High Yield Topics

Achilles Tendon Rupture

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Ovid: 5-Minute Sports Medicine Consult, The


Achilles Tendon Rupture
Carrie A. Jaworski
Lisa Palazollo
Basics
  • Achilles tendon ruptures are caused by laceration or by indirect forces applied to the tendon.
  • 3 types of indirect forces have been described:
    • Pushing off with the weight-bearing forefoot while extending the knee, such as with sprint starts and the pushoff in basketball
    • Sudden, unexpected dorsiflexion of the ankle, as when the foot slips in a hole
    • Violent dorsiflexion of a plantar flexed foot, as with a fall from a height
Description
  • Achilles tendon rupture is a complete disruption of the Achilles tendon, usually occurring 2–6 cm proximal to its calcaneal insertion, where blood supply is the poorest.
  • It can be associated with preexisting tendon degeneration and microtrauma.
  • It most commonly occurs in 30- to 40-year-old men.
  • Synonym(s): Heel-cord rupture; Achilles tear
Epidemiology
  • >75% of Achilles tendon ruptures occur in patients 30–40 yrs old while they partake in sports activities.
  • Males > Females: Ratio ranges from 1.7:1–19:1.
  • Left Achilles > right Achilles: Thought to be due to higher prevalence of right-side dominant individuals using left lower limb to push off during activity
Risk Factors
  • Disease processes: Connective tissue disorders, seronegative spondylopathies, rheumatoid arthritis, collagen vascular disease, diabetes mellitus, gout, hyperparathyroidism, renal insufficiency
  • Medications: Anabolic steroids or prolonged oral corticosteroid usage leads to degradation of collagen fibrils and decreased Achilles tendon strength. Corticosteroid injections weaken tendon structure. Fluoroquinolone antimicrobials lead to ischemia of tendon.
  • Disuse atrophy and sedentary lifestyle
  • Prolonged immobilization
  • Advanced age
  • History of Achilles tendonitis/tendinosis, regardless of history of injection therapy
  • Mechanical imbalances (ie, decreased flexibility of gastrocnemius-soleus complex)
  • Body weight/obesity
  • Possibility of genetic predisposition (possibility of association with HLA-B27, blood group 0)
Etiology
  • Is the largest tendon in the human body. It is designed to endure stresses up to 10 times the body's weight.
  • Is formed by the confluence of the tendons of the gastrocnemius and soleus muscles. The gastrocnemius medial and lateral heads originate from the medial and lateral femoral condyles, respectively. The soleus originates from a large attachment on the posterior tibia and fibula. Together, these tendons insert onto the calcaneus to form the Achilles tendon.
  • Receives its blood supply intrinsically from both the musculotendinous junction and the osteotendinous insertion site.
  • Additional vascular supply comes from an external source known as the paratenon. The paratenon is a thin layer of areolar tissue that encases the Achilles tendon. The further the tendon is from its musculotendinous origin and calcaneal insertion, the more it relies on the paratenon for vascular support.
  • The area with the poorest vascular supply is ∼2–6 cm proximal to the calcaneal insertion site.
  • Prior to inserting into the calcaneus, the Achilles tendon internally rotates, which imparts a structural torque stress in the tendon. This is thought to contribute to decreased vascularity in the tendon and ensuing tendon failure.
Diagnosis
History
  • Patients commonly report feeling as if they have been kicked or struck in the back of the heel, only to find no one is nearby.
  • May feel or hear a “pop” or snap
  • Pain with weight-bearing
  • Weakness or stiffness of posterior ankle
  • May give history of chronic Achilles tendinitis with or without history of injection therapy
Physical Exam
  • Acute complete rupture of the Achilles tendon involves a sudden, sharp pain behind the ankle, usually associated with a painful, palpable defect in the tendon.
  • Swelling and/or ecchymosis
  • “Hatchet strike” defect: Palpable, tender defect, usually 2–6 cm from the tendon insertion site
  • Positive Thompson test is diagnostic. Have patient lie prone or kneel with ankles clear of the table. Squeeze bulk of calf muscle and observe for plantar flexion. Perform on uninvolved side 1st for comparison. Absence of plantar flexion is consistent with complete tendon rupture.
  • Note that for the Achilles to function normally, only 25% of the fibers are needed; therefore, partial tears may be missed on examination.
  • Plantar flexion strength and ability to toe rise may be decreased compared to unaffected side.
  • Passive dorsiflexion may be increased compared to unaffected side.
  • These signs may be absent because of recruitment of other intact muscles, such as tibialis posterior, peroneus longus and brevis, and flexor digitorum and hallucis longus.
Diagnostic Tests & Interpretation
Imaging
  • Routine plain films should be obtained to avoid missing a calcaneal avulsion rupture, which would require surgical treatment. This finding usually can be appreciated on the lateral ankle radiograph.
  • US and MRI should be reserved for when the diagnosis of a complete rupture is questionable or if one is considering a partial tear.
Differential Diagnosis
  • Achilles tendinitis
  • Ankle sprain
  • Peritendinitis
  • Retrocalcaneal bursitis
  • Superficial Achilles bursitis
  • Periostitis
  • Plantar tendon rupture
  • Calcaneal avulsion
Treatment
  • Analgesia should be based on the patient's degree of pain.
  • Rest, ice, compression, and elevation (RICE) should be used in the initial treatment of complete and partial tears.
Additional Treatment
Additional Therapies
  • Both treatment approaches should be followed by a well-outlined rehabilitation program.
  • Advances in therapy should be supervised by the treating physician.
  • Cardiovascular fitness during treatment can be sustained through arm ergometer use, then recumbent cycling once no longer using crutches.
  • Once the cast is removed, active movement is initiated with the knee bent to 90 degrees; wound care and edema reduction is administered.
  • Progress to passive movement, but focus on limiting maximum stretch on the tendon while restoring normal ankle range of motion.
  • Slowly start strength exercises with isometrics, then progress to resisted range of motion exercises.
  • To restore functional activity, progress to closed kinetic chain exercises focusing on eccentric gastrocnemius strength.

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Ongoing Care
  • Controversy in the literature exists as to the best treatment approach for Achilles tendon rupture.
  • Careful patient selection is based on the patient's activity level and goals.
  • The 2 treatment options are surgical repair and casting.
  • Casting:
    • Offers quicker return to work
    • Fewer complications than surgery
    • Risk of re-rupture greater than with surgical repair: 10–30% for nonsurgical vs 1–4% for surgical repair
    • Risk of deep venous thrombosis (DVT) with prolonged casting; warfarin prophylaxis for high-risk patients
    • Usually recommended for less active or elderly patients, those with medical contraindications to surgery, or those with a history of multiple, chronic tears (1,2,3)[A]
    • Partial tears, or a tear in continuity diagnosed by MRI, also treated conservatively
    • The option exists to use a functional dorsal block splint that restricts dorsiflexion and gradually increases the amount of plantar flexion. Functional splints have been shown to help prevent gastrocnemius atrophy, quicker return to full dorsiflexion and better tolerance by patients than casting (4,5).
    • 0–4 wks: Long-leg cast with knee at 45 degrees and foot in gravity equinus. Can use short-leg cast non–weight-bearing (SLC NWB) if patient avoids any leg extension. This prevents pull on the Achilles from the gastrocnemius attachment at the femoral condyles.
    • 4–8 wks: Short-leg walking cast (SLWC) in slightly less equinus/neutral position
    • 8–10 wks: Continuous active motion (CAM) walker with gradual increases in dorsiflexion as tolerated. ∼10 degrees every 2–3 days. Discontinue CAM walker when full dorsiflexion is achieved.
    • 10 wks: 2–2.5-cm heel lift gradually decreased over next several weeks/months and aggressive rehabilitation for range of motion, then strengthening
    • 6 mos: Return to full activity
  • Open repair or closed, percutaneous technique:
    • Associated with a lower incidence of re-rupture (1,2,3,6)[A]
    • Increased restoration of calf strength/less loss of pushoff power
    • More likely to return to preinjury level: 57% surgical vs 29% nonsurgical
    • Surgical complications can include infection, DVT, pulmonary embolism, and death.
    • Other postoperative risks include delayed healing, scar adhesions, infection, persistent equinus, overlengthening, and fistulas.
    • Usually recommended for high-level athletes, those returning to high-risk activities (basketball, tennis, soccer, and sprinting), and for treatment of re-rupture
    • 0 wks: Surgical repair
    • 0–2 wks: SLC NWB in gravity equinus
    • 2–4 wks: CAM walker in 20 degrees plantar flexion and crutches
    • 4–8 wks: CAM walker with free plantar flexion and 0 degree dorsiflexion
    • 8 wks: Heel lift or elevated shoe and NWB resistive exercises
    • 12 wks: Resisted calf strengthening
    • 6 mos: Return to sports
Follow-Up Recommendations
  • The foot should be kept in slight plantar flexion and crutches should be used.
  • No activity until definitive treatment is under way and cleared by physician.
References
1. Cetti R, Christensen SE, Ejsted R, et al. Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature. Am J Sports Med. 1993;21:791–799.
2. Khan RJ. Treatment of acute Achilles tendon ruptures: a meta-analysis. J Bone Joint Surg Am. 2005;87:2202–2210.
3. Khan RJK, Fick DP, Keogh A, et al. Interventions for treating acute Achilles tendon ruptures. Cochrane Database of Systematic Reviews 2004, Issue 3. Art. No.: CD003674. DOI: 10.1002/14651858. CD003674.pub3 Accessed 8/31/09. http://www.cochrane.org/reviews/en/ab003674.html(A)
4. Saleh M, Marshall PD, Senior R, et al. The Sheffield splint for controlled early mobilisation after rupture of the calcaneal tendon: a prospective, randomised comparison with plaster treatment. J Bone Joint Surg Br. 1992;74:206–209.
5. Weber M, et al. Nonoperative treatment of acute rupture of the Achilles tendon. Results of a new protocol and comparison with operative treatment. Am J Sports Med. 2003;31:685–691. (B)
6. Metz R, Verleisdonk EJ, van der Heijden GJ, et al. Acute Achilles tendon rupture: minimally invasive surgery versus nonoperative treatment with immediate full weightbearing—a randomized controlled trial. Am J Sports Med. 2008;36:1688–1694.
Additional Reading
Metzl JA, Ahmad CS, Levine WN. The ruptured Achilles tendon: operative and non-operative treatment options. Curr Rev Musculoskelet Med. 2008;1:161–164.
Codes
ICD9
  • 727.67 Nontraumatic rupture of Achilles tendon
  • 845.09 Other ankle sprain
Clinical Pearls
  • The literature varies in its reported success and failure rates for both the surgical and nonsurgical approaches. Physicians need to be aware of both treatment options and their risks/benefits in order to help their patients make an informed decision (see “Long-Term Treatment”).
  • If casting is the treatment choice, typically 4 wks of non-weight-bearing, then 4 wks in an SLWC. After a patient has surgery, use of the CAM walker is preferred. Earlier mobilization can be utilized with these special braces to accelerate the healing by decreasing leg edema, increase range of motion, and restore normal gait pattern to return to functional activity. However, it is best to discuss surgical treatment approaches with your local orthopedic group to determine their philosophy (see “Long-Term Treatment”).


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