Lipoid Pneumonia

Fig. 20.5 Diffuse alveolar hemorrhage manifesting as crazy-paving appearance at thin-section CT in a 60-year-old man who had ischemic cardiomyopathy and received heparin and warfarin therapy. (aÐc) Lung window images of CT scans (2.5-mm section thickness) obtained at levels of main bronchi (a), cardiac ventricle (b), and liver dome (c),

respectively, show patchy and extensive areas of ground-glass opacity containing internal reticulation (crazy-paving appearance, arrows) in both lungs. Subpleural sparing is overt in all lung zones. (d) Coronal reformatted image (2.0-mm section thickness) also demonstrates crazypaving appearance (arrows) in both lungs with subpleural sparing

respiratory failure due to a severe inßammation caused by microbial degradation after antimicrobial therapy, the addition of corticosteroids is indicated for all patients with HIV infection and conÞrmed cases [10].

Lipoid Pneumonia

Pathology and Pathogenesis

There are two types of lipoid pneumonia: exogenous lipoid pneumonia and endogenous one (also called cholesterol pneumonia or golden pneumonia). Exogenous lipoid pneumonia is caused by repeated episodes of aspiration or inhalation of fat or oils, resulting in their accumulation within

alveolar macrophages that are incapable of metabolizing the fatty substances. Therefore, oil is repeatedly released into the alveoli, eliciting a foreign-body reaction. Mineral oil is the most common irritant.

Histologically, multiple round to oval cystic spaces (lipid vacuoles that are washed out during processing) surrounded by varying amounts of histiocytes and multinucleated foreign-body giant cells are found (Fig. 20.8). Endogenous lipoid pneumonia is usually associated with bronchial obstruction, thus resulting in the accumulation of cellular breakdown products including cholesterol and its esters from destroyed alveolar cell walls. These lipids are phagocytized by macrophages, which then accumulate within the alveolar spaces. Histologically, there are intraalveolar accumulation of foamy macrophages containing

Fig. 20.6 Pneumocystis jirovecii pneumonia in a 48-year-old man with asthma who received corticosteroid therapy. (a, b) Lung window images of CT scans (2.5-mm section thickness) obtained at levels of right middle lobar bronchus (a) and right inferior pulmonary vein (b), respectively, show diffuse ground-glass opacity harboring internal reticulation (crazy-paving appearance, arrows) in both lungs. Subpleural sparing is seen in all lung zones. (c) Coronal reformatted

image (2.0-mm section thickness) also demonstrates crazy-paving appearance (arrows) in both lungs with subpleural sparing. (d) HighmagniÞcation (×200) photomicrograph of transbronchial lung biopsy specimen obtained from right lower lobe discloses intra-alveolar foamy exudate (arrows) and mild interstitial inßammation and Þbrosis suggesting Pneumocystis pneumonia and acute lung injury

Þne lipid vacuoles (less than 1 μm) and eosinophilic proteinaceous materials derived from degenerating cells, including surfactant from type II pneumocytes, in the alveoli distal to the bronchial obstruction [13].

Symptoms and Signs

Symptoms can vary signiÞcantly among affected patients, ranging from asymptomatic to severe life-threatening disease

[14]. However, symptoms are usually mild. Chronic cough and dyspnea are the most common symptoms.

CT Findings

The most common CT Þndings of acute or chronic lipoid pneumonia are low attenuation areas of consolidation and a crazy-paving pattern (Fig. 20.8). The consolidation is most commonly seen within the dependent portions of the lungs.