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Tendinopathies

Tendinopathies: case study

The eccentric training programme first proposed by Alfredson (1998)(1) has gained widespread acclaim as we seek exercisebased rehabilitation for Achilles pain. However, this recipe will not work for everyone. The story of this 19-year-old sprinter with acute and severe tendoAchilles (TA) pain shows that we need a sophisticated approach to diagnosing the exact nature of the pathology before prescribing an off-the-shelf management programme.

The sprinter’s background

Sean was a talented junior athlete, who had been an under-age long jumper and track athlete (all distances up to 800 metres). He’d played competitive basketball up to the age of 16.

He came to see me with a four-day history of left-sided tendo-Achilles pain, after an arduous training session in preparation for the European track season. Just prior to the acute episode of pain, Sean had taken two weeks off training because of illness, and had gone straight back into plyometric drills.

He had been experiencing some mild TA pain and stiffness for the preceding two months but had not done anything about it. He was in good general health and had no personal or familial history of diabetes or inflammatory arthropathies.

The previous year, Sean had had a twomonth episode of central and left-sided nonspecific low back pain, which had been successfully managed conservatively. Around the same time, he’d also suffered three months of recurrent left-sided hamstring and calf tightness with no evidence of any muscle tear. This was successfully treated with nerve gliding physiotherapy techniques.

Sean was now in the pre-competitive phase of a periodised training programme. So in addition to his general conditioning and ‘core stability’ sessions, he was focusing on plyometrics and track speed sessions, especially starting-block work.

Sean’s pain was in the mid third of his left Achilles tendon, and he had general feelings of ‘tightness’ in left calf and hamstrings. He had ‘first step’ pain and stiffness in the mornings. Running was painful, especially at takeoff and when decelerating.

Investigation

Below is a summary of my findings: Lumbar spine and pelvis

* Posteriorly rotated left ilium (hip bone).

* Weak left gluteus maximus.

* Poor activation/isolation of transversus abdominis (deep abdominal stabiliser).

* Positive left active straight leg raise test (ASLR), demonstrating weakness in his ability to transfer load through his pelvis.

* Positive slump test on left (-30°) – possibly secondary to his history of low back pain.

Lower limb (static)

* Left-sided quadriceps and calf atrophy.

* Knee-to-wall measure of ankle dorsiflexion was 5cm on left (compared to 9cm on right).

* Active knee extension measure of hamstring length was -25o on left (-5° on right) .

* High and stiff medial longitudinal arch of the foot.

* Tight left gastrocnemius.

Lower limb (dynamic)

* Early left heel-off when walking (probably to protect against pain, but exacerbated by tight calf).

* Poor control of single-leg squat.

Pain

* Pain when walking (subjective score 3/10), with marked increase when he progressed speed to a run (6/10).

* Pain after four single-leg heel raises on left (single-leg heel raise endurance of 32 on right).

* Pain after one hop on left (8/10).

* Pain on palpation of mid-third of Achilles tendon.

* Some ‘lumpiness’ around the painful area, consitent with acute intratendinous swelling.

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Diagnosis

I was satisfied that the tendon was the source of Sean’s pain. The pain was localised and when I palpated away from the central part of the TA, it was pain-free, helping to exclude other secondary sources such as fat pad or the retrocalcaneal bursae.

I concluded that Sean’s signs and symptoms were consistent with acute proliferative Achilles tendinosis, a diagnosis confirmed by an ultrasound scan. This form of tendinosis is associated with palpable mid-tendon swelling and a rapid onset of symptoms brought on by loading, in contrast to the long history of grumbling pain that is a feature of chronic, degenerative tendinosis. This is an important point to recognise, because the treatment of these two conditions is very different, particularly in the early stages.

Current thinking about tendinopathy lends support to the notion of a maladaptive response to overload being responsible for tendon structure breakdown. In proliferative tendinopathy, the activity of tenocytes (the cells responsible for synthesising much of the tendon structure) increases, leading to an accumulation in ground substance, but lacking the structural integrity capable of withstanding load(2). Because the growth factor TNF (tumour necrosis factor) is thought to be key in this tenocyte proliferation(3), some elite sports physicians employ a ‘triple therapy’ of doxycyclin (an antibiotic), green tea and ibuprofen (an anti-inflammatory), all of which are said to inhibit the destructive cycle of tenocyte hyperactivity.

There is also an increase in the cartilage protein aggrecan within the tendon(4). This seems to be the body’s attempt to ‘toughen up’ the tendon by giving it cartilage-type properties. But aggrecan attracts water, which ‘swells’ the tendon, further cleaving apart the tendon scaffolding and reducing its ability to withstand load.

Sean had numerous risk factors for the development of acute Achilles tendon pain:

* Involvement in jumping sports as an adolescent.

* Biomechanical factors (see Table 1, above).

* Stress shielding, in which the collagen fibres in a tendon lose strength when de-loaded. This could well have occurred in the fortnight that Sean had off due to his illness. Going straight back into plyometrics after this was perhaps not the greatest of ideas.

While the past history of low back pain may not have been the primary factor in Sean’s Achilles problem, it probably played a role in the development of the altered muscle tone/lengths. This would affect the function and efficiency of the left-sided kinetic chain, potentially contributing to the increase in load placed upon the TA. It is the combined effect of these imbalances that might have been to powerful for Sean’s body to withstand.

Management plan

Sean was scheduled to compete in eight weeks’ time, so I needed to settle the acute symptoms quickly. My main aim initially therefore was to offload the aggravated tendon, using the following strategies:

* Decreasing TA excursion locally by limiting the amount of stretch put on the tendon and modifying the training load;

* Addressing the soft tissue restrictions;

* Reducing the lumbo-pelvic contributions to kinetic chain overload; l Beginning a lumbo-pelvic stability programme.

For a detailed summary of the management plan for weeks 1-2, see Table 2, over.

By the end of the second week, Sean’s walking was pain-free and his morning stiffness was reduced (although still present). He was able to run in a straight line without pain and his hop pain was 3/10.

His pelvic alignment had been corrected and maintained and he was reasonably proficient with his lumbopelvic local stabiliser contractions. His active knee extension had increased to -15 degrees and his knee-to-wall had increased to 7cm.

Weeks 3-5

My treatment aim now shifted to carefully increasing the load through the lower limb, remaining vigilant about any increase in symptoms, which I assessed using the VISA-A scale(5). For a summary of the treatment strategy during this period, see Table 3, page 7.

By the end of this period, Sean was only symptomatic when subjecting his Achilles to moderately high load. He was able to run at about 80% of his normal speed, although he did still have some pain on acceleration and deceleration.

His pain was worse when not wearing the SIJ compression belt, providing more evidence that distal symptoms can be influenced further up the kinetic chain. Facilitatory glutes taping also improved his tendon symptoms.

Encouragingly his slump test had almost normalised. His knee-to-wall measure was equal bilaterally, his active knee extension was -10 degrees on the left and he had maintained good pelvic alignment.

Weeks 6-10

Ideally we would be looking to settle the proliferative process gradually and build up tendon loading stresses to allow for tendon matrix remodelling. Unfortunately, Sean did not have that luxury of time: he needed to compete. The challenge to the sports physiotherapist in such cases is to enable the athlete to function at a level that the pathology ordinarily would not permit.

This strategy is not without risks, particularly if the athlete returns to high load activities prior to the resolution of the proliferation.

I needed progressively to load Sean’s Achilles to develop its ‘load-resilience’, at the same time progressing his lower limb and core strengthening/stability programmes.

We progressed the functional loading of the tendon over the next six weeks as follows:

* Straight line running (increasing speed and then adding off-line drills);

* Heel drops (moving from double leg to single leg and with increasing speed);

* Jumping (initially on the spot, then jumps for height and distance as well as on and off a step);

* Hopping (progressed as for jumping);

* Bounding (initially straight line and then incorporating changes in direction).

Sean performed these ‘tendon-loading’ sessions every three to four days and I monitored the 24-hour pain response closely to ensure we did not fall into the trap of overload. We were aiming for a pain report of 3/10 or lower. On the days that Sean reported pain of more than 3/10, he was not allowed to perform high tendon loading exercises.

Sean had a tendency to lose his lumbopelvic stability when fatigued (he would flex his lumbar spine) and so we needed to improve not just awareness of this but the endurance of his local muscular stabilisers under increasingly demanding conditions. He found taping and video feedback really helpful with this.

Sean’s lumbo-pelvic stability rehabilitation needed to be continued to the point where he was stable under both low and high load conditions with fatigue resistance in both the ‘inner’ and ‘outer’ units. He was continuing with the quads, glutes and calf hypertrophy and strength programme designed by his strength coach.

Ten weeks after he first presented, Sean was back to full competition and training. He was asymptomatic even with high tendon loading, although he did occasionally complain of niggles if he loaded the tendon on more than two consecutive days. His VISA-A score had climbed to 91/100 (from 16/100 10 weeks ago).

By this time, he had a negative ASLR and a negative slump test. He still had a calf strength deficit on the left side (heel raise = 33, compared to 42 on the right). All other dysfunctions that were noted at his initial presentation had been resolved.

His sprinting coach commented that his block starts were faster than ever and that his medial-lateral pelvic movement during running had reduced, both of which are excellent technical improvements which he attributed to the work Sean had put in during his rehabilitation.

Pitfalls for Sean to avoid

Given the sport that Sean is involved in, and the brutally unforgiving nature of the training required at elite level, Sean needs to be wise about how his training is scheduled, so that he does not overload the tendon (or any other area). His overall training and competition programme should be planned with this in mind, scheduling specific high, low and medium tendon loading days. Examples of high load activities in sprint training are:

* starting-block work

* bend running (particularly on the inside lanes because of the torsional stress placed on the tendon)

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l baton change-over practice (because of the rapid deceleration required). To build these considerations into the training programme clearly demands excellent communication between all members of Sean’s performance team. Sean must understand the importance of reporting any increases in his symptoms. It is advisable to monitor these symptoms with regular completion on the VISA-A scale.

Conclusion

Sean’s case demonstrated to me the value of addressing the entire kinetic chain in the management of a local tissue disorder. The rapid relief in his symptoms would not have been possible had treatment been focused solely on the Achilles, because it would have remained overloaded from the weight of his kinetic chain dysfunctions.

An eccentric loading programme would most likely have increased Sean’s symptoms. Acute proliferative Achilles tendinopathies need to be settled rather than subjected to the kind of load that eccentric training would involve. Our greater scientific understanding of tendinopathies gives sports clinicians a far better base from which to customise management strategies for every injured athlete.

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References

1. Alfredson H, Pietilä T et al ‘Heavy-Load Eccentric Calf Muscle Training For the Treatment of Chronic Achilles Tendinosis’. The American Journal of Sports Medicine 1988, 26, 360-366.

2. Cook JL, Feller, JA et al ‘Abnormal tenocyte morphology is more prevalent than collagen disruption in asymptomatic athletes’ patellar tendons’. Journal of Orthopaedic Research, 2004 22, 334-338.

3. Almekinders LC, Banes, AJ ‘The use of growth factors in tendinopathies’. In N Maffulli, P Renström, Leadbetter, WB (Eds), Tendon Injuries: Basic Science. 2005 New York: Springer.

4. Corps AN, Robinson AH et al ‘Increased expression of aggrecan and biglycan mRNA in Achilles tendinopathy’ 2006 Rheumatology, 45, 291-4.

5. Sayana MK, Maffulli N ‘VISA-A. An outcome measure for Achilles tendinopathy’. Journal of Bone and Joint Surgery British Volume 2005 87b (supp III), 375378.

Tendinopathies