Interstitial Pneumonia

Interstitial Pneumonia

Interstitial pneumonia is characterized histologically by a mononuclear inßammatory cell inÞltrate in the alveolar septa and interstitial tissue surrounding small parenchymal vessels (Figs. 26.7 and 26.8). The most common causes are

Mycoplasma pneumoniae, viruses, and Pneumocystis jiroveci. Because Mycoplasma pneumoniae pneumonia and

Pneumocystis pneumonia were described in other chapters, focused descriptions on viral pneumonias are rendered in this chapter.

The following are common pathologic Þndings in viral pneumonia: viruses can result in several pathologic forms of lower respiratory tract infection including tracheobronchitis,

a

c

cellular bronchiolitis, and pneumonia. Because viral organisms replicate within tissue cells, the most prominent histologic changes are observed in the epithelium and adjacent interstitium. In tracheobronchitis, airway walls are congested and lumen contains mononuclear cell inÞltrates. Degeneration and desquamation of the epithelial cells are seen. Cellular bronchiolitis, particularly important in children, appears with epithelial necrosis, neutrophilic exudate in the airway lumen, and predominantly mononuclear inÞltrates in its wall. Parenchymal involvement, the pneumonia, starts with the involvement of the lung adjacent to the terminal and respiratory bronchioles; however, extension throughout the lobule may occur (Fig. 26.7). Rapidly progressive pneumonia may occur particularly in the elderly and in

b

d

Fig. 26.7 Cytomegalovirus pneumonia over a follow-up period of 3 weeks in a 68-year-old woman with diffuse large B-cell lymphoma. (aÐc) Lung window images of CT scans (2.5-mm section thickness) obtained at levels of distal main bronchi (a), right inferior pulmonary vein (b), and cardiac ventricles (c), respectively, show bilateral bronchopneumonia pattern of lung abnormality comprising parenchymal opacity (arrows), tree-in-bud patterns (arrowheads), and variable-sized nodules (open arrows). (d) High-magniÞcation photomicrograph of

pathologic specimen obtained with transbronchial lung biopsy from left lower lobe discloses diffuse alveolar damage with Þbrinous exudate and interstitial Þbroblastic proliferation. Note suspicious viral inclusion (arrows) in atypical pneumocytes. (e) High-magniÞcation (×400) photomicrograph reveals a pneumocyte harboring intranuclear large viral inclusion (arrow), which is single, basophilic, and round to oval with peripheral halo. Inset: immunohistochemical staining (ABC methods, ×200) for cytomegalovirus showing many infected pneumocytes

e

Fig. 26.7 (continued)

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c

immunocompromised patients where the lungs histologically show diffuse alveolar damage comprising interstitial lymphocyte inÞltration, airspace hemorrhage, edema and Þbrin, type 2 cell hyperplasia, and hyaline membrane formation [5] (Figs. 26.7 and 26.8).

Viral pneumonia manifest radiologically as poorly deÞned nodules (airspace nodules of 4Ð10 mm in diameter) and patchy areas of peribronchial GGO and airspace consolidation. Because of the associated cellular bronchiolitis, hyperinßation is commonly present [5Ð7]. Progressive pneumonia shows the rapid conßuence of consolidation leading to diffuse alveolar damage, consisting of homogeneous or patchy unilateral or bilateral airspace consolidation and GGO or poorly deÞned small centrilobular nodules [5] (Figs. 26.7 and 26.8).

CT parenchymal lung abnormalities may be classiÞed into three main patterns according to the distribution and patterns of

b

d

Fig. 26.8 Adenovirus pneumonia in a 35-year-old woman with nonHodgkinÕs lymphoma who underwent hematopoietic stem cell transplantation 1 year ago. (a, b) Lung window images of thin-section (1.0-mm section thickness) CT scan obtained at levels of great vessels (a) and right inferior pulmonary vein (b), respectively, show extensive and patchy areas of ground-glass opacity (arrows) associated with interlobular septal thickening (arrowheads) and intralobular reticulation, forming so-called crazy-paving appearance in both lungs. (c) High-magniÞcation photomicrograph obtained with surgical lung

biopsy from left lower lobe displays intra-alveolar Þbrinous exudate forming hyaline membrane (arrows) and interstitial Þbroblastic proliferation (arrowheads) suggestive of mixed exudative and proliferative phase of diffuse alveolar damage (Reprinted from [11] with permission) (d) Photomicrographs of pathologic specimen (left, ×1,000) and after immunohistochemical staining for adenovirus (right, ×100) show alveolar lining cells with intranuclear inclusions (arrows, left) and poorly demarcated smudges (arrowheads, right) within nucleus, indicating positivity for adenovirus infection

Fig. 26.9 Inßuenza A (H1N1) pneumonia showing bronchopneumonia pattern in a 68-year-old woman with previous aortic valve replacement. (a) Lung window image of CT scan (2.5-mm section thickness) obtained at level of right bronchus intermedius shows multifocal areas of tree-in-bud signs (arrows) and lobular consolidation or poorly deÞned nodules (open arrows) in both lungs. Enlarged calciÞed and ruptured lymph nodes were seen in the bilateral hila and mediastina, indicating possible anthracoÞbrosis of airways on mediastinal window image. (b) CT scan obtained at level of right middle lobar bronchus demonstrates multifocal areas of tree-in-bud sign (arrows) and lobular area of ground-glass opacity (open arrow) in both lungs (Reprinted from Kang et al. [8] with permission)

Fig. 26.10 Inßuenza A (H1N1) pneumonia showing cryptogenic organizing pneumonia pattern in a 66-year-old man. (a) Lung window image of CT scan (2.5-mm section thickness) obtained at level of right upper lobar bronchus shows patchy areas of ground-glass opacity distributed mainly along bronchovascular bundles in both lungs. (b) Coronal reformatted (2.0-mm section thickness) CT scan also demonstrates parenchymal opacity lesions distributed along bronchovascular bundles (arrows) or subpleural (open arrows) lungs (Reprinted from Kang et al. [8] with permission)

the lung abnormalities: cryptogenic organizing pneumonia (COP), acute interstitial pneumonia (AIP), and bilateral extensive bronchopneumonia (Figs. 26.9, 26.10, and 26.11). This classiÞcation may help stratify patients with viral pneumonia in terms of their prognoses. In a particular viral pneumonia (inßuenza A [H1N1] pneumonia), patients with bronchopneumonia pattern have a tendency to belong to the mild illness group, whereas patients with AIP pattern show more severe clinical course in their outcome [8]. According to one study, CT Þndings in patients having a mild pneumonia course consist mainly of inßammatory lesions involving large or small airways with focal centrilobular small nodules with tree-in-bud sign and bronchiolar wall thickening [9]. Fatal cases of the same pneumonia present as areas of consolidation with or

without GGO on CT scans (AIP pattern) and the abnormalities are pathologically correlated with diffuse alveolar damage [10]. Therefore, it seems that pattern and extent of lung lesions observed at CT in viral pneumonias may be a determining factor for predicting patientÕs clinical course and prognosis [8].

The radiologic Þndings of adult viral pneumonias are variable and overlapping (Table 26.1). SpeciÞc organism diagnosis of a viral pneumonia cannot be made on the basis of imaging features alone. Clinical features such as patient age, immune status, time of year, illness in other family members, community outbreaks, onset, severity, duration of symptoms, and the presence of a rash remain as important aids in diagnosing viral causes of both atypical pneumonia and pneumonia in immunocompromised patients [5].

Fig. 26.11 Inßuenza A (H1N1) pneumonia showing acute interstitial pneumonia pattern in a 58-year-old woman with multiple myeloma. (a, b) Lung window images of CT scan (2.5-mm section thickness) obtained at level of right upper lobar bronchus (a) and lower lobar bronchi (b), respectively, show patchy and extensive parenchymal opacity

lesions without speciÞc zonal predominance in both lungs. Additionally, traction bronchiectasis is noted in right upper lobe, suggesting proliferative phase of diffuse alveolar damage. Lesions progressed on followup chest radiographs and patient died of the disease in following 6 days (Reprinted from Kang et al. [8] with permission)

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