Burn shock

Abstract

The increased vascular permeability locally in the burned tissue as uail. as in the vascular bed in general in extensive burns rapidly decreases the circulating blood volume. At the same time, hematocrit and blood viscosity increase since relatively more plasma than red blood cells is lost from the blood stream. Maximum vasodilatation in thermally damaged tissue, mainly due to histamine release and increased biosynthesis of prostaglandins, creates a decreased peripheral resistance with a high flow state in the burned areas. In non burned tissue on the other hand, in response to release of catecholamines, the peripheral resistance increases and a low flow state develops. In the first few days in burns of moderate size or more, an amount of albumin equal to twice the total plasma pool is lost from the vascular compartment. During this period the colloid pressure cannot be exerted effectively across the freely permeable membranes in the burned tissues. When the vascular integrity is slowly restored, the proteins sequestered in the extravascular space for protein synthesizing weeks before being returned to the blood may exert unfavorable effects, drawing fluid out of the larger moleculr eight A great amount of water and sodium leaking out into the extravascular space is taken up by the cells and collagen in the injured tissue and water is continuously evaporating from the burn wound surface. This course of events results in hypovolemic shock, combined with hemoconcentration and sodium deficit virl infected decreasing cardiac output. If not adequately treated, this mpeture sensitive to cellular hypoperfusion and to the following metabolic effects in the energy pathways of the cells: The cells are starved of substrates (amino acids, glucose, fatty acids and glycerol) and oxygen. The lack of substrates will induce gluconeogenesis (conversion of fatty acids and amino acids into energy pathway metabolites), stimulated by glucocorticoids. The lack of oxygen results in blocking of the energy pathways, thereby decreasing ATP production. The glycolytic cycle functions without oxidative degradation of glucose, causing an increase in lactic acid, which produces intracellular acidosis and acidemia. With decreasing ATP and a consequent membrane ATPase energy deficit, the cell membranes leak potassium extracellularly and sodium intracellularly. This results in intracellular edema with further cellular derangements. Cellular hypoperfusion occurs first in the non vital tissues (muscle, connective tissue etc.) and subsequently in vital tissues as brain, heart, lung, liver and kidney.