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

Pulmonary infarction occurs in the minority (10-15%) of patients with PE 2. It is more common in older patients with more comorbidities, young and otherwise healthy patients 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, higher the likelihood of developing lung infarction 1,2,4,5.

The lungs are not commonly infarcted, as they are supplied by two vascular systems with many anastomoses between them:

  • pulmonary vascular system
  • bronchial vascular system
    • consists of 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
    • bronchial arteries have the ability to increase their flow by up to 300% 

Thus, an occlusive pulmonary vascular lesion does not usually result in infarction because of alternative perfusion via collateral pathway.

Following an occlusive pulmonary embolus, the bronchial arteries are recruited as the primary source of perfusion for the pulmonary capillary network. The higher pressure of the bronchial arteries, in combination with locally increased vascular permeability and capillary endothelial injury, is thought to result in local pulmonary capillary haemorrhage. 

Usually these parenchymal findings are transient; the blood cells extravasated into the alveolar and bronchial cavities are resorbed, and the tissue regenerates with restitute ad integrum. However, the injury may progress to infarction in certain circumstances:

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

In these case, visceral perfusion is catastrophically compromised and the insult progresses to infarction. The necrotic parenchyma will be replaced by fibrous tissue and leads to a collagenous plate-like mass with pleural retraction 1,4,5.

The lungs are most at risk for infarction when distal vessels ≤3 mm in diameter are occluded, as opposed to central pulmonary artery occlusion 1,5. This is because there is more likely to be sufficient collateral circulation in a central obstruction.

In the acute/subacute setting, it may be difficult to differentiate ischemic pulmonary haemorrhage from actual lung infarction. The evolution of findings over time is helpful, as hemorrhage without infarction usually resolves within a week, while infarction evolves over months and results in parenchymal scarring.

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

Peripheral wedge shaped pulmonary consolidations are a classic manifestation of pulmonary infarct, particularly in the setting of a PE.

Recognized features include 2,3:

  • wedge-shaped (less often rounded) juxtapleural opacification (Hampton hump) without air bronchograms
  • consolidation with internal air lucencies, "bubbly consolidation"
    • represents non-infarcted aerated lung parenchyma co-existing side-by-side with infarcted lung in the same lobule 6
  • convex borders with a halo sign
    • secondary to adjacent haemorrhage
  • decreased in normal lung enhancement
    • may be scattered areas of low attenuation within the lesion (necrosis)
    • sometimes appears as hyperenhancement of the infarct perimeter
  • cavitation: may be seen in septic embolism and infection of a bland infarct (cavitatory pulmonary infarction)

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

For peripheral wedge-shaped lesions on CT, consider:

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Article information

rID: 12900
System: Chest, Vascular
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
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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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