[Initial shock from burns. Physiopathology: therapeutic principles]

Widespread destruction of the skin induces a large necrotic mass and a break of the skin barrier. It also leads to an intense inflammatory reaction. This activates keratinocytes, endothelial cells and neutrophils. Certain mediators (e.g. endothelin, histamine, bradykinin, serotonin, catecholamines, vasopressin, prostaglandins, cytokines and nitrogen monoxide) are thus released in large quantities and act both at the site of the burns and at a distance. The abnormally high level of albumin in the capillary wall and the increased capacity of absorption of the interstitial areas around the burns are the main abnormalities observed. This results in a hypovolemia associated with a hemoconcentration, hyponatremia, hypoalbuminemia, systemic vasoconstriction and myocardial malfunction, which is difficult to evidence. During the initial phase, the major risk is the appearance of hypovolemic shock, which is rapidly irreversible if early treatment is not administered. Vascular filling with iso- or hyper-osmolar sodium crystalloids, associated with buffer solutions, is the first line. There is still debate regarding the best moment at which to give albumin. A hyperkinetic shock may occur after several hours and despite the filling. The symptoms are tachycardia, increased heart rate and a dramatic decrease in systemic vascular resistance. This may lead to metabolic acidosis and multi-organ failure. Study of the hemodynamic profile of the patient allows the rational use of pressor amines and haemodialysis.