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Airspace Disease


Airspace Disease

Pulmonary Oedema

Definition

  • An excess of extravascular lung water

    • ▪

      Cardiogenic oedema: increased hydrostatic pressure moves fluid out of the vascular compartment ▸ this is commonly caused by left heart failure ▸ it is rarely caused by a reduction in plasma osmotic pressure (e.g. hypoalbuminaemia)

    • ▪

      Non-cardiogenic oedema: this is caused by an increased alveolar-capillary barrier permeability

      • –

        Causes: fluid overload ▸ drowning ▸ drug induced ▸ ARDS ▸ high altitude ▸ rapid re-expansion of a collapsed lung ▸ intracranial disease

Radiological Features

CXR/CT

Fluid passes from the intravascular compartment into the interstitium and then into the alveoli (i.e. interstitial oedema precedes frank airspace opacification)

  • Interstitial oedema: oedema fluid collecting in a subpleural space manifests as thickening of the interlobar fissures or as a costophrenic recess lamellar ‘effusion’

    • ▪

      Kerley B lines: thickened interlobular septa (1- to 2-mm wide, 30- to 60-mm long) ▸ this occurs within the sub-pleural lung and perpendicular to the pleural surface

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      Kerley A line: these are longer (up to 80–100 mm) and occasionally angulated ▸ they cross the inner of the lung (and tend to point medially towards the hilum)

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      Peribronchial cuffing: thickened and indistinct airway walls

      Cardiogenic oedema Non-cardiogenic oedema
      Distribution Central ‘bat's wing’ Tends to be more peripheral
      Septal lines Common Less common
      Peribronchial cuffing Common Less common
      Pleural effusions Common Less common
      Cardiomegaly Yes No
      Pulmonary vasculature Upper lobe diversion No redistribution

    • ▪

      Perihilar haze: loss of conspicuity of the central pulmonary vessels

  • Alveolar oedema: this generally spares the apices and extreme lung bases ▸ usually there is bilateral opacification (it can be unilateral) ▸ opacities may coalesce to produce a general ‘white-out’ (± air bronchograms) ▸ resolution of any airspace opacification may be rapid (over hours) ▸ the distribution of pulmonary oedema can vary with posture (dependent lung becomes more oedematous)

    • ▪

      ‘Butterfly’ or ‘bat's wing’ distribution: this occurs if the central lungs are predominantly affected

  • Additional signs:

    • ▪

      Cardiomegaly: this indicates chronic heart disease, compared with a normal cardiac size seen after an acute myocardial infarction

    • ▪

      Pleural effusions: these are often bilateral

    • ▪

      Unilateral oedema: this can be seen in patients placed in a lateral decubitus position for some time ▸ the distribution can be affected by coexisting disease (e.g. emphysema can lead to patchy oedema)

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      Redistribution of blood to the upper zones: this occurs with an elevated pulmonary venous pressure (when erect oedema accumulates in the dependent lung, compressing these vessels and increasing basal resistance to flow): the diameter of the upper lobe vessels > the lower lobe vessels ▸ diameter of pulmonary arteries > adjacent bronchi seen end on

Pearl

  • Thickened interlobular septa are not diagnostic of pulmonary oedema – they may also be caused by fibrosis or malignant infiltration (e.g. lymphangitis carcinomatosa)

CT signs of pulmonary oedema
Common findings

  • Ground-glass opacification (patchy or diffuse) ± consolidation

  • Smooth interlobular septal thickening

  • Peribronchovascular thickening

  • Vascular dilatation

Ancillary findings

  • Pleural effusions

  • Enlargement of mediastinal lymph nodes/‘hazy’ opacification of mediastinal fat (in heart failure)—reversible

Magnified view of the left costophrenic region demonstrating multiple interstitial (Kerley B) lines. Each line is roughly perpendicular to the chest wall and extends to the pleural surface. *

Peribronchial cuffing. The wall of the anterior segmental bronchus appears thickened and ill-defined (arrows) in early interstitial oedema due to (iatrogenic) fluid overload. *

Pulmonary oedema on CT. There is diffuse ground-glass opacification, smooth thickening of multiple interlobular septa and peribronchovascular cuffing. Bilateral pleural effusions are also seen. *

Upper lobe blood diversion. Vessels in the upper zones (arrows) are prominent in comparison to those in the lower lung zones. *

Pulmonary oedema on CXR demonstrating the characteristic ‘bat's wing’ distribution, with airspace opacification principally within the central lung. *

Generalized thickening of the interlobular septa on a background of ground-glass opacification in a patient with cardiogenic pulmonary oedema. ©2

Airspace Disease

Diffuse Pulmonary Haemorrhage

Definition

  • Airspace bleeding is a surprisingly frequent event ▸ the severity can vary from small symptomless bleeds to life-threatening episodes

  • Multiple causes (see table)

Clinical Presentation

  • Recurrent haemoptysis ▸ dyspnoea ▸ chronic cough ▸ intermittent pyrexia ▸ headache ▸ lethargy ▸ basal crackles ▸ clubbing

Radiological Features

  • Similar appearances regardless of cause

CXR

  • Acute phase: widespread ground-glass opacification or consolidation (mainly affecting the perihilar regions of the mid and lower zones)

  • Chronic phase : with repeated episodes ill-defined nodular or reticulonodular opacities are seen ± hilar lymph node enlargement

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