Pulmonary infarction

Pulmonary  infarction  (usually haemorrhagic) is most commonly caused by pulmonary embolism (PE) in combination with chronic left heart failure. It occurs in the minority (10-15%) of patients with PE 2.


The demographics of affected patients are older than those of patients with 'simple' pulmonary embolism (PE) as young patients with no co-morbidities are usually not affected. Risk factors for lung infarction in the setting of pulmonary embolism are coexisting cardiovascular disease and underlying malignancy.  Moreover, the greater the embolic burden, the greater the likelihood of developing lung infarction 1-2,4-5.



The lungs are generally infrequently infarcted due to them being supplied by two vascular systems with many anastomoses:

  • pulmonary vascular system
  • bronchial vascular system
    • consists of the bronchial arteries that are responsible for the majority of oxygen supply to the lung parenchyma
    • form a broad network with pre- and postcapillary anastomoses to the pulmonary system; the bronchial arteries have the ability to increase their flow up to 300% 


Lung infarction is seen more often when vessels of a diameter ≤ 3 mm are occluded, than in cases of central pulmonary artery occlusion 1, 5.

Following a pulmonary embolus, the bronchial arteries continue to supply the parenchyma with oxygen, but often they feed the pulmonary capillary network through anastomoses too. The higher pressure of the bronchial arteries compared to the pressure in the capillary system, in combination with locally increased vascular permeability and capillary endothelial injury leads to an extravasation of blood cells into the alveolar and bronchial cavities. Usually the blood cells will be resorbed and the tissue regenerates with restitute ad integrum.

This is not the case if:

  • reduce the flow in the bronchial arteries (e.g. shock, hypotension, use of vasodilators)
  • increase the pulmonary venous pressure (elevated pulmonary venous pressure, interstitial oedema)

In this case haemorrhage tends to progress into infarction. The necrotic parenchyma will be replaced by fibrous tissue and leads to a collagenous platelike mass with pleural retraction 1, 4-5.

Radiographic features

Chest radiograph

Typical chest x-ray findings include 2-3:

  • wedge shaped (less often rounded) pleurally based opacification (Hampton hump) without air bronchograms
  • more often in the lower lobes
  • in the case of pulmonary hemorrhage without infarction the opacities resolve, usually within a week, by maintaining their shape (the so called "melting sign")
  • in the case of infarction it requires months to heal and will leave a linear scar

 CT features include 2-3

  • like on plan film, wedge shaped (less often rounded) pleurally based opacification (Hampton hump) without air bronchograms
  • consolidation with internal air lucencies, "bubbly consolidation"; this represent non-infarcted aerated lung parenchyma co-existing side-by-side with infarcted lung in the same lobule 6
  • convex borders with a halo sign due to adjacent haemorrhage.
  • feeding vessel with visualisation of the thrombus
  • sometimes scattered areas of low attenuation within the lesion (necrosis) and sometimes enhancement of the perimeter of the infarct
  • cavitation: may seen in septic embolism and in infection of a bland infarct (cavitatory pulmonary infarction)

Treatment and prognosis

Content required

Differential diagnosis

For peripheral wedge shaped regions on CT consider.

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