Rare case of symptomatic calcific tendinopathy of the origin of rectus femoris tendon

Discussion

In discussion of the differentials, a rectus femoris strain was ruled in as a possibility because of the location of the pain being on the anterior aspect of the hip. Pain and weakness on hip flexion were also consistent with this, as well as positive Ely and Thomas tests. The X-ray findings of amorphous calcifications were more consistent with calcific tendinopathy, but there is certainly a likelihood that this was overlying a strain. An avulsion fracture of rectus femoris origin was less likely, given the X-ray findings and the predominance of pain, not the weakness, in our patient. Femoroacetabular impingement was a possibility given the positive FADIR test. However, X-ray findings did not show the usual structural changes associated with this condition. An acetabular labrum injury would have tied along with femoroacetabular impingement, but on its own it may occur as a chronic or acute injury in a runner, presenting with similar clinical findings. Certainly, this can coexist with calcific tendinopathy, but it bodes well as an indicator that the patient had excellent response to physical therapy and was able to get back to running 20 miles a week, without needing surgery. Early osteoarthritis or degenerative joint disease is always a possibility with athletes and active individuals, although in this particular patient the location of the pain, the absence of limitation in passive range of motion and end point pain on internal and external rotation, as well as radiographs showing no findings consistent with degenerative joint disease, pointed away from this diagnosis.

The distribution of case reports of CTRFT, although coming from a small group, appears to suggest a predilection for women in their late 30s–40s.1 Yun et al also describe a study of six patients with CTRFT with a 1:5 ratio of men:women and a mean age of 41 years.3 The reason for this epidemiological predisposition is unknown.

Zini et al suggest that powerful and repetitive hip movements, such as with kicking athletes and American football players, predispose to injury within the proximal rectus femoris tendon, which then potentially gives rise to calcification in the long term.4

While the exact pathophysiological process is unknown, there are postulations that repeated microtrauma from mechanical stress and/or tissue perfusion mismatches leads to localised hypoxia and fibrocartilaginous degradation of the tendon, where calcium then deposits as calcium hydroxyapatite crystals.5 Over time, these hydroxyapatite deposits can rupture and trigger an acute inflammatory reaction that leads to the clinical manifestation of pain and limitation of movement of the affected tendon.1 If left untreated and allowed to heal, there is evidence that the calcium deposits are eventually resorbed by macrophages, allowing for tendon healing.1 5 However, this is a prolonged process that can take up to several years to self-resolve and, in the interim, limits the patient’s functional ability.

Diagnosis of CTRFT is often confirmed on diagnostic imaging, after the clinical examination. Plain film X-ray imaging constructs a two-dimensional view that will display large calcium deposits as amorphous calcification, as was seen with our patient, but will not identify the exact location of crystal deposition for targeted therapy. CT allows for three-dimensional mapping of the crystal deposition; however, this presents the patient with higher cost and radiation exposure. MRI can also generate three-dimensional mapping and allow for ruling out other differential diagnoses, but is often more expensive than a CT scan. Hence, an alternate mode of diagnosis via ultrasonography has been described, which allows for live mapping of crystal deposition, as well as the potential for simultaneous local corticosteroid injection for treatment, with a milder price tag and no radiation exposure.1 6

Treatment of CTRFT, once confirmed, often begins with conservative measures including use of non-steroidal anti-inflammatory drugs (NSAIDs), rest and physical therapy. Localised corticosteroid injections are considered if conservative therapy fails to improve the condition.1 In the six patients that Yun et al reported on, five patients reported pain relief with corticosteroid injection within 2 days of the intervention, whereas one patient reported relief after 10 days of surgical intervention. However, all six patients had complete resolution and no recurrence after 16 weeks to 2 years of follow-up.3 Surgical intervention is reserved as a last-resort option in cases of persistent pain due to CTRFT, which failed all other less-invasive interventions. More recently, Lee et al described the possible use of extracorporeal shockwave therapy as a non-invasive intervention for calcific tendinopathy, with measurable success and resolution of pain.6 In addition, De Zordo et al used an ultrasound-guided perforation and lavage technique to safely and successfully treat calcific tendinopathy of various tendons, including the rectus femoris.7 Finally, Zini et al proposed arthroscopic excision of calcification as another less-invasive option, before open surgical intervention.4

Our patient was an avid runner who likely sustained repeated microtraumas within her left rectus femoris tendon that, over time, led to deposition of calcium hydroxyapatite crystals. As this triggered repeated acute inflammatory reactions, this may have led to significant pain and limitation, most pronounced with hip flexion that involved the rectus femoris. With activity reduction and the use of NSAIDs, the inflammation eventually resolved and led to the resolution of her symptoms—a successful example of an initial conservative strategy to manage CTRFT.