Current Pedorthics | July-August 2018 | Vol.50, Issue 4 | Page 56

Understanding Achilles Tendinopathy for Improved Results in Orthotic Therapy
disease processes ( 6 ). Pathological changes such as calcification of tendons , lipid accumulation , and inflammation can also cause tendons to degenerate ( 3 ). Historically , tendon ruptures occur in areas of the tendon that have both decreased blood flow and an increased lipid accumulation such as the Achilles tendon ( 4 ). Pain upon ambulation and / or with descending staircases is the number one complaint of patients , especially the elderly , who seek treatment for tendon degeneration ( 5 ). In younger adults most tendon damages are due to forceful rupture of the tendon . Achilles tendon ruptures occur in young athletes ; especially in sports such as tennis , basketball , diving , running and track ( 7 ). Causes are usually related to inappropriate warm up , chronic corticosteroids use , over exertion of the tendon , and use of certain antibiotics such as quinolones . The mechanism of rupture is forced dorsiflexion of the foot or direct trauma to the Achilles tendon . It can also occur from tendon degeneration associated with a long standing paratendinosis . It has been described as a snapping sound with the feeling of being kicked or shot in the area ( 7 ). Achilles tendinopathy accounts for 9 % of all injuries in runners ( 10 ). The most common area of the tendon rupture is called the watershed area , about 3-6 cm above the Achilles insertion point on the back of the heel where blood flow to the tendon is at its lowest .
II . TYPES OF ACHILLES TENDINOPATHY
Many etiologies exist that result in pain and or swelling in the area of the insertion of the Achilles tendon : tendonitis , tendinosis , paratendinopathy , Achilles rupture , Haglund ’ s deformity , retrocalcaneal exostosis , retrocalcaneal bursitis , xanthomas , and enthesopathies should all be in your differential . According to Amis , equinus is the major culprit or contributing factor to most biomechanical problems in the foot and ankle . He calls his theory the splitsecond effect . The split-second effect is divided into two components : ankle dorsiflexion and knee extension . The ankle dorsiflexion component of the split-second effect occurs at the last half of midstance . It starts when the foot in swing phase passes the stance phase foot and ends when the foot lifts the heel from the ground . If , at this point in time , the stance phase foot fails to adequately dorsiflex , ankle forces increase significantly , peak faster and last longer . This damages the soft tissues and joints . Repetitive stresses result in tendon degeneration over time . If knee extension is restricted by a tight gastrocnemius at the same time that the ankle fails to adequately dorsiflex , additional forces are generated in an already taught Achilles tendon . When tight gastrocnemius muscles prevent normal ankle dorsiflexion , the knee has to compensate by flexing or hyperextending . Unless this occurs , the already taut Achilles tendon is further stretched because of the proximal origin of the gastrocnemius ( 22 ). A third component of the mechanism , excessive contact phase pronation of the subtalar joint , causes what Amis calls " a whip like force " to occur at the medial Achilles tendon . This motion places a third split-second overload on the tendon completing the injury which can be a sudden ballistic injury or a cumulative moderate overload that results in an eventual injury ( 20 ).
The terms tendonitis , tendinosis , and paratenitis are easily confused . In 1998 Maffulli proposed these tendon pathologies should be referred to by a broader term – tendinopathies . He further stated these specific names should only be used after examining tissue via histology ( 24 ). Tendinosis presents with pain and swelling of the Achilles near its insertion on the calcaneus . Animal models have demonstrated that , with repetitive stress , tendon degeneration can occur in as little as 2-3 weeks ( Khan ). Histological studies have shown an increase in tenocytes , an absence of inflammatory cells , and disorganization of the
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