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References

31

 

 

Table 2.1 Common diseases manifesting as lung mass

Disease

Key points for differential diagnosis

Malignant condition

 

Lung caner

Wash-in values of >25 HU, lobulated

 

or spiculated margin, and absence of

 

a satellite nodule

BALT lymphoma

Consolidation or nodule with air

 

bronchograms

Pulmonary sarcoma

Large mass with heterogeneous

 

enhancement

Nontumorous condition

 

Benign tumor

 

Rounded atelectasis

Round mass abutting a thickened

 

pleura, comet tail sign

Progressive massive

Mass with irregular margin and

Þbrosis

associated paracicatricial

 

emphysema, low SI on T2WI

Actinomycosis

Consolidation or mass containing

 

central low attenuation and

 

peripheral enhancement

Semi-invasive aspergillosis

 

Note: BALT bronchus-associated lymphoid tissue, HU HounsÞeld unit,

SI signal intensity, T2WI T2-weighted images

CT Findings

In acute disease, actinomycosis manifests as a small, poorly deÞned, and peripheral pulmonary nodule with or without interlobular septal thickening on CT. With progression of infection, the pulmonary nodule gradually increases in extent to manifest as an airspace consolidation or a mass. Typically, consolidation or mass contains central areas of low attenuation with peripheral enhancement [6] (Fig. 2.5). Other CT Þndings include hilar or mediastinal lymphadenopathy, localized pleural thickening, or pleural effusion.

CT–Pathology Comparisons

Pulmonary parenchymal infection is characterized pathologically by bronchopneumonia with focal or multifocal abscess formation. The low-attenuation areas on contrastenhanced CT represent abscesses or dilated bronchi containing inßammatory exudate; the enhancing rim corresponds to vascular granulation tissue in the abscess wall or hyperplastic bronchial vessels in the mucosa of draining airways [6].

Pulmonary Actinomycosis

Pathology and Pathogenesis

Actinomycosis is an infection caused by the anaerobic Þlamentous bacteria Actinomyces species. Acute bronchopneumonia with abscess formation is the initial reaction, and the process typically progresses to Þbrosis. The process is often associated with localized interlobular septal and pleural thickening. In rare cases, infection can cause an endobronchial infection. The endobronchial form reßects actinomycosis colonization of preexisting obstructive broncholiths or endobronchial foreign bodies, which causes the inßammation of the adjacent airway and results in distal obstructive pneumonia. Broncholiths are formed by erosion of calciÞed lymph nodes into the airway as a result of a granulomatous process [19].

Symptoms and Signs

Patients with small nodule or mass-like consolidation are often asymptomatic. The most frequent respiratory symptom is chronic cough. Constitutional symptoms of low-grade fever, weight loss, and fatigue may be the main complaints prior to the detection of lung lesion, which mimic the clinical features of malignancy, tuberculosis, and fungal infection. As disease progresses, most patients develop productive cough and pleuritic chest pain. In more advanced case, discharge of characteristic Òsulfur granuleÓ from the Þstula tract on the chest wall from the pleural cavity can be found.

Patient Prognosis

Pulmonary actinomycosis responds well to prolonged antibiotic treatment. Standard treatment is initial parenteral antibiotic administration for 4Ð6 weeks followed by at least 6 months of oral antibiotic therapy. In mild case, treatment duration can be shortened [20]. Adjunctive surgical resection may be necessary in the case with severe pleural and chest wall involvement.

References

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