Which term describes the collapse of a previously inflated area of lung tissue?

DIFFERENTIAL DIAGNOSIS

Causes of Acute Diffuse Pulmonary Consolidation

Acute diffuse pulmonary consolidation is nonspecific in neonates, as it is in adults, and can represent blood, pus, or water. In the neonate, the specific considerations include edema, which may be secondary to the development of patent ductus arteriosus (Fig. 3-11); pulmonary hemorrhage, to which surfactant therapy predisposes; worsening surfactant deficiency (during the first several days of life but not later); or developing neonatal pneumonia (Table 3-2). Diffuse microatelectasis is another possibility because neonates have the propensity to artifactually demonstrate diffuse lung opacity on low lung volume films (expiratory technique; Fig. 3-12A. B); this should not be mistaken for another cause of consolidation. Such radiographs showing low lung volumes offer little information concerning the pulmonary status of the patient and should be repeated when clinically indicated.

Differentiation of Lung Collapse from Consolidation

Many causes of pulmonary consolidation also cause a degree of collapse. Lobar pneumonia is typically associated with volume loss of about 25%. Volume loss of more than this would support predominant collapse over consolidation. Sometimes consolidation is associated with no volume loss or occasionally with lobar expansion, for example, in gram-negative pneumonia or proximal bronchial obstruction with fluid accumulation within the distal lung (drowned lung). The patterns of individual lobar or lung consolidation mirror those of collapse of the same lobes, although there is less evidence of volume loss. The presence of air bronchograms supports the diagnosis of consolidation over collapse.

Discussion

Chronic, diffuse pulmonary consolidation is much less common than acute, diffuse consolidation. Chronic consolidation is usually focal or multifocal rather than diffuse.

Alveolar proteinosis is an uncommon condition of unknown origin that is often diffuse. Occasionally, alveolar proteinosis may be caused by inhalation of large quantities of silica dust (i.e., silicoproteinosis) or be associated with marked immunosuppression. Alveolar proteinosis is characterized on high-resolution CT by the presence of smooth septal lines and intralobular lines superimposed on the ground-glass opacities, resulting in a crazy-paving pattern.

Organizing pneumonia most commonly results in a patchy, bilateral consolidation that has a predominantly peribronchial and peripheral distribution on CT, but it occasionally may be diffuse. Similarly, chronic eosinophilic pneumonia typically results in consolidation mainly in the peripheral lung regions, but it may occasionally be diffuse.

Bilateral consolidation that progresses slowly over several months should raise the possibility of lymphoma or bronchioloalveolar cell carcinoma.

Pathology

Necropsy reveals well-demarcated areas of pulmonary consolidation in the cranial and ventral areas of the lungs (Eckhoff et al., 1998; Finnie et al., 1999; Percy and Barthold, 2007). Histologically, necrotizing bronchitis/bronchiolitis is evident with pronounced desquamation of the epithelium and predominantly mononuclear cell infiltration. Airway occlusion by necrotic epithelial cell debris, leukocytes, and fibrin is seen (see Figure 23.1). In infected epithelial cells of the bronchi, nuclei contain distinctive round to oval basophilic inclusions that are 7–15 µm in diameter. Electron microscopy of pneumonic lesions reveals classic intranuclear adenoviral arrays in epithelial cells. Typical lesions have been observed in the airways of non-symptomatic animals (Crippa et al., 1997; Hankenson et al., 2010).

IMAGING

Pathological features

The macroscopic appearances vary from a localised tan or grey tumour to areas of apparent pulmonary consolidation (Fig. 12.4.9). Preserved bronchovascular bundles can sometimes be seen on the cut surface.

Microscopically, the tumours consist of small lymphocytes, which may be centrocyte-like, lymphocyte-like or monocytoid, although all are thought to be variations of the same neoplastic cell (Fig. 12.4.10A). They first proliferate around the bronchovascular bundles and then spread out in the connective tissue planes alongside blood vessels and their accompanying lymphatics. At this stage there is prominent involvement of the interlobular septa (Fig. 12.4.10B) and there may be pleural infiltration. As the disease progresses there is invasion of the alveolar walls, which are first expanded and then destroyed leading to filling of the air spaces and obliteration of the alveolar architecture (Fig. 12.4.10C, D).100 This ultimately results in a tumour mass in which only the larger airways and blood vessels are spared. The latter may be infiltrated101 but not on the scale seen with the angiocentric lymphoproliferative disorders. Ultimately, the tumour cells also infiltrate the pleura and bronchial cartilage. Hyaline sclerosis is common and lymphoid follicles are often evident, particularly when stains for the CD21 marker of follicular dendritic cells are employed (Fig. 12.4.11). Epithelioid and giant cell granulomas may rarely be observed (Fig. 12.4.12) and lymphoepithelial lesions are often present, recognition of which is facilitated by cytokeratin staining (Fig. 12.4.13). Giant lamellar bodies derived from type II pneumocytes may be seen within the tumour, possibly related to airway obstruction (Fig. 12.4.14).102 Amyloid is present in up to 10% of cases.5,6,103,104 Necrosis is rarely observed.

Pathology

Gross necropsy lesions included bronchopneumonia with profuse yellow watery bronchial exudate (Smith and Damit, 1982) and pulmonary congestion and consolidation with multifocal abscesses ranging from miliary to 2.5 cm in diameter (Retnasabapathy and Joseph, 1966; Butler et al., 1971; Mutalib et al., 1984). Multifocal abscesses in the liver, spleen, trachea, and stomach were observed in many cases (Kaufmann et al., 1970; Butler et al., 1971; Mutalib et al., 1984). Subcutaneous abscesses and abscessed peripheral lymph nodes were noted in macaques (Kaufmann et al., 1970). Swollen metacarpal joints containing exudate and peripheral lymphadenopathy with edema occurred in a chimpanzee (Butler et al., 1971). Exudation was noted around surgical implants (Kaufmann et al., 1970; Butler et al., 1971). The scoliotic lesion at T10–T13 in the paraplegic rhesus monkey was associated with spinal cord compression, mild exudation in the vertebral canal, and fibrosis of vertebral bodies (Fritz et al., 1986).

Multifocal microabscesses in the lung, liver, spleen, stomach, lymph nodes, and/or trachea were the primary microscopic lesion (Retnasabapathy and Joseph, 1966; Kaufmann et al., 1970; Butler et al., 1971; Mutalib et al., 1984; Fritz et al., 1986). Gram-negative bacteria could be visualized in the necrotic centers of the abscesses in some cases (Kaufmann et al., 1970). Acute suppurative bronchopneumonia was characterized by neutrophilic infiltration within and around bronchioles (Butler et al., 1971; Mutalib et al., 1984). Suppurative inflammation extended into surrounding alveoli, and the alveolar septae were thickened. Acute and chronic osteomyelitis occurred in affected thoracic vertebrae and metacarpal bones (Butler et al., 1971; Fritz et al., 1986).

IMAGING STUDIES

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Chest x-ray may be normal; suggestive findings include elevated diaphragm, pleural effusion, dilation of pulmonary artery, infiltrate or consolidation, abrupt vessel cut-off, or atelectasis. A wedge-shaped consolidation in the middle and lower lobes is suggestive of a pulmonary infarction and is known as “Hampton's hump.”

Lung scan (in patient with normal chest x-ray examination):

A normal lung scan rules out PE.

A ventilation-perfusion mismatch is suggestive of PE, and a lung scan interpretation of high probability is confirmatory.

If the clinical suspicion of PE is high and the lung scan is interpreted as low probability, moderate probability, or indeterminate, a pulmonary arteriogram is diagnostic; a positive arteriogram confirms diagnosis; a positive compressive duplex ultrasonography for DVT obviates the need for an arteriogram, because treatment with IV anticoagulants is indicated in these patients; the overall sensitivity of compressive ultrasonography for DVT in patients with PE is 29%, specificity 97%; adding ultrasonography in patients with a nondiagnostic lung scan prevents 9% of angiographies; however, this improvement in efficacy is achieved at the cost of unnecessary anticoagulant therapy in 26% of patients who have false-positive ultrasonography results.

Spiral CT is an excellent modality for diagnosing PE. It may be used in place of the lung scan and is favored in patients with baseline lung abnormalities on initial chest x-ray. It has the added advantage of detecting other pulmonary pathology that can mimic pulmonary embolism.

Angiography: pulmonary angiography is the gold standard; however, it is invasive, expensive, and not readily available in some clinical settings. False-positive pulmonary angiograms may result from mediastinal disorders such as radiation fibrosis and tumors. CT angiography is an accurate, noninvasive tool in the diagnosis of PE at the main, lobar, and segmental pulmonary artery levels. A major advantage of CT angiography over standard pulmonary angiography is its ability to diagnose intrathoracic disease other than PE that may account for the patient's clinical picture. It is also less invasive, less costly, and more widely available. Its major shortcoming is its poor sensitivity for subsegmental emboli. Gadolinium-enhanced magnetic resonance angiography of the pulmonary arteries has a moderate sensitivity and high specificity for the diagnosis of PE; MRA is best reserved for selected patients when CT scan and/or lung scan are inconclusive and the risk of pulmonary angiography is high.

Pathology

PVM replicates exclusively in the respiratory tract and reaches peak titers in the lung 6–8 days after infection. Although pulmonary consolidation can occur in experimentally infected mice, gross lesions are rare during natural infection. Histological lesions can occur in the upper and lower respiratory tract. They consist of mild necrotizing rhinitis, necrotizing bronchiolitis, and interstitial pneumonia, which usually occur within 2 weeks after exposure to virus and are largely resolved by 3 weeks. The predominant inflammatory infiltrate is comprised of mononuclear cells, but some neutrophils are usually present. Immunohistochemistry on paraffin-embedded tissues can be used to detect viral antigen in bronchiolar epithelium, alveolar macrophages, and alveolar epithelium during acute infection. Residual lesions include nonsuppurative perivasculitis, which can persist for several weeks after acute infection has ceased. Severe progressive pneumonia, with wasting, can occur in immunodeficient mice. It is characterized by generalized pulmonary consolidation that reflects severe interstitial pneumonia with desquamated alveolar pneumocytes and leukocytes filling alveolar spaces (Fig. 3.24).