Pulmonary edema

Pulmonary edema is a broad descriptive term and is usually defined as an abnormal accumulation of fluid in the extravascular compartments of the lung ¹.

Pathology

One method of classifying pulmonary edema is as four main categories on the basis of pathophysiology which include:

• increased hydrostatic pressure edema
  • two pathophysiological and radiological phases are recognized in the development of pressure edema 
    • interstitial edema
    • alveolar flooding or alveolar edema
  • these phases are virtually identical for left-sided heart failure and fluid overload
• permeability edema with diffuse alveolar damage
• permeability edema without diffuse alveolar damage  
• mixed edema due to simultaneous increased hydrostatic pressure and permeability changes

It can arise from a range of cardiogenic and non-cardiogenic causes.

Causes

• cardiogenic pulmonary edema:
  • left heart failure
    • congestive cardiac failure
  • mitral regurgitation ^5,7
• non-cardiogenic pulmonary edema: 
  • fluid overload
  • pulmonary edema with acute asthma
  • post-obstructive pulmonary edema/post intubation pulmonary edema / negative pressure pulmonary edema
  • pulmonary edema in pulmonary thromboembolism
  • pulmonary edema due to air embolism
  • pulmonary veno-occlusive disease
  • near drowning pulmonary edema / asphyxiation pulmonary edema
  • ARDS - pulmonary edema with diffuse alveolar damage
  • heroin-induced pulmonary edema
  • pulmonary edema following administration of cytokines
  • transfusion-related acute lung injury
  • high-altitude pulmonary edema
  • neurogenic pulmonary edema
  • reperfusion pulmonary edema
  • pulmonary edema following lung transplantation
  • re-expansion pulmonary edema
  • post-pneumonectomy pulmonary edema
  • post lung volume reduction pulmonary edema
  • pulmonary edema from anti-snake venom administration ⁸

The causes of non-cardiogenic pulmonary edema can be recalled with the following mnemonic: NOTCARDIAC.

Radiographic features

Plain radiograph

The chest radiograph remains the most practical and useful method of radiologically assessing and quantifying pulmonary edema ^3-4.

Features useful for broadly assessing pulmonary edema on a plain chest radiograph include:

• upper lobe pulmonary venous diversion / pulmonary venous engorgement / stag's antler sign
• increased cardio-thoracic ratio / cardiac silhouette size: useful for assessing for an underlying cardiogenic cause or association
• features of pulmonary interstitial edema:
  • peri-bronchial cuffing and perihilar haze
  • septal lines / Kerley lines
  • thickening of interlobar fissures
• features of pulmonary alveolar edema:
  • air space opacification classically in a batwing distribution 
  • may have air bronchograms
• pleural effusions and fluid in interlobar fissures (including 'vanishing' pulmonary pseudotumour)

There is a general progression of signs on a plain radiograph that occurs as the pulmonary capillary wedge pressure (PCWP) increases (see pulmonary edema grading). Whether all or only some of these features can be appreciated on the plain chest radiograph, depend on the specific etiology ¹. Furthermore, pulmonary edema is usually a bilateral process, but it may uncommonly appear to be unilateral in certain situations and pathologies (see unilateral pulmonary edema). 

Ultrasound

The appearance of pulmonary edema is defined as a function of the perturbation of the air-fluid level in the lung, a spectrum of appearances coined the alveolar-interstitial syndromes. 

As subpleural interlobular septae thicken among air filled alveoli, they create an medium in which incident ultrasound waves will reverberate within, creating a short path reverberation artifact.  Referred to as B-lines, these are pathological when more than 3 appear, garnering the title lung rockets, and consistent with thickened interlobular septae. When spaced 7 mm apart they correlate with radiographic interstitial edema and when 3 mm apart with ground glass opacification. When surrounding alveoli become fluid filled, the resultant interface assumes a tissue-like pattern. The tissue-like sign and shred sign are pathognomic ¹⁰. 

Differential diagnosis

General imaging differential considerations include other causes of diffuse airspace opacification:

• diffuse pulmonary hemorrhage: has no dependent gradient and usually no pleural effusion
• diffuse pneumonia ⁶: usually no dependent gradient
• pulmonary alveolar proteinosis: usually no pleural effusion

See also

• pulmonary edema grading
• unilateral pulmonary edema
• bedside lung ultrasound in emergency