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  1. D M Silván1,
  2. F B Pazos1,
  3. A R Valero1,
  4. X D Justo1,
  5. T F Jaén2
  1. 1Clínica Traumatológica, Valladolid, Spain
  2. 2Clínica CEMTRO, Madrid, Spain


    Introduction Achilles tendinopathy (AT) is classically known to be very resistant to treatment. Although other diagnoses such as bursitis and insertional problems have been described, the most common pathology is mid-portion Achilles tendinopathy (55–66% of Achilles tendon disorders), which includes entities such as peritendinitis and tendon degeneration. Several factors have been described as a cause of AT. Intrinsic factors such as age, gender, rheumatic diseases, body mass index (BMI), cholesterol and glucose blood levels, or antibiotic intake may interact with other extrinsic factors such as malalignment, training errors, unloading or inappropriate load, in the development of degenerative tendinopathy. Although its management remains unclear, several conservative treatments have been proposed, with exercise and load management as the cornerstone for functional recovery. But the question is: can it be enough once the extracellular matrix and ground substance is profoundly affected?

    Methods A 33-year-old male amateur soccer player (176 cm, 78 kg BMI=25.2), presented to the clinic reporting 4 months of left Achilles pain, which started for the first time after 10 days of immobilisation following a gastrocnemius MTJ tear. He reported antibiotics intake 4 days before injury due to dental problems. The patient was unable to stand on the affected leg, had ankle ROM limitation (dorsiflexion=90°), gait alterations, 1 h of morning stiffness, and constant pain and difficulty with daily activities, with a VISA-A score of 8/100 and a SF-36 outcome of 40.18%, revealing high limitations in physical health measures. Imaging diagnosis (MRI and colour Doppler ultrasound) revealed a severe degenerative mid-portion Achilles tendinopathy, with a thickening of the affected tendon (143 mm) compared to the asymptomatic tendon (65 mm), showing severe neovascularisation, matrix disorganisation and hypoechoic areas. Blood analysis revealed no significant results in cholesterol (180 mg/dl) and glucose levels (77 mg/dl). Previous NSAIDs and physiotherapy (electrotherapy and manual therapy) had failed.

    The patient was managed with a conservative treatment programme, divided into 4 main areas: 1. Orthotics (4 cm of heel raise); 2. Medical treatment (ibuprofen post-exercise and a single methylprednisolone injection in paratenon at the beginning); 3. An intensive exercise programme (consisting of a progression from isometric to concentric then eccentric strengthening, combined with electrostimulation (ES)); and 4. Functional re-training and general health measures (aerobic exercise and weight loss). Follow-up measures were taken over 1 year, recording SF-36 results at the beginning and end, VISA-A score once a month, and colour Doppler ultrasound examination every 6 weeks. Progression criteria for exercise were tendon pain and morning stiffness.

    Results The patient reported a marked improvement in pain and function in the first 4 weeks of treatment (VISA-A=65), that consisted of isometric and concentric exercises, progressively adding external load, cycling, ES and stretching 3 times/week. Eccentric exercises were started in week 6, stretch-shorten cycle exercises in week 9, and he was able to run 14 weeks after the beginning of treatment (VISA-A=75). From then, the programme was modified once a week until he was able to play soccer in month 7 (VISA-A=100). He recovered full ankle ROM after 3 months, and had some minutes of morning stiffness until month 6. Colour Doppler ultrasound showed absence of neovascularisation after 12 weeks, and a progressive reduction of hypoechoic areas and a better fibre alignment was seen. One year later the tendon remained thickened, but had decreased from 143 to 125 mm (the paratenon was the most thickened structure), and SF-36 outcome also improved from 40.18% to 84.06%. BMI also decreased from 25.2 to 22.9.

    Discussion A progressive programme of exercises focused on tendon strengthening and recover of musculotendinous function was effective in the treatment of a severe degenerative Achilles tendinopathy. Medical and orthotic treatment might be important at the beginning to reduce pain, and causative factors such as antibiotics or previous immobilisation should be taken into account when designing a programme of exercises. Tendon structure recovered and was completely functional after 7 months, despite the tendon remaining thickened. In a severe degenerative tendinopathy like this, surgical treatment could be an option to restore tendon structure, but there are risks that should be taken into account. However, as shown in this case, exercise remains the most powerful stimuli for tendon function recover.

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