In acute calcific tendonitis, calcium hydroxyapatite deposition leads to a foreign body inflammatory response [1]. This inflammation can lead to accumulation of retropharyngeal fluid, low-grade fever, leukocytosis, and elevation of non-specific inflammatory markers such as ESR [1]. LCT is related to other more common forms of calcific tendonitis affecting the shoulder (supraspinatus tendon), wrist flexors (flexor carpi ulnaris), hip (gluteus maximus) and ankle (longus coli) [2].

LCT is a rare diagnosis that usually presents in the 3rd to 6th decade of life. Patients present with a relatively acute onset of neck pain and stiffness over several days. The pain is usually associated with difficulty or pain with swallowing and pain with neck movement. The precipitating etiology is unclear. As with this case, the presentation is often concerning for an acute infectious process such as retropharyngeal infection or infectious spondylitis. Unlike either of these more serious diagnoses, the natural course of LCT is spontaneous improvement over a period of 1-2 weeks.

Clinically, the most important pearl about LCT is to avoid mistaking it for a more serious etiology and risking unnecessary invasive intervention. The radiologic diagnosis of LCT is best made with a contrast CT of the neck which demonstrates tendinous calcium deposition in the superior portion of the longus colli. The calcium deposition can be subtle, but usually has a globular amorphous appearance as seen in this patient (arrows below)[3].