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 Indian J Med Microbiol  
 

Figure 5 (A-D): (A) Earliest changes of pulmonary edema (CVP 10-25 mmHg): redistribution of pulmonary veins- “cephalization” (curved white arrows). (B) With increasing pressure (CVP 20–25 mmHg), transudation of fluid around bronchi seen as peribronchial cuffing (curved black arrows). (C) Interstitial edema within lymphatics - Kerley B lines [thin, short lines 1–2 cm in length, at the periphery perpendicular to pleural surface] (black arrows). Other features seen are cardiomegaly, indistinctness of pulmonary vessels (asterisks), and early changes of perihilar bat wing opacities (white arrows). (D) At CVP 25- 30 mm Hg, fluid accumulates in alveoli producing classic perihilar batwing or angel wing consolidation (black arrow heads). Increased vascular pedicle width (black arrows) points to a likely underlying renal pathology (overhydration), leading to pulmonary edema

Figure 5 (A-D): (A) Earliest changes of pulmonary edema (CVP 10-25 mmHg): redistribution of pulmonary veins- “cephalization” (curved white arrows). (B) With increasing pressure (CVP 20–25 mmHg), transudation of fluid around bronchi seen as peribronchial cuffing (curved black arrows). (C) Interstitial edema within lymphatics - Kerley B lines [thin, short lines 1–2 cm in length, at the periphery perpendicular to pleural surface] (black arrows). Other features seen are cardiomegaly, indistinctness of pulmonary vessels (asterisks), and early changes of perihilar bat wing opacities (white arrows). (D) At CVP 25- 30 mm Hg, fluid accumulates in alveoli producing classic perihilar batwing or angel wing consolidation (black arrow heads). Increased vascular pedicle width (black arrows) points to a likely underlying renal pathology (overhydration), leading to pulmonary edema