Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This has rapidly resulted in a worldwide pandemic with significant increase in morbidity and mortality [1]. The imaging changes in COVID-19 pneumonia are diverse with the various atypical CT features being less clearly described. The study conducted herein explains the atypical CT features in COVID-19 pneumonia.
In our study, the most common presenting symptoms were fever and cough consistent with the study by Shi H et al. [7]. There was predilection towards males (78.5%) as seen in the study done by Huang C et al. [8]. The other predisposing conditions in our study were elderly patients (mean 53.4 years) and comorbidities which are consistent with the study by Shi H et al. [7]. The mortality rate in our study was 3%. All the deaths occurred in elderly patients who had comorbidities, consistent with previous reports (8) and had moderate-severe CT severity score. Hence, advanced age, male sex, presence of comorbidities and higher CT severity score might be risk factors for poor prognosis.
Based on current literature, the typical imaging features of COVID-19 pneumonia on CT include bilateral, multilobar GGOs with/without consolidation, and superimposed interlobar septal thickening [2, 3]. They show a peripheral, posterior, and basilar distribution [2]. In our study, majority of the patients (73.1%) showed typical CT features and only 21.1% patients showed atypical CT features with concurrent above classical findings. Among the atypical CT features, the most common was pulmonary cysts. The other features in the order of frequency included pleural effusion, nodules, bull’s eye/target sign, cavitation, spontaneous pneumothorax, hilar lymphadenopathy, spontaneous pneumo-mediastinum with subcutaneous emphysema, halo sign, empyema, and necrotizing pneumonia with abscess.
The incidence of pulmonary cysts in our study was 9.0% which is consistent with the study by Shi H et al. [7]. Recent studies speculate that the pulmonary cystic change in COVID-19 might be secondary to ischemic parenchymal damage, lung fibrosis and low lung compliance [9]. Another explanation is blockage of the bronchioles by mucus and mucus plugs followed by the over-inflation of the alveoli and resultant rupturing of the alveolar septum with subsequent formation of small cysts [10]. None of the patients in our study were on mechanical ventilation and hence ruling out barotrauma induced cystic changes [9]. The peripheral subpleural cysts are prone to rupture causing pneumothorax. Hence, in COVID-19 pneumonia, prominent identification of pulmonary cysts and close monitoring for complications are required. Figure 1 shows pulmonary cysts in a case of COVID-19 pneumonia.
The incidence of pleural effusion in our study was 5.7%. However the incidence of pleural effusion in COVID-19 has been reported to be varying as per the available literature [11]. According to the study by Shi et al., the prevalence of pleural effusion varies depending on the stage of the disease, with a reported prevalence of 13% in the third week after onset of symptoms [7]. Pleural effusion may also be predictive of worse prognosis [11]. The presence or absence of underlying medical conditions, study setting, disease stage, and concurrent superimposed bacterial pneumonia are to be considered in order to comment on the prevalence and etiology of pleural effusion in COVID-19 infection [12]. The presence of effusion in cases with no concurrent comorbidities can possibly be attributed to COVID-19 infection or superadded bacterial infection. Figure 2 shows bilateral pleural effusion in a case of COVID-19 pneumonia.
The bull’s eye/target sign consists of central ground glass opacity surrounded by an inner ring of air and an outer ring of ground glass as shown in Fig. 3. It is presumed that bull’s eye sign may be a variant of the reverse halo sign [13]. In our study, bull’s eye sign accounted to 1.3% of the cases. Only few case reports on COVID-19 with bull’s eye sign has been made in the literature [13–15]. It has been theorized that they represent regions of organizing pneumonia, with perilobular involvement and a tendency to be located peripherally within the lung parenchyma [13]. The bull’s eye sign/target sign in the presented cases likewise were all peripherally located in the lower lobes [13].
Lung cavitation due to COVID-19 pneumonia is an uncommon finding which usually is seen in the late stage [16, 17]. The incidence in our study was 1%. There are few reports of intrapulmonary cavities of COVID-19-infection [11, 16, 18, 19]. However majority of other reviews showed no cavitation in their study [7, 20–23]. The cavitation may be related to diffuse alveolar damage, intra-alveolar hemorrhage, and necrosis of parenchymal cells based on prior autopsy reports [24, 25]. Common causes of cavitary lung lesions must be investigated appropriately in all patients [26]. In our study, there was no laboratory evidence supporting bacterial infections. Hence, the possibility of COVID-19 independently resulting in cavitation is to be considered. Close monitoring is required for complications like hemorrhage within the cavity, rupture of peripheral cavity resulting in pneumothorax, and superadded bacterial infection resulting in an abscess. Figure 4 shows pulmonary cavity with clots in a case who presented with hemoptysis.
Spontaneous pneumomediastinum (SPM) refers to the presence of air in the mediastinum occurring in the absence of traumatic or an iatrogenic origin [2, 27]. In current limited research, only few case reports of SPM in COVID-19 have been made [2, 28–30]. The incidence of SPM in our study was 0.3% and isolated spontaneous pneumothorax was 0.6%. Chen N et al. showed incidence of isolated spontaneous pneumothorax of 1% in COVID-19 patients [20]. It is believed that the possible causes of SPM in COVID-19 were similar to those in SARS showing severe diffuse alveolar damage. This diffuse alveolar damage results in alveolar rupture which can be further precipitated by high interalveolar pressure caused by factors like artificial ventilation, coughing or straining. This results in air migration into the mediastinum through the Macklin effect [2, 31–33]. The SPM can lead to other complications such as pneumothorax, extensive subcutaneous emphysema, and an uncommon complication of lung infections [2]. In our study, none of the cases were mechanically ventilated at the time of initial CT imaging. One case with emphysematous changes showed SPM with pneumothorax and extensive subcutaneous emphysema as shown in the Fig. 5, which we believe would have occurred due to progression of pre-existing lung lesions resulting in rupture of subpleural bulla or secondary to alveolar rupture as described above. Isolated spontaneous pneumothorax in our study might be secondary to rupture of subpleural pulmonary cysts or due to alveolar rupture.
The halo sign represents area of consolidation/pulmonary nodule/mass surrounded by ground-glass opacity [34–36] as shown in the Fig. 6. The incidence of halo sign in our study was 0.3%. In current limited research, only few cases reports on the halo sign has been made in COVID-19 [11, 37, 38]. Based on the pathological findings as seen in some recent studies, extensive thrombotic damage of the pulmonary microcirculation can explain the “halo sign” of consolidations [34].
The incidence of hilar lymphadenopathy in our study was 0.6%. In the available current literature, only one case report with hilar lymphadenopathy has been reported in COVID-19 [39]. Few studies showed no presence of hilar lymphadenopathy in COVID-19 [21, 40]. Thoracic lymphadenopathy includes hilar and mediastinal group of lymph nodes. Mediastinal lymphadenopathy previously thought to be an atypical feature has been redefined as “not-atypical” feature of COVID-19 [7, 41]. However, hilar lymphadenopathy which is usually associated with fungal infections, mycobacterial infections, and sarcoidosis are seldom seen in COVID pneumonia [39]. Histopathological correlation was unavailable for our cases. Hence, bacterial or fungal co-infection cannot be ruled. Follow-up imaging is to be done to evaluate the persistence or resolution of hilar lymphadenopathy and is required to establish their clinical importance.
In our study, the incidence of pulmonary nodules was 4.3%. The reported incidence of nodules in COVID-19 has been found to be varying, 3 ~ 13% as per the available literature [42, 43]. The relation between COVID-19 and nodules are not fully understood. Further studies are required to know whether these are incidental nodules or atypical manifestation of COVID-19 pneumonia. Figure 7 shows a case with GGO nodule.
Empyema has significant clinical morbidity [44]. In our study, a case presented with loculated hydropneumothorax as shown in the Fig. 8. Later, pus-like pleural fluid was aspirated and sent for analysis which showed elevated glucose, protein, and chlorides with predominant neutrophils (90%). This confirms the superadded bacterial infection in COVID-19 pneumonia resulting in empyema. Isolated empyema in COVID-19 is seldom reported in the literature.
Necrotizing pneumonia is a severe complication of lung infection characterized by necrosis and liquefaction of lung parenchyma, likely secondary to ischemia caused by thrombosis of intrapulmonary vessels [45]. In viral pneumonias, necrotizing processes with development of cavities and air-fluid level in the initial areas of consolidation have been described before in the literature [46]. Similarly, COVID-19 which causes small vessel microthrombi and severe dysregulation of the host immune reaction can result in necrotizing pneumonia. Although bacterial and fungal lung abscesses are known to occur in COVID-19 in up to 11% and 3%, respectively, which were presumed to have formed after hospital admission [47]. Our study showed an incidence of only 0.3%. This discrepancy might be due to the differences in demographic features and hospital care. Figure 9 shows a case of necrotizing pneumonia with secondary cavitation and abscess formation.
