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BURN DISEASE. DETERMINATION, FLOW STAGES
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 common to distinguish the following phases: burn shock, burn toxemia, and burn septic toxemia, resulting in convalescence, or burn exhaustion. 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.
PATHOGENESIS OF BURN SHOCK
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 coordination 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 the compensatory abilities of the victim.
Another reason for the development of a microcirculation crisis in the area of a burn wound 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 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 life span of the remaining ones.
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.
CLINIC OF BURN SHOCK
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. Observed thirst. In severe shock, reflex paresis of the gastrointestinal tract often develops, which can cause vomiting. Due to a violation of water and electrolyte balance, seizures and muscle twitching often occur.
An important diagnostic sign is the reduction of 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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BURN DISEASE. DETERMINATION, FLOW STAGES
- Burn disease
Clinical manifestations. In a burn disease, the central and peripheral nervous system is involved in the pathological process, which undergoes significant both functional and morphological changes. In the first hours of a burn shock, approximately 25% of the victims experience excitement, alternating with inhibition of the shock. Deep reflexes are enhanced, may
- Burn disease
Clinic. Burn disease develops after thermal effects (II – IV degrees) by 10–15% or more than 50% of the body surface (with I degrees burns) with disorders of the vital activity of the whole organism (changes in the functions of the nervous system, internal organs, metabolism) and (current difference Phases of burn disease: burn shock, burn infection (toxemia), burn depletion
- Traumatic Disease. COMBAT FIRE INJURY. BURN DISEASE
Since prehistoric times, mankind has an acute problem of treating wounds and injuries resulting from armed conflicts, wars, natural disasters and man-made disasters. Out of five and a half thousand years of the development of human civilization, traced and studied by historical science, there were no significant armed conflicts on Earth for only 300 years. Practically
- BURNS. BURN DISEASE
DEFINITION. Burns are tissue damage caused by thermal, chemical, electrical, or radial energy. According to the etiological factor, burns are usually called thermal, chemical and radiation. EPIDEMIOLOGY High energy intensity of modern production, life, transport, wide use of high voltage current, aggressive chemical products and
- DETERMINATION OF THE STAGE OF ONCOGYNECOLOGICAL DISEASE THROUGH DIAGNOSTIC LAPAROTOMY
Modern oncogynecology requires precise determination of the stage of a malignant disease in order to select the most effective treatment method. Previously used non-invasive examination methods are now complemented by an extended diagnostic laparotomy. Many patients may actually have a more common process than is established with non-invasive examination methods.
- BURN DISEASE
- BURN DISEASE
- TREATMENT OF THE BURN DISEASE IN THE STAGE OF TOXEMIA AND SEPTICOTOXEMIA
The main principles of treatment are: 1. Detoxification The basis of detoxification therapy consists of two complementary directions: elimination of the source of intoxication and elimination of toxins from the internal media of the body. The source of intoxication is a burn wound (treatment tactics, see below - "Local treatment of burns"). Removal of toxic products absorbed into the blood and lymph
- Features of intensive care in other periods of burn disease
Period II (acute toxemia) of a burn disease is characterized by signs of intoxication and further circulatory disorders. On average, it lasts up to two weeks. After the burned-out shock comes out, the resorption of fluid from the lesion begins. In the bloodstream enters a large number of toxic substances, which contributes to the increase in the level of proteolytic enzymes. Developing
- Forms and stages of the disease
Each disease develops in a period of more or less time. Some diseases proceed very quickly, others - slowly. From the point of view of the rapidity of development of diseases, the most acute are distinguished - up to 4 days, acute - about 5–14 days, subacute - 15–40 days and chronic, lasting months and years. Separation is somewhat arbitrary, but the terms "subacute", "acute" and "chronic" disease are used.
- Task 28. HYPERTENSIVE III STAGE DISEASE
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- Problem 27. Hypertensive Disease I Stage
Pregnant Sh., 32 years old, was admitted to the maternity hospital for preeclampsia, at gestational age 24-25 weeks. Complaints of recurrent headaches in the occipital region. From anamnesis. Pregnancy the third first ended 6 years ago with urgent deliveries of a live, full-term baby. The second pregnancy ended 2 years ago with a medical abortion, without complications. Registered in female consultation with 14-15
- stages of the disease, clinic, laboratory diagnosis, treatment
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- Observation diary (course of illness)
This section of the case history is in the form of a diary. The existing form contains four headings: date, body temperature, the actual text of the diary (the course of the disease) and destination. Diary entries - medical art. In the diary should not be missed significant of what happened to the patient over the past period of time. Doctor's records should reflect the dynamics of the disease and the opinion
- Clinical protocol for the provision of medical care to patients with hypertension (essential hypertension) stage I — II
ICD-10 rubric: I0 – I5 Conditions in which medical aid should be provided Patients with GB I and II stages are subject to outpatient examination and treatment at the place of residence in district clinics by district physicians or family doctors. In severe cases, to exclude symptomatic (secondary) hypertension, additional examination and diagnosis refinement is carried out in urban cardiac,
- Progressive or stationary course of the disease
Hydrocephalus has a progressive or stationary (non-progressive) course. The stationary flow is observed with the compensation of pathological processes leading to hydrocephalus. When hydrocephalus occurs a kind of change in the psyche. At the onset of the disease, mechanical memory is good. Patients quickly memorize poems. Mostly mechanical memory (however, this feature is not