Introduction:

As the COVID-19 pandemic progresses, clinicians should be aware of the uncommon presentations of the disease, such is the case with pneumomediastinum. Recent evidence suggested that these can occur in the context of COVID-19 pneumonia, even in the absence of mechanical ventilation–related barotrauma (1)

We report 2 cases of spontaneous pneumomediastinum among 2 COVID-19 patients with fatal evolution.

Case reports:

Case 1:

The first case was an 84-year-old woman with a past medical history of hypertension. She presented to the emergency department (ED) with 7 days of marked chest pain, and dry cough with progressive dyspnea. On admission, her vital signs showed tachypnea at 22 breaths per minute, high temperature at 38.2°C, increased heart rate with 110 beats per minute, and desaturation at 85%. On physical examination, she had bilateral basal crackles and peripheral cyanosis. Laboratory results showed an elevated C-reactive protein (CRP) of 181 mg/L (normal range 0–6 mg/L). The suspicion of COVID-19 was confirmed by real-time reverse transcription polymerase chain reaction (RT-PCR) analysis of nasopharyngeal swab samples. Non-contrast chest computed tomography (CT) showed some ground-glass opacities of peripheral subpleural location, associated with multiple areas of consolidation in posterior segments of both lower lobes, with the presence of pneumomediastinum measuring 7mm. (Figure 1).

She received treatment with antibiotics and corticoid associated to oxygen supplementation with a reservoir mask. She did not receive non-invasive positive pressure ventilation.

After 10 days, she developed a septic choc and received nosocomial antibiotics with noradrenaline. However, despite the support measures, the patient died from respiratory failure 12 days after admission.

Case 2:

The second case was a 63-year-old man who was admitted to the ED for fever, cough that lasted for 6 days, chest tightness and shortness of breath that developed a day ago. He had no history of any specific diseases such as hypertension, diabetes, or any heart diseases nor had any traumatic injuries. The patient exhibited a clear consciousness, with the blood pressure of 130/62 mm Hg, and a pulse rate of 83 beats per minute. His oxygen saturation was only 80%, and 90% after applying an oxygen mask. His blood count showed leukocytosis at 12700 cells/μL. There were elevated blood levels for C-reactive protein at 188 mg/L. His RT-PCR was positive for SARSCoV-2 infection. Management included pharmacological treatment with azithromycin, ceftriaxone, levofloxacin and hydrocortisone as well as oxygen supplementation.

During his hospitalization, he presented progressive deterioration of respiratory function with dyspnea despite oxygen therapy.  A chest CT scan was performed and has shown: bilateral ground-glass opacities (90%), severe pneumomediastinum measuring 40mm with extensive subcutaneous emphysema mainly extending superiorly in the thorax and into the neck.

Unfortunately, his respiratory state worsened and the patient was intubated and put on regular prone positioning. Despite a prompt management, the patient died 10 days after hospitalization.

Discussion:

Pneumomediastinum in COVID-19 patients is most often caused by increased airway pressures, secondary to mechanical ventilation or airway obstruction (2). While not commonly seen in viral pneumonias, Spontaneous pneumomediastinum (SPM) has been described in patients with COVID-19 pneumonia, despite no history of mechanical ventilation. SPM is an uncommon presentation of COVID-19. Data on the incidence, pathogenesis, and outcomes of SPM during the recent SARS-CoV-2 pandemic are limited, and is confined to a few isolated case reports (3–5). SPM is define as by the presence of air in the mediastinum without evident causes - traumatic, iatrogenic, organ perforation or surgery (6). Although SPM is generally considered a benign and self-limiting condition, its appearance in viral pneumonia may be of clinical significance.

In case of pulmonary infections due to SARS-COV-2, the virus causes breakdown of the alveolar membrane integrity as it infects both type I and II pneumocytes (7). Therefore, the damage of alveolar membrane in coronavirus infections can be one of the mechanisms leading to alveolar rupture thus the occurrence of SPM.

Most commonly patients present with shortness of breath, cough and/or chest or neck pain. Our patients have almost the same symptoms. Physical signs can include tachycardia, tachypnoea, hypotension and subcutaneous emphysema (8). Pneumomediastinum may be visible on plain chest X-ray; however, it may only be detected on CT of the chest. In our cases, it was the CT scan which led us to the diagnosis.

The treatment approach is based on rest, oxygen therapy and analgesia (9). The association of pneumomediastinum with COVID- 19 does not imply a specific treatment, but should be fear as a potential aggravating factor specifically in case of extensive pulmonary lesions.

In fact, a recent case series described three cases of COVID-19 pneumonia that were complicated by SPM and pneumothorax, all of which were followed by a severe course of disease with fatal outcome (10). Our two patients unfortunately sustained the same evolution after a few days. So the spontaneous pneumomediastinum may be considered as a marker of severity in pulmonary infection by SARS-Cov 2.

Conclusion

SPM is a rare complication of COVID- 19 pneumonia and was associated with a severe course of disease in our patient. Future studies are warranted to assess whether SPM is an indicator of disease severity in COVID-19 pneumonia.

References

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