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Longus colli tendinitis: acute neck pain with retropharyngeal swelling
  1. Wan Qi Lim and
  2. Eu Chin Ho
  1. Otorhinolaryngology, Tan Tock Seng Hospital, Singapore
  1. Correspondence to Dr Wan Qi Lim; wanqi.lim{at}mohh.com.sg

Abstract

Longus colli tendinitis (LCT) has been described in several case reports, and is likely underdiagnosed due to its non-specific symptoms and self-limiting nature. It usually presents as acute neck pain with retropharyngeal swelling seen on nasoendoscopy and imaging studies. This may lead to unnecessary invasive interventions if physicians are unaware of the disease course. We discuss a case of LCT in a young woman who was treated at our institution, with recommendations on how to identify and treat such cases accurately without overtreatment.

  • Otolaryngology / ENT
  • Orthopaedics
  • General practice / family medicine
  • Emergency medicine
  • Radiology (diagnostics)

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Background

Longus colli tendinitis (LCT) has been described in several case reports and is likely underdiagnosed due to its non-specific symptoms and self-limiting nature. It usually presents as acute neck pain with retropharyngeal swelling seen on nasoendoscopy and imaging studies. This may lead to unnecessary invasive interventions if physicians are unaware of the disease course. We discuss a case of LCT in a young woman who was treated at our institution, with recommendations on how to identify and treat such cases accurately without overtreatment.

Case presentation

A woman in her late 30s with no significant past medical history presented with severe posterior neck pain and stiffness for 4 days, and odynophagia for 2 days. There was no haemoptysis, stridor nor dysphonia. She had no prior upper respiratory tract symptoms nor trauma.

She was afebrile and had unremarkable vitals. Her neck motion was limited by pain worsened with extension. There were no palpable neck swellings, and oral cavity was unremarkable. A flexible nasoendoscopy demonstrated left mild posterior pharyngeal wall swelling, with mobile vocal cords and patent airway.

Investigations

Leucocyte count was 12.6×109/L with normal differentials, C reactive protein (CRP) was 79.7 mg/L and blood sugar was 9.4 mmol/L.

A lateral neck radiograph showed loss of cervical lordosis with mild thickening of the prevertebral soft tissue at C2–C4 as well as calcium deposits anterior to the C1-C2 joint (figure 1A). Contrast-enhanced CT neck confirmed intratendinous calcific depositions anterior to C2–C5 and retropharyngeal fluid with no discernible rim enhancement (figure 1B). MRI C-spine highlighted prevertebral soft tissue oedema, with no foreign body, abscess or spondylodiscitis seen (figure 1C).

Figure 1

(A) X-ray of the lateral neck demonstrating loss of cervical lordosis, with mild thickening of the prevertebral soft tissue at the upper cervical vertebrae. Arrow points to calcium deposits seen anterior to the C1-C2 joint. (B) Sagittal view of contrast-enhanced CT of the neck: Retropharyngeal fluid with no discernible rim enhancement demonstrated from C2 to C4-C5 levels (bottom arrow), amorphous calcific densities seen anterior to the C1-C2 joint (top arrow). (C) Sagittal view of T2-weighted MRI of the neck, with arrow pointing towards oedema in the prevertebral soft tissues with no abscesses detected.

Differential diagnosis

With the distinctive history and radiological findings, a diagnosis of LCT was made. Other differentials include retropharyngeal abscess, pyogenic spondylitis or cervical spondylodiscitis, trauma and neoplasm. These were considered and ruled out after appropriate imaging was done.

This will be further discussed in this article.

Treatment

She was treated with non-steroidal anti-inflammatory drugs (NSAIDs) and a tapering dose of steroids. An antibiotic course was also completed due to our initial concerns of retropharyngeal abscess and raised inflammatory markers (CRP and leucocyte count).

Outcome and follow-up

By day 3, her symptoms had significantly resolved with improved range of motion including full neck extension. Repeat flexible nasoendoscopy on the same day showed resolution of posterior pharyngeal wall bulge. A CT neck on day 5 showed nearly complete resolution of the retropharyngeal oedema and fluid, with improvement in her CRP. The amorphous calcification was still present. She was discharged after 6 days with complete resolution of symptoms. Day 10 repeat CT neck showed interval improvement in calcification and complete resolution of retropharyngeal oedema.

Discussion

Acute calcific aseptic tendinitis of the longus colli muscle (LCM), is also known as calcific retropharyngeal tendinitis, calcific prevertebral tendinitis or LCT. For the purpose of our case report, we will be referring to the condition as LCT. LCT has been described in several case reports and was first described by Hartley1 in 1964 as an inflammation of the LCM secondary to calcium crystals deposition at its insertion, usually within the oblique portions of the muscle at C1-C2 levels. LCT is likely underdiagnosed2 due to its non-specific symptoms and self-limiting nature. This relatively benign condition mimics several other serious conditions such as retropharyngeal abscess, meningitis, spondylitis, traumatic injury, neoplastic disease, with unnecessary invasive procedures reported in literature such as trans-oral incision and drainage, and biopsies.3

LCT affects individuals between the ages of 30 years and 60 years with no gender preponderance. Horowitz et al estimated annual LCT incidence to be 0.50 cases per 100 000 person-years.2

LCT is a calcium hydroxyapatite deposition disease (CHADD)4 subtype with inflammation and calcium deposition at the insertion of the LCM tendon. The mechanism is still not fully understood,5 but may be caused by systemic or local metabolic derangements, with risks factors such as repetitive trauma, injury, necrosis, inflammation and genetics, similar to the idiopathic nature of CHADD.

The LCM is a paired prevertebral muscle extending from C1 to T3, with upper (superior oblique), lower (inferior oblique) and central (vertical) fibres that weakly flex and rotate the neck. The superior oblique fibres originate from the anterior tubercles of the transverse processes of C3-C5, insert into the anterior tubercle of C1, and are most commonly involved.6 Lower cervical (C4-C5, C5-6) involvement has also been described.7

Patients usually present with increasing throat and neck pain, odynophagia, with reduced range of neck motion especially in extension, and pain radiating up the occiput. Mild posterior pharyngeal wall bulging may be visualised with flexible nasoendoscopy.2 There may be associated mild fever and elevated inflammatory markers. Symptoms usually peak by day 4, with resolution of symptoms by 2 weeks.2 8

Contrast-enhanced CT is the imaging modality of choice,8 with good detection of C1-C2 intratendinous calcification which may not be appreciated on plain radiographs. CT also helps to demonstrate prevertebral effusion and exclude other differentials such as retropharyngeal abscesses, trauma or neoplastic aetiologies. Within emergency settings CT is more easily accessible and cheaper than MRI. The classical finding is amorphous calcification anterior to C1-C2 with prevertebral soft tissue oedema centred on the calcification and no rim-enhancing collection. MRI is not necessary for diagnosis and has poorer representation of calcification but can help characterise soft tissue abnormalities. As LCT is self-limiting, follow-up imaging is not essential but may help to demonstrate resolution of calcification or oedema.

Treatment includes NSAID therapy for 2–3 weeks or until symptom resolution, neck immobilisation with soft C-collar and supportive care with pain alleviation.9 Previous reports suggest that some patients with severe symptoms may obtain relief from a short course of tapered steroid therapy.10 Tapered doses of steroids such as methylprednisolone, prednisolone and dexamethasone have been used in case reports; however, specific dosages were rarely mentioned. Our patient was started on intravenous dexamethasone (8 mg once a day, then 4 mg three times per day) on admission in view of retropharyngeal swelling seen on nasoendoscopy, and severe pain. This was tapered down further (4 mg two times per day, to 4 mg once a day) over the next few days as her symptoms improved which also corresponded to an improvement in retropharyngeal swelling on repeat nasoendoscopy. Steroids were stopped when swelling had resolved. We recommend, if initiating a course of steroids without the benefit of nasoendoscopy, to wean the dose of steroids according to patient’s symptoms as the swelling and symptom severity is likely to be closely related.

Some case reports reported treatment with antibiotics as the condition was confused with a retropharyngeal abscess.10 However, as this condition is non-infective in nature, there is no role in starting antibiotic therapy.

In conclusion, LCT is self-limiting in nature, with all reported cases resolving spontaneously with neck immobilisation and NSAIDs.9 Some patients with severe symptoms obtain relief from a short course of steroid therapy.10 LCT should be considered if patients present with severe acute neck pain with characteristic radiological findings, to prevent unnecessary invasive procedures and delayed discharges.

Learning points

  • Think of longus colli tendinitis (LCT) when patients present with acute neck pain and suggestive features on imaging of retropharyngeal swelling with calcific deposits, without any rim-enhancing collection.

  • Retropharyngeal swelling with acute neck pain does not always equate to underlying infection.

  • Be aware of LCT so as to provide the most appropriate care.

  • Treatment includes non-steroidal anti-inflammatory drugs therapy, neck immobilisation, and may include adjunct therapy such as steroids for severe symptoms.

  • These patients should be treated conservatively; sometimes, less is more!

Ethics statements

Patient consent for publication

References

Footnotes

  • Contributors WQL performed the literature review and analysis of the previous case reports and patient data, and was the main contributor towards writing of the manuscript. ECH was the attending physician who guided WQL through the process of writing this report, as well as some final editing. All authors read and approved the final manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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