Case Presentation: An 82-year-old woman with a history of OA and asthma presented with 3-week dry cough, SOB, poor appetite, and generalized weakness. She saw her PCP prior to admission and was prescribed prednisone for suspected asthma exacerbation which she took for 2 days without improvement. On presentation, she had a low-grade fever of 100.2⁰F and SpO2 in the 60s. She had labored breathing with frequent coughs and decreased breath sounds bilaterally. Initial lab work notable for rapid COVID-19 PCR positive, SARS-COV-2-antibody negative, WBC 8300, procalcitonin 0.22, LDH 603, ferritin 1478.0, CRP 3.50, D-Dimer 0.99. CXR showed extensive interstitial thickening and parenchymal opacities throughout both lungs suggestive of COVID-19 pneumonia. The patient was placed on OptiFlow 60% FiO2 40L O2 with improved SpO2 to 95%. She met the criteria for severe disease and was started on dexamethasone 6mg daily, Remdesivir for 5 days, enoxaparin 40mg SQ daily, and prone-ventilation protocol. She received convalescent plasma on HD 2. Her clinical status continued to deteriorate by HD 5, requiring increased OptiFlow to 70% FiO2 50L O2, rising WBC to 16000, and jump in D-Dimer to 10.66. Subsequent CT PE was negative for PE but revealed extensive ground-glass consolidation in both lungs, as well as extensive pneumomediastinum and pneumopericardium most likely secondary to Macklin Effect. The pneumomediastinum was conservatively managed with general monitoring of respiratory status. A rapid response was called on HD 7 for continued desaturations with tachypnea, prompting further OptiFlow increase to 80% FiO2 60L O2. Given the patient’s worsening hypoxic respiratory failure and newly discovered pneumomediastinum, she was transferred to the MICU where she was eventually intubated with mechanical ventilation. She quickly developed worsening hypotension and shock due to COVID-19 ultimately requiring vasopressor support but without clinical improvement. She was switched to comfort cares on HD 19 and passed away the same day.
Discussion: We present a rare case of spontaneous pneumomediastinum in the context of severe COVID-19 pneumonia. The etiology of the pneumomediastinum was attributed to the Macklin Effect: alveolar rupture with dissection of air into the mediastinum. Interestingly, this phenomenon is typically seen in cases of barotrauma related to mechanical ventilation or significant history of vomiting/retching. In this case, the patient did not have any identifiable barotrauma prior to discovery of the pneumomediastinum. Possible explanations for the alveolar rupture in this case include direct alveolar destruction by the COVID-19 infection and/or secondary to increased endobronchial pressure with excess coughing against a closed glottis.
Conclusions: Although rare and usually self-limiting, spontaneous pneumomediastinum is a possible complication of COVID-19 pneumonia even in the absence of barotrauma. Early recognition and conservative management of pneumomediastinum can mitigate worsening of cardiorespiratory function and lead to enhanced clinical outcomes.