Andrew P. Molloy and Mark S. Myerson
DEFINITION
Chronic Achilles tendon ruptures are defined as those of greater than 3 months’ duration.
There are three indications for this technique:
A defect between healthy ends of tendon of at least 5 cm. Procedures using local tissue or autograft tendon augmentation generally suffice for lesser defects.
An expectation of recovery of function that would not be provided by Achilles tendon direct repair or advancement or flexor hallucis longus transfer
Failed reconstruction using autologous tendon advancement or augmentation
This technique may also be considered for patients with severe chronic Achilles tendinopathy that warrants resection of an extensive degenerated section of the tendon, leaving a gap similar to that observed in chronic Achilles tendon rupture.
ANATOMY
The Achilles tendon is the condensation of the two heads of the gastrocnemius and soleus muscles. The musculotendinous junction is about 6 to 8 cm from its insertion into the central third of the posterior calcaneus.
The enthesis is composed of cartilage and fibrocartilage, typically over an area of 6 cm2. The posterior calcaneal tuberosity and retrocalcaneal bursa lie anterosuperiorly.
The tendon is surrounded by paratenon consisting of both parietal and visceral layers. These relatively pliable layers provide tendon blood supply, nutrition, and lubrication. The approximate physiologic excursion of the Achilles tendon is 1.5 cm.
Blood supply, from vessels running the entire length of the paratenon, approach the tendon from its anterior surface via the mesotenon. The concentration and diameter of these vessels vary along the course of the paratenon, with the fewest being at the relatively hypovascular area 4 cm proximal to the insertion. The blood supply at the Achilles insertion on the calcaneus is also relatively avascular.4
PATHOGENESIS
Rupture occurs when the tendon is stressed beyond its yield point. The magnitude of this depends on the force and speed of loading, cross-sectional area of the tendon, and diminution of tendon quality by any pathologic process.
Predisposing factors
Achilles tendinopathy
Corticosteroids (oral or locally infiltrated), anabolic steroids
Low normal level of exercise, aging
Gout, hyperthyroidism, renal insufficiency, arteriosclerosis
Fluoroquinolones
Pathogenesis of tendinopathy and chronic tears
Chronic Achilles tendon tears most commonly occur with preexisting tendinopathy, tendinopathy that frequently was asymptomatic. Eighty percent of tears occur in the relatively hypovascular area 2 to 6 cm above the insertion; the second most common location for tendinopathy or chronic tears to develop is at the insertion on the calcaneus.
Tendinopathy is a result of microtrauma, hypovascularity, degeneration, and failure of healing. With progression, fibrovascular proliferation from the paratenon, accompanied by a marked lymphocytic and histiocytic response, develops in the degenerative tendon, leading to fibrinous and myxanthomatous degeneration of the Achilles tendon. These changes decrease the threshold for tendon rupture.
Pathologic changes in untreated ruptures
There is initial retraction of the tendon ends due to inherent muscle tension.
Within 2 weeks, fibrous organization of the tendon ends and hematoma occur.
There is a gradual transformation in shape of the tendon ends, with the distal and proximal portions respectively becoming more bulbous and conical. Moreover, the tendon ends tend to adhere to the investing fascia of the deep posterior compartment.
The hematoma in the gap between the tendon ends gradually organizes into fibrous scar tissue, which appears to reestablish tendon continuity but lacks contractile strength.
The fibroblasts remain disorganized rather than aligning in a physiologically correct longitudinal formation.
The resultant fibrous mass is rarely capable of withstanding the physiologic tensile forces of the gastrocnemius– soleus complex and thus develops further elongation and weakness.
Rupture of the Achilles tendon may lead to (1) loss of plantarflexion power, (2) lack of control of the second rocker during the stance phase of gait, and (3) subjective and objective decrease in ankle stability.12,13
NATURAL HISTORY
Most chronic ruptures present in older patients.
Occasionally a prodrome of Achilles tendon symptoms is reported; however, there may have been only the typical palpable and visual changes that occur with tendinopathy.
The patient will describe a sudden onset of pain of varying intensity either on stumbling (eccentric loading) or on push-off (concentric loading).
The pain is usually associated with swelling and weakness, although if the tendon was previously dysfunctional due to tendinopathy, the difference may be small.
Medical attention is often not sought because plantarflexion function, albeit weak, remains due to the contribution of the other ankle plantarflexors (flexor hallucis longus, flexor digitorum longus, peroneal tendons, and the posterior tibial tendon).
The amount of disability with an untreated rupture is often determined by the patient’s premorbid status.
A marked limp, inability to run, acquired pes planus, and difficulty climbing stairs are often noted.
Inability to repetitively perform a single leg raise and subjective weakness and instability are generally present.1,12,13
PATIENT HISTORY AND PHYSICAL FINDINGS
Physical examination methods include the following:
Thompson–Simmond test: Abnormal result signifies a functional tear of Achilles tendon.
Plantarflexion power: A score less than 4 indicates that a tear is likely; a score of 4 or 5 indicates that a tear is unlikely.
Palpation of gap in Achilles tendon: Mild = end-to-end repair; Moderate = V–Y advancement; severe = Achilles tendon allograft
A complete history and physical examination should be done to determine associated injuries and predisposing factors.
Inspection
Gap in tendon
Calf atrophy
Resting tension of the foot with the patient prone and knee flexed, relative to the uninjured contralateral extremity
Gait
Antalgic
Vertical oscillation of pelvis with increased hip and knee flexion13
Ankle instability13
Palpation of gap between tendon ends gives some indication of repair technique, should surgical reconstruction be considered.
1 to 2 cm: usually end-to-end repair with or without tenodesis augmentation
2 to 5 cm: usually V–Y advancement with or without tenodesis augmentation
More than 5 cm: autograft or allograft tendon transfer or reconstruction
Range of motion: excessive dorsiflexion (FIG 1)
Plantarflexion
May still be present due to recruitment of tibialis posterior, flexor hallucis longus, flexor digitorum longus, and peroneal tendons
Decreased power
Thompson–Simmond test11,14
FIG 1 • Excessive dorsiflexion due to chronic rupture of Achilles tendon.
Premorbid conditions: skin quality, smoking, neurovascular status, diabetes mellitus
IMAGING AND OTHER DIAGNOSTIC STUDIES
Imaging studies for chronic Achilles tendon ruptures are typically not indicated.
Plain radiographs may reveal calcification within the tendon, suggestive of a degenerative process leading to rupture.
Plain radiographs may also demonstrate a bony avulsion from the calcaneus.
Ultrasound and magnetic resonance imaging (MRI) are unnecessary but confirm clinical findings and provide some understanding of the extent of diseased tendon or gap in contrast to healthy tendon. This additional information may be useful in surgical planning for an Achilles tendon allograft since clinical examination may not accurately define the extent of diseased tendon that will need to be resected.
NONOPERATIVE MANAGEMENT
The extent of nonoperative treatment depends on level of symptoms and required level of functional improvement. Despite the seemingly devastating functional consequences of chronic Achilles tendon rupture, not all patients require a reconstructive procedure.
Bracing
The level of hindfoot and ankle stabilization required is determined by the power of plantarflexion power afforded by secondary muscles and to a lesser extent by the patient’s weight.
A relatively lightweight carbon-fiber ankle–foot orthosis (AFO) may enhance gait during push-off by transferring elastic recoil gained during dorsiflexion to plantarflexion to compensate for lack of Achilles tendon function. In our experience, this treatment is less suitable for heavier patients.
A clamshell AFO that encompasses the foot and ankle may be of greater benefit than a traditional AFO for patients with a combination of severe loss of plantarflexion function and poor ankle stability. The addition of an anterior component to the conventional AFO provides the advantage of resisting excessive ankle dorsiflexion.
In select patients, a double-upright brace attached to a stiffer-soled shoe and locked at the ankle may be as effective as a conventional or clamshell AFO.
Physical therapy
Physical therapy should focus on strengthening the secondary ankle plantarflexors (flexor hallucis longus, flexor digitorum longus, posterior tibial tendon, and peroneals)
Gait training, stabilization, and proprioception exercises
SURGICAL MANAGEMENT
Advantages of allograft versus autograft
No morbidity or loss of function and pain from donor site
Quality and amount of autogenous tendon may be insufficient
Shorter operative time as no harvesting is required
Satisfactory mechanical properties of allograft are proven8–10
Disadvantages
Cost
Theoretical risk of transmission of host infectious diseases2,3
Preoperative Planning
Vascular status is assessed.
The surgeon should ensure that the posterior lower leg skin is amenable to surgical intervention; if concern exists, the threshold for plastic surgery consultation should be low.
The contralateral limb is assessed for natural resting tension of the gastrocnemius–soleus complex.
Imaging studies, if obtained, may provide some understanding of the extent of degenerated Achilles tendon.
Positioning
Before positioning, a well-padded tourniquet is applied. This should be on the thigh as to prevent tethering of the gastrocnemius–soleus complex and potential inaccuracies in allograft tensioning.
We prefer a popliteal block for postoperative pain management in conjunction with general anesthesia to permit the patient to tolerate the thigh tourniquet. Depending on surgeon preference, a more proximal regional anesthetic, spinal, or epidural may be considered. The advantage to a popliteal block is improved leg function and potentially safer mobilization in the immediate postoperative period, since the proximal limb girdle muscle function is not forfeited.
Prone positioning with adequate padding, maintenance of airway, avoidance of brachial plexus tension, and safe positioning of the patient’s genitalia are all important.
The lower limb is prepared and draped in the standard sterile fashion to above the knee.
The limb is exsanguinated and the tourniquet is inflated. (Care must be taken to avoid excessive hip and lower back extension.)
Approach
A posterior approach to the distal lower leg is used with a midline incision of about 20 cm centered over the Achilles tendon and central posterior calcaneus. While this is our preferred technique, the surgical approach must respect prior surgical approaches to the Achilles tendon (FIG 2).
FIG 2 • Marked skin incision for allograft reconstruction.
TECHNIQUES
ALLOGRAFT RECONSTRUCTION OF CHRONIC ACHILLES TENDON RUPTURE
The Achilles tendon allograft tissue, comprising the distal Achilles tendon with its insertion into a block of allograft calcaneus, is carefully inspected to ensure it has been properly screened, has not expired, and is appropriate for the proposed procedure.
Make a longitudinal incision in the midline. If preexisting incisions are present, maintain a midline approach as best as possible while respecting the previous approach or approaches.
Create full-thickness flaps and retract only the deeper tissues to minimize wound complications.
Incise the tendon sheath longitudinally and reflect it.
Define and mobilize the tendon ends.
TECH FIG 1 • Intraoperative view after resection of diseased Achilles tendon.
Débride the proximal tendon end, leaving only healthy tendon. With allograft Achilles tendon reconstruction, the distal Achilles tendon stump is resected completely (TECH FIG 1).
Contour the block of allograft calcaneus attached to the Achilles allograft with a saw, rongeur, or both for insertion and fixation into the patient’s calcaneus.
Use an oscillating saw to create a matching corticocancellous trough in the posterior aspect of the patient’s calcaneus. We prefer to use a flexible chisel to fine-tune this trough, which will accommodate the allograft bone (TECH FIG 2).
After fully inserting the allograft’s bony portion into the patient’s calcaneal trough, secure the bony block using two fully threaded cancellous 4.0-mm titanium screws (DePuy ACE Screw System, Warsaw, IN) (TECH FIGS 3–5).
TECH FIG 2 • Preparation of posterior calcaneus for allograft.
TECH FIG 3 • Determining proper allograft fit.
TECH FIG 4 • Fixation of distal bone segment of allograft.
Insert a running nonabsorbable no. 2 whip suture (Ethibond, Ethicon, Somerville, NJ) on either side of the allograft tendon (TECH FIG 6).
By proximally tensioning the sutures, the ankle assumes a position of maximum equinus as the graft spans the defect. This tension is maintained until the allograft is adequately secured to the patient’s residual native Achilles tendon, with the no. 2 nonabsorbable suture being woven into the host tissue or secured to a symmetric no. 2 whip suture placed into the host tissue.
TECH FIG 5 • Intraoperative fluoroscopy of fixation of bony segment of allograft.
TECH FIG 6 • Intraoperative view of properly tensioned allograft reconstruction.
With healthy residual proximal host Achilles tendon, we recommend performing an end-to-end repair between allograft and host tendon. When the patient’s residual tendon is adequate but with suspect quality at the most distal portion of the host tissue, we routinely perform an overlapping, imbricated reconstruction.
Augment the repair or reconstruction with a running 2–0 Vicryl suture (Ethicon).
Close the paratenon with 4-0 Vicryl.
Reapproximate the subcutaneous layer with 4-0 Vicryl and close the skin with 4-0 nylon, while maintaining careful handling of the skin margins.
FIG 3 • Six-month follow-up after allograft reconstruction.
POSTOPERATIVE CARE
Immobilization in equinus in a bulky splint for 2 weeks
Suture removal at 2 weeks
Immobilization in a hinged cam walker (Bledsoe Platform Boot, Medical Technology Inc., Grand Prairie, TX) set to neutral dorsiflexion block and block at 20 degrees of plantarflexion. The foot is kept in equinus by inserting heel pads into the boot.
Partial weight bearing (25 kg) is commenced at 2 weeks. This is increased by increments of 25 kg per week until full weight bearing is achieved.
At 8 to 10 weeks the boot is swapped for a 1to 2-cm heel raise inside a shoe.
Gentle passive and active range-of-motion exercises and isometric exercises are commenced at 4 weeks.
Gentle passive stretching is started at 4 weeks and effort is gradually increased until at 10 weeks, standing calf-stretching exercises are commenced.
Elastic band exercises are started upon removal of the boot. Stationary bike riding is started at 10 to 12 weeks, with gradual progression of exercise up to 18 weeks, when active push-off exercises are initiated.
OUTCOMES
In our hands, outcomes with this technique have been satisfactory and without wound complications (FIG 3).
Typically, at 20 weeks the patient can perform single-leg toe-raises and begin jogging and light sporting activities, if previously able (FIG 4).
In our experience, most patients return to their preoperative exercise level and return to their prior occupation.
COMPLICATIONS
Infection
Wound dehiscence
Rupture of repair
FIG 4 • Single-leg toe-raise on affected side at 6-month postoperative stage.
Incorrect tensioning
Aseptic necrosis of graft
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