Release of reactive oxygen species, cytokines, prostaglandins, and other mediators follows. Damage-associated molecular patterns (DAMPs) activate local and systemic inflammatory responses. The immediate release of histamine and leukotrienes brings about peripheral vasodilation and contributes to the early drop in cardiac output that occurs even before significant plasma volume is lost. Successful management depends on understanding this trajectory ( Table 1).Ī complex interplay of inflammatory mediators steers the body’s transition through these phases in the response to injury. During the resuscitation period, which takes about 48 h to complete, a patient will pass through three phases with respect to hemodynamics. The mainstay of resuscitation is correction of hypovolemic shock by replacement of intravascular volume with intravenous crystalloid solution, augmented when needed by intravenous colloid solution. Collectively, these three processes contribute to decreased cardiac output and decreased end-organ perfusion. This is a complex phenomenon that features the following major features: (1) increased microvascular permeability, causing the loss of fluid similar to plasma from the intravascular space into the interstitium, resulting in hypovolemic shock (2) massive release of catecholamines, causing increased systemic vascular resistance and (3) a variable degree of myocardial dysfunction. Burn injuries involving 20% or more of the total body surface area (TBSA), or 10% TBSA in children or the elderly, are likely to result in burn shock.
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