Pathophysiology and metabolic response to injury and stress

As described originally by Cuthbertson [5], the metabolic response to injury includes an immediate shock or ebb phase and is associated with decreased intravascular volume, reduced tissue perfusion, low cardiac output, and relative hypometabolism, where total oxygen consumption is below normal levels [6]. Profound hypovolemia during this stage of injury may predispose or prime such patients for exacerbated hemodynamic and metabolic responses to subsequent injury after a second insult, such as endotoxemia, surgery, or further hypovolemia [7].

As successful restoration of adequate tissue perfusion is achieved, a physiologic state (the flow phase) of increased oxygen consumption and cardiac output is accompanied by increased muscle catabolism, erosion of lean body mass, and loss of body weight due to mobilization of fixed tissue stores of amino acids and other nutrients for biologic processes of seemingly higher biologic priority with inflammation that can last from days to weeks [2,3,6]. In patients with wounds, the catabolic phase gives way to a proliferative phase and maturation or remodeling of the wound. In the proliferative phase, fibroblasts are recruited to the inflammatory site, and extracellular matrix and collagen deposition occurs. Finally, in the maturation or remodeling phase, matrix metalloproteinases control extracellular matrix composition and facilitate cell migration to the epithelium.

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