Case Presentation: A 69-year-old male with past medical history of bipolar disorder, schizophrenia, and substance abuse presented to the ED with suicidal and homicidal ideations, and hallucinations. He tested positive for COVID-19 at an outside hospital a week prior to presentation. He endorsed subjective fevers and productive cough with non-bloody sputum and denied dyspnea, chest pain, nausea, vomiting, or recent travel. On admission, his vitals were remarkable for elevated blood pressure (187/77 mmHg) and tachypnea (26 breaths/minute). Physical exam showed lethargy and abdominal tenderness. Lab results showed elevated CRP (5.55 mg/dL, ref: < 0.50), ferritin (3695 ng/mL, ref: 30.0 - 400.0), and D-dimer (1.75 mg/L, ref: 0-0.69). CXR showed moderate patchy bilateral opacities consistent with COVID-19 pneumonia. Upon receiving 1mg of Ativan due to increased agitation, his oxygen saturation dropped to 88%, and he was placed on 2L nasal cannula (NC) and started on remdesivir. He also had a temperature of 103°F and dexamethasone was started. He further declined, requiring 55L flow and 80% FiO2 HFNC and 15L Oxymask. Elevated D-dimer and worsening oxygen needs prompted initiation of therapeutic enoxaparin. He was transferred to the MICU for increased oxygen requirements and worsening acute respiratory failure. In the MICU, dexamethasone and remdesivir were continued, and barcitinib was started. A few days later, his oxygen needs decreased to 50L flow and 50% FiO2 HFNC, and he was transferred to the inpatient floor. His D-dimer increased, and CT PE was negative for pulmonary embolism but showed extensive pneumomediastinum (SP) and subcutaneous emphysema. Cardiothoracic surgery was consulted, and conservative management and monitoring were recommended as he could not tolerate a procedure with ongoing psychiatric issues. Dexamethasone was tapered, and oxygen was weaned. Upon breathing successfully on room air, he was discharged.

Discussion: SP is a condition in which air is found in the mediastinum. It is a rare finding and is associated with asthma, chronic lung disease, infections, and mechanical ventilation. Although it is uncommon in viral pneumonias, there have been increased reports of SP with COVID-19 pneumonia. Although the mechanism is not completely elucidated, it is thought to be due to increased alveolar pressure and diffuse alveolar injury in the setting of severe COVID-19 pneumonia. In combination with a strong cough and increased work of breathing, this causes subpleural alveolar rupture [3]. Free air can dissect the peribronchovascular sheath and leak into the mediastinum. This phenomenon, called the “Macklin effect”, has been implicated as the cause of SP in closed thoracic lesions, asthma attacks, and Valsalva maneuvers [1]. This theory is not consistent with the absence of pneumothorax in high-resolution CT scans in certain cases of SP, as in our case (Figure 1). It is unclear how air can reach the mediastinum without causing a visible breach in the alveolar lung parenchyma [2]. Despite unclear mechanism, SP is usually a self-limiting condition. These patients should be monitored for SP-related cardiovascular and respiratory complications. Conservative management is usually sufficient.

Conclusions: SP cases in hospitalized patients with COVID-19 infection are increasing clinical interest in this rare condition. Despite an unclear mechanism, conservative management is usually all that is needed. Further research is necessary to investigate the pathogenesis of SP in COVID-19 infection.

IMAGE 1: Figure 1: CT scan confirming the presence of extensive pneumomediastinum and subcutaneous emphysema