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When surface burns are limited in area, the body’s response to injury is usually poorly pronounced. Deep and extensive burns are manifested by a general reaction of the body, called a burn disease. However, it must be remembered that superficial, but extensive, as well as small in size, but deep burns can cause quite serious pathophysiological disorders.

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


The pathogenesis of burn shock is based on complex pathophysiological and biochemical processes. The mass of tissue heated during a burn becomes a source of afferent impulsation, which leads to the uncoordination of the processes of excitation and inhibition in the central nervous system (CNS). The neuroendocrine response (stress response) leads to a powerful release into the blood of ACTH, antidiuretic hormone, catecholamines and corticosteroids. Pain impulses and endocrine stress response cause general vascular spasm, dramatically worsening the peripheral blood flow and microcirculation.

Psychomotor agitation due to unbearable pain is observed, 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 compensatory abilities of the victim.

Another reason for the development of a microcirculation crisis in the burn wound area is thrombosis of small vessels. There is a sharp increase in capillary permeability. In severe burns, the violation of permeability is so pronounced that colloidal substances with a mass of more than 150 thousand, i.e. albumin, go into extravascular space.

Neuro-endocrine stress response to trauma and hypovolemia leads to pronounced activation of the coagulation system, which sharply worsens the microcirculation and contributes to an increase in the necrosis zone due to a stasis zone in the affected area.
In parallel with the coagulation but somewhat slower, the anticoagulation system is activated. Developing fibrinolysis increases plasma loss and may cause secondary bleeding.

There are profound changes in the composition of blood and plasma. As a result of thermal hemolysis, up to 30% of erythrocytes circulating in the blood are destroyed, and the toxic effects of tissue decomposition products and biogenic amines lead to a significant reduction in the remaining lifetimes.

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 a decrease in the stroke 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 heart failure, which is the main clinical manifestation of the torpid phase of burn shock amid the continuing crisis of microcirculation.


The clinic of burn shock in the erectile phase does not have a pathognomonic picture. Of great importance is the state of the upper respiratory tract, since the burn of this area is equal in severity 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 is significantly reduced, the feeling of cold is increasing, the development of chills is possible. Tachycardia, dyspnea, and cyanosis persist, increasing as the shock deepens. There is marked thirst. In severe shock, reflex paresis of the gastrointestinal tract often develops, which can cause vomiting. Due to the violation of water and electrolyte balance often there are convulsions and muscle twitching.

An important diagnostic feature is a reduction in central venous pressure (CVP). His fall indicates the imminent development of heart failure.

However, the simplest and earlier prognostic sign is the development of oliguria, and then, possibly, anuria. The normal hourly amount of urine exceeds 30 ml / h (on average, about 50 ml / h). Pathological impurities appear in the urine - protein, cylinders, free hemoglobin, filtered through the kidneys during hemolysis.
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