At what area of ​​the burn does burn disease develop? Burn disease: stages, pathogenesis, treatment. Periods and clinic of burn disease

Burn disease – serious consequence for people injured by burns. However, not everyone develops this disease: the type and degree of burn, area, and depth of the damaged area are important; age of the victim; accompanying illnesses; absence/presence of additional factors.

Who most often develops burn disease and when?

1. Burn shock, signs and treatment

Burn shock– the reaction of the victim’s central nervous system to severe pain caused by a violation of the integrity of the skin, the thermal effect of the lesion. Symptoms and treatment here will depend on the severity of the burn.

General signs of the first period of burn disease:

  • The area of ​​damaged areas is more than 10%. If there is a simultaneous burn of the lungs and other organs of the respiratory system, burn shock can be diagnosed with 5% of skin damage.
  • Low/normal arterial pressure.
  • Frequent vomiting. It may have a thick, dark consistency - an unfavorable factor.
  • Changes in the smell of urine, its color (from cherry to black).

Before hospitalization, the disease in question can be diagnosed based on burned areas of the skin (more than 10%) and the presence of at least one of the above symptoms.

Treatment of burn shock involves A complex approach, aimed at:

  • Elimination pain. Removing excitement.
  • Normalization metabolic processes. The patient is prescribed corticosteroid hormones to monitor the activity of the stomach and intestines.
  • Neutralization of infection. The ideal option for placing a patient in a hospital is to provide him with a separate room, with a separate toilet/shower. Dressing (with sterile gauze/bandages) is recommended to be carried out within the patient's room. This will protect other patients from cross-infection. Throughout the patient's entire stay in the hospital (every 7-9 days), he needs to be administered antimicrobials. Since the body loses sensitivity to certain medications over time, it is necessary to determine the response to them.
  • Stabilization of functioning circulatory system. It is achieved through transfusion therapy, when, based on the patient’s body weight, age, and degree of burns, saline and salt-free solutions are infused into the victim every 8 hours. The total volume of these substances can vary from 4 to 14 liters. The fluid will be infused through a central vein using a catheter: until the wounds heal, the skin will not recover. The location of the catheter must be changed every 7 days to avoid suppuration. To control work urinary system a catheter is inserted into the urethra, and another one is inserted into the nose (to ensure Free access oxygen to patient's lungs). Plasma (infusion) is used as a bioactive substance.
  • Local treatment. It consists of regularly replacing dressings with sterile ones. Washing wounds is prohibited on the first day, as this can cause increased pain and worsen the patient’s condition.

2. Features of the treatment of acute burn toxemia

The great danger of this disease and the popular mortality rate during this period of burn disease is associated with negative influence breakdown products of toxins that form in the burn area.

The overall picture is complemented by microbial toxins, which together cause toxicosis in the victim.

Treatment of burn toxemia involves the following measures:

  • Detoxification. the main role allocated to transfusion therapy: daily protein-containing substances, various solutions (saline, glucose + insulin), and plasma substitutes are injected into the blood. In severe cases, accelerated diuresis is tried. For those diagnosed with liver problems, such therapy is replaced by plasmapheresem. Specific detoxification methods in the treatment of burn toxemia include infusion of immune plasma (antistaphylococcal, antiprotean, antipseudomonal) into the victim’s blood. This method is expensive.
  • Fighting germs. Only sterile dressings are used to wrap wounds. Antimicrobial dressings that contain antibiotics to help the wound dry out are popular. Bandages with ointment, unlike the previous ones, do not stick to the wound and do not destroy upper layer epithelium when removed. Antimicrobial drugs are prescribed intravenously as prescribed by a doctor.
  • Correction of hematopoietic processes. Pure red blood cells are used to replenish blood reserves.
  • Improving the functioning of the metabolic system: Use of vitamin C as an injection. Use 5 or more doses once.
  • Stimulation of wound healing. Steroid drugs are prescribed.
  • Diet With high content proteins, vitamins.

3. Treatment of burn septicotoxemia

In its symptoms and signs, the first stage of septicotoxemia is similar to the previous period of burn disease: active activity of microbes that caused inflammatory processes.

The second phase will depend on the degree and depth of the damage, but the general thing is the exhaustion of the patient. A feature of septicotoxemia is a number of complications that can significantly worsen the patient’s condition and lead to his death.

Most often, the occurrence of complications is associated with the development of infection in the body, which affects internal organs:

  • Inflammation lymph nodes : originates against the background of blood clotting disorders. Superficial burns may occur.
  • Purulent cellulite. Those victims who are obese are susceptible. This disease spreads quickly, takes a long time to treat, and can lead to death.
  • Sepsis. The infection strikes subcutaneous tissue, which contributes to the formation of pus in it. It is easy to treat this disease with fasciotomy if the latter is performed on time and correctly;
  • gangrene of the limbs. A predisposing factor is the tendency to form blood clots. It is more common in patients burned by flames with 20-25% of the skin burned.
  • Pneumonia. Among complications from the respiratory system, this disease is the most common; in half of the cases it ends in death. The victim receives pneumonia not during the burn, but several days later, as a result of the active proliferation of bacteria in the body, decline immune system.
  • Suppurative arthritis. It may occur a couple of months after the burn. Those who had problems with the musculoskeletal system before the burn are most susceptible to this disease.

Treatment for septicotoxemia is similar to treatment for burn toxemia: antibacterial drugs, transfusions (blood/plasma), vitamin therapy, steroid treatment, hormone therapy.

If the patient suffers from significant weight loss, protein is injected into his stomach using a special thin-walled tube (no more than 2 g per day).

4 Convalescence, beginning of recovery

This period in medicine is called convalescence, i.e. start of recovery.

The patient has a number of improvements:

  • Closure of wounds received during a burn.
  • Reduction/normalization of temperature.
  • The patient’s mental state stabilizes: the mood improves, the patient makes contact more easily.
  • Physical activity. In 33% of patients there is fast fatiguability after physical education, increased blood pressure, increased heart rate.
  • Restoring the functioning of all organs of the victim, except the kidneys. Kidney problems will be relevant for the victim for several years after the start of recovery.

It is very important for doctors to monitor the scarring process. With improper/pathological scarring, a number of diseases can occur, ranging from infectious to disorders in the functioning of the musculoskeletal system. After deep burns it is often necessary

Deep and extensive burns are manifested by a general body reaction called burn disease. However, it must be remembered that both superficial but extensive burns, as well as small 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 septicotoxemia, ending with convalescence or burn exhaustion.

Pathogenesis of burn shock. A mass of tissue heated during 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). The neuroendocrine response to afferent impulses (stress response) leads to a powerful release of ACTH, antidiuretic hormone, catecholamines and corticosteroids into the blood. Painful impulses and endocrine stress response cause general vascular spasm, which sharply worsens peripheral blood flow and microcirculation.

At this stage of the course of the disease, satisfactory central hemodynamic parameters are maintained, psychomotor agitation is often observed due to unbearably severe pain, that is, an erectile shock phase occurs, which can last from 1-2 to 4-6 hours depending on the depth and area of ​​the burn and compensatory capabilities of the victim.

Another reason for the development of a microcirculation crisis in the area of ​​a burn wound is thrombosis of small vessels, which continues to progress within 1-2 days after injury, which contributes to an increase in the area of ​​necrosis. With the addition of infection, thrombosis can intensify even more and necrosis deepens.

An important point in the pathogenesis of burn shock is a sharp increase in capillary permeability. This process lasts about 36 hours, but is most pronounced in the first 12 hours after injury. It is assumed that the increase in permeability is due to the accumulation in the tissue of histamine, prostaglandins E2, F2, their precursors and other biological active substances. In severe burns, the violation of permeability is so pronounced that colloidal substances with a mass of more than 150 thousand, i.e. albumins enter the extravascular space.

The neuroendocrine stress reaction to injury and hypovolemia lead to pronounced activation of the coagulation system, which sharply impairs microcirculation and contributes to an increase in the zone of necrosis due to the zone of stasis in the affected area. In parallel, plasma loss leads to depletion of proteins involved in blood clotting. Due to this, hypocoagulation develops, but it does not lead to an improvement in microcirculation, since progressive plasma loss aggravates hypovolemia. Parallel to the coagulation system, but somewhat more slowly, the anticoagulant system is activated. Developing fibrinolysis increases plasma loss and can cause secondary bleeding.

As a result of the evaporation of edematous fluid from the burn surface, a hyperosmotic zone is formed in the affected dermis, extracting water from the underlying tissues, forming vicious circle. With a deep burn area of ​​less than 30% of the body area, this process is limited to the burn wound, and with more extensive burns, it spreads to the capillaries of undamaged tissues, causing the deposition of fluid, proteins and electrolytes in the intercellular spaces.

In addition to changes in the functional properties of vessel walls, profound changes occur 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 effects of tissue breakdown products and biogenic amines lead to a significant reduction in the life span of the remaining ones. However, developing anemia is masked by hemoconcentration and initially manifests itself only as bilirubinemia and urobilinuria.

Hypovolemia, hypoxia, toxemia lead to the development of metabolic disorders and dysfunction of vital functions. important organs. First of all, this concerns the functional state of the heart muscle.

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

Burn Shock Clinic.

During the erectile phase of shock, patients rush about on the bed, moan, often complain of cold, tremble, experience severe thirst, but after taking liquid they often vomit. The skin is pale. Body temperature is normal or moderately reduced. Pulse up to 110-120 beats per minute, blood pressure within physiological norm, either slightly increased or decreased. Thus, clinical data at this stage do not provide sufficient information to predict the further course of the disease, and most importantly, to assess the possibility of development and severity of the torpid phase of shock. The forecast has to be based on indirect data, the main of which, as already mentioned, are the area and depth of the burn - 15% or more in terms of a deep burn. The condition of the upper respiratory tract is of great importance, since a burn in this area is equal in severity to a deep burn of 5 - 15% of the body surface. In addition, it is necessary to take into account that in children and elderly people, as well as in cases of burn damage to richly innervated areas (face, hands, perineum), shock may develop when a much smaller area of ​​the body is affected.

As the torpid phase of shock develops, psychomotor agitation gives way to retardation and apathy. The pain is significantly reduced, the feeling of cold increases, and chills may develop. Tachycardia, shortness of breath and cyanosis persist, increasing as the shock deepens. There is pronounced thirst. In severe shock, reflex paresis of the gastrointestinal tract often develops, which can cause vomiting. Due to water-electrolyte imbalance, cramps and muscle twitching often occur.

An important diagnostic sign is a decrease in central venous pressure (CVP). Its fall indicates the rapid development of heart failure, manifested by a drop in blood pressure, threadlike pulse, and disorders of consciousness.

However, the simplest and earliest prognostic sign is the development of oliguria, and then, possibly, anuria. The normal hourly amount of urine exceeds 30 ml/h (average - about 50 ml/h). With the development of burn shock, this amount decreases. Pathological impurities appear in the urine - protein, casts, free hemoglobin, filtered through the kidneys with the development of hemolysis. In conditions of increasing acidosis, it can precipitate, clogging the renal tubules. At the same time, renal failure is significantly aggravated, which sharply aggravates general state victim due to the toxic effects of accumulating nitrogenous waste.

The severity of the torpid phase of burn shock can vary. There are 3 degrees of severity:

1st degree - “mild” shock- for burns up to 20% of the body area. Moderate condition. Consciousness is preserved. Paleness of the skin. Pulse 90-100 beats/min, blood pressure within the physiological norm. Urine more than 30 ml per hour. Hematocrit no more than 50% Blood hemoglobin no more than 150-170 g/l.

2nd degree - "severe" shock- for burns up to 40% of the body area. The condition is serious. Consciousness is clear. Pale skin with cyanosis. Pulse 100-120 beats/min, blood pressure is reduced, but systolic is more than 70 mm Hg. Art. Oliguria (less than 30 ml per hour) and hematuria are noted. Anuria is possible. Hematocrit more than 50%; hemoglobin 160-200 g/l. Metabolic acidosis.

3rd degree - "extremely severe" shock- for burns of more than 60% of the body area, deep lesions - more than 40%. The condition is extremely serious, consciousness is confused. The skin is pale with a marbled tint. Pulse is thread-like, more than 120 beats/min; blood pressure is below 70 mm Hg. Art. Hematocrit 60-70%, hemoglobin - 200-240 g/l. Oligo-anuria develops, urine is dark brown in color with a burning smell.

When a victim has burns, deep (from 10%) or superficial (from 15%), we can talk about the development of the disease of the same name, the severity of which is determined by the area/depth of the lesion. The outcome/prognosis of burn disease will depend on these parameters. Not small role Where the source of damage is located and what age category it belongs to also plays a role.

A burn disease occurs in four periods:

  1. State of shock – up to 72 hours;
  2. Toxemia acute course– up to two weeks;
  3. The development of septicotoxemia lasts up to several months.
    • The period of rejection of necrotic tissue, depending on the severity of the lesion, the likelihood of complications and the therapeutic measures taken;
  4. Recovery.

Mechanism of development of burn disease

The disease develops when a large number of elements of cellular decay and toxins enter the blood, which are formed from a massive necrotic focus and tissue paranecrosis.

Proteolytic enzymes, prostaglandins, potassium, serotonin, sodium and histamine sharply increase their levels in the blood, increasing capillary permeability. Plasma, penetrating through the walls of blood vessels, leaves the channel, accumulating in the tissues, which leads to a decrease in the volume of circulating blood. Constricting blood vessels release catecholamine, adrenaline and norepinephrine into the blood. Internal organs begin to suffer from a lack of blood supply and hypovolemic shock occurs.

The blood thickens, water-salt exchange is disrupted. The failure of the most important organs is aggravated to a pathological level. Since the systems (endocrine and immune) are depleted, and the influence of tissue decay of a toxic nature on them is constantly increasing.

Causes

Among the basics of the development of burn disease:

  • loss of plasma - the blood thickens, blood circulation is significantly impaired;
  • dysfunction of blood cells due to the victim’s high body temperature;
  • general disorders, including death:
    • with the development of neuro-reflex shock, due to strong pain syndrome and feelings of fear in case of burn injury.

Stages of burn disease

The periods of the disease are limited to four stages:

  1. Stage I – burn shock.
    • In the first (shock) period, which begins immediately after the defeat, metabolic processes are disrupted, the central nervous system is in a state of excitement. The victim becomes inhibited and loses the ability to truly perceive reality. With an increase in hemoglobin levels in the blood, there is a high probability of developing hypoproteinemia or hyperkalemia.
  2. Stage II – acute toxemia.
    • During this period, tissues begin to die, forming toxic substances that cause infection, thickening of the blood and failure of water-salt metabolism. The work of many internal organs deviates from the norm, leukocytosis manifests itself with a decrease in the level of hemoglobin and red blood cells in the blood.
  3. Stage III – septicotoxemia.
    • The third phase is the period of counteraction to infection. Here the development of suppuration is noted. Scabs form. The density of urine becomes less. With a favorable picture of the disease, the wound site is gradually restored. As the condition worsened, the development of pneumonia and sepsis was recorded.
  4. Stage IV – convalescence.
    • The final period of improvement in the patient’s physiological condition is the phase of stabilization of temperature and metabolism. The patient gradually recovers, his health returns to normal.

Characteristic symptoms

Each period of a burn disease is characterized by the manifestation of its own symptoms.

Signs of a shock period

At the first stage of burn disease, the victim experiences:

  • excessive mobility;
  • agitation turning into lethargy;
  • thirst;
  • uncontrollable vomiting;
  • increased heart rate;
  • pallor;
  • dark cherry colored urine;
  • lack of urination;
  • decreased body temperature;
  • trembling/chills

Manifestations of the toxemia stage

The second period is characterized by:

  • insomnia;
  • fever;
  • delusions/hallucinations;
  • confusion;
  • convulsions;
  • bedsores.

There is a high probability of developing complications in the form of pleurisy, intestinal obstruction, toxic hepatitis, pneumonia. Digestive disorders and of cardio-vascular system.

Symptoms of the septicotoxemia stage

The third period of the disease is expressed:

  • loss of appetite;
  • weakness;
  • muscle atrophy;
  • exhaustion;
  • slow healing of lesions;
  • suppuration/bleeding of wound surfaces;
  • accompanying symptoms of disease complications.

Recovery phase

At the last stage of burn disease, the following is restored:

  • level of exchange;
  • work of internal organs;
  • circulatory and nervous system;
  • temperature;
  • damaged tissue;
  • psycho-emotional background.

However, in rare cases, relapses and complications are possible.

First aid

In case of emergency anti-burn measures, the following actions are indicated:

  1. For a thermal burn:
    • early interruption of contact between the victim and the affected object;
    • removing smoldering parts of the victim’s clothing and tissue around the wound;
    • calling an ambulance;
    • cooling procedures with cool water (the effect of water on the wound should last about half an hour);
    • cover the burn with a clean cloth;
    • if your fingers are damaged, place a cloth soaked in cool water between them and only then apply a bandage;
    • give the victim a pain reliever;
    • Give him plenty of fluids.
  2. If the burn is chemical, then after abundantly washing the wound, lubricate it:
    • glycerin (burn with carbolic acid);
    • not a strong solution of acetic/citric acid (for alkaline burns);
    • 2% soap or soda solution (for acid burns).
  3. When there is a burn to the respiratory tract, it is necessary:
    • do not allow the victim to talk or drink;
    • help to take a reclining position, calming and ensuring peace for the patient;
    • make sure that he has access to fresh air;
    • do not leave the injured person until the ambulance arrives.

Prohibited actions

In case of burn injuries, you must not:

  • tear off the tissue adhering to the wound surface so as not to aggravate the depth of the lesion and to prevent causing additional pain to the victim;
  • treat the wound with brilliant green, iodine, and other antiseptics;
  • apply talc, cream or ointment to an open wound;
  • open blisters and clean them;
  • lose the victim from sight, since in a state of shock a person is not always adequate in his actions.

Diagnostics

When diagnosing a burn disease, the area of ​​the affected surface and the depth of the damage are determined. Hemodynamic parameters and the condition of the victim himself are taken into account.

To assess the functioning of internal organs, a number of studies are carried out:

  • blood test for biochemistry/general;
  • General urine test.

To determine a pathological complication it is necessary to obtain the following results:

  • gastroscopy;
  • electrocardiograms;
  • radiography;
  • echocardiography;
  • magnetic resonance imaging of the heart.

Treatment

Each stage of burn disease has its own therapeutic measures.

Treatment of burn shock

  1. Warmth is recommended for the victim. You can cover it with a blanket. Heating pads and active warming agents are contraindicated.
  2. Drink plenty of drinks other than distilled water.
  3. Insertion of catheters (into a vein, into the nose and into the bladder).
  4. In case of vomiting, remove the stomach contents with an aspiration probe.
  5. At severe bloating abdomen, flatulence, insertion of a gas outlet tube into the anus.
  6. Analgesic and antihistamine therapy: Metamizole sodium, Trimeperidine, Droperidol, Diphenhydramine, Promethazine.
  7. Taking osmotic diuretics.
  8. Novocaine blockade of a body area depending on the location of the lesion.
  9. Infusion-transfusion therapy to correct hemostasis.
  10. Use of solutions of Hydrocortisone, Prednisolone, Cocarboxylase, Trifosadenine, ascorbic acid, Korglykon, glucose, Niketamide, Aminophylline according to indications and in prescribed dosages.

Treatment of burn toxemia

Detoxification treatment:

  1. Intravenously: Hemodez, Reopoliglyukin, Ringer's solution, Lactasol;
  2. For medicinal and preventive measures in case of metabolic disorders: Albumin, Blood transfusions, casein hydrolyzate, Aminopeptide, nicotinic acid, B vitamins, ascorbic acid.

Healing burn septicotoxemia

  1. Antibacterial therapy.
  2. Steroid (Methandrostenolone, Retabolil) and non-steroidal (potassium salt, orotic acid) drugs.
  3. Regeneration stimulants (Pentoxyl, Methyluracil).
  4. Locally - dry wet-dry dressings with an antiseptic.

Possible complications

A week after the incident, the development of a burn disease can result in pathologies of an infectious nature: sepsis, bedsores or pneumonia. Later, after a few months, a malfunction may be detected digestive organs, heart, circulatory system.

After a serious burn, it is possible to develop:

  • myocardial infarction;
  • anemia;
  • pyelitis;
  • nephrosonephritis;
  • parenchymal/viral hepatitis;
  • kidney amyloidosis;
  • erosive gastritis;
  • intestinal bleeding;
  • angina pectoris;
  • jade;
  • skin problems such as erysipelas inflammatory processes, itching, dermatitis, scarring.

There is a high probability of developing general exhaustion, toxic edema lungs or myocarditis.

Prevention of infectious diseases

To prevent the development of infectious complications during a burn, it is necessary to take antibiotics - second generation cephalosporins.

It is advisable to stimulate the immune system:

  • plasma transfusion (other blood products);
  • vaccination against staphylococcus;
  • vitamin therapy;
  • introduction of recombinant human interleukin-2;
  • carrying out aseptic procedures;
  • emergency tetanus prophylaxis.

Burns that are limited in area cause predominantly local damage. As a result, sometimes a quickly passing general reaction occurs.

For extensive burns (over 10-20% - in people of average age group, over 5% - in children and people over 60 years old) a complex of general and local disorders occurs in the body, the consequence of which is the development of burn disease.

The following periods are distinguished during its course:.
1. Burn shock(1-3 days after injury).
2. Acute burn toxemia(3-9 days after injury).
3. Septicotoxemia(9th day and until the integrity of the skin is restored and infectious complications are eliminated).
4. Convalescence(until the restoration of motor functions and the ability to self-care).

N. Frank (1960) proposed a prognostic indicator - lesion severity index(ITP), based on an assessment of the depth and extent of the lesion and expressed in arbitrary units. In this case, each percentage of the surface of the burn II - ША st. is equivalent to 1 index unit, and deep III B-IV Art. - 3 units. First degree burns are not taken into account.

In the presence of burns of the respiratory tract, 30 units are added to the ITP.

In persons aged 16 to 50 years with a lesion severity index of up to 60 units, the prognosis is favorable, 60-120 units - doubtful, and over 120 units - unfavorable.

In children and patients over 50 years of age with ITP up to 29 units. the prognosis is favorable, 30-60 units. - doubtful and more than 60 units. - unfavorable.

Burn shock is based on hemodynamic disorders with a predominant disruption of microcirculation and metabolic processes in the victim’s body.

During the period of burn shock (the first 2-3 days), circulatory disorders are of particular importance. Already in the first hours after receiving extensive burns, the volume of circulating blood decreases due to a drop in both the volume of circulating plasma and the volume of circulating red blood cells. The main reason for the decrease in the volume of circulating plasma is a sharp increase in capillary permeability in the burned area. Another reason for the early drop in cardiac output after severe burns is deterioration in myocardial contractility.

Circulatory disorders, including those in the hepatoportal system, are the main causes of liver dysfunction: antitoxic, protein-forming, excretory. Impaired liver function is indicated by increased serum bilirubin levels and hyperglycemia.

Clinical manifestations of burn shock do not have characteristic diagnostic signs.

In a victim in a state of shock, blood pressure does not change noticeably, the patient is conscious and in early period gives the impression of a seriously ill person, since compensatory repeated mechanisms during this period are still able to compensate for the main disturbances of homeostasis. If a patient with burns is unconscious, it is necessary to find out the cause and exclude combined lesions (traumatic brain injury, combustion products, alcohol or drug intoxication, etc.).

It should be borne in mind that burn shock in children and people over 60 years of age can occur with a smaller area of ​​damage (from 5% of the body surface) and be more severe.

After the burnt person comes out of shock, fluid resorption from the lesion begins, which leads to the rapid spread of toxic substances in the body. 2-3 days after a severe burn, symptoms of intoxication come to the fore: body temperature rises, various disorders appear in the central nervous system.

In the development of acute burn toxemia, a certain role belongs to bacterial factor. Possibility of self-charging and pathogenesis " colonization» wounds are very high. The very specificity of thermal injury contributes to the creation of favorable conditions for the generalization of infection. The loss of the victim’s skin, disorganization of the most important neurotrophic and metabolic functions of the body, a sharp decrease and prolonged suppression of protective factors of the immune system lead to the spread of infection at the burn site.

The end of the period of burn toxemia in severe burns enters the third stage - septicotoxemia, when an infection spreads through the body through a hematogenous route, which often leads to death. This period of burn disease is observed only with extensive and deep burns. At the beginning of this period, burn septicotoxemia is caused by the rejection of necrosis in the wound and suppuration. Subsequently, after the rejection of necrosis and the development of granulation tissue, all disorders are associated with significant protein losses through the wound and ongoing suppuration.

In the fourth stage of burn disease - stage convalescence- restoration of lost motor functions occurs. This rehabilitation period can be quite long. Often there is a need for reconstructive surgery.

With extensive and deep burns, a clinically pronounced general reaction of the body develops; it begins in the first hours after injury and continues for some time after full recovery skin. In this case, general disorders can be so serious that they can cause severe complications and lead to death.

Burn disease- a set of clinical symptoms, general reactions body and dysfunction of internal organs due to thermal damage to the skin and underlying tissues.

Signs of burn disease are observed with superficial burns of more than 15-25% of the body surface and deep burns of more than 10%. The main factor determining the severity of a burn disease, its outcome and prognosis is the area of ​​deep burns. Great importance have the age of the victim and the location of the burn. In people old age and children, deep damage to even 5% of the body surface can be fatal.

There were many theories about the pathogenesis of burn disease.

Dupuytren explained the development general violations in the body and the onset of death in case of burns by the development of neuro-reflex shock associated with severe pain irritation and fear during injury.

Baradok and Troyanov linked the development common symptoms with loss of plasma, leading to blood thickening and poor circulation.

They expressed thoughts about dysfunction of erythrocytes during elevated temperature bodies, etc.

There are four periods during a burn disease.

I period - burn shock. It begins immediately or in the first hours after injury, and can last up to 3 days.

II period - acute toxemia. Continues for 10-15 days after the burn injury.

III period - septicotoxemia. The beginning of the period is associated with the rejection of necrotic tissue. Depends on the severity of the burn, the development of complications, the nature therapeutic measures. Duration from 2-3 weeks to 2-3 months.

IV period - convalescence. Occurs after spontaneous healing of wounds or surgical restoration of the skin.

The presented division of the course of burn disease into periods is somewhat arbitrary, since it is not always possible to draw a clear boundary between them. Much depends on the severity of the injury, the individual characteristics of the victim, the treatment performed and the timing of surgical restoration of the skin for deep burns. However, the allocation different periods burn disease is necessary to understand the processes occurring in the body and take special measures to combat the developed pathological condition.

Burn shock

Burn shock- a pathological process that develops with extensive thermal damage skin and underlying tissues, it continues depending on the area and depth of the lesion, timeliness and adequacy of treatment for up to 72 hours.

Pathogenesis

Specific features burn shock, distinguishing it from traumatic shock, are as follows:

No blood loss;

Severe plasma loss;

Hemolysis;

Peculiarities of renal dysfunction.

Blood pressure in burn shock, in contrast to typical traumatic shock, decreases somewhat later after injury.

In the development of burn shock, two main pathogenetic mechanisms should be distinguished (Fig. 14-5):

Excessive afferent (painful) impulse leads to a change in the functions of the central nervous system, characterized first by excitation and then inhibition of the cortex and subcortical layer, irritation of the center of the sympathetic nervous system, increased activity endocrine glands. The latter, in turn, causes an increase in the flow of ACTH, pituitary antidiuretic hormone, catecholamines, corticosteroids and other hormones into the blood. This leads to spasm peripheral vessels while maintaining the vascular tone of vital organs, blood redistribution occurs and the volume of blood volume decreases.

Due to thermal damage to the skin and underlying tissues under the influence of inflammatory mediators, both local and severe general disorders occur: severe plasma loss, impaired microcirculation, massive hemolysis, changes in water-electrolyte balance and acid-base balance, impaired renal function.

Rice. 14-5.Pathogenesis of burn shock

The leading pathogenetic factor of burn shock is plasma loss. The loss of plasma is largely associated with an increase in the permeability of capillary walls due to the accumulation of vasoactive substances (histamine and serotonin) in burn tissue. A large amount of plasma sweats through the capillaries, swelling of the tissues of the affected area occurs, and the volume of blood volume decreases even more. Vascular permeability is impaired immediately after a burn, but reaches a clinically significant value after 6-8 hours, when a decrease in blood volume becomes apparent.

Developing hypovolemia becomes the cause of hemodynamic disorders, causing further microcirculation disorder in the kidneys, liver, pancreas. This is also facilitated by developing hemoconcentration and rheological disorders. Microcirculatory disorders cause secondary necrosis in the thermally affected zone, the formation of acute erosions and ulcers in the gastrointestinal tract, early pneumonia, dysfunction of the liver, kidneys, heart, etc.

The development of hemolysis is one of the reasons for the increase in potassium content in the blood plasma, which, due to damage to cell membranes, leads to the movement of sodium into the cells. As a result, intracellular edema develops.

Changes in water-electrolyte and acid-base balance. In the first hours after a burn, the volume of extracellular fluid decreases by 15-20% or more due to intense evaporation from the surface of the burn, through healthy skin, with breathing and vomit.

The circulation of water and electrolytes is normalized by aldosterone and antidiuretic hormone. An increase in their content leads to an increase in the reabsorption of water and sodium in the renal tubules. Gradually developing metabolic acidosis.

Renal dysfunction. The cause of oliguria is a reduction in renal blood flow due to spasm of renal vessels, a decrease in blood volume, a violation of the rheological properties of the blood, as well as the action of hemolysis products and endotoxins.

Clinical picture

By clinical course There are three degrees of burn shock.

Burn shock I degree

Observed in young and middle-aged people with an uncomplicated medical history with burns of 15-20% of the body surface. If the lesion is predominantly superficial, victims experience severe pain and burning at the burn site. Therefore, in the first minutes, and sometimes even hours, they are somewhat excited. Heart rate - up to 90 per minute. Blood pressure is slightly elevated or normal. Breathing is not impaired. Hourly diuresis is not reduced. If infusion therapy is not carried out or its start is delayed by 6-8 hours, oliguria and moderate hemoconcentration may develop.

Second degree burn shock

It develops when 21-60% of the body surface is damaged and is characterized by a rapid increase in lethargy and adynamia with preserved consciousness. Tachycardia up to 100-120 per minute. A tendency towards arterial hypotension is noted; blood pressure remains stable only when infusion therapy and the use of cardiotonic drugs.

The victims are chilly and their body temperature is below normal. Thirst and dyspeptic symptoms are characteristic. Possible paresis gastrointestinal tract. Urination decreases. Diuresis is maintained only with the help of medications. Hemoconcentration is pronounced (hematocrit increases to 60-65%). From the first hours after injury, moderate metabolic acidosis with respiratory compensation is determined.

Burn shock III degree

Develops with thermal damage to more than 60% of the body surface. The condition of the victims is extremely serious. 1-3 hours after the injury, consciousness becomes confused. Lethargy and stupor set in. The pulse is threadlike, blood pressure drops to 80 mm Hg. and lower, which is accompanied by a critical deterioration in the perfusion of internal organs and their hypoxia. Breathing is shallow. Unfavorable clinical sign extremely severe burn shock is considered paresis of the gastrointestinal tract - nausea, hiccups, repeated vomiting, and often coloration often develop coffee grounds(bleeding from erosions and acute stomach ulcers).

Severe disorders microcirculation and increased permeability of cell membranes lead to life-threatening dysfunctions of organs and systems; they are most clearly manifested by disorders of kidney function in the form of oliguria and anuria. Already in the first portions of urine, micro or macro hematuria is detected, then the urine becomes dark brown (like “meat slop”), and anuria develops quite quickly.

Hemoconcentration develops after 2-3 hours, the hematocrit can exceed 70%. Hyperkalemia and decompensated acidosis increase. Body temperature drops to 36 °C and below. From laboratory parameters, unfavorable in prognosis, first of all, it is necessary to note pronounced mixed acidosis with a deficiency of buffer bases.

Acute burn toxemia

With a favorable course, burn shock gradually passes into the stage of toxemia. This stage reaches its maximum development on the 2-3rd day after the burn and lasts 10-15 days. The end of this period coincides with the beginning of the suppurative process in burn wounds.

Toxemia can develop after burn shock or without previous shock. With deep lesions, burn toxemia turns into III stage burn disease - septicotoxemia; with lighter (mostly superficial) burns it ends in recovery.

Pathogenesis

After relief of shock and normalization of blood circulation, rapid absorption of active substances from the burn area begins. Despite a large number of studies, the pathogenesis of burn toxemia remains unclear.

Many studies were based on the opinion of V.N. Avdakov, who in 1876 suggested that thermal damage to the skin leads to the formation of a specific toxin in it. Since ancient times, the development of burn toxemia has been associated with the appearance in the body of victims of nonspecific toxins: histamine, serotonin, prostaglandins, which are important in the genesis of microcirculatory disorders.

The nature of the toxins produced in the body during a burn has now been determined. One of them - glycoproteins with antigen specificity.Toxic effect is caused by inhibition of ATPase and loss of the ability of tissues to use ATP energy.

Other toxins - lipoproteins(so-called “burn toxins”) - are formed from endoplasmic membranes that lose water under the influence of heat. The toxic effect on tissue leads to the loss of glycogen by cells.

The leading role in the pathogenesis of acute toxemia belongs to toxic oligopeptides(the so-called “medium molecules”). Their toxic effect due to the inhibitory effect of molecules of average mass on the phagocytic activity of lymphocytes and disruption of processes tissue respiration. The content of medium molecules clearly correlates with severity clinical manifestations toxemia.

Toxic effects can occur when proteolytic enzymes are activated and the activity of their inhibitors decreases. The effect of proteolytic enzymes on tissue leads to increased protein breakdown, which is accompanied by an increase in urea and creatinine levels in the blood.

The products of hemolysis of erythrocytes and fibrin breakdown have a toxic effect on the body of a burnt person.

In the development of intoxication syndrome, in addition to toxic products, a known role belongs to bacterial factor. The source of infection can be the microflora of one’s own normal skin, upper respiratory tract, exogenous flora hospital environment. The spread of bacteria in tissues is facilitated by the absence of skin, poor circulation, destruction and thrombosis of blood vessels, and weakening of the body's defenses.

Clinical picture

The nature of the course of toxemia is determined by the area of ​​damage, depth and localization of the burn. Victims with superficial and dermal burns usually feel satisfactory. With deep widespread burns, the first sign of toxemia is fever. Most often, the temperature curve is noted in the form of irregular waves with peaks up to 38-39 ° C. Hyperthermia above 40 °C usually has a central origin and is explained by impaired thermoregulation due to circulatory disorders, hypoxia and cerebral edema.

In addition to fever, other symptoms of intoxication are also detected: pallor of the skin, tachycardia, sometimes a tendency to arterial hypotension, weakness, nausea, and possible vomiting.

In approximately a third of patients, central nervous system disorders associated with the development of cerebral edema are registered (the tone of the cerebral vessels decreases, the development of venous stasis with increase intracranial pressure and cerebral edema). Clinically, this manifests itself as a psychotic state with disorientation in time and space, as well as hallucinations. Oculomotor disorders and asymmetry of facial muscles appear.

From the cardiovascular system, the development of myocarditis is possible, with dullness of heart sounds, systolic murmur, expansion of the boundaries of the heart and signs of heart failure.

Changes in kidney function depend on the severity of the burn injury. The normalization of renal blood flow, which occurs after the patient has recovered from shock, persists for burns of less than 30% of the body surface.

In case of more severe damage, impaired renal function cannot be restored - the clinical picture of acute renal failure develops.

IN clinical analysis blood, high leukocytosis with a shift in the leukocyte formula to the left is noted. It is possible to develop moderate anemia associated with hemolysis of red blood cells and inhibition of erythropoiesis. On the 4-6th day after receiving a burn, the hemoglobin content decreases to 80-100 g/l.

In biochemical blood tests at this time, hypoproteinemia, hyperbilirubinemia, and increased transaminase activity are noted.

Almost all victims experience proteinuria, microhematuria, and disturbances in electrolyte metabolism.

Septicotoxemia

Septicotoxemia develops with extensive IIIa degree burns and deep burns. The clinically pronounced picture of septicotoxemia usually appears 10-14 days after the burn, but its development is also possible earlier.

Pathogenesis

At the end of the period of toxemia, the body gradually begins to recover and put into action defense mechanisms: specific characteristics appear in the blood humoral factors protection (burn antibodies), the activity of phagocytosis increases, they are gradually delimited and rejected necrotic tissue, granulation tissue develops, serving as an obstacle to the penetration of bacteria and their toxins. It is advisable to divide this period into two phases:

The phase of the beginning of scab rejection until the wound is completely cleansed after 2-3 weeks;

The phase of existence of granulating wounds until they are completely healed.

The first phase has much in common with toxemia. Wound cleansing is accompanied by inflammatory reaction. The main pathogenetic factor determining clinical symptoms, - resorption of products of tissue decay and vital activity of microorganisms.

In the second phase, against the background of a sharp depression of the immune system, the regeneration process slows down, and infectious complications develop. An important symptom During this period, hypoproteinemia becomes difficult to compensate for (protein loss up to 7-8 g/day).

With deep burns of more than 10% of the body surface area, burn exhaustion develops to varying degrees as a result of a long course of burn disease, and until this time the condition of the victims remains satisfactory.

Clinical picture

Clinical symptoms of septicotoxemia are associated with the nature and phase of the wound process.

In the first phase, the condition of the patients remains serious. Sleep disturbances are possible, patients are irritable and tearful. Appetite is reduced. All signs of purulent intoxication are observed: high fever, tachycardia, weakness, chills, etc. During this period, anemia continues to develop, associated with inhibition of erythropoiesis, bleeding from granulating wounds and sometimes internal organs. IN leukocyte formula the shift to the left increases up to the myelocytes. Eosinophilopenia and lymphocytopenia are considered unfavorable prognostic signs. The development of toxic hepatitis phenomena is possible: icterus of the skin and sclera, enlarged liver, hyperbilirubinemia, increased activity of transferases, and the appearance of urobilin in the urine. Renal dysfunction persists or progresses, pyelonephritis develops - infectious complication burn disease.

The second phase of septicotoxemia is characterized by the appearance various complications. The most common of these is pneumonia. The mechanism of its development is associated with microembolism of pulmonary microvessels and tissue hypoxia against the background of circulatory disorders.

The course of a burn disease can lead to digestive disorders. Often there is the development of acute ulcers of the gastrointestinal tract - Curling ulcers. In their pathogenesis, the main role is played by microcirculatory disorders in the mucous membrane: ischemia, thrombosis, septic emboli. Most often, damage to the mucous membrane of the bulb occurs duodenum and the antrum of the stomach. A dangerous complication these ulcers become bleeding.

If burn exhaustion develops, the wounds do not heal, granulations do not fully mature, and epithelization is absent. Extensive infected wounds maintain constant intoxication and hypoproteinemia caused by the loss of protein with wound discharge. A kind of vicious circle arises.

Against this background, resistance to infection is reduced. Generalization of the infection is very likely - burn sepsis, often leading to the death of the victim. There are early sepsis, which develops during the period of rapid inflammation in the burn wound and its cleansing from necrosis, and late sepsis - 5-6 weeks after the injury, when the wounds are cleared of dead tissue.

Timely and adequate treatment, aimed at early rejection of necrotic masses and closure of the burn wound, as well as preventive antibacterial and immunocorrective therapy can prevent the development of septicotoxemia or minimize its clinical manifestations.

Convalescence

Elimination of a burn wound does not mean full recovery the victim. Certain violations persist on the part of internal organs and systems. In addition, the newly created skin still differs in properties from healthy skin.

At the same time, the root cause of burn disease - the burn wound - has already been eliminated, and the final stage (convalescence) has begun and means the gradual restoration of previously impaired functions. The condition of the patients improves, body temperature decreases. The psyche is normalized, although symptoms may persist bad dream and fatigue. This period is characterized by still insufficient compensatory ability of the cardiovascular system: even with minor physical activity severe tachycardia, decreased or increased blood pressure develop. Most often in this period, impaired renal function is noted: in 10% of burned patients, signs of pyelonephritis, amyloidosis or urolithiasis are detected.

With the restoration of the skin, the content of hemoglobin, erythrocytes and leukocytes is normalized.

At a normal general level, qualitative changes in the protein composition of the blood remain.

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