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PATHOGENESIS AND CLINIC OF BURNING TOXIMIA AND SEPTICOTOXEMIA

The basis of the pathogenesis of burn toxemia is resorption of tissue breakdown products from a burn wound into the blood and lymph. This process is particularly pronounced in the first few days after receiving the burn, when granulations have not yet formed, which are the "wound barrier" in the path of absorption of toxins.

It has now been found that the pathogenesis of intoxication from the very beginning of the microbial factor is of essential importance. Any burn wound is primarily infected. Wet burn scab permeable to germs. In combination with a significant inhibition of all the body's defenses characteristic of a severe burn injury, the infectious process has a pronounced tendency to spread and generalize, i.e. development of burn sepsis. Thus, the release of individual stages of toxemia and septicotoxemia during a burn disease is largely conditional. The development of suppuration of a burn scab is considered to be the criterion for the change of toxemia with septicotoxemia.

The duration of the period of burn toxemia on average from 2 to 4 to 10 to 15 days. The end of this period coincides with the onset of marked suppuration in burn wounds. With deep and extensive lesions, toxemia proceeds to the third stage of the course of a burn disease - septicotoxemia, with lighter ones - it ends with recovery.

The leading signs of burn toxemia are fever with a body temperature of 38–39 ° C without chills or with minor chills, without significant differences in morning and evening temperatures, with moderate tachycardia and tachypnea.
The use of antibiotics and antipyretic drugs does not have a significant effect on the temperature response. Severe intoxication, in which the functions of all organs and systems suffer.

The clinic of burn septicoxemia depends on the severity and localization of purulent-septic processes and developing complications. The leading syndrome of this stage of the disease is purulent-resorptive fever, which disappears when cleansing wounds from necrosis and pus, decreases when prescribing antipyretic drugs.

An important symptom of the third stage of burn disease is difficult to replenish the loss of protein due to purulent-septic process. Continuing or progressive intoxication in combination with dystrophic lesions in vital organs leads to the depletion of the reparative capabilities of the body. Progression of exhaustion, often the development of sepsis. Burn wounds cease to heal, granulations become sluggish, dull, with gray bloom and abundant purulent discharge. Skin grafts cease to take root. This condition has received the name of BURN OF LOSS. The prognosis of its development and the absence of intensive treatment becomes unfavorable.
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PATHOGENESIS AND CLINIC OF BURNING TOXIMIA AND SEPTICOTOXEMIA

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