title: [Traumatic shock--physiopathologic aspects].
abstract: Traumatic shock is a complex phenomenon that represents the culminating element of a series of events. It is, in fact, the outcome of an imbalance-decompensation of the organism's defence mechanisms, in which the oxygen supply to the mitochondria is hampered by a macro and/or microcirculation failure. Basically, it is a form of hypovolemic shock in which further factors have a role, including the activation of inflammation mediators. It should also be stressed that part of the cellular damage is caused by tissue reperfusion. Good hemodynamic compensation is maintained with loss of up to 30% of the circulation mass but, beyond this amount, a fall of the cardiac index, peripheral pO2, and an increase of blood lactates will ensue. Hypoxia causes capillary injury and increased permeability, resulting in the formation of edema and finally in loss of the self-regulating power of the microcirculation. Moreover, it strongly stimulates pro-inflammatory activation of the macrophages and the release of vasoactive substances, such as prostaglandins and thromboxanes. The inflammatory response is triggered by cascade systems (such as the complement, coagulation, kinins, fibrinolysis), cell elements (endothelium, leukocytes, macrophages, monocytes, mast cells) and the release of mediators (cytokines, proteolytic enzymes, histamine, etc.) and others interacting factors. In severe trauma, the inflammatory process extends beyond the local limits, maintaining and aggravating the state of shock and causing a Systemic Inflammatory Response Syndrome (SIRS), with involvement and injury of healthy organs and tissues even at a distance from the site of trauma, raising a risk of onset of ARDS (Acute Respiratory Distress Syndrome), sepsis, MODS (Multiple Organ Dysfunction Syndrome). Tissue reperfusion (reoxygenation) also induces the production of toxic metabolites, such as hydroxylated anions, superoxide, hydrogen peroxide: peroxidation of the phospholipid cell membranes alters the barrier functions, permitting entry of substances such as calcium, which interfere with the intracellular enzymatic systems.
authors.affiliation: Università degli Studi di Bari, Dipartimento Di Scienze Chirurgiche Generali e Specialistiche, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Fabiano
authors.forename: A
authors.initials: A
authors.lastname: Pezzolla
authors.forename: M A
authors.initials: MA
authors.lastname: Filograna
authors.forename: F
authors.initials: F
authors.lastname: Ferrarese
mesh_terms: D002199:Capillary Permeability; D006801:Humans; D020896:Hypovolemia / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism*; D009102:Multiple Organ Failure / Q000503:physiopathology; D011453:Prostaglandins / Q000378:metabolism; D012128:Respiratory Distress Syndrome / Q000503:physiopathology; D012772:Shock, Septic / Q000503:physiopathology; D012774:Shock, Traumatic / Q000378:metabolism / Q000503:physiopathology*; D018746:Systemic Inflammatory Response Syndrome / Q000503:physiopathology; D013931:Thromboxanes / Q000378:metabolism
chemical_list: D018836:Inflammation Mediators; D011453:Prostaglandins; D013931:Thromboxanes