Normally, oxygen and carbon dioxide diffuse across the capillary and alveolar membranes and the interstitial space (top). Fluid impairs this diffusion, resulting in less oxygenated blood (bottom).<unk>  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<unk>  edema in more serious cases. As a result of these and other pathological processes,<unk>  progresses over time and can cause hypoxia (insufficient oxygen). Bleeding and edema In<unk> s, 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.<unk>  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. In normal gas exchange, carbon dioxide diffuses across the endothelium of the capillaries, the interstitial space, and across the alveolar epithelium; oxygen diffuses in the other direction. Fluid accumulation interferes with gas exchange, and can cause the alveoli to fill with proteins and collapse due to edema and bleeding. The larger the area of the injury, the more severe respiratory compromise will be. Consolidation and collapse<unk>  can cause parts of the lung to consolidate, alveoli to collapse, and atelectasis (partial or total lung collapse) to occur. Consolidation occurs when the parts of the lung that are normally filled with air fill with material from the pathological condition, such as blood. Over a period of hours after the injury, the alveoli in the injured area thicken and may become consolidated. A decrease in the amount of surfactant produced also contributes to the collapse and consolidation of alveoli; inactivation of surfactant increases their surface tension. Reduced production of surfactant can also occur in surrounding tissue that was not originally injured. Inflammation of the lungs, which can result when components of blood enter the tissue due to<unk> , can also cause parts of the lung to collapse. Macrophages, neutrophils, and other inflammatory cells and blood components can enter the lung tissue and release factors that lead to inflammation, increasing the likelihood of respiratory failure. In response to inflammation, excess mucus is produced, potentially plugging parts of the lung and leading to their collapse. 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<unk> ; 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.<unk>  hypoxic vasoconstriction, in which blood vessels near the hypoxic alveoli constrict (narrow their diameter) in response to the lowered oxygen levels, can occur in<unk> . 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. If it is severe enough, the hypoxemia resulting from fluid in the alveoli cannot be corrected just by giving supplemental oxygen; this problem is the cause of a large portion of the fatalities that result from trauma.
Pulmonary contusion
Hemothorax
Pulmonary hematoma
Diaphragmatic rupture
Urinothorax
Hemopneumothorax
Hydropneumothorax
Flail chest