Even when only one side of the chest is injured, inflammation may also affect the other lung. Uninjured lung tissue may develop edema, thickening of the septa of the alveoli, and other changes. If this inflammation is severe enough, it can lead to dysfunction of the lungs like that seen in acute respiratory distress syndrome. Ventilation/perfusion mismatch
Normally, the ratio of ventilation to perfusion is about one-to-one; the volume of air entering the alveoli (ventilation) is about equal to that of blood in the capillaries around them (perfusion). This ratio is reduced in pulmonary contusion; fluid-filled alveoli cannot fill with air, oxygen does not fully saturate the hemoglobin, and the blood leaves the lung without being fully oxygenated. Insufficient inflation of the lungs, which can result from inadequate mechanical ventilation or an associated injury such as flail chest, can also contribute to the ventilation/perfusion mismatch. As the mismatch between ventilation and perfusion grows, blood oxygen saturation is reduced. Pulmonary hypoxic vasoconstriction, in which blood vessels near the hypoxic alveoli constrict (narrow their diameter) in response to the lowered oxygen levels, can occur in pulmonary contusion. The vascular resistance increases in the contused part of the lung, leading to a decrease in the amount of blood that flows into it,  directing blood to better-ventilated areas. Although reducing blood flow to the unventilated alveoli is a way to compensate for the fact that blood passing unventilated alveoli is not oxygenated, the oxygenation of the blood remains lower than normal.
An adults more bony chest wall absorbs more of the force itself rather than transmitting it. Thus children commonly get pulmonary contusions without fractures overlying them, while elderly people are more likely to develop fractures than contusions. One study found that pulmonary contusions were accompanied by fractures 62% of the time in children and 80% of the time in adults. Pathophysiology
Pulmonary contusion results in bleeding and fluid leakage into lung tissue, which can become stiffened and lose its normal elasticity. The water content of the lung increases over the first 72 hours after injury, potentially leading to frank pulmonary edema in more serious cases. As a result of these and other pathological processes, pulmonary contusion progresses over time and can cause hypoxia (insufficient oxygen). Bleeding and edema
In contusions, torn capillaries leak fluid into the tissues around them. The membrane between alveoli and capillaries is torn; damage to this capillary–alveolar membrane and small blood vessels causes blood and fluids to leak into the alveoli and the interstitial space (the space surrounding cells) of the lung. With more severe trauma, there is a greater amount of edema, bleeding, and tearing of the alveoli. Pulmonary contusion is characterized by microhemorrhages (tiny bleeds) that occur when the alveoli are traumatically separated from airway structures and blood vessels. Blood initially collects in the interstitial space, and then edema occurs by an hour or two after injury. An area of bleeding in the contused lung is commonly surrounded by an area of edema.