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A pulmonary contusion, also known as lung contusion, is a bruise of the lung, caused by chest trauma. As a result of damage to capillaries , blood and other fluids accumulate in the lung tissue. The excess fluid interferes with gas exchange , potentially leading to inadequate oxygen levels ( hypoxia ).
An injury that is potentially more serious than pulmonary contusion, pulmonary laceration involves disruption of the architecture of the lung, [2] while pulmonary contusion does not. [3] Pulmonary laceration is commonly caused by penetrating trauma but may also result from forces involved in blunt trauma such as shear stress.
A pulmonary contusion is another cause of bleeding within the lung tissue, but these result from microhemorrhages, multiple small bleeds, and the bleeding is not a discrete mass but rather occurs within the lung tissue. An indication of more severe damage to the lung than pulmonary contusion, a hematoma also takes longer to clear. [3]
Diffuse alveolar damage (DAD) is a histologic term used to describe specific changes that occur to the structure of the lungs during injury or disease.Most often DAD is described in association with the early stages of acute respiratory distress syndrome (). [1]
VALI is most common in people receiving mechanical ventilation for acute lung injury or acute respiratory distress syndrome (ALI/ARDS). [1] 24 percent of people mechanically ventilated will develop VALI for reasons other than ALI or ARDS. [1] The incidence is probably higher among people who already have ALI/ARDS, but estimates vary widely. [1]
Cardiogenic pulmonary edema and ARDS are common causes of a fluid-filled lung. Diffuse alveolar hemorrhage is a rarer cause of diffuse GGO seen in some types of vasculitis, autoimmune conditions, and bleeding disorders. [6] Inflammation and fibrosis can also cause diffuse GGOs.
The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. [1]
It is often impossible to distinguish TRALI from acute respiratory distress syndrome (ARDS). The typical presentation of TRALI is the sudden development of shortness of breath, severe hypoxemia (O 2 saturation <90% in room air), low blood pressure, and fever that develop within 6 hours after transfusion and usually resolve with supportive care within 48 to 96 hours.