Acute calcific tendinitis of the longus colli muscle is an aseptic inflammatory response to the deposition of calcium hydroxyapatite crystals in the longus colli tendon. The longus colli is a prevertebral muscle that flexes and rotates the neck. The deposition tends to occur predominantly in the superior fibres extending from the transverse process at C3–C5 to the anterior tubercle of C1 (atlas) (1–4).
The aetiology of the condition remains unclear. One hypothesis is that trauma, degeneration, or ischaemia of the tendon predisposes to the deposition of crystals in an attempt to compensate for reduced tendon quality. Rupture and release of the crystals induces a strong inflammatory foreign body response in the surrounding soft tissue. The crystals are resorbed over the course of one to two weeks, and symptoms usually resolve after a few days (1, 2). One study found a mean symptom duration of 4.6 days (3). The condition responds well to non-steroidal anti-inflammatory drugs, and possibly to steroids in severe cases (1–4). An epidemiological study from 2013 reported the incidence as 0.5 per 100 000 but stated that the condition was also likely to be underreported. The condition typically affects those aged 30–60 years (5).
Calcific tendinitis of the longus colli muscle is also referred to in the literature as prevertebral calcific tendinitis, retropharyngeal tendinitis or longus colli tendinitis, and is characterised by acute and severe pain in the neck and throat and reduced mobility of the neck. Fever, mild leukocytosis and elevated CRP and sedimentation rate may also be present (1–4).
The condition may mimic several other infectious conditions, such as retropharyngeal abscess and spondylodiscitis. Imaging is essential for diagnosis, as this case report illustrates. The gold standard is cervical CT with intravenous contrast, which reveals the pathognomonic calcifications in the superior fibres of the longus colli tendon at C1–C2 (1–4) – as seen in our patient (Figure 1).
The amount of calcium can vary and does not correspond to the degree of inflammation (2). Secondary inflammatory changes may also be present, such as retropharyngeal effusion and oedema in prevertebral soft tissue, as seen on both CT and MRI in this patient (Figures 1 and 2). In patients with retropharyngeal abscess, contrast enhancement would be expected around the fluid collection, and possibly gas bubbles and local lymphadenopathy; these will be absent in cases of calcific tendinitis (2, 4). Our patient was nevertheless given antibiotics, as infection could not be completely ruled out.
The antibiotics were soon discontinued, however, as the patient's symptoms resolved more rapidly than would be expected with an infection, reinforcing suspicion of calcific tendinitis.
Cervical MRI was also performed to rule out spondylodiscitis. MRI has high sensitivity for detecting inflammatory changes in and around the longus colli muscle, but is less sensitive than CT for detecting calcifications, and is therefore not the first choice (2).
This case report illustrates that calcific tendinitis of the longus colli muscle has a characteristic appearance on CT and should be suspected by clinicians and radiologists in patients with acute neck pain and stiffness, and odynophagia. Knowledge of the condition can reduce pain and unnecessary medical or surgical interventions.