Presentation
Acute onset of dyspnea 1 week ago. Past medical history includes alcoholism.
Patient Data
Note: This case has been tagged as "legacy" as it no longer meets image preparation and/or other case publication guidelines.
Right perihilar haziness (compare it with the normal contralateral hilum) with peribronchial cuffing and interlobular septal thickening (Kerley B lines).
Alveolar edema (note the distribution of the upper opacity, lying on the minor/horizontal fissure, this finding suggests a gravitational effect typical of pulmonary edema)
Bilateral pleural effusions.
Yellow arrows: Right perihilar haziness.
Green arrows: Interlobular septal thickening (Kerley B line) and peribronchial cuffing.
Red arrows: Alveolar edema (note the distribution of the upper opacity, lying on the minor fissure, this finding suggests a gravitational effect typical of pulmonary edema)
Blue arrows: Bilateral pleural effusion with right blunted costophrenic angle and superior margin of left pleural effusion.
Multiple CT images displayed with the lung window setting showing typical findings of pulmonary edema.
Coronal:
Red arrows: Pulmonary opacification lying on the minor fissure, this finding suggests a gravitational effect typical of pulmonary edema.
Blue arrow: Kerley A line.
Black arrows: Kerley B line.
Axial:
Red arrows: Thickening of bronchial walls
Blue arrows: Note the sparing of the peripheral lung with multiple central and perihilar ground-glass opacities.
Note the presence of cardiomegaly and bilateral pleural effusions.
Cardiomegaly with a very enlarged left ventricle, displacing the interventricular septum towards the right ventricle, as well as an enlarged left atrium.
Bilateral pleural effusions.
One day after the first chest plain film: Reduction of the right perihilar haze, alveolar edema and bilateral pleural effusions.
Two days after the first plain film: Resolution of the findings mentioned in the first x-ray with a persistent blunt left costophrenic angle representing small remnant pleural effusion.
Case Discussion
Pulmonary edema occurs when an increased hydrostatic pressure causes the passage of fluid from vessels to interstitium and alveolar space or when there is an injury to the lung parenchyma or vasculature which facilitates fluid movement.
There are several types of pulmonary edema, if we review its pathophysiology: increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema (increased hydrostatic pressure plus permeability changes):
- increased hydrostatic pressure: batwing edema (cardiogenic), asymmetric pulmonary edema (cardiogenic or underlying chronic pulmonary diseases), acute asthma, postobstructive pulmonary edema (relief from an airway obstruction), pulmonary thromboembolism (chronic overperfusion of non-affected lobes or in less than 10% of acute thromboembolism), veno-occlusive disease (lethal condition), near-drowning edema (mild cases).
- permeability edema with diffuse alveolar damage: diffuse alveolar damage (DAD) can be caused by an underlying pulmonary disease or by an extrapulmonary disease or agent (sepsis, pancreatitis, toxic gas, gastric fluid, blood transfusion etc.)
- permeability edema without diffuse alveolar damage: heroin-induced edema (10% mortality rate: depression of respiratory center, hypoxia and acidosis which cause permeability changes), administration of cytokines, high-altitude edema (secondary to acute and persistent hypoxia).
- mixed edema: neurogenic pulmonary edema (severe brain lesion), reperfusion pulmonary edema (thromboendarterectomy after massive thromboembolism), post-lung transplantation edema (the first 3 days, probably related to hypoxia), postreduction pulmonary edema (severe emphysema), re-expansion pulmonary edema, postpneumonectomy edema, air/gas embolism.
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