Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)1 belongs to the family of Coronaviridae and is responsible for the current outbreak of Coronavirus disease 2019 (COVID-19).2 COVID-19 cases were first reported as pneumonia of unknown cause in Wuhan, China.3 With increasing spread across the world, it was declared as a pandemic by the World Health Organization in March 2020.
Similar to other respiratory viral illnesses, COVID-19 most commonly presents with symptoms of fever, fatigue, cough, and dyspnea.4,5 Severe COVID-19 with high mortality mostly, but not exclusively, occurs in elderly patients and individuals with comorbidities such as hypertension, diabetes, cardiovascular disease, cancer, or obesity.4–6 The most frequently reported complications of COVID-19 include acute respiratory distress syndrome (ARDS), acute cardiac injury, arrhythmia, septic shock, acute kidney injury, and secondary infections.4,5,7,8
As COVID-19 continues to spread globally, health care professionals are increasingly being urged to utilize computed tomography (CT) and chest radiographs as screening and/or diagnostic tools. Data from China emerged in late February 2020, which concluded that “CT imaging has a high sensitivity for the diagnosis of COVID-19,”9 but data outside of China during early stages of the outbreak have been less convincing, considering significant overlap in imaging features that might be seen during an influenza epidemic and, in particular, with many false-negative tests.10 Current thinking is that the positive predictive value of CT will be low unless the disease prevalence is high, as it was in Wuhan.10 Viral testing remains the only specific method of diagnosis to date,11 but has its own challenges with imperfect sensitivity.9,12,13
The American College of Radiology recommends that CT not be used as a first-line tool for screening or diagnosing COVID-19, and should be reserved only for hospitalized symptomatic patients with specific indications for chest CT.11 Portable radiography may be considered in patients if deemed medically necessary.11 The Fleischner Society recently issued a consensus statement on the role of chest imaging in patient management during the COVID-19 pandemic, which states that imaging is indicated in patients with COVID-19 and worsening respiratory status. Imaging is also indicated as a triage tool for patients with suspected COVID-19 who present with moderate-severe clinical features and a high pre-test probability of disease in a resource-constrained environment.14 Although imaging should not be used for first-line screening or diagnosis, if a patient imaged for other reasons has findings suggestive of COVID-19 and negative testing, this should prompt repeat testing. In all scenarios, radiologists should be familiar with the typical imaging findings seen in COVID-19 along with mimics that could potentially confound the diagnosis.
IMAGING FINDINGS OF COVID-19
Numerous studies have shown a wide variety of imaging findings seen in COVID-19, most commonly including ground-glass, consolidative, or nodular opacities; with the distribution pattern being peripheral, bilateral, and multi-lobar.15 Additional findings include crazy paving pattern, interlobular septal thickening, bronchiectasis, or subpleural involvement15 along with other unclear distribution patterns.16 “Crazy paving” is used to describe the pattern of thickened interlobular and intralobular lines superimposed on a background of ground-glass opacities (GGO), resembling irregularly shaped paving stones.17 The Radiological Society of North America (RSNA) recently published an expert consensus statement in an attempt to reduce report variability among radiologists and to better aid in the management of these patients.18 In this consensus statement, imaging findings are divided into 4 main categories: typical, indeterminate, atypical, and negative, to convey a relative likelihood that these findings are attributable to COVID-19 pneumonia.
The “negative for pneumonia” category has imaging features that lack any parenchymal abnormality to suggest an infectious process, such as GGO or consolidation.18 It is vital to understand that imaging may be negative in the early stages of COVID-19, and that many conditions may present with imaging findings similar to those that have been described to occur in COVID-19 pneumonia.
“Typical” features of COVID-19 pneumonia (Fig. 1) are those that are more frequently and specifically reported in the current literature. These include GGO in a peripheral, bilateral distribution, with or without consolidation or visible intralobular lines (crazy paving pattern).18 GGO can also be multifocal with a rounded morphology in a similar distribution.18
Although radiographic changes may be absent or mild in early disease, findings may change over the course of the disease. Later stage infections (6 to 12 d) are usually characterized by greater total (often bilateral) lung involvement, coalescence of GGO into dense consolidations that can progress to ARDS.16,19 Findings that have been described to occur more commonly in later stages of disease include GGO with a reticular pattern, vacuolar sign (lucency within GGO), fibrotic streaks, air bronchogram, bronchus distortion, a subpleural line, a subpleural transparent line, and pleural effusion (Figs. 2, 3).20 As patients recover, this is followed by progressive organization into more linear opacities and sometimes resolution of all abnormalities.16,19
MIMICS OF COVID-19: TYPICAL FINDINGS
Frequently encountered conditions with overlapping imaging features with those that are typical of COVID-19 include other viral pneumonias, chronic eosinophilic pneumonia (CEP), and disease processes that result in an organizing pneumonia pattern of lung injury.
Several RNA and DNA viruses can cause respiratory illnesses in humans. RNA viruses that typically present from late autumn to early spring include Influenza A and B, Human Metapneumovirus (HMPV), and Coronavirus. DNA viruses such as Adenovirus tend to manifest in late winter, spring, and early summer. Other DNA viruses including Herpes Simplex Virus, Cytomegalovirus, and Varicella occur more often in immunocompromised patients.21 Symptoms reported include high fever, dry cough, runny nose and/or congestion, lethargy, and myalgias.22
RNA viruses, specifically Influenza A and B, are responsible for annual outbreaks of pneumonia during the winter months.21,22 HMPV causes about 4% of the community-acquired pneumonias in adults and in those with chronic obstructive pulmonary disease exacerbation, and can account for 9% of infections in patients with hematologic malignancy.23 Coronaviruses initially appeared with the SARS-CoV epidemic in autumn 2002 and Middle East respiratory syndrome-related coronavirus (MERS-CoV) in autumn 2012, and more recently COVID-19.3,22,24,25 Most patients with Coronavirus pneumonias (SARS-CoV, MERS-CoV, and COVID-19) will have imaging findings similar to the aforementioned findings typical of COVID-19.3
Imaging patterns of viral pneumonias range from poorly defined centrilobular nodules and patchy peribronchial GGO to peripheral consolidation with air bronchograms (Fig. 4).21–23 Influenza pneumonia presents with centrilobular nodules and branching linear opacities, with or without consolidation on radiographs. Patchy areas of consolidation rapidly coalesce over days.21,22 On CT, bilateral peribronchovascular and subpleural GGO with or without septal thickening (crazy paving) can be seen (Fig. 5).23 Influenza A avian subtype (H5N1, H7N9) pneumonias can undergo pseudocavitation and pneumatocele formation and may be associated with lymphadenopathy.26
HMPV pneumonia shows multifocal consolidation on chest radiographs. On CT, HMPV pneumonia manifests as GGO, small centrilobular nodules, and multifocal areas of consolidation in a bilateral asymmetric distribution.21–23 Many patients with HMPV do not undergo imaging due to mild symptoms; those that do are typically patients who are either immunocompromised or who may have chronic obstructive pulmonary disease exacerbation, cystic fibrosis, or asthma.23
Adenovirus is more prevalent in children and only accounts for 1% of respiratory infections in adults.21 On imaging, adenovirus pneumonia manifests as patchy GGO, centrilobular nodules, and peribronchial consolidation.21,22 Sequelae of adenovirus can include bronchial wall thickening, bronchiectasis, and postinfectious bronchiolitis obliterans. The latter is most often seen in children after adenovirus infection.21
Although most viral pneumonias resolve without complication, some viral pneumonias may result in significant lung injury with a pattern of diffuse alveolar damage (DAD) resulting in fibrosis.22 Influenza A has been shown to have fibrotic interstitial changes after the initial infection.3 Coronavirus pneumonias can result in fibrotic changes after pneumonia, likely due to lung injury and DAD.22,24 Adenovirus in solid organ and stem cell transplant patients has an incidence of 3% to 47%, with increased risk for developing ARDS as a complication of adenovirus pneumonia.21
CEP is one of a heterogenous group of eosinophilic lung diseases and can result in an imaging appearance similar to that of COVID-19. CEP is an idiopathic condition with gradual onset of clinical symptoms of restrictive lung disease. It most commonly affects middle-aged patients, approximately half of whom have a history of asthma.27 Histologically, CEP is characterized by accumulation of eosinophils and lymphocytes in the alveoli and interstitium, with interstitial fibrosis. The percentage of eosinophils in bronchoalveolar lavage fluid is very high.27
The typical CT finding in CEP is nonsegmental peripheral airspace consolidation, with an upper lobe predominance (Fig. 6). Less commonly encountered findings that predominate in later stages of disease include GGO, reticulation, and nodules. Pleural effusion is uncommon. CT performed at least 2 months after symptom onset may show linear bands parallel to the pleural surface.27
Treatment consists of systemic corticosteroids, with patients experiencing complete recovery in a matter of days. Long-term prognosis is considered excellent, although most patients require maintenance therapy with low-dose oral corticosteroids to prevent relapses.28
Organizing pneumonia is a pattern of lung injury resulting from a spectrum of causes, such as infection (including COVID-19), inflammatory disease, radiation therapy, drugs, toxins, or autoimmune disease.29 Idiopathic forms are referred to as cryptogenic organizing pneumonia.
Lung injury in organizing pneumonia can be either focal or diffuse. Injury to alveolar epithelium leads to fibroblast migration, starting the process of “organization.” If the inciting factor is removed and the basement membrane is intact, there is remodeling of the fibroblastic tissue into normal pulmonary parenchyma. On the contrary, if the culprit stimulus persists and there is prolonged distortion of basement membranes, eventually, organized fibroblastic tissue leads to irreversible fibrosis.30
Patients present with shortness of breath, nonproductive cough, lethargy, low-grade fever, and weight loss.31 The diagnosis is made on the basis of a combination of clinical presentation, lack of response to multiple antibiotic regimens, negative cultures, and imaging findings. It is imperative to note that some etiologies of organizing pneumonia may clinically overlap with COVID-19. These include infections such as pneumococcus, influenza, and pneumocystis carinii, and respiratory involvement in systemic lupus erythematous and rheumatic fever.32,33
The accuracy of CT has been described to be up to 79% for the diagnosis of organizing pneumonia.29 In 62% to 90% cases of organizing pneumonia, pulmonary involvement is diffuse and bilateral. There is generally a lower lobe predilection with peripheral consolidations and GGO in a peribronchial distribution (Fig. 7).31 Unilateral pulmonary involvement, although less common (10% to 38%), is manifested by a solitary pulmonary nodule, single consolidation, and/or GGO in a peribronchial location, with associated bronchiectasis and architectural distortion. In addition to consolidation, peribronchial nodules of varying sizes can be seen in both diffuse and unilateral lung involvement.30
Although descriptors such as reverse halo sign and atoll sign were initially reported to be specific for organizing pneumonias,29,34,35 it is now known that these can also be seen in a host of infectious, noninfectious, and granulomatous processes. The “reverse halo” sign is described as ring of consolidation around a central GGO. If this ring is interrupted at one location, it is referred to as an “Atoll sign.”30
Treatment consists of removal of the inciting stimulus and corticosteroid therapy for 6 to 12 months, and the prognosis is generally favorable.31 Nevertheless, if the initial lung injury is severe, irreversible fibrosis can ensue.
MIMICS OF COVID-19: INDETERMINATE FINDINGS
As per the RSNA consensus statement, “atypical” imaging findings of COVID-19 (Fig. 8) pneumonia are those that are not commonly reported with this disease and more indicative of other disease processes. They lack the typical and indeterminate features. Atypical CT findings include isolated lobar or segmental consolidation without GGO, lung cavitation, discrete nodules (tree-in-bud opacities and centrilobular nodules), and pleural effusion.18 These are more commonly seen in bacterial pneumonia, a variety of community-acquired pneumonias, and aspiration. Such findings are unlikely to create a diagnostic dilemma and should suggest alternative diagnoses other than COVID-19 pneumonia.
Imaging findings that have been reported in COVID-19, but are nonspecific, fall into the “indeterminate” category, including diffuse, multifocal, perihilar or unilateral GGO, with or without consolidation, and lacking a specific distribution pattern. Few very small nonrounded and nonperipheral GGO are also included in this category.18 Similar findings have also been described in pneumocystis pneumonia, hypersensitivity pneumonitis, diffuse alveolar hemorrhage (DAH), pulmonary edema, and pulmonary alveolar proteinosis (PAP), which may present a diagnostic challenge.
Pneumocystis Jirovecii Pneumonia (PJP)
PJP is a fungus that causes pneumonia in immunocompromised hosts and is the most common opportunistic infection among individuals with AIDS. Since the introduction of highly active anti-retroviral therapy and PJP chemoprophylaxis in HIV-infected patients, patients without HIV infection account for a majority of PJP cases in industrialized countries.36 This includes patients with primary immunodeficiency or hematologic malignancies, solid organ and bone marrow transplant recipients, collagen vascular disorders, and those undergoing treatment with corticosteroids or chemotherapy.36 HIV-infected patients typically present with insidious onset of respiratory symptoms, whereas PJP infection in patients without HIV infection presents acutely with severe hypoxia and rapid deterioration of respiratory function requiring mechanical ventilation, overlapping with the clinical presentation of patients with COVID-19.37
On CT, PJP is characterized by extensive GGO, which is most commonly in a central distribution with peripheral sparing but may also be diffuse (Fig. 9). In more advanced disease, consolidation and crazy paving may develop. Pulmonary cysts develop in up to one third of cases and are associated with an increased risk of spontaneous pneumothorax.36
First-line therapy for PJP is oral trimethoprim-sulfamethoxazole (TMP-SMX), with the addition of corticosteroids for patients with HIV infection. Mortality rates of PJP remain high despite treatment, with survival rates of 86% to 92% in HIV-infected patients, and 51% to 80% in those without HIV infection.37
Hypersensitivity Pneumonitis (HP)
HP is an inflammatory reaction in the lungs caused by repeated inhalation of triggering particles. Chronic and severe cases can lead to pulmonary fibrosis. The offending particles are small enough to reach the lung parenchyma (1 to 5 μm) and elicit an immune response.38 Numerous types of exposures can cause this entity, often related to occupation, but also seen with recreational activities or contaminated air systems. Many antigens have been described as triggers, including plant and animal products, chemicals, chemotherapies, and aerosolized microorganisms. Development of this disease is multifactorial, and likely related to the levels and duration of exposure, type of antigen, and inherent host characteristics.39 Smokers are less likely to develop HP as their lungs are frequently and repeatedly exposed to antigens.
The diagnosis is made by combining clinical and radiographic features: exposure to triggering antigen, classic signs and symptoms, abnormal pulmonary function tests, and abnormal chest imaging. The sensitivity of chest radiography for the detection of HP is low and radiographs may be normal. If abnormal, findings depend on the phase of acuity. Early disease can manifest as numerous poorly defined small nodular opacities throughout both lungs and may spare apices and bases. Pulmonary edema pattern of patchy or diffuse GGO can also be seen. Later stages of disease are characterized by irreversible lung damage or fibrosis with reticulation and honeycombing and upper lobe predominant volume loss. Cardiomegaly can be seen as a result of cor pulmonale.40
CT has superior sensitivity, with abnormal findings in 90% of patients with clinical features of HP. Findings that can be seen by CT (Fig. 10) include GGO, which can be bilateral and symmetric, or patchy in the mid to lower lungs or in a bronchovascular pattern; numerous often poorly defined centrilobular nodules; mosaic attenuation; and a combination of patchy GGO, normal lung, and air trapping, known as the “head cheese sign.” Later stage disease may show a spectrum of fibrosis from reticulation to honeycombing, mediastinal lymphadenopathy, pulmonary arterial enlargement, midlung predominant, or diffuse centrilobular emphysema sparing the extreme apices and bases, and traction bronchiectasis and bronchiolectasis.38
Treatment entails removal of the offending antigen and steroids, if indicated. Prognosis is generally worse if fibrosis or severe respiratory impairment is present.41
DAH is an uncommon condition describing bleeding into pulmonary alveoli, caused by injury to the alveolar microcirculation. Clinical symptoms often include severe hemoptysis, anemia, and hypoxemic respiratory failure.42
DAH is associated with various disease entities, reflecting several histologic subtypes. The most common subtype is small-vessel vasculitis (ie, pulmonary capillaritis), typically resulting from seropositive systemic vasculitides or connective tissue disorders. Other subtypes are bland pulmonary hemorrhage and DAD.42
In one case review of DAH, capillaritis occurred in 88% of cases. The most common clinical cause was granulomatosis with polyangiitis (formerly Wegener’s granulomatosis) (32%), followed by Goodpasture syndrome (13%), idiopathic pulmonary hemosiderosis (13%), collagen vascular diseases (13%), and microscopic polyangiitis (9%).43
The imaging findings of DAH can vary with underlying disease etiology and chronicity. In up to 50% of cases, imaging of the lungs appears normal during the acute phase. Radiographic findings of acute alveolar hemorrhage include central and basilar predominant airspace opacities, with sparing of the costophrenic angles. The corresponding findings on CT are patchy GGO without significant interlobular septal thickening. CT findings in the subacute phase (within 48 h) include interlobular and intralobular interstitial thickening. If septal thickening occurs in the setting of pre-existing GGO, a crazy paving pattern is seen. Airspace opacities and septal thickening typically resolve within 2 weeks. If hemorrhagic episodes are chronic or recurrent, pulmonary fibrosis may develop. Chronic CT findings include regional architectural distortion with lobular sparing, on a background of coarse septal thickening and interstitial fibrosis.44
Granulomatosis with polyangiitis (formerly Wegener’s granulomatosis) is the most common cause of DAH on imaging (Fig. 11). It is a multisystemic necrotizing vasculitis associated with the presence of c-ANCA serum antibody. The classic imaging appearance is bilateral peribronchovascular nodules and masses, which may cavitate, surrounded by a halo of ground-glass opacity. GGO and consolidation, when they occur, indicate underlying DAH. Associated arteriolar vasculitis may cause a mosaic perfusion pattern. Focal or diffuse airway stenosis is an uncommon late-stage complication.44
On the basis of imaging findings seen in DAH, the differential diagnosis commonly overlaps with pulmonary edema and infection, including COVID-19. Cardiogenic pulmonary edema is often accompanied by cardiomegaly and rapidly changing radiologic findings, over the course of hours. The airspace opacities of DAH typically improve over the course of days. Pleural effusions are commonly seen in acute pulmonary edema, but they are uncommon in DAH. Also, unlike in pulmonary edema, radiographic findings in DAH are generally not gravity dependent. To differentiate from infectious etiologies, the presence of fever, cough, and leukocytosis are important.44
Bronchoalveolar lavage confirms the diagnosis of DAH. However, lung biopsy is often required to elucidate underlying histologic subtype. DAH treatment aims to directly address the underlying etiology and usually includes corticosteroids, immunosuppressive agents, and plasmapheresis.42
Pulmonary edema is defined as abnormally increased fluid within the extravascular spaces of the lung. In terms of pathophysiology, pulmonary edema may be classified as increased hydrostatic pressure (ie, cardiogenic), permeability with DAD (ie, ARDS), permeability without DAD, and mixed edema with increased hydrostatic pressure and permeability changes.45 The 2 most common clinical presentations resulting in pulmonary edema are congestive heart failure and fluid overload. The numerous other causes of pulmonary edema include postobstructive, acute asthma exacerbation, acute/chronic pulmonary embolism, veno-occlusive disease, near drowning, drug reaction, high-altitude sickness, inhalational injury, neurogenic, and reperfusion.45
Generally, pulmonary edema develops in 2 phases: interstitial and alveolar. These correspond with imaging findings on radiograph and CT (Fig. 12). Interstitial pulmonary edema manifests as distended pulmonary arteries and veins, interlobular septal thickening, and peribronchovascular interstitial thickening. Alveolar pulmonary edema is seen as airspace GGO or consolidation.46 The combination of septal thickening and GGO can result in a crazy paving pattern on CT, which may mimic the findings of COVID-19. Classically, cardiogenic pulmonary edema demonstrates central distribution of acute pulmonary opacities (ie, bat’s wing appearance), whereas permeability edema shows dependent distribution of opacities. In most cases of cardiogenic pulmonary edema, associated extrapulmonary imaging findings include cardiomegaly and pleural effusions.46
PAP is a rare condition that leads to abnormal intra-alveolar accumulation of surfactant due to altered surfactant homeostasis. This accumulation of surfactant can be either due to overproduction of phospholipids by pneumocytes, impaired clearance of surfactant by macrophages, or a combination of both.47
Adult patients with PAP may be asymptomatic or present with nonspecific symptoms of dyspnea, dry cough, fatigue, and weight loss, which may overlap with the clinical presentation of COVID-19.47,48 The most common elevated serologic marker in PAP is lactate dehydrogenase. Cases of idiopathic PAP also tend to have antibodies against granulocyte-macrophage colony-stimulating factor.47
Classically, imaging findings appear more severe than clinical presentation. Chest radiographs in patients with PAP most commonly demonstrate symmetric bilateral central lung opacities (GGO, reticular, or nodular) with relative sparing of the lung apices and costophrenic angles.47 Unilateral involvement or extensive diffuse consolidation are less common manifestations. Chest CT characteristically demonstrates widespread crazy paving with wide areas of regional or zonal predominance, and sharply marginated areas of geographic or lobular sparing (Fig. 13).47,48 Although these CT findings are characteristic of PAP, they are nonspecific and can be seen with several infectious, hemorrhagic, and idiopathic conditions, including COVID-19.
Treatment for PAP depends on the particular subtype of the disease. Idiopathic PAP requires sequential therapeutic whole-lung lavage, secondary PAP requires removing the offending agent, and congenital PAP typically requires lung transplant.47
As global rates of COVID-19 continue to rise, radiologists need to be aware of its imaging features, and those of common conditions that may mimic COVID-19 pneumonia. Although imaging is not currently recommended to play a diagnostic role, recognition of this entity as an incidental finding or in the setting of negative testing has diagnostic and management implications, and public health importance for managing staff exposures, patient isolation, and appropriate facility decontamination. At the very least, detection of imaging features that are typical of COVID-19 should prompt confirmation of the diagnosis with laboratory testing and further clinical evaluation.
1. Gorbalenya AE, Baker SC, Baric RS, et al. Severe acute respiratory syndrome-related coronavirus: the species and its viruses–a statement of the Coronavirus Study Group. bioRxiv. Published online February.
3. Hosseiny M, Kooraki S, Gholamrezanezhad A, et al. Radiology perspective of coronavirus disease 2019 (COVID-19): lessons from severe acute respiratory syndrome and Middle East respiratory syndrome. Am J Roentgenol. 2020;214:1–5.
4. Wang D, Hu B, Hu C, et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020;323:1061–1069.
5. Guan W-j, Ni Z-y, Hu Y, et al. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med. 2020;382:1708–1720.
6. Muniyappa R, Gubbi S. COVID-19 pandemic, coronaviruses, and diabetes mellitus. Am J Physiol Endocrinol Metab. 2020;318:E736–E741.
7. Wang Y, Wang Y, Chen Y, et al. Unique epidemiological and clinical features of the emerging 2019 novel coronavirus pneumonia (COVID-19) implicate special control measures. J Med Virol. 2020;92:568–576.
8. Lai C-C, Shih T-P, Ko W-C, et al. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and corona virus disease-2019 (COVID-19): the epidemic and the challenges. Int J Antimicrob Agents. 2020;55:105924.
9. Ai T, Yang Z, Hou H, et al. Correlation of chest CT and RT-PCR testing in coronavirus disease 2019 (COVID-19) in China: a report of 1014 cases. Radiology. 2020;296:32–40.
10. Hope MD, Raptis CA, Shah A, et al. A role for CT in COVID-19? What data really tell us so far. Lancet. 2020;395:1189–1190.
11. American College of Radiology (ACR). Recommendations for the use of chest radiography and computed tomography (CT) for suspected COVID-19 infection. Available at: https://www.acr.org/Advocacy-and-Economics/ACR-Position-Statements/Recommendations-for-Chest-Radiography-and-CT-for-Suspected-COVID19-Infection
. Accessed March 22, 2020.
12. Prinzi A. False negatives and reinfections: the challenges of SARS-CoV-2 RT-PCR testing. American Society of Microbiology. 2020. Available at: https://asm.org/Articles/2020/April/False-Negatives-and-Reinfections-the-Challenges-of
. Accessed April 27, 2020.
13. Yang Y, Yang M, Shen C, et al. Laboratory diagnosis and monitoring the viral shedding of 2019-nCoV infections. MedRxiv. 2020:493.
14. Rubin GD, Ryerson CJ, Haramati LB, et al. The role of chest imaging in patient management during the COVID-19 pandemic: a multinational consensus statement from the Fleischner Society. Chest. 2020;158:106–116.
15. Salehi S, Abedi A, Balakrishnan S, et al. Coronavirus disease 2019 (COVID-19): a systematic review of imaging findings in 919 patients. AJR Am J Roentgenol. 2020;215:1–7.
16. Bernheim A, Mei X, Huang M, et al. Chest CT findings in coronavirus disease-19 (COVID-19): relationship to duration of infection. Radiology. 2020;295:685–691.
17. Hansell DM, Bankier AA, MacMahon H, et al. Fleischner Society: glossary of terms for thoracic imaging. Radiology. 2008;246:697–722.
18. Simpson S, Kay FU, Abbara S, et al. Radiological Society of North America Expert Consensus Statement on reporting chest CT findings related to COVID-19. Endorsed by the Society of Thoracic Radiology, the American College of Radiology, and RSNA. Radiology. 2020;2:e200152.
19. Wang Y, Dong C, Hu Y, et al. Temporal changes of CT findings in 90 patients with COVID-19 pneumonia: a longitudinal study. Radiology. 2020;296:200843.
20. Zhou S, Wang Y, Zhu T, et al. CT features of coronavirus disease 2019 (COVID-19) pneumonia in 62 patients in Wuhan, China. Am J Roentgenol. 2020;214:1–8.
21. Franquet T. Imaging of pulmonary viral pneumonia. Radiology. 2011;260:18–39.
22. Koo HJ, Lim S, Choe J, et al. Radiographic and CT features of viral pneumonia. Radiographics. 2018;38:719–739.
23. Koo HJ, Lee HN, Choi SH, et al. Clinical and radiologic characteristics of human metapneumovirus infections in adults, South Korea. Emerg Infect Dis. 2019;25:15–24.
24. Lan B, Lu P, Zeng Y, et al. Clinical imaging research of the first Middle East respiratory syndrome in China. Radiol Infect Dis. 2015;2:173–176.
25. NIH. COVID-19, MERS & SARS. 2020. Available at: https://www.niaid.nih.gov/diseases-conditions/covid-19
. Accessed May 8, 2020.
26. Zeng Z, Huang X-R, Lu P-X, et al. Imaging manifestations and pathological analysis of severe pneumonia caused by human infected avian influenza (H7N9). Radiol Infect Dis. 2015;1:64–69.
27. Jeong YJ, Kim K-I, Seo IJ, et al. Eosinophilic lung diseases: a clinical, radiologic, and pathologic overview. Radiographics. 2007;27:617–637.
28. Durieu J, Wallaert B, Tonnel A. Long-term follow-up of pulmonary function in chronic eosinophilic pneumonia. Groupe d’Etude en Pathologie Interstitielle de la Societe de Pathologie Thoracique du Nord. Eur Respir J. 1997;10:286–291.
29. Mehrian P, Shahnazi M, Dahaj AA, et al. The spectrum of presentations of cryptogenic organizing pneumonia in high resolution computed tomography. Pol J Radiol. 2014;79:456–460.
30. Kligerman SJ, Franks TJ, Galvin JR. From the radiologic pathology archives: organization and fibrosis as a response to lung injury in diffuse alveolar damage, organizing pneumonia, and acute fibrinous and organizing pneumonia. Radiographics. 2013;33:1951–1975.
31. Lee JW, Lee KS, Lee HY, et al. Cryptogenic organizing pneumonia: serial high-resolution CT findings in 22 patients. Am J Roentgenol. 2010;195:916–922.
32. Cordier J-F. Organising pneumonia. Thorax. 2000;55:318–328.
33. Lalani TA, Kanne JP, Hatfield GA, et al. Imaging findings in systemic lupus erythematosus. Radiographics. 2004;24:1069–1086.
34. Kim SJ, Lee KS, Ryu YH, et al. Reversed halo sign on high-resolution CT of cryptogenic organizing pneumonia: diagnostic implications. Am J Roentgenol. 2003;180:1251–1254.
35. Marchiori E, Zanetti G, Meirelles GSP, et al. The reversed halo sign on high-resolution CT in infectious and noninfectious pulmonary diseases. Am J Roentgenol. 2011;197:W69–W75.
36. Catherinot E, Lanternier F, Bougnoux M-E, et al. Pneumocystis jirovecii
pneumonia. Infect Dis Clin North Am. 2010;24:107–138.
37. Kanne JP, Yandow DR, Meyer CA. Pneumocystis jiroveci
pneumonia: high-resolution CT findings in patients with and without HIV infection. Am J Roentgenol. 2012;198:W555–W561.
38. Hirschmann JV, Pipavath SN, Godwin JD. Hypersensitivity pneumonitis: a historical, clinical, and radiologic review. Radiographics. 2009;29:1921–1938.
39. Yi ES. Hypersensitivity pneumonitis. Crit Rev Clin Lab Sci. 2002;39:581–629.
40. Unger G, Scanlon G, Fink J, et al. A radiologic approach to hypersensitivity pneumonias. Radiol Clin North Am. 1973;11:339–356.
41. Vourlekis JS, Schwarz MI, Cherniack RM, et al. The effect of pulmonary fibrosis on survival in patients with hypersensitivity pneumonitis. Am J Med. 2004;116:662–668.
42. Lara AR, Schwarz MI. Diffuse alveolar hemorrhage. Chest. 2010;137:1164–1171.
43. Travis WD, Colby TV, Lombard C, et al. A clinicopathologic study of 34 cases of diffuse pulmonary hemorrhage with lung biopsy confirmation. Am J Surg Pathol. 1990;14:1112–1125.
44. Lichtenberger JP III, Digumarthy SR, Abbott GF, et al. Diffuse pulmonary hemorrhage: clues to the diagnosis. Curr Probl Diagn Radiol. 2014;43:128–139.
45. Gluecker T, Capasso P, Schnyder P, et al. Clinical and radiologic features of pulmonary edema. Radiographics. 1999;19:1507–1531.
46. Levesque M-H, Montesi SB, Sharma A. Diffuse parenchymal abnormalities in acutely dyspneic patients. J Thorac Imaging. 2015;30:220–232.
47. Frazier AA, Franks TJ, Cooke EO, et al. Pulmonary alveolar proteinosis. RadioGraphics. 2008;28:883–899.
48. Holbert JM, Costello P, Li W, et al. CT features of pulmonary alveolar proteinosis. Am J Roentgenol. 2001;176:1287–1294.