Case Study

Tendon injury and the continuum. What hurts, and why?

July 21, 2020

Tendon injury: multiple findings within the same tendon.


A 62 year old competitive badminton player presented having injured his left Achilles while playing approximately 6 weeks earlier. He had been sore since the injury despite conservative management and was referred for an ultrasound examination of the left Achilles.

Ultrasound examination (Philips iU22, L12-5 MHz and 15-7 MHz Hockey Stick transducers) of the left calf was performed. The examination suggested Achilles tendinopathy, including a partial tear and reactive component, and associated paratenonitis.

Key findings (Images A-C) included: “the Achilles tendon has fusiform thickening (10 mm AP thickness), the medial part is reduced echogenic with loss of fibrillar echopattern, increased vascularity, paratenon thickening with vascularity, and an ill-defined laminar intrasubstance tear (approx. 19 mm long x 5 mm axial). The abnormal tendon has 70 mm² cross sectional area compared with a total tendon cross sectional area of 157 mm². The lateral part of the tendon maintained a fibrillar echopattern but also had collagen fascicular discontinuity and microcystic change.

When reassessed approximately two months later, the Achilles tendon showed significant change consistent with resolution of reactive tendinopathy, paratenonitis, and healing of the intrasubstance tear.

Key findings (Images D-F) included: “the Achilles tendon thickening has reduced (AP thickness 7.9 mm now 10 mm previously), the medial abnormal area is less prominent, and now has microcystic change and collagen fascicular discontinuity. Only one vessel is within the tendon, no paratenon vessels and the ill-defined laminar intrasubstance tear (19 mm long x 5 mm axial) is no longer identified. The total tendon cross sectional area is reduced to 126 mm² compared to 157 mm².


This case illustrates some important aspects regarding planning the management of tendinopathy within a continuum model, according to Cook and her collaborators.  Two key points to examine are the source of nociception, including findings of structural change and vascularity, and the distribution of tendon pathology within a tendon and in this case, the paratenon.

Tendinitis is a term that implies that a tendon is inflamed, and more than that, that the cause of pain is the inflammation itself.1  This is not to say that inflammation is not present within an injured  tendon, and in fact inflammatory cytokines are known drivers of tendon cell changes.1–3 Rather, the search for the illusive nociceptive driver of tendon pain appears to currently rest with the tendon cell itself when in the reactive state rather than with inflammatory mediators.3

Related to this point is the fact that the painful, reactive tendon appears to thicken in a homogeneous way without disorganisation of structure, while a tendon with structural evidence  of disrepair, such as collagen fascicular discontinuity, may also be thickened.4 Pain experienced by patients in either of these stages of the continuum appear due to the reactive tendon cells themselves, and the decision made to manage pain, structure, or both.cf3 Further, the presence of vascularity within a tendon does not appear to be diagnostic of tendon pain, where neovascular structures were apparent in both painful and painless tendons.5 It would therefore be tempting to suggest that neovascularisation isn’t important, notwithstanding evidence that neovessels may be partially responsible for tendon degeneration,6,7 and to ignore them in our management planning.

You will have noted that vascularity decreased over two months. This may suggest that while some vascularity was likely associated with degenerative tendinopathy, the paratenonitis in fact represented an injury superimposed on the structurally compromised tendon. Snedeker & Foolen8cite evidence showing that in the presence of injury, cells from the epitenon and endotenon migrate into the wound in order to promote healing, and this is likely to be represented by vascular structures arising from the paratenon. We suggest that vascularity within tendons should therefore be monitored, especially in the presence of paratenonitis.

Degenerative tendons may have areas that are reactive, ‘reactive on degenerative tendinopathy’3 and therefore painful. Further, a tendon may exhibit several stages of the continuum concurrently.4  Add to that the evidence of tears the ultrasound imaging provided, and this case illustrates that while the continuum model of tendinopathy is helpful in directing management of tendon pain and structural compromise, there is still much to consider in a tendon patient.


Coming in the next post:

The next case will unpack a presentation that is found in up to 5% of people during routine imaging of the shoulder, and we think maybe more.  Hint: it’s not something that is within the subacromial ‘space’.




  1. Rees JD, Stride M, Scott A. Tendons–time to revisit inflammation. Br J Sports Med. 2014 Nov;48(21):1553–7.
  2. Dean BJF, Gettings P, Dakin SG, Carr AJ. Are inflammatory cells increased in painful human tendinopathy? A systematic review. Br J Sports Med. 2016 Feb;50(4):216–20.
  3. Cook JL, Rio E, Purdam CR, Docking SI. Revisiting the continuum model of tendon pathology: what is its merit in clinicalpractice and research? Br J Sports Med. 2016 Oct;50(19):1187–91.
  4. Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinicalpresentation of load-induced tendinopathy. Br J Sports Med. 2009 Jun;43(6):409–16.
  5. Tol JL, Spiezia F, Maffulli N. Neovascularization in Achilles tendinopathy: have we been chasing a red herring? Vol. 20, Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA. Germany; 2012. p. 1891–4.
  6. Järvinen TA. Neovascularisation in tendinopathy: from eradication to stabilisation? Vol. 54, British journal of sports medicine. 2020. p. 1–2.
  7. Tempfer H, Traweger A. Tendon Vasculature in Health and Disease. Front Physiol. 2015;6:330.
  8. Snedeker JG, Foolen J. Tendon injury and repair – A perspective on the basic mechanisms of tendon diseaseand future clinical therapy. Acta Biomater. 2017 Nov;63:18–36.


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