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Just completed a lower limb tendon course in Melbourne with a great group of therapist, looking forward to Perth and Melbourne courses over the next few weeks.
Special blog edition for tendinopathy blog no 8 this week... an article that I have recently written for the Australian Sports Physio magazine about clinical reasoning in Achilles tendon rehab, with a focus on the key factors that we should consider. Definitely joined some dots in my mind when I was writing it!
Here it is...hope you enjoy
All the best
How do we maximise patient outcomes in tendinopathy management? Is it about better rehabilitation, retraining their movements, or identifying other factors that are not related to load but impact on pain? Probably all of the above. As thinking clinicians, we strive to answer these questions and to treat every Achilles tendinopathy patient slightly differently to maximise their treatment outcome. Sometimes we can clearly see the ‘big fish’, other times we cannot. There is significant skill in identifying relevant factors that will influence patient outcome.
This short article will consider a simple model for identifying key factors, building on an existing model by Coombes et al. (2009)7. These authors focused on lateral elbow tendinopathy and highlight changes in the tendon, pain system and motor system (see figure below). They suggest that clinicians ‘should seek to identify the relative expression of local pathology, pain and motor system dysfunction in individual patients, so that treatment strategies may be better matched to the clinical presentation’. A very sensible suggestion. Here we will attempt to apply this thinking to Achilles tendinopathy conservative management.
Pain system considerations
Typical tendon pain is associated with sudden changes in tendon energy storage and compressive loads, warms up or improves with activity, and is localised to the tendon5, 23. These features may be less clear if other tissues are involved, for example, the paratenon, and it is important to identify contribution from other tissues as management may vary (e.g. anti-inflammatory treatments for a paratenon component). The focus of this article is not on diagnosis, but rather other factors to consider when in the presence of ‘typical’ tendon pain.
1. Pain mechanisms and individual factors
In the Coombes model they define pain system changes as ‘arising in both the peripheral and central nervous systems, possibly involving both nociceptive and non-nociceptive processes’. Let’s broaden this category to include pain mechanisms and an individual’s sensitivity to pain.
There are arguments that there is a nociceptive driver because tendon pain is load-related and does not display key features of central sensitisation such as spreading or shifting pain23. What is important to remember, however, is that there is always a central component to pain – the brain can amplify or dull nociceptive danger signals19. Take the example of a runner with an obsessive personality. They introduce a new speed session to their training and feel Achilles tendon pain the following day. PANIC sets in. They don’t move, they stress about the pain, they catasrophise, perhaps they see the wrong clinician who tells them they may have done very serious damage and need to rest. The pain is amplified. The point is even short term tendon pain can be centrally modulated and this may or may not involve typical features of central sensitisation (spreading and shifting pain, absent or disproportionate load-pain relationship).
In a very recent study, conditioned pain modulation (the phenomenon of a reduction in pain after a painful stimulus, in this case cold water immersion) was impaired among Achilles tendinopathy patients, indicating a change in central pain processing27. These patients had typical load-related and localised Achilles pain. The point is central modulation may be a feature of Achilles tendinopathy even when symptoms are typical.
As clinicians, we need to be aware of factors that may influence the emergence, modulation and persistence of pain. These include reduced sleep, obesity, stress/anxiety, fears and beliefs, family and work circumstances, behaviours (e.g. fear avoidance), negative coping strategies (e.g. ignoring pain or losing hope), diet, autoimmune issues (e.g. irritable bowel), fatigue21. An example from the Achilles tendinopathy literature comes from a study by Silbernagel et al. (2011)25. They found that calf raise function (calf raise work) was negatively associated with fear avoidance beliefs measured with the Tampa Scale. Currently we are focused on managing tendon load and biomechanics but a priority for all tendinopathy patients should be to understand and then manage (where possible) factors that influence pain. Addressing motivation, reassurance, education, strategies for improving sleep and stress, considering diet, general exercise and health can go a very long way.
Where do classic tendon risk factors fit in? These include load (change in energy storage and compressive load), biomechanical factors and systemic factors such as lipid levels, obesity and age. Of course we should consider these, and I will discuss biomechanics below. Systemic factors are thought to influence tendon capacity to withstand load, but it is easy to also see the overlap with factors that influence pain.
2. Irritability and load tolerance
A key consideration in managing Achilles pain is identifying movements and functions that are sensitised (painful) and the response to load. Typically, Achilles pain flares after energy storage loading (e.g. the day after a run). If the flare lasts for more than 24 hours this is defined as ‘irritable’ pain17. Patients with irritable pain are commonly sensitised to hopping and sometimes calf raises. Although they may be sensitised, lower load activities such as calf raises do not typically cause a flare in Achilles tendon pain; but in some patients they may - ruling out other tissue diagnoses, this is most likely explained by dominant central pain mechanisms.
Regardless of pain mechanisms, defining which movement and functions are sensitised, and irritability to load, will guide management, perhaps more than any other factor. The goal is to achieve load tolerance to movement and functions relevant to the individual. Load tolerance is a concept related to irritability. A person is load tolerance to a movement or function if it can be performed with minimal pain, and there is less than 24 hours of pain flare post the activity17. Minimal pain is often defined as less 3 or 5 or out of 10, but another approach is to ask patient not to exercise beyond what they are willing to accept.
What is the best way to achieve load tolerance? Key interventions include load modification (reducing load that leads to irritable tendon pain flare in the short term), education as discussed above, as well as exercise. A recent study in the patellar tendon showed a greater post exercise analgesic effect with isometric compared with isotonic exercise22. An interesting finding in this study was motor cortex inhibition in the patellar tendon group that improved alongside pain improvement, suggesting motor cortex inhibition (a central motor adaptation) is part of the tendinopathy pain experience.
3. Progressively loading the sensitised tendon
Progressing on from isometric exercise, the common approach in tendinopathy rehabilitation is to progressively load the sensitised tendon, including the introduction of isotonic and tendon energy storage loads1, 3, 10. An interesting phenomenon from the Achilles tendinopathy rehabilitation literature is that outcomes seem to be similar when comparing different loading programs16. Bayer et al. (2015)3 recently found that whether you do Alfredson eccentrics or heavy slow resistance loading (see figure below) pain and function outcome (VISA scale) at 12 months were similar. These are hugely different programs; the HSR program involves much higher load and has been shown to have a greater effect on tendon turnover in the patellar tendon than a the Alfredson eccentric program13. This suggests that tendon adaptation may not explain clinical outcome. There are likely to be muscle effects that we know parallel clinical improvements in Achilles tendinopathy rehabilitation16, but also pain system effects such as reduced peripheral sensitisation or also changes in self efficacy, fear of movement and central sensitisation20. The fact that virtually all studies in the literature progress rehabilitation based on load tolerance (much like a graded exposure approach) supports pain system mechanisms.
Pain system key point: We often think about biomechanics and load with tendons. Addressing cognitive-emotional and other factors that influence pain and targeting our loading towards the pain system as well as tissues can be very powerful.
Motor system and biomechanics considerations
Motor system impairments vary greatly between Achilles tendinopathy patients. Common impairments reported in the literature include reduced calf muscle function (e.g. peak torque) (ref) and reduced hopping performance18, 28. Reduced calf muscle torque has also been shown to precede pain, so may be a risk for Achilles tendinopathy15. Silbernagel et al. (2006)26 showed that these deficits remain after a comprehensive rehabilitation program. This suggests that full restoration of motor impairments in not necessary for improvement in Achilles tendon pain.
Several biomechanical factors have been associated with Achilles tendinopathy including increased or decreased dorsiflexion range of motion (e.g.12), foot pronation (e.g. 24), and poor running technique (e.g. overstride, excessive dorsiflexion in midstance)2. It is difficult to know whether these precede or are secondary to pain as most studies are cross-sectional. Addressing these factors may improve kinetic chain function or reduce Achilles tendon load. For example, peak DF in running is proportional to Achilles load11, and excessive dorsiflexion can be addressed in several ways. First, run retraining (increase step rate) can reduce peak DF range in midstance14. Alternatively, through range eccentric training has been shown to improve calf function closer to end range (shifting the length tension curve) meaning the Achilles tendon is supported by a stronger muscle in this excessive DF range8. Yet another approach would be to address hip flexor restriction or weakness that may limit hip extension in terminal stance, therefore causing excessive ankle DF.
Motor system and biomechanics key point: Motor impairments and biomechanics are often but not always relevant. We should address obvious deficits (which requires careful and thorough assessment).
Now let’s not forget the tendon. Aside from potentially assisting to confirm diagnosis, how does knowing the state of the tissues actually help our conservative management reasoning? The popular continuum model proposes that reactive tendinopathy (increased cells and ground substance) precedes degenerative pathology (matrix disruption, neurovascular ingrowth)6. (Please note, I am referring to reactive and degenerative pathology very distinctly from pain.) Reactive pathology is thought to be reversible so it makes sense to try and prevent progression to degenerative pathology6. This involves good education and carefully planned load progression (i.e. avoiding peaks and troughs). We could also argue for loading a degenerative tendon in an attempt to adapt the matrix and improve tendon function6. We know that heavy isometric and isotonic load will adapt normal tendon over 8 or more weeks4, but little is known about pathological tendon. Tendon pathology on imaging (ultrasound and MRI) does not seem to change appreciably with rehabilitation9, but this does not rule out improved quality of the remaining normal tendon; so there may be a rationale to load degenerative tendon. The key question is whether knowing the imaging stage is essential. Probably not, because you are going to be careful with load progressions anyway, and heavy load may well be part of the equation for load tolerance or biomechanical reasons.
Tendon tissue key point: tendon pathology is a consideration but arguably has little influence on rehabilitation clinical reasoning.
Achilles tendinopathy is a complex pain state involving peripheral and central pain mechanisms. A sensible first step is to address factors that may influence pain including stress, fear, fatigue, sleep, among many others, in order to create an environment that supports recovery. Regardless of pain mechanisms, the primary approach is graded exposure - limit sensitised postures and movement (in the short term) and then progressively load to develop ‘load tolerance’. The motor system and biomechanics may be critical considerations some of the time. And the tendon tissue state is probably the least important consideration in conservative management reasoning. This is Achilles tendinopathy rehabilitation turned on its head; consider pain and the person first.
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Clinical gems and awesome management models. Your patients will love you for it!