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Pulmonary infarction due to pulmonary embolism

Cleveland Clinic Journal of Medicine. 2018 November;85(11):848-852 | 10.3949/ccjm.85a.17132
November 1, 2018|Cleveland Clinic Journal of Medicine
Melda Sonmez, MD;Loutfi S. Aboussouan, MD;Carol Farver, MD;Sudish C. Murthy, MD, PhD;Roop Kaw, MD
Author and Disclosure Information

Melda Sonmez, MD
Medical Student, Koc University School of Medicine, Istanbul, Turkey

Loutfi S. Aboussouan, MD
Department of Pulmonary, Allergy, and Critical Care Medicine, Cleveland Clinic; Associate Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Carol Farver, MD
Department of Pathology, Cleveland Clinic; Professor of Pathology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Sudish C. Murthy, MD, PhD
Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic; Professor of Surgery, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Roop Kaw, MD
Departments of Hospital Medicine and Outcomes Research Anesthesiology, Cleveland Clinic; Associate Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western University, Cleveland, OH

Address: Roop Kaw MD, Departments of Hospital Medicine and Outcomes Research Anesthesiology, M2 Annex, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; kawr@ccf.org

RISK FACTORS FOR PULMONARY INFARCTION

4. Which statement about risk factors for pulmonary infarction in pulmonary embolism is incorrect?

  • Heart failure may be a risk factor for pulmonary infarction
  • Pulmonary hemorrhage is a risk factor for pulmonary infarction
  • Pulmonary infarction is more common with more proximal sites of pulmonary embolism
  • Collateral circulation may protect against pulmonary infarction

Infarction is more common with emboli that are distal rather than proximal.

Dalen et al15 suggested that after pulmonary embolism, pulmonary hemorrhage is an important contributor to the development of pulmonary infarction independent of the presence or absence of associated cardiac or pulmonary disease, but that the effect depends on the site of obstruction.

This idea was first proposed in 1913, when Karsner and Ghoreyeb17 showed that when pulmonary arteries are completely obstructed, the bronchial arteries take over, except when the embolism is present in a small branch of the pulmonary artery. This is because the physiologic anastomosis between the pulmonary artery and the bronchial arteries is located at the precapillary level of the pulmonary artery, and the bronchial circulation does not take over until the pulmonary arterial pressure in the area of the embolism drops to zero.

Using CT data, Kirchner et al5 confirmed that the risk of pulmonary infarction is higher if the obstruction is peripheral, ie, distal.

Using autopsy data, Tsao et al18 reported a higher risk of pulmonary infarction in embolic occlusion of pulmonary vessels less than 3 mm in diameter.

Collateral circulation has been shown to protect against pulmonary infarction. For example, Miniati et al14 showed that healthy young patients with pulmonary embolism were more prone to develop pulmonary infarction, probably because they had less efficient collateral systems in the peripheral lung fields. In lung transplant recipients, it has been shown that the risk of infarction decreased with development of collateral circulation.19

Dalen et al,15 however, attributed delayed resolution of pulmonary hemorrhage (as measured by resolution of infiltrate on chest radiography) to higher underlying pulmonary venous pressure in patients with heart failure and consequent pulmonary infarction. In comparison, healthy patients without cardiac or pulmonary disease have faster resolution of pulmonary hemorrhage when present, and less likelihood of pulmonary infarction (and death in submassive pulmonary embolism).

Data on the management of infected pulmonary infarction are limited. Mortality rates have been as high as 41% with noninfected and 73% with infected cavitary infarctions.4 Some authors have advocated early surgical resection in view of high rates of failure of medical treatment due to lack of blood supply within the cavity and continued risk of infection.

KEY POINTS

In patients with a recently diagnosed pulmonary embolism and concurrent symptoms of bacterial pneumonia, a diagnosis of cavitary pulmonary infarction should be considered.

Consolidations that are pleural-based with sharp, rounded margins and with focal areas of central hyperlucencies representing hemorrhage on the mediastinal windows on CT are more likely to represent a pulmonary infarct.20

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