Imaging of Pulmonary Viral Pneumonia 1 - SIRM

STATE OF THE ART: Imaging of Pulmonary Viral PneumoniaFranquetFigure 19Figure 19: (a) Bedside chest radiograph in a patient with severe hantavirus pulmonary syndrome shows extensive bilateral interstitial opacities.(b) Frontal chest radiograph obtained 6 hours later demonstrates rapid progression to diffuse perihilar and lower lung consolidation ,refl ecting associated diffuse alveolar damage. (Images courtesy of Loren Ketai, MD, Albuquerque, NM.)edema, fibrin, and variable numbersof inflammatory cells) and proliferative(eg, proliferation of reparative type IIpneumocytes, fibroblastic thickening ofthe alveolar septa with severe airspacedisorganization, and distortion of lungarchitecture) stages of diffuse alveolardamage ( 18 ).Chest radiographs may be initiallynormal but progressively worsen, displayingsigns of pulmonary edema andacute respiratory distress syndrome( 125 , 126 ). The findings at chest radiographymay represent differences inthe extent of alveolar epithelial damageseen in hantavirus pulmonary syndromeand acute respiratory distresssyndrome ( 127 ). The lack of peripheraldistribution of initial airspace disease,the prominence of interstitial edema,and the presence of pleural effusionsearly in the disease process are in contrastto the typical radiographic findingsin acute respiratory distress syndrome( 126 ) ( Fig 19 ).The CT appearances of hantaviruspulmonary syndrome consist of extensivebilateral ground-glass opacities,thickened interlobular septa, few poorlydefined small nodules, bronchial wallthick ening, and small bilateral pleuraleffusions ( 128 ).SARS.— SARS caused by SARSassociated coronavirus is a systemic infectionthat clinically manifests as progressivepneumonia ( 129 – 131 ). SARS was firstdetected in the Guangdong Province ofChina in late 2002, with major outbreaksin Hong Kong, Guangdong, Singapore,and Toronto and Vancouver, Canada( 132 ). More than 8000 people were affected,with a mortality rate of 10%.The typical clinical manifestation ofSARS-associated coronavirus includesan incubation period of 2–10 days, earlysystemic symptoms followed within 2–7days by dry cough or shortness of breath,the development of radiographically confirmedpneumonia by day 7–10, and, inmany cases, lymphocytopenia ( 133 , 134 ).Criteria for the confirmation of SARSat laboratory analysis include detectionof antibodies in a convalescent-phaseblood serum sample, detection of SARSassociatedcoronavirus in a clinical specimenwith reverse transcriptase PCR, orisolation of SARS-associated coronavirusin a cultured clinical specimen ( 135 ).Histologically, acute diffuse alveolardamage with airspace edema is the mostprominent feature in patients who diebefore the 10th day after onset of illness.Hyaline membranes, interstitial edema,interstitial infiltrates of inflammatorycells, and bronchiolar injury with lossof cilia are other observed features( 136 , 137 ). Patients who die after the 10thday of illness present with a mixture ofacute changes and those of the organizingphase of diffuse alveolar damage ( 19 )( Fig 5 ).The imaging features of SARS-associatedcoronavirus infection consist ofunilateral or bilateral ground-glass opacities,focal unilateral or bilateral areasof consolidation, or a mixture of both.In the areas of ground-glass opacification,thickening of the intralobular interstitiumor interlobular septa may bepresent ( Fig 20 ). If marked septal thickeningoccurs, a crazy-paving appearanceresults ( 134 , 138 – 141 ). Cavitation,calcification, a reticular or nodular patternof opacification, lymphadenopathy,or pleural effusion are not features ofSARS ( 14 ).Selected DNA VirusesAdenovirus.— Human adenoviruses arenonenveloped, double-stranded DNAviruses belonging to the family Adenoviridae.More than 50 serotypes havebeen described, and approximately halfof these serotypes are known humanpathogens. Depending on the serotype,adenovirus may cause respiratory diseaseRadiology: Volume 260: Number 1—July 2011 n radiology.rsna.org 29