Insufficient preparation, overstrain, lack of general conditioning contribute to Achilles tendon ruptures. Participants in any sport involving repetitive impact loading associated with jumping are at an increased risk for Achilles tendon ruptures. Approximately 75% of all Achilles tendon ruptures occur during sporting events. This overexertion most commonly occurs while playing basketball, baseball or soccer.
Advancing age is definitely shown to correlate with Achilles tendon overuse injuries. The average victim of a complete Achilles tendon rupture does not engage in highly competitive professional athletics. Rather, the patient is usually the so-called "weekend warrior."
Inappropriate footwear with insufficient heel height, rigid soles, inadequate shock absorption, or wedging from uneven wear can magnify the stresses exerted on the tendon during activity.
Training errors include sudden increases in training intensity, excessive training, training on hard surfaces, and running on sloping, hard or slippery roads.
Mechanism of Injury
The weekend warrior ruptures the Achilles tendon in 1 of 3 ways. Most often, they occur when pushing off the weightbearing foot while extending the knee joint, which occurs during sprinting or jumping. Because the right-handed warrior is apt to push off with the left leg, left Achilles tendon rupture is more prevalent in this population. Approximately 17% of ruptures occur when the warrior suddenly and unexpectedly dorsiflexes his ankle when stepping into a hole, falling forward, or slipping on a ladder. Approximately, 10% of ruptures result from jumping/falling from a height and violently dorsiflexing the plantarflexed foot.
The incidence is higher in males than females.
Drug- and Disease-Related Risk Factors
Both corticosteroids and anabolic steroids as well as fluoroquinolones have been implicated in playing a role in Achilles tendon ruptures. The injection of corticosteroids into the tendons of rats has been shown to cause tendons necrosis. Although injection into peritendinous areas is less detrimental, corticosteroids, nonetheless, inhibit healing. In addition, corticosteroids may mask painful symptoms, causing the individual to overexert a weakened tendon.
Furthermore, both anabolic steroids and fluoroquinolones cause dysplasia of collagen fibrils, which, in turn, decrease tendon tensile strength.
Other reported causes of Achilles tendon ruptures include gout, hyperthyroid, renal insufficiency, and arteriosclerosis.
Along with gathering a detailed history, a careful physical exam is critical to diagnosing an Achilles tendon rupture. The classic findings are a palpable and painful defect 2 cm to 6 cm proximal to the tendo-calcaneal insertion. The reason for this distribution of injuries is not entirely clear, although some studies suggest that the blood flow in this vicinity is relatively poor. Also, the leg bruises in the area of the tear and the patient has weak plantarflexion.
Despite the seemingly straightforward history and physical, about 25% of Achilles tendon ruptures are missed during the patient's first visit. Although the patient initially feels the pain of a violent kick, or even a "gunshot," pain may not be present on palpation. In addition, the typical ecchymosis and edema may not be present early. If swelling is present, it can obliterate any palpable defect. The physician may incorrectly diagnose a "partial tear" if the patient can still plantarflex his ankle. This paradox is due to the functional flexor hallucis longus, flexor digitorum longus, posterior tibial, and peroneal tendons.
These pitfalls can be avoided by using a few simple tests. First, the patient should be instructed to perform repetitive heel rises. Despite the other functioning plantarflexors, the patient with a torn Achilles tendon will be unsuccessful in this attempt.
The well-known Thompson test can aid in the diagnosis. This is done by simply squeezing the midcalf of the affected leg, which is kneeling (90-degree angle) on a chair while the opposite leg remains standing. It may also be performed with the patient in the prone position if the patient is fully relaxed. The absence of ankle plantarflexion is suggestive of a complete Achilles tendon rupture and is termed a "positive" Thompson test.
Figure 1. With an intact Achilles tendon (left), squeezing the calf will result in plantarflexion of the foot. With a ruptured Achilles tendon (right), no plantar flexion in noted.
O'Brien described a test in which a 25-gauge needle is placed 10 cm proximal to the superior border of the calcaneus such that it penetrates the Achilles tendon. The ankle is then alternated with passive dorsiflexion and plantarflexion movements. If the needle end tilts such that it points in the direction opposite the movement, then the Achilles tendon is noted to be intact. However, if it remains relatively still, a rupture is the diagnosis.
Ultrasonography and MRI
A careful history and physical examination as described above should result in an accurate diagnosis in more than 90% of patients. If the diagnosis remains questionable, either ultrasound or MRI can be helpful.
Ultrasound scanning will show an intact Achilles tendon as a hypoechogenic ribbon-like image contained within 2 hyperechoic bands. When torn, the distal stump will be grossly thickened and contain an irregular echogenic pattern. This correlates with the operative findings of a degenerative stump surrounded by inflammatory cells. The site of the tear will also show a hyperechogenic area consistent with a partially organized hematoma. Ultrasound is noninvasive, inexpensive, nonionizing, and fast. Unfortunately, it may not be sensitive in differentiating between partial and complete tears and its interpretation often requires a steep learning curve.
On MRI, an intact Achilles tendon will have low signal intensity on all pulse sequences; any increased signal intensity within the tendon is viewed as abnormal. The sagittal T1 images can differentiate fat from hemorrhage. It will show high signal intensity at a rupture site filled with edema and hemorrhage. In contrast, sagittal T2 images are best for delineating the size of the gap and the condition/orientation of the torn fibers. Although more time consuming and expensive, MRI is generally superior to ultrasound in differentiating hemorrhage from tendon at the rupture site as well as differentiating partial from complete tears.
TREATMENT OF ACUTE ACHILLES TENDON RUPTURES
The choice of treatment for acute ruptures of the Achilles tendon continues to be controversial.
Nonsurgical treatment usually begins with cast immobilization with the foot in 20 degrees of plantarflexion for 6-8 weeks. Some have advocated the use of ultrasonography to asses whether the diastasis of the tendon is adequately closed at this position. At 6-8 weeks, the patient is weaned from the cast and gentle range of motion exercises are performed. As the patient begins walking, a 2 cm heel lift is used for one month and a 1 cm heel lift is used for the second month. Strengthening exercises are started a 8 - 10 weeks, with a resumption of sports at 4 - 6 months. It may take 12 or more months to gain maximum strength and some residual weakness in common.
Surgery has been the first choice of treatment for Achilles tendon ruptures in young fit individuals at this time. Advances in surgical techniques and new postoperative rehabilitation protocols have resulted in studies showing the advantages of direct tendon repair.
With conservative treatment, extensive scarring often fills the gap between the torn tendons. This leads to a lengthened tendon, which, in turn, leads to decreased push-off strength. Surgical treatment of Achilles tendon rupture resulted in increased strength.
Direct repair results in less calf atrophy when compared with nonsurgical treatment. Those undergoing direct repair lose only approximately 3% of their strength when undergoing isokinetic testing and about 90% of athletes are able to return to their respective sports at a similar level at 6 months postoperatively. A higher number of patients return to their pre-injury athletic level.
In addition, surgical repair appears to significantly increase the strength in those suffering re-ruptures. Those treated surgically for the second time increased their level of strength by 85% compared with a 50% strength gain in those treated conservatively.
The most significant benefit of surgical repair is the decreased re-rupture rate. Studies have analyzed the differences in the rate of re-rupture for nonsurgical versus surgical treatment. The studies have reported re-rupture rates as high as 18 to 30% for Achilles ruptures treated nonsurgically. The re-rupture rates for those treated with surgical repair ranged from 1-4%.
Currently, with greater attention paid to surgical technique and post-operative care, the complication rate for patients treated surgically (12%) is less than for patients treated nonsurgically (18%). Most of the post-operative complications are minor and involve minor wound healing problems. This has not been found to influence the long-term outcome of these patients.
Increased operative treatment also leads to more experience in treating complications effectively. For example, it is now shown that physical therapy can overcome many of the problems associated with adhesions between the repair site and the skin.
Moreover, the vast majority of superficial wound infections can be treated effectively with limited weight bearing, oral antibiotics, and silver sulfadiazine (Silvadene). Once the tissue granulates, the wound can simply be treated with wet to dry dressing changes; only in rare circumstances is additional reconstructive surgery necessary.
Those favoring surgical treatment also point out the relatively uncomplicated nature of the procedure. There is no evidence showing that primary augmentation is more effective than simple end-to-end repair in acute tears. Therefore, more extensive procedures using tendon transfers, flaps, or mesh are best left for use with delayed tears, in which the repair will be under tension due to the chronically retracted ends.
The patient is placed in the prone position with both prepped feet dangling from the end of the table. By placing the table in Trendelenburg, the feet receive less blood flow. An 8-cm to 10-cm longitudinal incision is made just medial to the Achilles tendon. A posterior lateral incision would place the sural nerve at risk and a mid-posterior incision can result in suture interference from the tendon repair site. After dissecting through the subcutaneous tissues, the paratenon is cut longitudinally with Mayo scissors.
As the ruptured ends often have a "mop-end" appearance, some surgeons will wait one week before repair in order to allow the ends to better consolidate. After juxtaposing the ends, the tendon is sewn together with non-absorbable suture. Prior to tying the suture ends, the tendon's dynamic resting tension is optimized by comparing it with the control side. A circumferential stitch is used to further strengthen the repair site. After closing the paratenon, the plantaris fascia can be fanned out over the repair site to help prevent adhesions with the undersurface of the skin. The subcutaneous tissue is then approximated with absorbable suture and the skin sewn together in a nylon mattress fashion. A fasciotomy of the deep posterior compartment can facilitate closure in cases with excessive skin tension. This allows for improved closure of the paratenon as well.
Usually, postoperative rehabilitation involved wearing a splint with the ankle in equinus during the immediate postoperative period. A cast is then placed within a few days and continued for 6 weeks.
The patient is seen in the office at 2-week intervals during which the cast is changed and placed in an increasingly more dorsiflexed position. After 4 to 6 weeks in the cast, it is advanced to a plantigrade position.
At 6 weeks, the cast is removed and the patient is placed in a removable Achilles brace. Weightbearing can be started at this point. The wedges in the Achilles brace are removed every 1-2 weeks, gradually bringing the ankle to a plantigrade position over a 4-6 week period. At 10-12 weeks after repair, normal walking is permitted with a heel lift in the shoe until 12 weeks after repair. Return to sports is usually permitted at 4-6 months.
In certain circumstances, a more functional rehabilitation program may be followed. This would depend on the perceived strength of the repair at the time of surgery. It is further restricted to the compliant well-motivated athlete.
This protocols use a walking boot for 6 weeks allowing full range of motion with the exception of dorsiflexion beyond neutral. The patient performs progressive exercises and is allowed to bear weight, as tolerated with crutches. The program involves use of the bicycle at 3 weeks, the pool at 4 weeks, and push off strengthening exercises with a stair climbing device at 8 weeks. At 2 months, the patient can perform heel rises, jog, and increase push-off strengthening activities.
- Accompanying the increased popularity of weekend recreational sporting contests is an increased incidence of Achilles tendon ruptures.
- These usually occur in otherwise sedentary males who are in their 30s or 40s.
- Although the history and physical remain the most accurate way to diagnose the injury, MRI and ultrasonography can prove helpful in select circumstances.
- The current preferred treatment in young and otherwise healthy patients is surgical repair.
- Conservative treatment remains an acceptable alternative in older patients who have fewer physical demands.
- Improved rehabilitation protocols have enhanced recovery for patients who receive either nonsurgical or surgical treatment.
- Atkinson, TS, Easley, M: Complete ruptures of the Achilles tendon. Medscape Orthopaedics & Sports Medicine 5(3), 2001. © 2001 Medscape, Inc.
- Saltzman, CL, Tearse, DS: Achilles tendon injuries. JAAOS, 6(5), 317-325, 1998.
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