Deep cervical cellulitis: the shadow cast by NSAIDs

Deep cervical cellulitis (DCC) represents major infectious emergencies that are life-threatening due to rapid progression within the fascial spaces of the head and neck. While the etiology is classically of odontogenic or pharyngeal origin, the precipitating and aggravating role of non-steroidal anti-inflammatory drugs (NSAIDs) is increasingly highlighted in scientific literature. These molecules, by inhibiting the cyclo-oxygenase pathway, alter leukocyte chemotaxis and early immune defense mechanisms. For the practitioner, the risk is twofold: a masking of initial clinical signs and an acceleration of tissue destruction, promoting deep and extensive bacterial spread.

Objective and hypothesis of the case study

This case report documents an exceptional clinical presentation in a 45-year-old patient with no prior medical history, whose infection occurred following the intake of NSAIDs for an extra-oral reason (ankle sprain). The objective is to illustrate the severity of a rare multi-compartmental extension, reaching not only the mediastinum but also the retroperitoneum, accompanied by venous thrombosis. The central hypothesis examined by the authors is that the administration of NSAIDs acted as a catalyst, masking the initial pain and allowing an unusual downward spread of the infection beyond the cervicothoracic junction, in the absence of an obvious infectious portal of entry.

Case report methodology

This work reports the clinical and radiological analysis of a single patient, an immunocompetent 45-year-old woman with no medical history (absence of diabetes, immunosuppression, or chronic kidney disease). The case documents the progression of a cervical infection that occurred three days after initiating medical treatment with analgesics and non-steroidal anti-inflammatory drugs (NSAIDs) for a sprained ankle.

The evaluation and diagnostic protocol was based on the following steps:

• Clinical examination: Thorough investigation looking for an infectious entry point (dental caries, periodontopathies or ENT foci) and evaluation of the cervical swelling.
• Biological evaluation: Analysis of the inflammatory syndrome including a complete blood count (showing 18,500/µL leukocytes including 15,200/µL neutrophils) and C-reactive protein measurement (CRP initially at 245 mg/L).
• Medical imaging: Cervico-thoracic computed tomography (CT) scan with iodinated contrast injection to map the extension of cellulitis within the fascial spaces and detect vascular complications.
• Therapeutic follow-up: Monitoring of clinical and biological evolution, with control imaging (CT scan) performed at 2 weeks to confirm the regression of infiltration and venous recanalization.

Biological profile and inflammatory markers

Upon admission, the biological assessment of this 45-year-old patient revealed a massive inflammatory syndrome. The analyses showed severe leukocytosis and a marked elevation of C-reactive protein (CRP), reflecting the aggressiveness of the infectious process following the initiation of treatment with non-steroidal anti-inflammatory drugs (NSAIDs).

Renal and hepatic functions were initially preserved, confirming the absence of early multi-organ failure despite the extent of the infection.

Radiological evaluation: anatomical extension and vascular complications

The cervico-thoracic CT angiography revealed extensive left laterocervical cellulitis with diffuse infiltration of the fascial planes (fat stranding). The examination showed an exceptionally rare anatomical progression due to its depth and caudal direction:

• Mass effect: Significant compression of the upper aero-digestive tract by inflammatory edema.
• Mediastinal extension: Crossing of the cervico-thoracic junction with invasion of the mediastinum.
• Retroperitoneal extension: Downward progression of the infectious process reaching the retroperitoneal space.
• Vascular involvement: Identification of a localized venous thrombosis affecting the initial portions of the left internal jugular vein and the left subclavian vein.

Imaging did not reveal signs of associated septic pulmonary embolism, despite the presence of venous thrombosis. No localized purulent collection or circumscribed abscess was visible at the time of initial diagnosis, with the clinical picture presenting as a diffuse phlegmonous infiltration.

Chronology and aggravating factors

The medical history established a close temporal correlation between the intake of NSAIDs for an ankle sprain and the symptomatic explosion. Clinical signs (swelling, dysphagia, and cervical stiffness) manifested only three days after the start of anti-inflammatory treatment, illustrating the rapidity of bacterial spread facilitated by the inhibition of the early immune response.

The danger of immune masking by NSAIDs

This clinical case illustrates the danger of administering non-steroidal anti-inflammatory drugs (NSAIDs) in the presence of an infectious focus, even if clinically silent. By inhibiting the cyclooxygenase pathway, NSAIDs suppress prostaglandins and thromboxane A2, which are essential for leukocyte recruitment and phagocytosis. For the practitioner, this mechanism creates a masking effect: pain decreases while bacterial proliferation intensifies, facilitating aggressive fascial destruction.

An exceptional anatomical extension

The most striking aspect of this study lies in the spread of the infection. While descending mediastinitis is a known complication of deep cervical cellulitis, the extension to the retroperitoneum observed here is described as exceptionally rare. The CT scan revealed multi-compartmental infiltration reaching the abdominal level, complicated by venous thrombosis of the internal jugular vein and the subclavian vein. This case serves as a reminder that the absence of an obvious dental or ENT portal of entry during the initial examination does not rule out a life-threatening cervico-facial emergency.

Limits and clinical analysis

As the study is a single case report (n=1), it does not allow for the generalization of prevalence, but it highlights a major pharmacological risk. A notable limitation is the absence of an identified entry point, which is atypical for deep cervical cellulitis (generally odontogenic or pharyngeal). This suggests that a latent infection may have been fulgurantly exacerbated by the treatment of the ankle sprain.

Study summary

This clinical case reports deep cervical cellulitis with an exceptional extension towards the mediastinum and retroperitoneum in a 45-year-old patient, following the intake of NSAIDs. Imaging and biology revealed severe multi-compartmental involvement (CRP 245 mg/L, leukocytes 18,500/µL) associated with venous thrombosis of the internal jugular and subclavian veins.

In concrete terms, for the practitioner:

• NSAID Vigilance: Formally proscribe NSAIDs in the presence of any suspicion of cervicofacial infection; they inhibit the early immune response and mask clinical signs, facilitating lightning-fast bacterial progression.
• Assessment of extension: In the presence of cervical cellulitis associated with recent NSAID intake, suspect deep (mediastinal) spread even in the absence of an obvious dental or ENT portal of entry.
• Radiological emergency: A major inflammatory syndrome must systematically lead to a contrast-enhanced cervico-thoracic CT scan to map the fascial spaces and detect potential vascular or necrotic complications.

Technical lexicon of the study

• Deep cervical cellulitis (DCC): Fulminant infection of the fascial spaces of the neck, characterized by rapid spread and life-threatening risk.
• Fat stranding: Radiological sign on CT scan showing densification of peri-fascial fat, reflecting active inflammatory or edematous infiltration.
• Leukocyte chemotaxis: Process of recruiting white blood cells to the infectious site, which NSAIDs inhibit by blocking prostaglandin synthesis, thus masking clinical warning signs.
• Descending necrotizing mediastinitis: Caudal extension of a cervical infection towards the mediastinum, facilitated by the continuity of the cervicothoracic fascial spaces.
• Phlegmonous infiltration: Diffuse and non-collected inflammation of soft tissues, distinguished from an abscess by the absence of an individualized purulent cavity on imaging.
• Jugular vein thrombosis: Vascular complication caused by intense perivascular inflammation, leading here to partial occlusion of the internal jugular and subclavian veins.

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