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.
Highlights
Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and necrosis of the lung parenchyma
(1) The reported annual incidence of pulmonary embolism (PE) varies between 75 and 269 cases per 100,000 persons, and mortality rates as high as 28% have been described. [1,2,3,4] the dual blood supply to the lungs, i.e. the pulmonary and the bronchial circulation, is thought to be protective against pulmonary ischemia, pulmonary infarction can be found in 10 to 50% of all patients with PE. [5] This wide range is the result of the difference in definition of pulmonary infarction used in literature, which varies from pulmonary infarction as a clinical syndrome to a radiological finding or a histological phenomenon
The presence and extent of local collateral circulation was recognized to play a vital role whether or not infarction occurs. [9,11,13] It is thought that, these bron chopulmonary anastomoses are present in every individual, they are usually not functional in healthy conditions. [13,19] When changes in hydrostatic pressure in the lung vasculature are perceived, for example when the pressure within a pulmonary artery falls considerably distal to an embolic obstruction, it is thought that an increase in bronchial blood flow, together with an increase in vasoactive substances cause these anastomoses to dilate, allowing blood supply by the bronchial circulation. [8,19,20]
Summary
Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and necrosis of the lung parenchyma. It is most often caused by acute pulmonary embolism (PE), a frequently occurring and potentially life-threatening disease. [5] This wide range is the result of the difference in definition of pulmonary infarction used in literature, which varies from pulmonary infarction as a clinical syndrome to a radiological finding or a histological phenomenon Literature on this complication is limited, and pulmonary infarction is scarcely addressed in PE guidelines, if at all. In this review we will summarize current knowledge on the patho physiology, epidemiology, diagnosis and prognosis of pulmonary infarction in the setting of acute PE (Fig. 1)
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