OCS Field Guide: A PT Podcast

Midportion Achilles Tendinopathy CPG: Pathology, Epidemiology, and Diagnosis

November 08, 2022 David Smelser and Austin Kercheville Season 1 Episode 33
OCS Field Guide: A PT Podcast
Midportion Achilles Tendinopathy CPG: Pathology, Epidemiology, and Diagnosis
Show Notes Transcript Chapter Markers

We have a ton of information on midportion Achilles tendinopathy, which means it is likely to be an ankle/foot diagnosis that shows up quite a bit on the OCS exam. Today we walk through the first half of the 2018 CPG, including pathoanatomic factors, epidemiology, risk factors, clinical course, diagnosis, and outcome measures.

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Hello, future orthopedic specialists, and welcome back. Today we’re going to take a look at the Midportion Achilles Tendinopathy CPG. There has been a lot of interesting work done in the area of Achilles tendinopathy research, so I’m excited to take a look at this diagnosis with you. We’re going to cover the first half of the CPG today, and we will cover the treatment section in our next episode.

A quick note as we get started: you will see that this CPG is specific to midportion Achilles tendinopathy. This is distinct (and much better studied) than insertional Achilles tendinopathy. Throughout this CPG and this episode, when we say “Achilles tendinopathy,” we’re talking about the midportion variety. Let’s start by looking at pathoanatomic factors and epidemiology.

Achilles tendinopathy is usually considered an overload pathology. The CPG indicates that it appears to be caused by “an excessive mechanical stressor, such as tensile loading and/or shearing, which initiates pathological changes in the tendon. These pathological changes can include tenocyte proliferation with tendon thickening, neovascularity, collagen fibril thinning and disorganization, increase of non- collagenic and fibrocartilage matrix, fat deposition, altered fluid movement, and overproduction of nitric acid with tissue apoptosis. Failure to control hyperthermia that results during exercise, as tendons convert some of the stored energy to heat, can also contribute by causing local cell death.” To summarize those features in slightly more natural terms, once the process gets started, we note extra tenocytes—or cells which lay down tendon tissue—and neovascularity—or the proliferation of new small blood vessels—both of which appear to be connected to the tendon thickening usually noted in Achilles tendinopathy. We also have collagen thinning, disorganization and increase in non-collagenic and fibrocartilage matrix, and fat deposition, all of which contributes to a weaker tendon and less efficient load transfer. We also have altered fluid movement, overproduction of nitric acid, and abnormally high amounts of heat, which causes cell death. The CPG says, “These changes lead to a decrease in tendon stiffness and strength, ineffective force transfer, thereby affecting central nervous system motor control.” Understanding this process—and being able to explain it to your patients—helps explain why tendinopathies tend to respond well to loading to rebuild tendon stiffness, which we will talk about shortly. Also remember that pathophysiology (together with pain science) is 10% of the exam, so you should have a general grasp on what is going on whenever we have this much insight into a pathological process. Note that while inflammation can be present at different points in this process, it is actually tissue changes occurring in the tendon that drive this pathological process, not inflammation. Interestingly, the CPG notes that the extent or severity of these tendon changes is NOT consistently related to the severity of the clinical presentation, so seeing a significantly thicker tendon during physical exam or with imaging does not necessarily correlate to worse patient presentation.

In addition to these basic tissue changes, the CPG also notes that the plantaris tendon and peritendinous nerve structures may impinge on the medial aspect of the thickened Achilles tendon, which may contribute to pain. Studies have noted that genetic variations representing an abnormal neuronal phenotype has been linked to Achilles tendinopathy. Apparently when these individuals experience a tendon injury, the nearby nerves grow into the tendon and are abnormally sensitive to pain mediators. Other genetic factors that cause abnormal collagen production may also play a role as well.

Most often, Achilles tendinopoathy affects active individuals. Runners appear to be the most commonly affected cohort, but athletes from a wide variety of sports can also be affected. Symptoms usually appear during training rather than during competition. And although athletes are the most commonly affected, sedentary individuals can develop Achilles tendinopathy as well. The mean age of Achilles disorders in general is 30 to 50 years old. 

Let’s talk risk factors. The CPG notes that risk is multifactorial and appears to be a combination of intrinsic and extrinsic factors. They cite evidence for a huge number of risk factors. Some of these include: older age, obesity, hypertension, hyperlipidemia, diabetes, presence of any systemic disease, genetic factors, altered foot biomechanics, abnormal subtalar range of motion, abnormal dorsiflexion range of motion, decreased plantarflexor strength, neuromuscular deficits in the LE in general and the gluteal muscles specifically, abnormal LE kinematics, use of rigid insoles compared to shock-absorbing insoles, fluoroquinolone antibiotic use, environment, playing surfaces, and the physical demands of sport participation. That’s way too much to memorize, and I think in general you can see that just about anything that could affect the Achilles tendon has some evidence to show that it does affect the Achilles tendon. I will call your attention to a couple specific factors here that stand out to me. You will note that hyperlipidemia is a risk factor. We’ve seen for a while now that high cholesterol causes fatty deposits to develop in the body’s tendons, and it tends to affect the Achilles tendon more than others. So hyperlipidemia is a significant risk factor for Achilles tendinopathy, and it’s also a significant risk factor for Achilles tears, ruptures, and rotator cuff tendon tears. Next, note the risk factor related to insoles. A very large military study gave some new recruits rigid insoles and others shock absorbing insoles, and the group with shock absorbing insoles had 50% fewer cases of Achilles tendinopathy. So using shock absorbing footwear or insoles is a potentially promising preventative treatment. Lastly, note that fluoroquinolone use is associated with Achilles tendinopathy. This is an antibiotic; the generic names typically end with “-floxacin,” and one common brand name in this class is Cipro. For decades now we’ve been able to directly link fluoroquinolone use to Achilles tendinopathies and tendon tears and ruptures, so we think it would be a very good idea to remember the link between fluoroquinolones and tendon injuries for the OCS. If you want more information about this and other medications we think are important to know, we have a bonus episode on that very topic on our Patreon.

Next we will talk about clinical course. The clinical course of Achilles tendinopathy is quite varied. It seems that most episodes are very brief, but some can be very long. In one study of elite soccer players, median missed participation due to Achilles tendinopathy was 10 days, and the mean was 23 days. In a large cohort of runners, median time to recovery was 82 days, with a minimum of 21 days and a maximum of 479 days. So you can see that most athletes have fairly brief episodes, but some will have chronic problems. The good news is that 5-year outcomes are pretty good. Most people managed with heavy load calf strengthening demonstrate good recovery that lasted at 5-year follow-up, although some of those individuals continued to have some mild pain. So for prognosis, you should know that most people have fairly brief episodes of tendinopathy, and most who are treated with heavy exercise will have good long-term outcomes, but there are a few who will continue to have some chronic pain and difficulties. The CPG reads, “While most patients will improve, mixed levels of recovery can be anticipated.”

Let’s move on to diagnosis. With C-level evidence, the CPG recommends that the following symptoms and findings be used to rule in midportion Achilles tendinopathy: gradual onset of pain located 2 to 6 cm proximal to the Achilles tendon insertion, pain with palpation of the Achilles tendon, a positive arc sign, and a positive Royal London Hospital Test. A positive arc sign is when you have the patient lie prone with their foot off the table, identify the area that is the most swollen, ask the patient to dorsiflex and plantarflex, and see if the enlargement moves up and down with the tendon. If it does, this is a positive test. In essence, you’re concluding that the swelling is in the tendon and isn’t something else, like a callous on the skin. A positive Royal London Hospital test starts with the patient in the same position and the foot relaxed and slightly plantarflexed. Here, the therapist palpates to find the part of the tendon that is the most tender to palpation. Once the most tender area is identified, the therapist asks the patient to actively dorsiflex their foot while continuing to palpate the tender area. If the pain is decreased during active dorsiflexion, you have a positive test and should suspect tendinopathy. Individuals with Achilles tendinopathy tend to report significantly decreased or absent pain during an active Achilles stretch.

The CPG offers quite a few other diagnoses to consider in your differential diagnosis. They do not offer specific recommendations for ruling in or out these conditions other than saying that they should be considered if the presentation doesn’t fit everything we’ve just covered, or if symptoms are not improving with interventions. These other conditions include: acute Achilles tendon rupture, partial tear of the Achilles tendon, retrocalcaneal bursitis, posterior ankle impingement, irritation or neuroma of the sural nerve, os trigonum syndrome, accessory soleus muscle, Achilles tendon ossification, systemic inflammatory disease, involvement of the plantaris tendon, fascial tears, and insertional Achilles tendinopathy. I will take a quick stab at giving you some key differentiators to most of these even though the CPG doesn’t. An acute Achilles rupture is usually going to be palpable, and patients tend to have a positive Thompson test, meaning you squeeze their calf and their foot does not plantarflex in response. A partial tear will again be palpably different than tendinopathy; with a tear, you will feel a divot instead of thickening. Retrocalcaneal bursitis is tricky, but you might suspect it if the Achilles tendon isn’t thickened or if you can palpate the fluid-filled retrocalcaneal bursa. Posterior ankle impingement won’t have a tender, swollen area on the Achilles tendon, and it is going to present with pain during full plantarflexion, whereas Achilles tendinopathy will also have pain in a neutral foot position. Insertional Achilles tendinopathy will have a similar history, but the pain will be at or near the insertion instead of 2 to 6 cm proximal to the insertion. You can see that the key in these tends to be palpation of the Achilles tendon. Systemic conditions that can present with heel pain include ankylosing spondylitis, rheumatoid arthritis, and psoriatic arthritis, so look for signs of those as well.

I will also add to this list that if you are dealing with a child who has heel pain, your primary suspicion should be Sever’s disease, also called calcaneal apophysitis, which is a condition affecting the calcaneal growth plate in obese or very active 8- to 15-year-olds.

If you’re stuck clinically and need imaging to assess for some of these diagnoses, the CPG recommends ultrasound imaging or MRI. They note that there is conflicting evidence between the severity of tendon abnormalities on imaging and severity of symptoms, so don’t expect an ugly looking tendon to fare worse than a case that appears more mild on imaging.

Finally, they remind us that we should refer to an appropriate provider if we suspect rupture or systemic inflammatory diseases or anything else that would require more than PT intervention.

Next, let’s talk about outcome measures. We’ll cover patient-reported outcome measures first, and then functional outcome measures. To measure symptom severity, the CPG recommends the VISA-A, which stands for the Victorian Institute of Sport Assessment-Achilles. No MCID is mentioned here or in the earlier version of the CPG, but you should know that on the VISA-A, 100% represents full recovery, and a score of at least 80% usually represents good recovery and possible indication for discharge to self-management. For function, the CPG recommends the FAAM, or Foot and Ankle Ability Measure, and the LEFS, or Lower Extremity Functional Scale. The FAAM has an ADL subscale with an MCID of 8 and a sport subscale with an MCID of 9. Just like with the VISA-A, this instrument runs from 0% to 100%, where 100% represents no dysfunction. The Lower Extremity Functional Scale, or LEFS, is scored from 0 to 80, where higher scores indicate a higher level of function. The MCID is not reported in the CPG, but it is reported elsewhere as 9 points. You will notice that a lot of outcome measures have MCIDs of 9 points, which should really help simplify your studying.

So to summarize, the VISA-A was developed specifically to assess symptom severity with Achilles tendinopathy, and the FAAM was developed to assess function of the foot and ankle. Both of them run from 0 to 100%, with 100% representing no symptoms or dysfunction. The LEFS is a general lower extremity functional measure that runs from 0 to 80, with 80 representing full function. The MCID of the FAAM and the LEFS is both about 9—although technically the MCID of the FAAM’s ADL sub scale is 8, if you really want to be picky about it.

For functional tests and physical impairment measures, the CPG recommends using hop testing, heel raise endurance testing, ankle dorsiflexion ROM, subtalar joint ROM, plantarflexion strength and endurance, static arch height, forefoot alignment, and pain with palpation. Most of these make sense: the ones that jump out to me are static arch height and forefoot alignment, which are not measures that I would instinctively take. So for exam measures, think about the measures you would typically take for ankle strength and ROM, and add static arch height and forefoot alignment to that list.

Let’s wrap up with some practice questions.

A 42-year-old male recreational soccer player presents for initial evaluation at an outpatient clinic with a chief complaint of heel pain. He reports that the onset was insidious with no mechanism of injury. At first it was bothering him only after practice, but now it’s bothering him after about 10 minutes of practice. He reports sensations of stiffness and loss of calf strength. Which of the following examination procedures would be most helpful in differentiating between the patient’s most likely diagnoses?

A. Hop testing
B. Palpation of the Achilles tendon
C. Thompson test
D. Windlass test

The correct answer is B. palpation of the Achilles tendon. Hope testing is a recommended physical measure, but it does not help you differentiate between different Achilles or heel pathologies. Thompson test would help you determine if there was a full thickness Achilles rupture, but that is an unlikely diagnosis because there is no mechanism of injury and onset was gradual. Windlass test would help rule in plantar fasciitis, which is a possible diagnosis because we don’t have an exact location of the pain. However, Achilles palpation is going to help differentiate between far more diagnoses, including insertional Achilles tendonitis, partial Achilles tears, and retrocalcaneal bursitis.

The next question pertains to the same patient. You note that the patient is taking multiple medications. Which of the following medications could be implicated as a cause of this   injury?

A. Loratadine
B. Meloxicam
C. Metoprolol
D. Moxifloxacin

The correct answer is D. moxifloxacin. Recall that medications ending in -floxacin are fluoroquinolones, which are particularly implicated in Achilles tendonopathies, tears, and ruptures. Loratidine is the generic name for Claritin; it’s just an antihistamine. Meloxicam is an NSAID, and metoprolol is a blood pressure medication.

Last question: at initial evaluation, the patient scored a 62% on the VISA-A. After four weeks of treatment with therapeutic exercise, he now scores an 86%. Which of the following next steps is most appropriate?

A. Decrease load intensity of therapeutic exercise
B. Continue treatment with same plan
C. Discharge to HEP with progression of therapeutic exercise
D. Refer for MRI to evaluate for other conditions

The correct answer is C. discharge to HEP. This question hinges on your understanding that on the VISA-A, high scores are better, and greater than 80% is an indication for possible discharge to self-management. If the score had decreased, we might want to consider changing the intervention or referring for further testing. If the score had improved but did not meet a threshold for discharge, we would want to continue treatment. However, since we have improved and met a threshold for potential discharge, C. discharge to HEP is the best choice here.

That wraps up the first half of the CPG. We will be back soon with the second half: mid portion achilles tendinopathy treatment.

Pathoanatomic Factors & Epidemiology
Risk Factors
Clinical Course
Outcome Measures
Practice Questions