Pulmonary infarction in acute pulmonary embolism

Abstract

Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma. It is most commonly caused by acute pulmonary embolism (PE), with a reported incidence of around 30%. Following an occlusion of the pulmonary artery, the bronchial arteries are recruited as primary source of perfusion of the pulmonary capillaries. The relatively higher blood pressure in the bronchial circulation causes an increase in the capillary blood flow, leading to extravasation of erythrocytes (i.e. alveolar hemorrhage). If this hemorrhage cannot be resorbed, it results in tissue necrosis and infarction. Different definitions of pulmonary infarction are used in literature (clinical, radiological and histological), although the diagnosis is nowadays mostly based on radiological characteristics. Notably, the infarcted area is only replaced by a fibrotic scar over a period of months. Hence and formally, the diagnosis of pulmonary infarction cannot be confirmed upon diagnosis of acute PE. Little is known of the impact and relevance of pulmonary infarction in acute PE, and whether specific management strategies should be applied to prevent and/ or treat complications such as pain, pneumonia or post-PE syndrome. In this review we will summarize current knowledge on the pathophysiology, epidemiology, diagnosis and prognosis of pulmonary infarction in the setting of acute PE. We highlight the need for dedicated studies to overcome the current knowledge gaps.

Peripheral Pulmonary Lesions in Confirmed Pulmonary Arterial Embolism

“…The embolic obstruction of the pulmonary artery may lead initially to hemorrhage in subsequent alveoli 19 . At this stage, the hemorrhagic area could be supplied by bronchial arteries and bronchopulmonary anastomoses 19 . In the case of inadequate systemic bronchial‐arterial supply (for example, due to congestive heart failure), this area is replaced by necrotic tissue 19 .…”

“…At this stage, the hemorrhagic area could be supplied by bronchial arteries and bronchopulmonary anastomoses 19 . In the case of inadequate systemic bronchial‐arterial supply (for example, due to congestive heart failure), this area is replaced by necrotic tissue 19 . The different pathological findings may be the explanation for different perfusion patterns on baseline CEUS and during follow‐up examinations 19 .…”

“…19 In the case of inadequate systemic bronchial-arterial supply (for example, due to congestive heart failure), this area is replaced by necrotic tissue. 19 The different pathological findings may be the explanation for different perfusion patterns on baseline CEUS and during follow-up examinations. 19 Lesions with homogeneous enhancement on baseline CEUS may show patterns of inhomogeneous/absent enhancement on follow-up CEUS in terms of secondary perfusion disturbance.…”

“…19 The different pathological findings may be the explanation for different perfusion patterns on baseline CEUS and during follow-up examinations. 19 Lesions with homogeneous enhancement on baseline CEUS may show patterns of inhomogeneous/absent enhancement on follow-up CEUS in terms of secondary perfusion disturbance. Furthermore, in lesions with inhomogeneous/absent enhancement on the baseline CEUS, reperfusion of nonperfused areas on follow-up CEUS indicated reparative processes and fibrinolysis.…”

“…17,18 The reason for delayed regression of PPLs due to pulmonary infarcts may be the development of necrotic tissue due to perfusion disturbance. 19 The aim of this study was to describe the B-LUS and CEUS follow-up patterns of PPLs in patients with confirmed PE.…”