Pulmonary embolism, spontaneous pneumomediastinum and subcutaneous emphysema in a patient with COVID-19 disease: A case report

Abstract

The pathophysiology of pulmonary embolism (PE) and pneumomediastinum (PNM) in COVID-19 patients remain unclear. Studies indicate that the infection of the endothelial cells by the virus perpetuates a storm of cytokines and thrombogenic factors, which cause endothelium injury. We present a unique, to our knowledge, case of a patient aged 56 years with COVID-19 pneumonia who was admitted with dyspnea, desaturation, and fever. His situation was complicated by both PNM and PE. He received appropriate treatment with a therapeutic dose of low molecular weight heparin, and exhibited clinical improvement and resolution of the subcutaneous emphysema. Clinicians should suspect both PE and PNM within the differential diagnosis in cases of COVID-19 patients with pleuritic pain, dyspnea, and respiratory failure, after the tenth day from the onset of symptoms. INTRODUCTION The SARS-CoV-2 pandemic, known as COVID-19, has affected more than 94 million people globally, to date. The risk of thrombosis is increased in these patients. In a United States registry of patients with COVID-19, thrombotic complications occurred in 35.3% of hospitalized critically-ill patients1. However, spontaneous pneumomediastinum (PNM) and subcutaneous emphysema (SE) are rare complications with limited reported cases in the international literature to date2. CASE PRESENTATION A man aged 56 years, ex-smoker with an unremarkable medical background, presented to the Emergency Room with a six-day history of fever and dyspnea. The realtime reverse transcription polymerase chain reaction (RTPCR) for SARS-CoV-2 was positive three days before. On physical examination, he had a low-grade temperature of 37.6°C, tachypnea (RR=35/min) and desaturation (SpO2 88% on FiO2 0.21). The rest of his vital signs were as follows: blood pressure of 130/70 mmHg and heart rate 85 beats per minute. During auscultation, he had crackles at the base of the lungs bilaterally. Chest x-ray showed widespread pulmonary infiltrates (Figure 1a). The baseline laboratory blood tests showed raised inflammatory markers suggestive of acute infection (Table 1). On admission, we used the standard therapy with intravenous azithromycin, and dexamethasone 8 mg/d, subcutaneous prophylactic low molecular weight heparin (LMWH), and supplemental oxygen via nasal cannula (6 L/min). A chest computed tomography (CT) was performed that showed diffuse ground-glass infiltrations in the basal part of the lower lobes (Figure 2a). On the third hospitalization day, intravenous remdesivir was added to the therapeutic scheme following a decrease in the aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels (98 IU/L and 112 IU/L, respectively). His condition deteriorated 3 days later with fever up to 38.5°C, gradual increase in oxygen demands, and raised inflammatory markers. A new chest x-ray was ordered on the sixth hospitalization day, which revealed cervical subcutaneous emphysema and radiolucent shades parallel to trachea and the left cardiac border. The latter is a characteristic feature of pneumomediastinum, known as ‘double wall sign’ (Figure 1b). These findings were confirmed by a new chest CT scan (Figure 2b). In addition, it showed interstitial emphysema with a small amount of air around the bronchi and pulmonary vessels in the area of the left hilum due to bronchial or alveolar rupture. We escalated the oxygen delivery method to a AFFILIATION 1 Respiratory Department, Papageorgiou General Hospital, Thessaloniki, Greece 2 Plastic and Reconstructive Surgery Department, Papageorgiou General Hospital, Thessaloniki, Greece 3 1st Department of Internal Medicine, Papageorgiou General Hospital, Thessaloniki, Greece CORRESPONDENCE TO Despoina Moumtzi. Respiratory Department, Papageorgiou General Hospital, 564 29, Thessaloniki, Greece. E-mail: dmoumtzi@ hotmail.com ORCID ID: https://orcid. org/0000-0001-6967-2313