A 63-year-old female non-smoker with a history of hypertension and chronic kidney disease was admitted to our hospital for dyspnea, fever (39.1°C), and myalgia. Coronavirus disease 2019 (COVID-19) infection was confirmed by positive detection of severe acute respiratory syndrome coronavirus 2 RNA from a nasopharyngeal swab. At admission, the chest computed tomography (CT) scan showed bilateral, patchy ground-glass opacities (Figure 1A and B). The patient was treated with dexamethasone (6 mg/day), enoxaparin (prophylactic dose), and tocilizumab (800 mg intravenously). One week after admission, desaturation (75% on ambient air) and tachypnea (34 breaths/min) developed. A CT scan performed at that time showed subtotal bilateral ground-glass attenuation (Figure 1C and D). The patient was treated with non-invasive ventilation (continuous positive airway pressure, 8–12 cmH2O, with a fraction of inspired oxygen of 60–90%) and, after 4 weeks of continuous positive airway pressure, therapy was weaned successfully to mask oxygen.
Thoracic computed tomographic scans (A, B) at admission showing diffuse bilateral ground-glass opacities predominantly involving the left lower lobe; (C, D) 2 weeks after admission showing diffuse subtotal bilateral ground-glass attenuation and linear opacities; (E, F) 6 weeks after admission showing extensive bilateral thick-walled, irregularly shaped cavities, with several coalescing into a larger one; and (G, H) 8 weeks after admission showing persistent bilateral cavitary lesions. (A, C, E, G) Coronal views. (B, D, F, H) Axial views below the carina.
Citation: The American Journal of Tropical Medicine and Hygiene 106, 1; 10.4269/ajtmh.21-0949
One week later, the patient developed fever and had increased levels of C-reactive protein (175 U/mL) and white blood cells (15.3 × 109 cells/L). Chest CT scan showed extensive bilateral, thick-walled cavities, with several coalescing into a larger one (Figure 1E and F). Empiric antibacterial therapy was started and lasted for 2 weeks (amoxicillin–clavulanic acid and levofloxacin, followed with moxifloxacin). Our patient did not receive empiric antifungal coverage. Culture of multiple respiratory specimens showed only Staphylococcus haemolyticus in a low titer in one sample, and culture on Sabouraud agar remained sterile. The procalcitonin levels were low in all samples performed (≤ 0.1 ng/mL). Polymerase chain reaction assay for Aspergillus was negative in two sputum samples. Serum galactomannan was performed twice, but showed low levels (≤ 0.2 µg/L). Acid-fast bacilli were negative on smear, so Mycobacterium tuberculosis infection was not identified. Repeated blood cultures also showed no growth. The patient was managed conservatively, all inflammatory markers decreased significantly, and a CT scan 8 weeks after admission did not change significantly (Figure 1G and H). The patient was discharged home with continuous oxygen at 5 L/min.
Pulmonary cavitary lesions are rare manifestations of COVID-19 pneumonia.1 According to one case series, the overall prevalence of this complication is ≈3% of patients who developed COVID-19 pneumonia.2 The mechanisms of pulmonary cavitary lesions in COVID-19 are still unknown. Possible causes of cavitation are bacterial, fungal, or mycobacterial infections,3 but in our patient all these factors were excluded. Another plausible cause of cavitary lesions is distal pulmonary embolism or thrombosis, which can lead to pulmonary infarction.4,5 Pulmonary cavitation can be associated with secondary complications such as pneumothorax, hemoptysis, and superinfection; therefore, close follow-up of patients is necessary.
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