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PNEUMONIA

Patients with severe pneumonia complicated by sepsis, respiratory failure, hypotension, or shock are seen frequently in the ICU. While many patients will have acquired pneumonia outside of the hospital, a substantial number will have nosocomial pneumonia, defined as lower respiratory tract infection occurring more than 48 hours after admission. Nosocomial pneumonia is the second most common nosocomial infection in the United States and is associated with high morbidity and mortality. Factors contributing to the high incidence of nosocomial pneumonias include endotracheal intubation or tracheostomy, prolonged mechanical ventilation, aspiration, and impaired host defenses. Inappropriate use of antimicrobials and emerging patterns of resistance has created additional treatment challenges.

Most radiologists sort the radiographic appearance of pneumonia into 3 categories that may aid in differentiation: lobar (alveolar or air space) pneumonia, lobular pneumonia (bronchopneumonia), and interstitial pneumonia. Lobar pneumonia is characterized on x-ray by relatively homogeneous regions of increased lung opacity and air bronchograms. The entire lobe does not need to be involved, and since the airways are not primarily involved, volume loss is not a frequent finding. Streptococcus pneumonia is the classic lobar pneumonia, although other organisms produce a similar pattern. Lobular pneumonia (bronchopneumonia) results from inflammation involving the terminal and respiratory bronchioles. The distribution is more segmental and patchy-appearing, affecting some lobules while sparing others. Mild volume loss may also be present. The most common organisms producing typical bronchopneumonia are Staphylococcus aureus and Pseudomonas species. Interstitial pneumonia is typically caused by viruses, Mycoplasma pneumoniae or, in immunocompromised patients, Pneumocystis jiroveci. Chest radiographs demonstrate an increase in linear or reticular markings in the lung parenchyma with peribronchial thickening.

Radiographic Features

Plain Films

The chest radiograph assesses for the presence and extent of pneumonia, as well as the existence of associated complications such as parapneumonic effusions, pneumatoceles, cavitation, and abscess formation. It also helps to gauge response to antibiotic therapy. A persistent pneumonia on the radiograph despite adequate therapy may raise suspicion for mimics of infectious pneumonia, including cryptogenic organizing pneumonia or bronchioalveolar carcinoma, or the presence of an obstructing mass.

The silhouette sign on the chest radiograph is useful for determining the site of pneumonia. When consolidation is adjacent to a structure of soft tissue density (eg, the heart or the diaphragm), the margin of the soft tissue structure will be obscured by the opaque lung. Thus, a right middle lobe consolidation may cause loss of the margin of the right heart border, lingular consolidation may cause loss of the left heart border, and lower lobe pneumonia may obliterate the diaphragmatic contour.

Cavitation and abscess formation are also important complications of pneumonia caused by necrosis of the pulmonary parenchyma. Typical causative agents include anaerobes and gram-negative organisms, but cavitation can also be caused by staphylococci, Mycobacterium tuberculosis, atypical mycobacteria, and fungi. Lung abscesses may also be polymicrobial. Complications of lung abscess include sepsis, cerebral abscess, hemorrhage, and spillage of contents of the cavity into uninfected lung or pleural space. A lung abscess usually appears as a rounded, focal mass with a thickened (5-15 mm), irregular wall and an air-fluid level. An air crescent sign (crescentic radiolucency around lung parenchyma) or a halo sign (pulmonary opacity surrounded by a zone of ground-glass attenuation) may also be present (Figure 11–11). Abscesses may be surrounded by adjacent parenchymal consolidation (Figure 11–12) or appear as areas of lucency within an area of consolidation.

Figure 11–11

Pulmonary aspergillosis with cavitation. Chest radiograph demonstrates a pulmonary opacity surrounded by a zone of ground-glass attenuation (halo sign, white arrow) and a crescent-shaped air density surrounding a parenchymal opacity (crescent sign, red arrow).

Figure 11–12

Cavitary pneumonia. Posteroanterior (A) and lateral (B) chest radiographs demonstrate consolidation with cavitation (arrows) in the superior segment of the left lower lobe. (Reproduced with permission from Bongard FS, Sue D, Vintch J: Current Diagnosis and Treatment Critical Care, 3rd edition. New York: McGraw-Hill Education; 2008.)

Pneumatoceles (Figure 11–13) are associated with pneumonia and are caused by alveolar rupture and resulting formation of subpleural air collections. Radiographically, they appear as single or multiple cysts with thin, smooth walls that often change in size and location on serial imaging. The most common causative agent is S aureus. Complications include pneumothorax and secondary infection.

Figure 11–13

Pneumatocele in Staphylococcus pneumonia.

Computed Tomography

The cross-sectional imaging plane and superior contrast resolution make CT useful in the evaluation of complicated inflammatory diseases. Cavitation, which may be obscured on plain films, is easily identified on CT.

Localization of parenchymal diseases facilitates the direction of invasive studies such as bronchoscopy or open lung biopsy. Superimposed pleural and parenchymal processes are more easily differentiated on CT than on plain films (Figure 11–14). The administration of intravenous contrast material can further facilitate the differentiation of pleural and parenchymal disease; pleural lesions will exhibit little to no enhancement with contrast, whereas parenchyma will demonstrate enhancement as well as the presence of blood vessels.

Figure 11–14

Pneumonia with loculated empyema. A. CT shows a loculated pleural effusion in the left hemithorax (arrows). B. Dense consolidation with air bronchograms in the left lower lobe. The consolidated lung enhances with contrast and is easily distinguished from the surrounding pleural effusion. (Reproduced with permission from Bongard FS, Sue D, Vintch J: Current Diagnosis and Treatment Critical Care, 3rd edition. New York: McGraw-Hill Education; 2008.)

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