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

Clinical presentation

The clinical presentation of pulmonary oedema includes:

• acute breathlessness

• orthopnoea

• paroxysmal nocturnal dyspnoea (PND)

• foaming at the mouth

• distress

Pathology

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

• increased hydrostatic pressure oedema

  • two pathophysiological and radiological phases are recognised in the development of pressure oedema 

    • interstitial oedema

    • alveolar flooding or alveolar oedema

  • these phases are virtually identical for left heart failure and fluid overload

• permeability oedema with diffuse alveolar damage (DAD)

• permeability oedema without diffuse alveolar damage (DAD)

• mixed oedema due to simultaneous increased hydrostatic pressure and permeability changes

Aetiology

Broadly causes can be classified as cardiogenic and non-cardiogenic:

• cardiogenic pulmonary oedema:

  • left heart failure

    • ​congestive cardiac failure

  • mitral regurgitation ⁵

  • aortic stenosis

  • arrhythmias

  • myocardial pathology

    • myocarditis

    • cardiomyopathy

• non-cardiogenic pulmonary oedema: 

  • fluid overload

  • pulmonary oedema with acute asthma

  • postobstructive pulmonary oedema / postintubation pulmonary oedema/negative pressure pulmonary oedema

  • pulmonary oedema in pulmonary thromboembolism

  • pulmonary oedema due to air embolism

  • pulmonary veno-occlusive disease

  • near-drowning pulmonary oedema / asphyxiation pulmonary oedema

  • ARDS: pulmonary oedema with diffuse alveolar damage

  • heroin-induced pulmonary oedema

  • pulmonary oedema following administration of cytokines

  • transfusion-related acute lung injury

  • high-altitude pulmonary oedema

  • neurogenic pulmonary oedema

  • reperfusion pulmonary oedema

  • pulmonary oedema following lung transplantation

  • re-expansion pulmonary oedema

  • post-pneumonectomy pulmonary oedema

  • post lung volume reduction pulmonary oedema

  • pulmonary oedema from anti-snake venom administration ⁸

  • activity-related

    • swimming-induced pulmonary oedema ¹¹

    • immersion pulmonary oedema

    • exercise-induced pulmonary oedema

  • acute selenium toxicity

The causes of non-cardiogenic pulmonary oedema 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 oedema ^3,4.

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

• upper lobe pulmonary venous diversion (stag's antler sign)

• increased cardiothoracic ratio/cardiac silhouette size: useful for assessing for an underlying cardiogenic cause or association

• features of pulmonary interstitial oedema:

  • peribronchial cuffing and perihilar haze

  • septal (Kerley) lines

  • thickening of interlobar fissures

• features of pulmonary alveolar oedema:

  • air space opacification classically in a batwing distribution 

  • may have air bronchograms

• pleural effusions and fluid in interlobar fissures (including 'vanishing' pulmonary pseudotumour)

A useful mnemonic is ABCDE.

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

CT

Interstitial pulmonary oedema is most commonly demonstrated by the following CT signs ⁷:

• ground glass opacification

• bronchovascular bundle thickening (due to increased vascular diameter and/or peribronchovascular thickening)

• interlobular septal thickening

Alveolar oedema is demonstrated by airspace consolidation in addition to the above findings.

Pleural effusions are a frequent accompanying finding in cardiogenic/hydrostatic pulmonary oedema.

Mediastinal and/or hilar lymph node enlargement can occur with congestive cardiac failure ¹².

Ultrasound

The appearance of pulmonary oedema 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 septa thicken among air-filled alveoli, they create a 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 three appear, garnering the title lung rockets, and consistent with thickened interlobular septa. When spaced 7 mm apart they correlate with radiographic interstitial oedema 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 pathognomonic ¹⁰. 

Differential diagnosis

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

• diffuse pulmonary haemorrhage: 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 oedema grading

• unilateral pulmonary oedema

• bedside lung ultrasound in emergency