. Insertional calcific tendinitis and degenerative tendinosis occur more commonly in patients who are obese and sedentary.
For noninsertional tendinitis one must distinguish between paratenonitis and degenerative tendinosis. Patients typically report gradual onset of pain, edema, and warmth proximal to the tendon insertion, initially following exercise, then during exercise, after which they may occur during activities of daily living. Athletic individuals may note symptoms after a change in their routine, such as increasing mileage, or an alteration of the running or shoe surface. Patients with tendinosis often report a history as described, but present with complaints which are more isolated, and a palpable nodule in the tendon. Symptoms of insertional achilles tendinitis are similar to those described above, however the focus is more distal, at the site of tendon insertion. Symptoms are aggravated by shoewear from direct pressure of the heel counter on the inflamed tendon, and worsened when walking uphill or ascending and descending stairs. All these symptoms are magnified after a period of rest, when a rapid return of symptoms occurs. The clinical presentation of Haglund deformity and retrocalcaneal bursitis is similar to that of insertional tendinitis, again aggravated by shoewear and dorsiflexion of the ankle as when walking uphill. Preen on bursitis is anatomically different, and lies posterior to the tendon and anterior to the skin, occurring predominantly in females wearing fashionable shoewear.
More diffuse edema and tenderness is noted along the tendon, 4 cm to 6 cm proximal to the insertion. In paratenonitis, the tendon is tender to palpation, and gliding the tendon between the fingers and the skin elicits crepitus and marked pain. This contrasts with tendinosis, where a fusiform palpable nodule is present in the same location. The combination of paratenonitis with tendinosis may also occur with features of both entities; edema, tenderness, crepitation and erythema may be present with a palpable tendon nodule. Patients with insertional achilles tendinitis have tenderness and signs of inflammation isolated to the insertion site on the calcaneus, typically associated with a bony prominence. Dorsiflexion of the ankle is limited due to pain at the insertion site. A Haglund deformity is a specific condition, and is a bone prominence of the superior lateral posterior calcaneus. This is not always associated with edema, and warmth, and if so, there is usually associated retrocalcaneal bursitis.
Various imaging studies are quite helpful with each of these conditions: plain radiographs for insertional tendinitis, and magnetic resonance imaging (MRI) or ultrasound for the various types of noninsertional tendinitis. MRI is an important study to clarify the extent of degenerative tendinosis but is not helpful in cases of paratenonitis, where ultrasound, which is a more dynamic test, helps clarify the extent of the disorder.
Plain radiographs may reveal posterior spurs and calcification in the distal extent of the tendon and bony overgrowth or cystic changes in the calcaneus consistent with chronic inflammation. Although we do not use MRI to diagnose insertional tendinitis, it may help to define the extent of the disease at the insertion site, with signal change in the distal tendon and calcaneus. There is no imaging study to adequately diagnose Haglund deformity, although a lateral radiograph demonstrates a prominence of the calcaneus and a loss of fluency between the achilles tendon and the calcaneal prominence associated with retrocalcaneal bursitis.
Identifying acute and chronic disease is important in management. Acute situations may be managed with rest and subsequent rehabilitation, while chronic situations may benefit from immediate rehabilitation, unless tendon compromise warrants surgical intervention. In general, the nonoperative treatments recommended for all inflammatory conditions of the achilles tendon is similar, with a heel lift, walking boot, or a cast with slight equinus, nonsteroidal anti-inflammatory drugs (NSAIDs), and gentle range of motion and stretching exercise in combination with modalities (ultrasound, electric stimulation, iontophoresis). Once acute symptoms resolve, gastrocnemius-soleus strengthening is advocated, followed by a gradual return to running and athletic activities. Since excessive pronation is commonly associated with paratenonitis, consideration may be given to use of a rigid orthotic arch support.
For recalcitrant cases of paratendinitis, surgery should be considered, and for these patients, the thickened crural fascia and tendon adhesions are excised, with removal the thickened paratenon with a fairly rapid resumption of activities including running. Alternatively, as more recently described, multiple percutaneous tenotomy may be performed to improve the vascularity of the tendon and enhance healing. If a degenerative tendinosis is present either in isolation or in combination with paratenonitis, a gentle physical therapy program may be initiated, although immobilization is the mainstay of initial treatment. Surgical management of tendinosis involves debridement of all the degenerated and necrotic tendon. A medial incision is made over the fusiform swollen tendon, the tendon split longitudinally, and the necrotic segment identified and excised. The problem with surgical management here is knowing where to start and stop the debridement, since if a significant amount of tendon is debrided (in excess of ½ to 2/3 of the tendon) consideration must be given to an augmenting the tendon. We recommend using the FHL muscle and tendon as a free tendon transfer since the muscle of the FHL is then in proximity with the dysvascular achilles tendon and may enhance healing. The FHL is detached either in the foot, or as distally in the ankle as possible, and then either passed through a drill hole in the calcaneus, or attached with a suture anchor to the calcaneus. It is essential to tension the FHL tendon accurately with this transfer procedure.
The treatment for insertional achilles tendinitis is typically nonoperative and is generally successful. Although immobilization may be used during the acute phase, this may be difficult if the boot or cast irritates the posterior heel. In these cases a boot with an open or soft posterior heel area may be used. Most patients do well with an open back "clog" type shoe, with a 2.5 cm to 3 cm heel to take the load off the tendon insertion. If this shoe is not tolerated, it is unlikely that other nonoperative treatments will alleviate pain. Nonsteroidal medication may be used, however, corticosteroid injections are contraindicated. Topical anti-inflammatory modalities with the aid of a physical therapist is helpful. Once the acute phase resolves, patients can resume more regular shoewear, although a 1 cm heel lift and a shoe with a soft heel counters is recommended. For the running athlete, decreased mileage, avoidance of hills, and cross-training are combined with a progressive physical therapy program, including gentle stretching and strengthening. If these treatments fail, then surgery may be considered using a variety of alternative techniques and incisions determined by the underlying pathology and maximum location of pain. We recommend a vertical longitudinal tendon splitting incision made in the central tendon and diseased portions of tendon are debrided and excised. Once the central third of the tendon is removed, the large posterior heel spur is identified and resected along with an ostectomy of the posterior calcaneus. If more than one half of the tendon insertion is debrided, it should be re-attached to the bone, preferably with a suture anchor. The divided tendon is repaired with side-to-side sutures. Following suture removal, a walker boot is used for 6 weeks followed by the use of a heel lift and physical therapy modalities. Patients should understand that it may take up to one year to regain full function following surgical treatment of calcific insertional tendinitis.
Nonoperative treatment is often successful in the management of Haglund’s Deformity and Retrocalcaneal Bursitis, using a combination of a heel lift, achilles stretching, physical therapy modalities, and avoidance of walking/running uphill. Rarely we may use a single injection of corticosteroid into the retrocalcaneal bursa. This may have a dramatic effect, but should not be repeated since the retrocalcaneal bursa is in anatomic proximity to the distal achilles tendon insertion. Surgical treatment involves excision of both the bursa and the superolateral bony prominence, and is therefore performed through a short vertical lateral incision taking care to avoid injury to the sural nerve.
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