Pulmonary infarction

Pulmonary infarction is most commonly caused by pulmonary embolism (PE) in combination with chronic left heart failure.

The demographics of affected patients are older than those of patients with 'simple' pulmonary embolism (PE) as young patients with no comorbidities are usually not affected. Pulmonary infarction occurs in the minority (10-15%) of patients with PE 2. 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.

Typical chest radiographic findings include 2-3:

  • wedge-shaped (less often rounded) juxtapleural opacification (Hampton hump) without air bronchograms
  • more often in the lower lobes
  • in the case of pulmonary haemorrhage 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 plain radiographs, wedge-shaped (less often rounded) juxtapleural 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)

Providing cardiopulmonary support is the initial treatment. Anticoagulation is done in patients without risk of active bleeding. If the emboli are large, thrombolysis is an option. In some cases, embolectomy and placement of vena caval filters are required.

For peripheral wedge-shaped lesions on CT, consider:

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Article information

rID: 12900
Systems: Vascular, Chest
Section: Gamuts
Synonyms or Alternate Spellings:
  • Lung infarction
  • Pulmonary infarct
  • Lung infarct
  • Lung infarctions
  • Lung infarcts
  • Pulmonary infarcts
  • Infarction of the lung
  • Infarction of lung

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Cases and figures

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    Case 1: pulmonary embolism with lung infarction
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    At least three il...
    Case 2
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    Case 2
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    Case 6: infarction with cavitation
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    Case 7: infarction from pulmonary emboli
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    Case 8
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