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BURIAL DISEASE. DEFINITION, STAGES OF THE CURRENT

With limited surface burns, the body's response to trauma is usually not very pronounced. Deep and extensive burns are manifested by a general reaction of the body, called burn disease. However, it must be remembered that both superficial and extensive, as well as small in area, but deep burns can cause quite serious pathophysiological disturbances.

During the burn disease it is customary to distinguish the following phases: burn shock, burn toxemia and burn septicotoxemia, resulting in convalescence, or burn-out depletion. However, the commonality of many moments of pathogenesis and the complexity of processes occurring in the body do not always allow one to clearly distinguish separate phases from the general course of the disease. Thus, toxemia can sometimes develop before the patient leaves the state of shock. Possible options for the transition of severe shock directly into septicotoxemia.

PATHOGENESIS OF BURIAL SHOCK

At the heart of the pathogenesis of burn shock are complex pathophysiological and biochemical processes. The mass of tissue heated with a burn becomes a source of afferent impulses, which leads to discoordination of the processes of excitation and inhibition in the central nervous system (CNS). Neuroendocrine response (stress reaction) leads to a powerful release into the blood of ACTH, antidiuretic hormone, catecholamines and corticosteroids. Painful impulsation and endocrine stress reaction cause a common vascular spasm, sharply worsening peripheral blood flow and microcirculation.

There is psychomotor agitation because of intolerable pain, that is, the erectile phase of shock, which can last from 1-2 to 4-6 hours, depending on the depth and area of ​​the burn and the compensatory capabilities of the victim.

Another cause of the microcirculation crisis in the area of ​​the burn wound is thrombosis of small vessels. There is a sharp increase in the permeability of capillaries. With severe burns, permeability disturbance is so pronounced that colloidal substances with a mass of more than 150,000, i.е. albumins, go into extravascular space.

Nervous-endocrine stress reaction to trauma and hypovolemia lead to a pronounced activation of the coagulation system, which dramatically worsens microcirculation and promotes an increase in the necrosis zone due to the stasis zone in the lesion area.
In parallel, the anticoagulant system is activated somewhat more slowly. Developing fibrinolysis increases plasmolysis and can cause secondary bleeding.

There are profound changes in the composition of blood and plasma. Due to thermal hemolysis, up to 30% of red blood cells circulating in the blood are destroyed, and the toxic effect of the decay products of tissues and biogenic amines leads to a significant reduction in the lifetimes of the remaining.

Hypovolemia, hypoxia, toxemia lead to the development of metabolic disorders and impaired function of vital organs. First of all, it concerns the functional state of the heart muscle.

Simultaneously with the reduction of the shock volume of the heart, there is a decrease in regional perfusion of the liver, kidneys, brain and the heart itself, which leads to the development of renal, hepatic and worsening of heart failure, which is the main clinical manifestation of the torpid phase of burn shock when the microcirculation crisis persists.

CLINIC OF BURIAL SHOCK

The clinic of burn shock in the erectile phase has no pathognomonic picture. Of great importance is the condition of the upper respiratory tract, since the burn of this area is equated with gravity to a deep burn of 5-15% of the body surface.

As the torpid phase of shock develops, psychomotor agitation is replaced by inhibition and apathy. The pain significantly decreases, the feeling of cold increases, chills develop. Tachycardia, dyspnea and cyanosis persist, intensifying as the shock deepens. A marked thirst is observed. In severe shock, reflex paresis of the gastrointestinal tract often develops, which can cause vomiting. Owing to the violation of the water-electrolyte balance, convulsions and muscle twitching often occur.

An important diagnostic feature is the reduction in central venous pressure (CVP). Its fall testifies to the rapid development of heart failure.

However, the most simple and earlier prognostic sign is the development of oliguria, and then, perhaps, anuria. The normal hourly amount of urine exceeds 30 ml / h (average - about 50 ml / h). In the urine appear pathological impurities - protein, cylinders, free hemoglobin, filtered through the kidneys during the development of hemolysis.
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BURIAL DISEASE. DEFINITION, STAGES OF THE CURRENT

  1. Burn disease
    Clinical manifestations. In case of burn disease, the central and peripheral nervous system is involved in the pathological process, which undergoes significant functional and morphological changes. In the first hours of burn shock, about 25% of the affected people are experiencing excitement, which is replaced with a slowing of the shock by inhibition. Deep reflexes in this case are increased, can
  2. Burn disease
    Clinic. Burn disease develops after the thermal effects (II-IV degree) by 10-15% or more than 50% of the body surface (with burns of the 1st degree) with disorders of the vital activity of the whole organism (changes in the functions of the nervous system, internal organs, metabolism) and (flow difference The phases of burn disease: burn shock, burn infection (toxemia), burnout
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    Period II (acute toxemia) of burn disease is characterized by intoxication and further circulatory disorders. On average, it lasts up to two weeks. After the burn out of shock, resorption of the liquid begins from the lesion. A large number of toxic substances enter the vascular bed, which is facilitated by an increase in the level of proteolytic enzymes. Developing
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