Achilles Tendinopathy 112752 am_846862.pptx

Achilles Tendinopathy 112752 am_846862.pptx

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  ACHILLES TENDINOPATHY OYETADE OREOLUWA
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  OUTLINE • INTRODUCTION • TYPES •MECHANISM OF INJURY • PATHOPHYSIOLOGY • RISK FACTORS • DIAGNOSIS • DIFFERENTIAL DIAGNOSIS • MANAGEMENT • PREVENTION • REFERENCES
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  INTRODUCTION • Achilles tendinopathyis a painful overuse injury of Achilles tendon. This injury is commin among athletes. • Among elite track and field athletes, 43% reported having either current or prior symptoms of Achilles tendinopathy. (Highest prevalence (83%) in middle- distance runners) • 63% of injuries are found in general public which are sport related.
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  TYPES • Achilles tendinopathyis a clinical diagnosis and majority of the patients come with a combination of localized pain, swelling of the Achilles tendon and loss of function. • According to location of pain, Achilles tendinopathy can be classified as; 1. Insertional tendinopathy (20-25%) 2. Non-Insertional or Midportion tendinopathy (55-63%) 3. Proximal muscilotendinous junction type (9-25%) • Patient can present with symptoms at the insertion and midpoint concurrently. • 30% patients have bilateral pain.
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  MECHANISM OF INJURY •Achilles tendon is a mechanoresponsive structure • The most common cause of athletes is excessive loading with inadequate recovery. • An increase work or daiky activity can contribute to excessive loading. • A fixed forefoot equinus results in compensation at the ankle joint by dorsiflexion and may result an overuse injury to the tendon. • Compensation at the subtalar joint for imbalance of foot places on the tendon. The subtalar joint may compensate by exerting the calcaneus with increase load over the tendon. • A rigid plantar-flexed first metatarsal or cavovarus places strain on lateral side of the tendon.
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  MECHANISM OF INJURY
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  PATHOLOGY • The mainpathology is a failed healing response with degeneration and haphazard proliferation of tenocytes. disruption of collagen fibers and increase in non-collagenous matrix. • Histopathologically the samples show unequal and irregular crimping and loosening and increased waviness of collagen fibers, with an increase of type III collagen fibers. • Hypoxic, hyaline degeneration, calcification,fibro-cartilaginous and bony metaplasia can coexist.
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  RISK FACTORS • INTRINSIC 1.Tendon vascularity 2. Dyslipidemia 3. Pes cavus 4. Deficits in Hip neuro-muscular control 5. Obesity 6. Lateral ankle instability 7. Weakness & lack of flexibility of the gastrocnemius-soleus complex. • EXTRINSIC 1. Excessive loading of the tendon 2. Fluroquinolone 3. Corticosteriods 4. Training load errors.
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  SYMPTOMS & SIGNS •SYMPTOMS  Gradual onset of pain with activity & reduced function  Stiffness in morning and after prolonged sitting or after a period of inactivity.  Deficit in strength & performance. • SIGNS  Tenderness  Sometimes a nodular swelling can be palpated  The ARC sign  The Royal London Hospital Test.
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  DIAGNOSTIC TESTS Blood Investigations. •CBC, ESR, CRP • LFT • Uric acid • FBS, PPBS, HbA1c • Lipid Profile.
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  FUNCTIONAL IMPAIRMENTS 1. Rangeof motion: Decreased dorsiflexion (Non-weight bearing- Goniometer, Weight bearing- Ankle-lunge test), limitation of planter flexion, inversion and eversion. 2. Calf muscle endurance: Decreased. Assessment done by Heel-Rise test. The Limb symmetry index can be calculated to compare the degree of functional deficit between limbs. 3. Calf Muscle strength: Strength deficit is seen due to reduced plantar-flexor strength. Dynamometry can be used to meadure isometric and dynamic strength. Isokinetic dynamometry is used to assess ankle plantar-flexor and dorsiflexor strength. 4. Jumping ability: Single-legged hopping and drop- countermovement jump can be used to measure function and degree of pain during activity.
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  MANAGEMENT • Achilles tendinopathyis difficult to treat. Management of AT lacks evidence-based support, and payients are at risk of long term morbidity with unpredictable clinical outcome. • Non-operative care should be implemented for a minimum of three to six months prior to considering surgery.
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  CONSERVATIVE MANAGEMENT PHARMACOLOGICAL 1. NSAIDS:Commonly used and shows modest efficacy. Effective in only acute cases. Analgesic effect of NSAIDS can impose further damage to the tendon and delay definitive healing. 2. NITRIC OXIDE: Can be administered by an adhesive patch (in case of midportion AT). Topical GTN is effective in chronic cases of non-insertional AT and treatment benefits upto 3 years. 3. INJECTIONS: Several substances have been used for AT injections. Steroid, Dextrose, aprotinin, sclerosing agnts, Local anaesthetic or PRP can be given. Helps in reducting pain, improving activity level and reducing tendon thickness. High volume injections are found to be more efficacious than platelet rich plasma in short term.
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