ARDSthe first marker of multiple organ failure

The alterations of capillary permeability, and the activation of phagocytic and endothelial cells, are not limited to the lungs, but are seen elsewhere in the organism following infections and shock states. They also occur in organs after successive cycles of ischemia and reperfusion, as a result of mitochondrial dysfunction. This leads to falls in ATP synthesis and increased levels of intracellular calcium. The result is cellular edema, activation of enzymes, and production of active oxygen species. The contribution of this mechanism (ischemia-reperfusion) depends on the given organ's sensitivity to hypoperfusion; however, some degree of altered capillary permeability and cellular activation is present in virtually all organs. The clinical expression of this lesion, and of the inflammatory reaction that accompanies it, can be discrete despite the organ's exquisite sensitivity (such as the pancreas), while the clinical syndrome of respiratory failure is readily apparent in the lung early in the disease process. Among the organs damaged first are the kidneys, the heart, and the brain (dysfunction of these systems is well described during and after shock states), and also the intestines, the liver, and the pancreas. Altered mucosal permeability of the digestive tract implies the possibility of translocation of bacteria, toxins, and active digestive enzymes. Failure of hepatic macrophages promotes penetration of micro-organisms via the portal circulation, decreased metabolism of inflammatory mediators and products of cellular destruction (such as hemoglobin), and reduced synthesis of normal proteins. Pancreatic lesions involve penetration of active digestive enzymes into the circulation (trypsin, elastase, lipase, amylase, etc.). Some of these enzymes (such as trypsin) can activate the complement and coagulation cascades, destroy proteins and peptides, and contribute to saturating endogenous antiproteases, with establishment of a protease-antiprotease imbalance.

Once localized inflammatory reactions become excessive and poorly controlled, they lead to dispersal of mediators towards other sites and to the systemic inflammatory response syndrome. This can progress to frank multiple organ failure, frequently complicated by sepsis. Under these circumstances, ARDS becomes the earliest and easiest to diagnose aspect of a simultaneous syndrome of widespread visceral failure, as opposed to an isolated clinical entity.

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