44 Achilles Tendon Rupture



10.1055/b-0040-176985

44 Achilles Tendon Rupture

Jannat M. Khan, D. Landry Jarvis, Alejandro Marquez-Lara, and Eben A. Carroll

Introduction


Achilles tendon ruptures represent a spectrum of acute and chronic injuries. While acute injuries are more often associated with sports activity, chronic ruptures occur in the setting of chronic tendinopathy. Although the cause of Achilles tendinopathy is likely multifactorial, it has been associated with repetitive stress, such as running, and chronic metabolic conditions affecting the extracellular matrix of the Achilles tendon. Understanding the differences between these two conditions is essential to develop an appropriate treatment strategy and optimize patient outcomes (▶Video 44.1).



I. Preoperative




  1. History and physical examination




    1. Peak incidence in the third to fifth decade of life.



    2. Higher incidence among males (5:1) with positive correlation of Achilles tendon pathology among obese, and elderly population (> 60 years old).



    3. Common among nonathletes participating in intermittent high-performance activity (“Weekend Warrior”).



    4. At the time of injury, the patient may feel a snap sensation, hear an audible pop, and have instant pain that gradually dissipates.



    5. Visible limp with difficulty with plantar flexion and weight bearing.



    6. Etiology not clear but can be divided into degenerative theory or traumatic mechanical theory.



    7. Risk of degenerative injury—recent oral or intrasubstance fluoroquinolones and corticosteroids, long-standing paratendinitis, or recent Achilles surgery.




      1. Degeneration postulated to occur due to impaired blood flow to the tendon, which may lead to hypoxia and altered metabolism.



      2. Rupture can occur without application of excessive loads.



    8. Injury may be due to direct or indirect acute trauma:




      1. Direct—blow, laceration, or crush injury.



      2. Indirect—obliquely loaded at a short initial length with maximum muscle contraction when pushing off weight-bearing foot with knee in extension (most common), that is, lunging for a ball with a giving way sensation.




        • i. Sharp unexpected dorsiflexion, that is, fall in hole.



        • ii. Strong dorsiflexion force on a plantar-flexed ankle, that is, falling from a height.



    9. Ecchymosis and edema.



    10. Excessive dorsiflexion at rest.



    11. Unable to stand on toes.



    12. The American Academy of Orthopaedic Surgeons (AAOS) Clinical Practice Guidelines states that diagnosis made with two or more positive findings following examinations:




      1. Thompson’s test (when compression of calf in prone position does not elicit passive plantar flexion): 96% sensitive (▶ Fig. 44.1 ).

        Fig. 44.1 Clinical picture demonstrating the Thompson test. Note the absence of dorsiflexion with compression of the calf muscle.


      2. Decreased plantar flexion strength.



      3. Positive sulcus sign (palpable defect distal to insertion site).



      4. Matles’ test (increased passive ankle dorsiflexion at rest): 88% sensitive (▶ Fig. 44.2 ).

        Fig. 44.2 Clinical photograph demonstrating Matles’ positive for right leg. (Adapted from Wikimedia commons, public domain.)


  2. Anatomy




    1. Achilles tendon is the strongest and largest tendon in the human body.



    2. Gastrocnemius–soleus complex (GSC):




      1. Formed by conjoined tendon of the gastrocnemius and soleus muscles.



      2. Integral in knee flexion, foot plantar flexion, and hindfoot inversion.



      3. Tendon spans three different joints including the knee, tibiotalar, and subtalar joints.



      4. Gastrocnemius arises from posterior femoral condyles: acts as an effective plantar flexor with knee in extension.



      5. Soleus arises from the posterior aspect of the tibia, fibula, and interosseous membrane only traversing the ankle joint: acts as an effective plantar flexor with knee in flexion.



      6. GSC inserts over the broad posterosuperior aspect of the calcaneal tuberosity.



    3. Seventy-five percent of ruptures occur 2 to 6 cm proximal to the calcaneus.




      1. Tenuous vascular supply in this watershed area.




        • i. Proximal—intramuscular arterial branches of posterior tibial artery.



        • ii. Distal—interosseous arteriole branches from peroneal artery.



      2. High-peak stresses (70 MPa) experienced in this area. Most tendons experience stress below 30 MPa.



    4. Extracellular matrix:




      1. Matrix metalloproteinase (MMP 1–3)—increase in MMP1 is associated with degradation of type I collagen and matrix remodeling.



      2. Transglutaminase (TG):




        • i. Implicated in organogenesis, tissue repair, and tissue stabilization.



        • ii. Decrease in TG associated with reparative tendon’s capabilities.



  3. Imaging




    1. X-ray:




      1. Helps assess Kager’s triangle, which is the space between Achilles tendon, posterior tibia, and superior calcaneus (▶ Fig. 44.3 ). Irregular configuration in chronic ruptures.

        Fig. 44.3 Lateral plain film radiograph demonstrating normal-appearing space between the Achilles tendon, posterior tibia, and superior calcaneus (Kager’s triangle).


    2. Ultrasound:




      1. Help differentiate partial and complete tears.



      2. Hypoechoic signal proximal to insertion of Achilles tendon.



      3. Greater than 5 mm gap noted between tendon edges indicates surgical intervention.



      4. Not recommended if suspicion of partial tendon tear (only 50% sensitive).



    3. MRI:




      1. Discontinuous Achilles tendon due to tear denoted by hypointense signal proximal to insertion in T1, hyperintense signal in T2 MRI.



      2. Disruption of signal in tendon substance on T1.



      3. Generalized high signal on T2 (▶ Fig. 44.4a, b ).

        Fig. 44.4 (a) Sagittal cut of T2 MRI demonstrating acute achilles tendon rupture at the watershed area. (b) Sagittal cut T2 MRI demonstrating acute achilles tendon rupture at the calcaneus insertion.


      4. Recommended to reserve use for the following patient populations:




        • i. Inconclusive clinical examination findings.



        • ii. Subacute or chronic tears occurring more than 4 weeks prior to presentation.



        • iii. Prior tears with concern for scar tissue in order to develop an appropriate surgical plan.



  4. Classification




    1. Kawada classification (▶ Table 44.1 ):





























      Table 44.1 Kuwada’s classification of Achilles tendon ruptures

      Type


      Injury


      Treatment


      I


      Partial tear (< 50%)


      Nonoperative treatment


      II


      Complete rupture with <3 cm tendinous gap


      End-to-end anastomosis


      III


      Tendon (flexor hallucis longus) flap with or without synthetic graft augmentation, V-Y advancement, a Bosworth turndown, tendon transfer


      Complete rupture with 3–6 cm tendinous gap


      IV


      Complete rupture with >6 cm tendinous gap


      Gastrocnemius recession with tendon or synthetic graft




      1. Derived from direct visualization of Achilles tendon; unclear if correlates with MRI.



      2. Developed to help guide treatment based on the completeness of the tear and the amount of gapping.

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Jun 26, 2020 | Posted by in ORTHOPEDIC | Comments Off on 44 Achilles Tendon Rupture
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