Secondary specialized education of a medical profile. Critical impairment of vital activity in surgical patients General impairment of vital activity of a surgical patient

General dysfunctions in acute surgical diseases of the abdominal organs are mainly caused by intoxication.

Endogenous intoxication- (Latin in in, inside + Greek toxikon poison) - a disruption of life caused by toxic substances formed in the body itself.

Endotoxicosis(endotoxicoses; Greek endō inside + toxikon poison + -ōsis) - complications of various diseases associated with disruption of homeostasis due to the accumulation in the body of endogenous toxic substances with pronounced biological activity. In clinical practice, endotoxemia is usually considered as a syndrome of endogenous intoxication that occurs with acute or chronic failure of the body's natural detoxification system (inability to effectively remove metabolic products). In contrast to intoxication, endotoxemia refers to an already formed state of poisoning with substances of an endogenous nature, and the term “intoxication” refers to the entire pathological process of intense self-poisoning of the body.

To refer to the processes of eliminating endotoxemia, the terms “detoxification” and “detoxification” are used. The latter term is more often used to describe therapeutic methods of enhancing the natural processes of cleansing the body.

Clinical signs of endotoxicosis have been known for a long time. In almost any disease, especially of an infectious nature, children and adults develop symptoms characteristic of “endogenous intoxication”: weakness, stupor, nausea and vomiting, loss of appetite and weight loss, sweating, pale skin, tachycardia, hypotension, etc. These most typical signs are usually divided into groups. The phenomena of neuropathy (encephalopathy), which are based on dysfunctions of the nervous system (neurotoxicosis), are often the first prodromal symptoms of developing intoxication, since the most highly differentiated nerve cells of the brain are especially sensitive to metabolic disorders and hypoxia. In children, dysfunctions of the nervous system are most severe with the development of psychomotor agitation, convulsions, soporous or even comatose states. In infectious diseases, a feverish state with signs of intoxication psychosis is typical. Manifestations of cardiovasopathy can be in the nature of mild asthenovegetative disorders and severe circulatory disorders of a hypodynamic type (decrease in stroke volume of the heart, increase in total peripheral vascular resistance, cardiac rhythm and conduction disturbances), usually accompanied by respiratory failure (shortness of breath, cyanosis of the mucous membranes, metabolic acidosis). Hepato- and nephropathy are most often manifested by proteinuria, oliguria, azotemia, and sometimes liver enlargement and jaundice are noted.

Laboratory diagnostics. To assess the severity of toxemia and monitor the dynamics of its development, quite a few laboratory tests have been proposed. One of the first to use integral indicators of blood plasma (lymph) toxicity was the leukocyte intoxication index and the neutrophil shift index.

For laboratory assessment of the severity of homeostasis disorders accompanying endotoxemia, traditional methods are used that characterize the main functions of the affected organ (for example, in case of nephropathy, the composition of urine, the concentration of creatinine, urea in plasma, etc. are examined; in case of hepatopathy, a blood test is performed for bilirubin, transaminases, proteins, cholesterol etc.) or a certain body system that usually suffers from endotoxicosis. This is primarily the acid-base state, osmolarity, rheological data (relative viscosity, aggregation of erythrocytes and platelets) and basic immunological indicators (level of T- and B-lymphocytes, immunoglobulins of class G, A, M, etc.).

Some laboratory biochemical tests are specific for this type of lesions that cause endotoxemia, for example, determination of myoglobin in the blood and urine in case of injury, enzyme activity in case of pancreatitis, bacteremia in case of sepsis.

1) etiological, which aims to accelerate the removal of toxic substances from the body using methods of enhancing natural detoxification and methods of “artificial detoxification”;

2) pathogenetic, associated with the need to reduce the intensity of catabolic processes and the activity of proteolytic enzymes, increase the immunological defense of the body;

3) symptomatic, with the task of maintaining the function of the cardiovascular and respiratory systems.

In addition, the entire arsenal of treatments for the underlying disease, which led to the development of endotoxemia, is simultaneously used. Most often this is antibacterial treatment, specific pharmacotherapy, surgical treatment, etc.

For the purpose of detoxification, intravenous infusion therapy (solutions of glucose, electrolytes, hemodez) is most widely used, often in combination with the method of forced diuresis using osmotic diuretics (urea, mannitol in a dose of 1-1.5 g/kg) in the form of hypertonic solutions (15-20%) or saluretics (furosemide in a dose of up to 500-800 mg per day).

To remove toxins from the blood, hemofiltration is used ( hemodialysis )or hemosorption, as well as plasmapheresis surgery (purification of blood plasma). In cases of overhydration of the body or high concentrations of toxins in the blood and lymph, it is recommended lymphatic drainage and cleansing the resulting lymph (lymphosorption) with its subsequent return to the body (intravenous drip infusions) to avoid possible loss of proteins.

The greatest effectiveness of detoxification is achieved with the combined use of several methods and the use of various biological media (blood, lymph) for cleansing.

Pathogenetic treatment of endotoxemia consists of the use of antiproteolytic drugs (contrical, trasylol or ingitril), antioxidants (tocopherol), immunostimulants (T-activin).

Ultraviolet irradiation of blood in a dose of up to 100-120 has the greatest effect in this regard. J, carried out daily in the amount of 5-6 procedures.

Detoxification and pathogenetic treatment should be carried out under the control of the dynamics of the concentration of SM and other laboratory indicators of endotoxemia until they are stable and normalized.

Forecast is largely related to the possibilities of using modern methods of artificial detoxification in the early stages of the development of endotoxemia.

Acute respiratory failure– a syndrome based on dysfunction of external respiration, leading to insufficient oxygen supply or retention of CO2 in the body. this condition is characterized by arterial hypoxemia or hypercapnia, or both.

The etiopathogenetic mechanisms of acute respiratory disorders, as well as the manifestation of the syndrome, have many features. Unlike chronic, acute respiratory failure is a decompensated condition in which hypoxemia, hypercapnia rapidly progress, and blood pH decreases. Disturbances in the transport of oxygen and CO2 are accompanied by changes in the functions of cells and organs. Acute respiratory failure is one of the manifestations of a critical condition, in which, even with timely and correct treatment, death is possible.

Clinical forms of acute respiratory failure

Etiology and pathogenesis

Acute respiratory failure occurs when there are disturbances in the chain of regulatory mechanisms, including central regulation of respiration and neuromuscular transmission, leading to changes in alveolar ventilation - one of the main mechanisms of gas exchange. Other factors of pulmonary dysfunction include lesions of the lungs (pulmonary parenchyma, capillaries and alveoli), accompanied by significant gas exchange disorders. It should be added that the “mechanics of breathing”, that is, the work of the lungs as an air pump, can also be impaired, for example, as a result of injury or deformation of the chest, pneumonia and hydrothorax, high position of the diaphragm, weakness of the respiratory muscles and (or) airway obstruction. The lungs are a “target” organ that responds to any changes in metabolism. Mediators of critical conditions pass through the pulmonary filter, causing damage to the ultrastructure of the lung tissue. Pulmonary dysfunction of varying degrees always occurs with severe impacts - trauma, shock or sepsis. Thus, the etiological factors of acute respiratory failure are extremely extensive and varied.

In intensive care practice, there are two types of acute respiratory failure: ventilation (hypercapnic) And parenchymal (hypoxemic).

Ventilatory respiratory failure manifested by a decrease in alveolar ventilation. This form of respiratory failure is accompanied by an increase in CO2 in the blood, respiratory acidosis, and arterial hypoxemia.

Causes of ventilation respiratory failure:

 Suppression of the respiratory center by narcotic, sedative drugs, barbiturates, or in connection with diseases and (or) traumatic brain injury (heart attack, cerebral edema, increased intracranial pressure, after-effects of cerebral anoxia, coma of various etiologies);

 Impaired conduction of nerve impulses to the respiratory muscles (due to traumatic injury to the spinal cord, infection such as polio, peripheral neuritis, or neuromuscular blockade caused by muscle relaxants, myasthenia gravis and other factors);

 Weakness or dysfunction of the respiratory muscles, “fatigue” of the diaphragm is a common cause of acute respiratory failure in patients in intensive care units.

 Impaired breathing can be observed with trauma or deformation of the chest, pneumothorax, pleural effusion, or lack of excursion of the diaphragm.

Ventilation respiratory failure often occurs in the immediate postoperative period. Factors contributing to ventilation failure include obesity, old age, smoking, cachexia, and kyphoscoliosis. The increased formation of CO2 in tissues, observed during hyperthermia, hypermetabolism, mainly with carbohydrate energy supply, is not always compensated by an increased volume of pulmonary ventilation.

Parenchymal respiratory failure is characterized by the development of arterial hypoxemia against the background of reduced, normal or increased CO2 levels in the blood. It develops as a result of damage to the lung tissue, pulmonary edema, severe pneumonia, acid aspiration syndrome and many other reasons and leads to severe hypoxemia. The main pathogenetic links of this form of acute respiratory failure are pulmonary shunt (discharge of blood from right to left), discrepancy between ventilation and blood flow, and disruption of diffusion processes.

Causes of parenchymal respiratory insufficiency:

 Trauma, sepsis, systemic inflammatory reaction (released inflammatory mediators: tumor necrosis factor, proinflammatory cytokines, thromboxane, NO, arachidonic acid metabolites, impaired oxygen transport when pulmonary functional units are damaged by oxygen radicals passing through the pulmonary filter;

 Multiple organ failure syndrome (in these cases, lung damage usually occurs);

 Adult respiratory distress syndrome;

 Severe forms of pneumonia;

 Pulmonary contusion;

 Atelectasis;

 Pulmonary edema (caused by an increase in hydrostatic pressure in the pulmonary capillaries or the permeability of the capillary wall);

 Severe form of bronchial asthma;

 Pulmonary embolism;

 Massive bronchopulmonary aspiration.

The identification of two forms of acute respiratory failure is to a certain extent arbitrary. Often one form turns into another. A combination of both forms is also possible.

Clinical picture Acute respiratory failure may be erased during an external examination of the patient and even absent, but it can also be extremely pronounced.

Ventilatory respiratory failure against the background of coma caused by the action of opiates, sedative drugs, anesthesia, is accompanied by minor signs (miosis, shallow breathing). An increase in Pco2 leads to stimulation of the respiratory center, which will most likely result in an increase in all parameters of external respiration. However, this does not happen when exposed to drugs. If active oxygenation is carried out under these conditions, a further decrease in ventilation volume, even apnea, may occur. With the development of ventilation respiratory failure in a patient with initially clear consciousness, blood pressure rises (often up to 200 mmHg and above), and brain symptoms appear. Very characteristic symptoms of hypercapnia are significant sweating, bronchial hypersecretion and lethargy. If you help the patient cough and eliminate bronchial obstruction, then lethargy disappears. Hypercapnia is also characterized by oliguria, which is always observed with severe respiratory acidosis.

Decompensation of the condition occurs at the moment when the high level of Pco2 in the blood ceases to stimulate the respiratory center. Signs of decompensation in advanced cases include a sharp decrease in minute ventilation, circulatory disorders and the development of coma, which, with progressive hypercapnia, is CO2 narcosis. Pco2 in this case reaches 100 mmHg, but coma can occur earlier - due to hypoxemia. At this stage, it is necessary to carry out artificial ventilation of the lungs with high FiO2. The development of shock against the background of a coma means the beginning of rapid damage to the cellular structures of the brain, internal organs and tissues.

Parenchymal respiratory failure is often not accompanied by symptoms of respiratory failure, with the exception of changes in arterial blood tests indicating a decrease in Po2. it is characterized by a gradual or rapidly progressive course, mild clinical symptoms and the possibility of death within a short time. Initially, tachycardia develops with moderate arterial hypertension, nonspecific neurological manifestations are possible: inadequacy of thinking, confusion of consciousness and speech, lethargy, and so on. Cyanosis is a relatively subjective factor, observed only in the late stage of acute respiratory failure. And corresponding to a significant decrease in saturation and oxygen tension in arterial blood (SaO2< 80%, Po2 < 50ммHg). Внезапно нарушается сознание и развивается кома (гипоксическая) с отсутствием рефлексов, падением артериального давления, остановкой сердечной деятельности. Продолжительность гипоксемической формы острой дахательной недостаточности может колебаться от нескольких минут (при аспирации, асфиксии, синдроме Мендельсона) до нескольких часов и дней (респираторный дистресс синдром взрослых).

Clinical signs of progressive respiratory failure:

 Breathing disorders (shortness of breath, gradual decrease in tidal and minute breathing volumes, oligopnea, mild cyanosis);

 Increasing neurological symptoms (indifference, aggressiveness, agitation, lethargy, coma);

 Disorders of the cardiovascular system (tachycardia, persistent increase in blood pressure during hypercapnia, decompensation of the cardiovascular system and cardiac arrest).

Clinical signs of acute respiratory failure:

 Acute respiratory failure (oligoproe, tachypnea, bradypnea, apnea, pathological rhythms);

 Progressive respiratory hypoxemia (Po2< 50 мм Hg при дыхании воздухом);

 Progressive hypercapnia (Pco2< 50 мм Hg);

 pH< 7,30.

All these signs are not always detected. The presence of at least two of them allows a diagnosis to be made.

Acute heart failure- This is a sudden onset of muscular failure of the ventricles of the heart. This condition can be aggravated by the dissonance between the decreased functioning of one and the normal function of another part of the heart. Sudden onset of cardiac weakness can be fatal.

The causes of acute cardiac dysfunction are myocardial infarction, diffuse myocarditis, excessive physical activity, intercurrent infection, as well as other pathological conditions in which hypercatecholaminemia, a violation of the ionic composition of the intracellular fluid, conduction disturbances, especially in the atrieventricular system (Morgagni-Edams-Stokes attacks) are observed. ), disturbance of excitability (attacks of paroxysmal tachycardia, paroxysmal flutter and atrial fibrillation and ventricular fibrillation leading to asystole).

Symptoms of acute heart failure

The clinical picture of acute heart failure, accompanied by a drop in cardiac output and a sharp decrease in blood supply to the arterial system, is very reminiscent of the picture of acute vascular circulatory failure, which is why it is sometimes referred to as acute cardiac collapse, or cardiogenic shock. Patients experience extreme weakness, a state close to fainting), pallor, cyanosis, coldness of the extremities, and very low pulse filling. Recognition of acute weakness of the heart is based primarily on the detection of changes in the heart (expansion of the boundaries of the heart, arrhythmia, pre-diastolic gallop rhythm). In this case, shortness of breath, swelling of the neck veins, congestive wheezing in the lungs, and cyanosis are observed. A sharp slowdown (less than 40 per minute) or increased heart rate (more than 160 per minute) is more characteristic of cardiac weakness than vascular weakness. Blood pressure is reduced. There are symptoms of organ ischemia with symptoms of venous congestion due to the disproportion between the total mass of circulating blood and its effective volume.

Acute syndrome right ventricular failure most clearly manifested in cases of blockage of the pulmonary artery trunk or its large branch due to the introduction of a blood clot from the veins of the legs, pelvis, or less often from the right ventricle or atrium. The patient suddenly develops shortness of breath, cyanosis, sweat, a feeling of constriction or pain in the heart area, the pulse becomes very small and frequent, and blood pressure drops. Soon, if the patient remains alive, venous pressure increases, the neck veins swell, and then the liver enlarges, an accent of the second tone on the pulmonary artery and a gallop rhythm are heard. X-ray reveals an enlargement of the right ventricle and expansion of the conus of the pulmonary artery. After 1-2 days, signs of heart attack and pneumonia may appear.

Acute right ventricular failure can be observed in patients with acute myocardial infarction of the posterior wall with concomitant pneumosclerosis and pulmonary emphysema. Along with the clinical picture of myocardial infarction, they experience cyanosis, congestion in the systemic circulation, and sudden enlargement of the liver. Sometimes patients are admitted to the surgical department with a diagnosis of acute abdomen and acute cholecystitis due to severe pain in the right hypochondrium due to stretching of the liver capsule.

Acute left ventricular failure clinically manifested by cardiac asthma and pulmonary edema.

Cardiac asthma is an attack of asthma.

It should be borne in mind that the clinical picture of acute left ventricular failure also develops in cases of mechanical closure of the left atrioventricular orifice by a moving thrombus in mitral stenosis. Characteristic is the disappearance of the arterial pulse along with a noticeable strong heartbeat, the appearance of acute pain in the heart area, shortness of breath, increasing cyanosis with subsequent loss of consciousness and the development in most cases of reflex collapse. Prolonged closure of the atrioventricular orifice by a thrombus usually leads to the death of patients.

Similarly, with mitral stenosis, acute functional failure syndrome of the left atrium is often observed. This happens when the defect is compensated by increased work of the left atrium while the contractile function of the right ventricle is preserved. With excessive physical stress, sudden stagnation of blood in the vessels of the lungs can occur and an attack of cardiac asthma may occur, which can develop into acute pulmonary edema. Sometimes such attacks are repeated frequently, appear suddenly and disappear just as suddenly, which confirms the great importance of the reflex influence from the atria to the pulmonary vessels.

Until now, all the mechanisms of development of cardiac asthma have not been deciphered. Convincing data have been obtained on the role of the central and autonomic nervous systems in the occurrence of these attacks. Hormonal factors also have a big influence.

It is known that attacks of cardiac asthma and pulmonary edema can occur when the cardiac probe irritates the pulmonary artery receptors during cardiac probing.

With physical exertion, excitement, fever, pregnancy, etc., there is an increased need for oxygen in the body, increased cardiac activity and increased cardiac output, which in patients with existing heart lesions can lead to suddenly developing weakness of the left side of the heart. A decompensated difference in the ejection of blood from the right and left parts of the heart leads to overflow of the pulmonary circulation. Pathological reflexes due to hemodynamic disturbances lead to the fact that the production of glucocorticoids decreases, and mineralocorticoids increase. This, in turn, increases vascular permeability and causes sodium and water retention in the body, which further worsens hemodynamic parameters.

It is necessary to take into account one more factor that can play a big role in the development of these complications - a violation of lymph circulation in the lung tissue, expansion of the anastomoses between the veins of the large and small circle.

Long-term increase in capillary pressure in the lungs above 30 mmHg. Art. causes fluid to leak from the capillaries into the alveoli and can lead to pulmonary edema. At the same time, as shown in the experiment, a short-term increase in capillary pressure in the lungs, reaching 50 mm Hg. Art. and more, does not always lead to pulmonary edema. This indicates that capillary pressure is not the only factor influencing the development of pulmonary edema. A significant role in the development of pulmonary edema belongs to the permeability of the alveolar and capillary walls and the degree of precapillary pressure. Thickening and fibrosis of the alveolar wall may prevent the development of pulmonary edema at high capillary pressure. With increased capillary permeability (anoxemia, infections, anaphylactic shock, etc.), pulmonary edema can develop even when the capillary pressure is significantly below 30 mm Hg. Art. Pulmonary edema occurs in patients with a small difference between the pressure in the pulmonary artery and pulmonary capillaries and low pulmonary arteriolar resistance. When the pressure gradient between the pulmonary artery and the pulmonary capillaries is high, there is a high pulmonary arteriolar resistance, which creates a protective barrier that protects the pulmonary capillaries from overflowing with blood, a sharp increase in pressure in them, and, consequently, from the occurrence of cardiac asthma or pulmonary edema . In patients with pronounced narrowing of the left venous ostium, development of muscle fibers in the pulmonary arterioles, proliferation of fibrous tissue in the intima of vessels, thickening of the pulmonary capillaries, hypertrophy of the fibrous base with partial loss of elasticity of the pulmonary tissue were noted. In this regard, the pulmonary capillaries move away from the alveolar membrane, and the alveolar membranes themselves thicken. This restructuring begins when the pressure in the pulmonary artery increases to 50 mm Hg. Art. and higher and is most pronounced in the pulmonary vessels with an increase in pulmonary arterial pressure to 90 mm Hg. Art. and higher.

These changes reduce the permeability of blood vessels and alveolar membranes. However, these morphological changes in patients with mitral stenosis do not exclude the possibility of them developing attacks of suffocation or pulmonary edema. Capillary extravasation is also possible with these changes, but at a higher “critical” level of pulmonary capillary pressure necessary for the occurrence of capillary extravasation and the passage of tissue fluid through the altered alveolar membranes.

Clinic for cardiac asthma and pulmonary edema characterized initially by the occurrence of severe suffocation and severe cyanosis. A large number of scattered dry and moist rales are detected in the lungs. There is bubbling breathing, a cough with the release of foamy sputum (often blood-stained). Blood pressure often decreases.

Acute renal failure (ARF)- this is a sudden, potentially reversible, significant decrease or complete cessation of all (secretory, excretory and filtration) functions of the kidneys. Every second patient with acute renal failure needs hemodialysis. Currently, there is a trend in which acute renal failure is identified as one of the manifestations of multiple organ failure syndrome.

CAUSES

All the reasons that cause the development of acute renal failure can be divided into three large groups:

1. Extrarenal (extrarenal) causes- lead to a decrease in blood volume and a sharp decrease in renal blood flow, which can cause irreversible death of renal tissue cells. Extrarenal causes of acute renal failure include: severe extensive operations, especially in weakened or elderly patients; injuries accompanied by painful shock and hypovolemia; sepsis; massive blood transfusion; extensive burns; uncontrollable vomiting; uncontrolled use of diuretics; cardiac tamponade.

2. Renal (renal) causes- include ischemic and toxic damage to the renal tissue, acute inflammation of the renal parenchyma or damage to the renal vessels, which cause necrosis of the renal tissue. Renal causes of acute renal failure include: acute glomerulonephritis; acute tubular necrosis; rheumatic kidney damage; blood diseases; poisoning with mercury, copper, cadmium salts, poisonous mushrooms, organic fertilizers; malignant arterial hypertension; lupus nephritis; uncontrolled use of drugs from the group of sulfonamides, antitumor drugs, aminoglycosides, NSAIDs.

3. Subrenal (postrenal) causes– are associated with a violation of the outflow of urine, which leads to the accumulation of urine in the collecting system, edema and necrosis of renal tissue cells. Renal causes of acute renal failure include: bilateral obstruction of the ureters by stones or blood clots; urethritis and periurethritis; tumors of the ureters, prostate, bladder; prolonged compression of the ureters in trauma, surgical interventions on the abdominal organs.

CLASSIFICATION

Depending on the causes of development, prerenal, renal and postrenal acute renal failure are distinguished, respectively.

SYMPTOMS

With acute renal failure, there is a sharp disruption of all functions performed by the kidneys. The loss of the kidneys' ability to maintain the balance of electrolytes in the blood is accompanied by an increase in the concentration of calcium and potassium ions and chlorine, as well as the accumulation of protein metabolic products and an increase in the level of urea and creatinine in the blood. Violation of the secretory function of the kidneys causes the development of anemia and thrombocytopenia. As a consequence of impaired renal excretory function, one of the main symptoms of acute renal failure develops - oliguria (decreased urine output) up to anuria (complete absence of urine). The condition of patients with acute renal failure is usually moderate or severe, disturbances of consciousness occur (lethargy or excessive agitation), swelling of the extremities, cardiac arrhythmias, nausea and vomiting, and an increase in the size of the liver is determined.

The clinical course of acute renal failure is divided into several stages, successively replacing each other.

1. At the initial stage of acute renal failure, which usually lasts several hours, less often several days, circulatory collapse develops, accompanied by severe ischemia of the renal tissue. The patient's condition may be different; it is determined by the main cause of the development of acute renal failure.

2. At the stage of oligoanuria, there is a sharp reduction in urine volume (no more than 0.5 liters of urine per day) or a complete absence of urination. This stage usually develops within three days from the onset of acute renal failure, but can extend to 5-10 days. Moreover, the later acute renal failure develops and the longer its duration, the worse the prognosis of the disease and the higher the likelihood of death. With prolonged oligoanuria, the patient becomes lethargic and lethargic, and may fall into a coma. Due to pronounced suppression of immunity, the risk of secondary infection with the development of pneumonia, stomatitis, mumps, etc. increases.

3. During the diuretic stage, there is a gradual increase in urine volume, reaching about 5 liters of urine per day. The duration of the diuretic stage is usually 10-14 days, during which a gradual regression of the symptoms of renal failure occurs and the electrolyte balance of the blood is restored.

4. At the recovery stage, further restoration of all kidney functions occurs. It may take 6 months to a year to fully restore kidney function.

Acute liver failure develops as a result of massive necrosis of hepatocytes, which leads to a sharp deterioration in liver function in patients without previous liver disease. The main symptom of acute renal failure is hepatic encephalopathy (HE), which has a decisive influence on the course of acute renal failure and the prognosis of the disease.

One can talk about acute renal failure if encephalopathy develops within 8 weeks from the onset of the first symptoms of acute hepatocellular insufficiency. If PE develops within 8 to 24 weeks from the onset of the first symptoms of liver damage, then we should talk about subacute liver failure. In addition, it is advisable to isolate hyperacute liver failure, which develops within 7 days from the onset of jaundice. Mortality in acute renal failure, according to various authors, ranges from 50 to 90%.

The main etiological factors for the development of acute renal failure are:

1. Viral hepatitis.

2. Drug poisoning (paracetamol).

3. Poisoning with hepatotoxic poisons (mushrooms, alcohol substitutes, etc.).

4. Wilson–Konovalov disease.

5. Acute fatty degeneration of the liver in pregnant women.

Main symptoms and complications of acute renal failure

Hepatic Encephalopathy is a complex of potentially reversible neuropsychiatric disorders resulting from acute or chronic liver failure and/or portosystemic shunting.

According to most researchers, PE develops due to the penetration of endogenous neurotoxins through the blood-brain barrier (BBB) ​​and their effects on astroglia as a result of liver cell deficiency. In addition, the amino acid imbalance that occurs with liver failure affects the development of PE. As a result, the permeability of the BBB, the activity of ion channels changes, neurotransmission and the provision of neurons with macroergic compounds are disturbed. These changes underlie the clinical manifestations of PE.

Hyperammonemia in liver diseases is associated with a decrease in the synthesis of urea and glutamine in it, as well as with portosystemic shunting of the blood. Ammonia in a non-ionized form (1–3% of the total amount of ammonia in the blood) easily penetrates the BBB, stimulating the transport of aromatic amino acids to the brain, resulting in increased synthesis of false neurotransmitters and serotonin.

According to some authors, in addition to ammonia, neurotoxins involved in the pathogenesis of PE include mercaptans, short- and medium-chain fatty acids, and phenols formed from the corresponding substrates under the influence of intestinal bacteria. The mechanisms of their action are similar and are associated with the inhibition of neuronal Na +, K + -ATPase and an increase in the transport of aromatic amino acids to the brain. Short- and medium-chain fatty acids, in addition, inhibit the synthesis of urea in the liver, which contributes to hyperammonemia.

Finally, there are indications of the role of the inhibitory neurotransmitter g-aminobutyric acid (GABA) of intestinal origin in the pathogenesis of PE, the excessive supply of which to the brain under conditions of astroglial edema also leads to an increase in neuropsychic disorders characteristic of PE.

It is important to note that a clear relationship between the concentrations of each of the listed metabolites involved in the pathogenesis of PE and the severity of encephalopathy has not been established. Thus, PE appears to be the result of a complex effect and mutual reinforcement of several factors: endogenous neurotoxins, among which ammonia is of leading importance, amino acid imbalance and changes in the functional activity of neurotransmitters and their receptors.

The development of encephalopathy in patients with acute renal failure is dominated by factors of parenchymal liver failure, the outcome of which is often endogenous hepatic coma. Provoking factors in this case are the increased breakdown of proteins contained in the diet, or when blood protein enters during gastrointestinal bleeding, irrational use of medications, alcoholic excesses, surgical interventions, concomitant infections, etc. Encephalopathy in patients with cirrhosis of the liver can be episodic with spontaneous resolution or intermittent, lasting many months or even years. In accordance with the criteria of the International Association for the Study of Liver Diseases (Brighton, UK, 1992) and the standardization of nomenclature, diagnostic signs and prognosis of liver and biliary tract diseases (C. Leevy et al., 1994), latent and clinically pronounced (4 stages) PE are distinguished .

1. General symptoms of acute renal failure: nausea, vomiting, anorexia, hyperthermia, malaise and progressive fatigue.

2. Jaundice is a mirror of the degree of liver failure. Bilirubin levels may increase to 900 µmol/L.

3. “Liver odor” from the mouth (smell of rotten meat).

4. Flopping tremor. Determined in conscious patients. In addition, it can be recorded with uremia, respiratory failure, low levels of potassium in the blood plasma, as well as intoxication with a number of drugs.

5. Ascites and edema (associated with a decrease in albumin levels in the blood).

6. Deficiency of coagulation factors due to a decrease in their production by the liver. The platelet count also decreases. As a result, gastrointestinal bleeding and diapedetic bleeding from the nasopharynx, retroperitoneal space, and injection sites often develop.

7. Metabolic disorders. Typically, hypoglycemia develops as a result of gluconeogenesis and an increase in insulin levels.

8. Cardiovascular complications:

hyperdynamic circulation (reminiscent of septic shock) - increased cardiac index, low peripheral resistance, arterial hypotension;

hypovolemia;

enlarged heart;

pulmonary edema;

arrhythmias (atrial fibrillation and ventricular extrasystoles);

pericarditis, myocarditis and bradycardia develop in the terminal phase of acute liver failure.

9. Sepsis. The septic state is aggravated by the phenomena of immunological dysfunction. The most common pathogens are Staphylococcus aureus/Streptococci, intestinal flora.

10. Renal failure (hepatorenal syndrome). Most patients with acute renal failure have renal failure, which is manifested by oliguria and increased blood creatinine levels. In cases of acetaminaphen poisoning, renal failure also develops as a result of the direct toxic effect of the drug. Tubular damage can develop as a result of hypotension and hypovolemia. Blood urea levels in acute renal failure are usually low as a result of decreased synthesis in the liver.

Differential diagnosis of acute (fulminant) liver failure should be made with bacterial meningitis, brain abscess, and encephalitis.

LESSON PLAN #40

date according to the calendar-thematic plan

Groups: General Medicine

Discipline: Surgery with the basics of traumatology

Number of hours: 2

Topic of the training session:

Type of training session: lesson on learning new educational material

Type of training session: lecture

Goals of training, development and education: formation of knowledge about the main stages of dying, the procedure for carrying out resuscitation measures; idea of ​​post-resuscitation illness;

formation of knowledge about the etiology, pathogenesis, clinic of traumatic shock, rules for the provision of primary care, principles of treatment and patient care.

Education: on the specified topic.

Development: independent thinking, imagination, memory, attention,student speech (enrichment of vocabulary words and professional terms)

Upbringing: responsibility for the life and health of a sick person in the process of professional activity.

As a result of mastering the educational material, students should: know the main stages of dying, their clinical symptoms, the procedure for resuscitation; have an idea about postresuscitation illness.

Logistics support of the training session: presentation, situational tasks, tests

PROGRESS OF THE CLASS

Organizational and educational moment: checking attendance at classes, appearance, availability of protective equipment, clothing, familiarization with the lesson plan;

Student Survey

Familiarization with the topic, setting learning goals and objectives

Presentation of new material,V polls(sequence and methods of presentation):

Fixing the material : solving situational problems, test control

Reflection: self-assessment of students’ work in class;

Homework: pp. 196-200 pp. 385-399

Literature:

1. Kolb L.I., Leonovich S.I., Yaromich I.V. General surgery. - Minsk: Higher school, 2008.

2. Gritsuk I.R. Surgery.- Minsk: New Knowledge LLC, 2004

4. L.I.Kolb, S.I.Leonovich, E.L.Kolb Nursing in surgery, Minsk, Higher School, 2007

5. Order of the Ministry of Health of the Republic of Belarus No. 109 “Hygienic requirements for the design, equipment and maintenance of healthcare organizations and for the implementation of sanitary, hygienic and anti-epidemic measures for the prevention of infectious diseases in healthcare organizations.

6. Order of the Ministry of Health of the Republic of Belarus No. 165 "On disinfection, sterilization by healthcare institutions

Teacher: L.G.Lagodich

LECTURE NOTES

Lecture topic: General disorders of the body's vital functions in surgery.

Questions:

1. Definition of terminal states. The main stages of dying. Preagonal states, agony. Clinical death, signs.

2. Resuscitation measures for terminal conditions. The procedure for resuscitation measures, effectiveness criteria. Conditions for terminating resuscitation measures.

3. Post-resuscitation illness. Organization of observation and care for patients. Biological death. Ascertainment of death.

4. Rules for handling a corpse.

1. Definition of terminal states. The main stages of dying. Preagonal states, agony. Clinical death, signs.

Terminal states - pathological conditions based on increasing hypoxia of all tissues (primarily the brain), acidosis and intoxication with products of impaired metabolism.

During terminal conditions, the functions of the cardiovascular system, respiration, central nervous system, kidneys, liver, hormonal system, and metabolism collapse. The most significant is the decline of the functions of the central nervous system. Increasing hypoxia and subsequent anoxia in brain cells (primarily the cerebral cortex) lead to destructive changes in its cells. In principle, these changes are reversible and, when normal oxygen supply to tissues is restored, do not lead to life-threatening conditions. But with continued anoxia, they turn into irreversible degenerative changes, which are accompanied by hydrolysis of proteins and, ultimately, their autolysis develops. The least resistant to this are the tissues of the brain and spinal cord; only 4–6 minutes of anoxia are necessary for irreversible changes to occur in the cerebral cortex. The subcortical region and spinal cord can function somewhat longer. The severity of terminal conditions and their duration depend on the severity and speed of development of hypoxia and anoxia.

Terminal conditions include:

Severe shock (IV degree shock)

Transcendent coma

Collapse

Preagonal state

Terminal pause

Agony

Clinical death

Terminal states in their development have3 stages:

1. Preagonal state;

– Terminal pause (since it does not always happen, it is not included in the classification, but it is still worth taking into account);

2. Agonal state;

3. Clinical death.

The main stages of dying. Preagonal states, agony. Clinical death, signs.

Ordinary dying, so to speak, consists of several stages that successively replace each other.Stages of dying:

1. Preagonal state . It is characterized by profound disturbances in the activity of the central nervous system, manifested by the victim’s lethargy, low blood pressure, cyanosis, pallor or “marbling” of the skin. This condition can last quite a long time, especially in the context of medical care. Pulse and blood pressure are low or not detected at all. It often happens at this stage terminal pause. It manifests itself as a sudden short-term sharp improvement in consciousness: the patient regains consciousness, may ask for a drink, blood pressure and pulse are restored. But all this is the remnants of the body’s compensatory capabilities put together. The pause is short-lived, lasting minutes, after which the next stage begins.

2. Next stage -agony . The last stage of dying, in which the main functions of the body as a whole are still manifested - breathing, blood circulation and the governing activity of the central nervous system. Agony is characterized by a general deregulation of body functions, therefore the provision of tissues with nutrients, but mainly oxygen, is sharply reduced. Increasing hypoxia leads to the cessation of respiratory and circulatory functions, after which the body enters the next stage of dying. With powerful destructive effects on the body, the agonal period may be absent (as well as the preagonal period) or may not last long; with some types and mechanisms of death, it can last for several hours or even more.

3. The next stage of the dying process isclinical death . At this stage, the functions of the body as a whole have already ceased, and it is from this moment that the person is considered dead. However, the tissues retain minimal metabolic processes that maintain their viability. The stage of clinical death is characterized by the fact that an already dead person can still be brought back to life by restarting the mechanisms of breathing and blood circulation. Under normal room conditions, the duration of this period is 6-8 minutes, which is determined by the time during which the functions of the cerebral cortex can be fully restored.

4. Biological death - this is the final stage of the dying of the organism as a whole, replacing clinical death. It is characterized by irreversible changes in the central nervous system, gradually spreading to other tissues.

From the moment of clinical death, postmorbid (post-mortem) changes in the human body begin to develop, which are caused by the cessation of the functions of the body as a biological system. They exist in parallel with ongoing life processes in individual tissues.

2. Resuscitation measures for terminal conditions. The procedure for resuscitation measures, effectiveness criteria. Conditions for terminating resuscitation measures.

The distinction between clinical death (the reversible stage of dying) and biological death (the irreversible stage of dying) was decisive for the development of resuscitation - a science that studies the mechanisms of dying and revival of a dying organism. The term “resuscitation” itself was first introduced in 1961 by V. A. Negovsky at the international congress of traumatologists in Budapest. Anima is the soul, re is the reverse action, thus - resuscitation is the forced return of the soul to the body.

The formation of resuscitation in the 60-70s is considered by many to be a sign of revolutionary changes in medicine. This is due to overcoming the traditional criteria of human death - cessation of breathing and heartbeat - and reaching the level of acceptance of a new criterion - “brain death”.

Methods and techniques for performing mechanical ventilation. Direct and indirect cardiac massage. Criteria for the effectiveness of resuscitation measures.

Artificial respiration (artificial pulmonary ventilation - mechanical ventilation). Need for artificial respiration occurs in cases where breathing is absent or impaired to such an extent that it threatens the patient’s life. Artificial respiration is an emergency first aid measure for drowning, suffocation (asphyxia from hanging), electric shock, heat and sunstroke, and some poisonings. In case of clinical death, i.e. in the absence of independent breathing and heartbeat, artificial respiration is carried out simultaneously with cardiac massage. The duration of artificial respiration depends on the severity of respiratory disorders, and it should continue until independent breathing is completely restored. If obvious signs of death, such as cadaveric spots, appear, artificial respiration should be stopped.

The best method of artificial respiration, of course, is to connect special devices to the patient’s respiratory tract, which can inject the patient with up to 1000-1500 ml of fresh air for each breath. But non-specialists, of course, do not have such devices at hand. Old methods of artificial respiration (Sylvester, Schaeffer, etc.), which are based on various chest compression techniques, turned out to be insufficiently effective, since, firstly, they do not clear the airways from a sunken tongue, and secondly, with with their help, no more than 200-250 ml of air enters the lungs in 1 breath.

Currently, the most effective methods of artificial respiration are considered to be mouth-to-mouth and mouth-to-nose blowing (see figure on the left).

The rescuer forcefully exhales air from his lungs into the patient's lungs, temporarily becoming a breathing apparatus. Of course, this is not the fresh air with 21% oxygen that we breathe. However, as studies by resuscitators have shown, the air exhaled by a healthy person still contains 16-17% oxygen, which is enough to carry out full artificial respiration, especially in extreme conditions.

So, if the patient does not have his own breathing movements, he must immediately begin artificial respiration! If there is any doubt whether the victim is breathing or not, you must, without hesitation, start “breathing for him” and not waste precious minutes looking for a mirror, putting it to your mouth, etc.

In order to blow “the air of his exhalation” into the patient’s lungs, the rescuer is forced to touch the victim’s face with his lips. From hygienic and ethical considerations, the following technique can be considered the most rational:

1) take a handkerchief or any other piece of cloth (preferably gauze);

2) bite (tear) a hole in the middle;

3) expand it with your fingers to 2-3 cm;

4) place the fabric with the hole on the patient’s nose or mouth (depending on the chosen method of ID); 5) press your lips tightly to the victim’s face through the tissue, and blow through the hole in this tissue.

Artificial respiration "mouth to mouth":

1. The rescuer stands on the side of the victim’s head (preferably on the left). If the patient is lying on the floor, you have to kneel.

2. Quickly clears the victim’s oropharynx of vomit. If the victim's jaws are tightly clenched, the rescuer moves them apart, if necessary, using a mouth retractor tool.

3. Then, placing one hand on the victim’s forehead and the other on the back of the head, he hyperextends (that is, tilts back) the patient’s head, while the mouth, as a rule, opens. To stabilize this position of the body, it is advisable to place a cushion from the victim’s clothing under the shoulder blades.

4. The rescuer takes a deep breath, slightly holds his exhalation and, bending over to the victim, completely seals the area of ​​his mouth with his lips, creating, as it were, an air-impermeable dome over the patient’s mouth. In this case, the patient’s nostrils must be closed with the thumb and forefinger of the hand lying on his forehead, or covered with his cheek, which is much more difficult to do. Lack of tightness is a common mistake during artificial respiration. In this case, air leakage through the nose or corners of the victim’s mouth negates all the efforts of the rescuer.

After sealing, the rescuer exhales quickly, forcefully, blowing air into the patient's airways and lungs. The exhalation should last about 1 s and reach 1-1.5 liters in volume in order to cause sufficient stimulation of the respiratory center. In this case, it is necessary to continuously monitor whether the victim’s chest rises well during artificial inhalation. If the amplitude of such respiratory movements is insufficient, it means that the volume of air blown in is small or the tongue sinks.

After the end of exhalation, the rescuer unbends and releases the victim’s mouth, in no case stopping the hyperextension of his head, because otherwise the tongue will sink and there will be no full independent exhalation. The patient's exhalation should last about 2 seconds, in any case, it is better that it be twice as long as the inhalation. In the pause before the next inhalation, the rescuer needs to take 1-2 small regular inhalations and exhalations “for himself.” The cycle is repeated at first with a frequency of 10-12 per minute.

If a large amount of air gets into the stomach, rather than into the lungs, the swelling of the latter will make it difficult to save the patient. Therefore, it is advisable to periodically empty his stomach of air by pressing on the epigastric (epigastric) region.

Artificial respiration "mouth to nose" carried out if the patient's teeth are clenched or there is injury to the lips or jaws. The rescuer, placing one hand on the victim’s forehead and the other on his chin, hyperextends his head and simultaneously presses his lower jaw to his upper jaw. With the fingers of the hand supporting the chin, he should press the lower lip, thereby sealing the victim’s mouth. After a deep breath, the rescuer covers the victim’s nose with his lips, creating the same air-tight dome over it. Then the rescuer performs a strong blowing of air through the nostrils (1-1.5 liters), while monitoring the movement of the chest.

After the end of artificial inhalation, it is necessary to empty not only the nose, but also the patient’s mouth; the soft palate can prevent air from escaping through the nose, and then with the mouth closed, there will be no exhalation at all! During such an exhalation, it is necessary to maintain the head hyperextended (i.e., tilted back), otherwise a sunken tongue will interfere with exhalation. The duration of exhalation is about 2 s. During the pause, the rescuer takes 1-2 small breaths and exhales “for himself.”

Artificial respiration should be carried out without interruption for more than 3-4 seconds until full spontaneous breathing is restored or until a doctor appears and gives other instructions. It is necessary to continuously check the effectiveness of artificial respiration (good inflation of the patient’s chest, absence of bloating, gradual pinkening of the facial skin). Always make sure that vomit does not appear in the mouth and nasopharynx, and if this happens, before the next inhalation, use a finger wrapped in a cloth to clear the victim’s airways through the mouth. As artificial respiration is carried out, the rescuer may become dizzy due to the lack of carbon dioxide in his body. Therefore, it is better for two rescuers to carry out air injection, changing every 2-3 minutes. If this is not possible, then every 2-3 minutes you should reduce your breaths to 4-5 per minute, so that during this period the level of carbon dioxide in the blood and brain of the person performing artificial respiration rises.

When performing artificial respiration on a victim with respiratory arrest, it is necessary to check every minute whether he has also suffered cardiac arrest. To do this, you need to periodically feel the pulse in the neck with two fingers in the triangle between the windpipe (laryngeal cartilage, which is sometimes called the Adam's apple) and the sternocleidomastoid (sternocleidomastoid) muscle. The rescuer places two fingers on the lateral surface of the laryngeal cartilage, and then “slides” them into the hollow between the cartilage and the sternocleidomastoid muscle. It is in the depths of this triangle that the carotid artery should pulsate.

If there is no pulsation in the carotid artery, you must immediately begin chest compressions, combining it with artificial respiration. If you skip the moment of cardiac arrest and perform only artificial respiration on the patient without cardiac massage for 1-2 minutes, then, as a rule, it will not be possible to save the victim.

Ventilation using equipment is a special topic in practical classes.

Features of artificial respiration in children. To restore breathing in children under 1 year of age, artificial ventilation is carried out using the mouth-to-mouth and nose method, in children over 1 year of age - using the mouth-to-mouth method. Both methods are carried out with the child in the supine position; for children under 1 year of age, a low cushion (folded blanket) is placed under the back or the upper body is slightly raised with an arm placed under the back, and the child’s head is thrown back. The person providing assistance takes a breath (shallow!), hermetically covers the child’s mouth and nose or (in children over 1 year old) only the mouth, and blows air into the child’s respiratory tract, the volume of which should be smaller the younger the child is (for example, in a newborn it is equal to 30-40 ml). When there is a sufficient volume of air blown in and the air enters the lungs (and not the stomach), movements of the chest appear. Having finished insufflation, you need to make sure that the chest descends. Blowing in a volume of air that is too large for a child can lead to serious consequences - rupture of the alveoli of the lung tissue and the release of air into the pleural cavity. The frequency of insufflations should correspond to the age-related frequency of respiratory movements, which decreases with age. On average, the respiratory rate is 1 minute in newborns and children up to 4 months. Life - 40, at 4-6 months. - 40-35, at 7 months. - 2 years old - 35-30, 2-4 years old - 30-25, 4-6 years old - about 25, 6-12 years old - 22-20, 12-15 years old - 20-18.

Heart massage - a method of resuming and artificially maintaining blood circulation in the body through rhythmic compression of the heart, promoting the movement of blood from its cavities into the great vessels. Used in cases of sudden cessation of cardiac activity.

Indications for cardiac massage are determined primarily by general indications for resuscitation, i.e. in the case when there is at least the slightest chance to restore not only independent cardiac activity, but also all other vital functions of the body. Cardiac massage is not indicated in the absence of blood circulation in the body for a long period of time (biological death) and in the development of irreversible changes in organs that cannot be subsequently replaced by transplantation. Cardiac massage is inappropriate if the patient has injuries to organs that are clearly incompatible with life (primarily the brain); for precisely and predetermined terminal stages of cancer and some other incurable diseases. Cardiac massage is not required and when suddenly stopped blood circulation can be restored using electrical defibrillation in the first seconds of ventricular fibrillation of the heart, established during monitor monitoring of the patient’s heart activity, or by applying a jerky blow to the patient’s chest in the area of ​​​​the projection of the heart in case of sudden and documented cardioscope screen of his asystole.

A distinction is made between direct (open, transthoracic) cardiac massage, performed with one or two hands through an incision in the chest, and indirect (closed, external) cardiac massage, performed by rhythmic compression of the chest and compression of the heart between the sternum and spine displaced in the anteroposterior direction.

Mechanism of actiondirect cardiac massage lies in the fact that when the heart is compressed, the blood located in its cavities flows from the right ventricle into the pulmonary trunk and, with simultaneous artificial ventilation of the lungs, is saturated with oxygen in the lungs and returns to the left atrium and left ventricle; From the left ventricle, oxygenated blood enters the systemic circulation, and therefore to the brain and heart. Restoring the energy resources of the myocardium as a result makes it possible to resume the contractility of the heart and its independent activity during circulatory arrest as a result of ventricular asystole, as well as ventricular fibrillation, which is successfully eliminated.

Indirect cardiac massage can be performed both by human hands and with the help of special massage devices.

Direct cardiac massage is often more effective than indirect one, because allows you to directly monitor the state of the heart, feel the tone of the myocardium and promptly eliminate its atony by intracardially injecting solutions of adrenaline or calcium chloride, without damaging the branches of the coronary arteries, since it is possible to visually select an avascular area of ​​the heart. However, with the exception of a few situations (for example, multiple rib fractures, massive blood loss and the inability to quickly eliminate hypovolemia - an “empty” heart), preference should be given to indirect massage, because To perform a thoracotomy, even in an operating room, certain conditions and time are required, and the time factor in intensive care is decisive. Indirect cardiac massage can be started almost immediately after circulatory arrest is determined and can be performed by any previously trained person.

Monitoring the efficiency of blood circulation , created by cardiac massage, is determined by three signs: - the occurrence of pulsation of the carotid arteries in time with the massage,

Constriction of the pupils,

And the appearance of independent breaths.

The effectiveness of chest compressions is ensured by the correct choice of the place where force is applied to the victim’s chest (the lower half of the sternum immediately above the xiphoid process).

The massager’s hands must be correctly positioned (the proximal part of the palm of one hand is placed on the lower half of the sternum, and the palm of the other is placed on the back of the first, perpendicular to its axis; the fingers of the first hand should be slightly raised and not put pressure on the victim’s chest) (see. diagrams on the left). They should be straight at the elbow joints. The person performing the massage should stand quite high (sometimes on a chair, stool, stand, if the patient is lying on a high bed or on the operating table), as if hanging with his body over the victim and putting pressure on the sternum not only with the force of his hands, but also with the weight of his body. The pressing force should be sufficient to move the sternum towards the spine by 4-6 cm. The pace of the massage should be such as to provide at least 60 heart compressions per minute. When performing resuscitation by two persons, the massager compresses the chest 5 times with a frequency of approximately 1 time per 1 s, after which the second person providing assistance makes one vigorous and quick exhalation from the mouth to the mouth or nose of the victim. 12 such cycles are carried out in 1 minute. If resuscitation is carried out by one person, then the specified mode of resuscitation measures becomes impossible; the resuscitator is forced to perform indirect cardiac massage at a more frequent rhythm - approximately 15 heart compressions in 12 s, then 2 vigorous blows of air into the lungs in 3 s; 4 such cycles are performed in 1 minute, resulting in 60 heart compressions and 8 breaths. Indirect cardiac massage can only be effective if properly combined with artificial ventilation.

Monitoring the effectiveness of indirect cardiac massage carried out continuously as it progresses. To do this, lift the patient’s upper eyelid with a finger and monitor the width of the pupil. If, within 60-90 seconds of performing a cardiac massage, pulsation in the carotid arteries is not felt, the pupil does not narrow and respiratory movements (even minimal) do not appear, it is necessary to analyze whether the rules for performing a cardiac massage are strictly followed, resort to medication to eliminate myocardial atony, or switch (if conditions exist) to direct cardiac massage.

If signs of the effectiveness of chest compressions appear, but there is no tendency to restore independent cardiac activity, the presence of ventricular fibrillation of the heart should be assumed, which is clarified using electrocardiography. Based on the pattern of fibrillation oscillations, the stage of ventricular fibrillation of the heart is determined and indications for defibrillation are established, which should be as early as possible, but not premature.

Failure to comply with the rules for performing chest compressions can lead to complications such as rib fractures, development of pneumo- and hemothorax, liver rupture, etc.

There are somedifferences in performing chest compressions in adults, children and newborns . For children aged 2-10 years, it can be performed with one hand, for newborns - with two fingers, but at a more frequent rhythm (90 per 1 minute in combination with 20 blows of air into the lungs per 1 minute).

3. Post-resuscitation illness. Organization of observation and care for patients. Biological death. Ascertainment of death.

If the resuscitation measures are effective, spontaneous breathing and heart contractions are restored to the patient. He is entering a periodpost-resuscitation illness.

Post-resuscitation period.

In the post-resuscitation period, several stages are distinguished:

1. The stage of temporary stabilization of functions occurs 10-12 hours from the start of resuscitation and is characterized by the appearance of consciousness, stabilization of breathing, blood circulation, and metabolism. Regardless of the further prognosis, the patient's condition improves.

2. The stage of repeated deterioration of the condition begins at the end of the first, beginning of the second day. The patient's general condition worsens, hypoxia increases due to respiratory failure, hypercoagulation develops, hypovolemia due to plasma loss with increased vascular permeability. Microthrombosis and fat embolism disrupt microperfusion of internal organs. At this stage, a number of severe syndromes develop, from which “post-resuscitation illness” is formed and delayed death may occur.

3. Stage of normalization of functions.

Biological death. Ascertainment of death.

Biological death (or true death) is the irreversible cessation of physiological processes in cells and tissues. Irreversible cessation usually means “irreversible within the framework of modern medical technologies” cessation of processes. Over time, medicine’s ability to resuscitate dead patients changes, as a result of which the borderline of death is pushed into the future. From the point of view of scientists who support cryonics and nanomedicine, most people who are dying now can be revived in the future if the structure of their brain is preserved now.

TO early signs of biological death cadaveric spotswith localization in sloping places of the body, then occursrigor mortis , then cadaveric relaxation, cadaveric decomposition . Rigor mortis and cadaveric decomposition usually begin in the muscles of the face and upper extremities. The time of appearance and duration of these signs depend on the initial background, temperature and humidity of the environment, and the reasons for the development of irreversible changes in the body.

The biological death of a subject does not mean the immediate biological death of the tissues and organs that make up his body. The time before death of the tissues that make up the human body is mainly determined by their ability to survive under conditions of hypoxia and anoxia. This ability is different for different tissues and organs. The shortest life time under anoxic conditions is observed in brain tissue, more precisely, in the cerebral cortex and subcortical structures. The stem sections and spinal cord have greater resistance, or rather resistance to anoxia. Other tissues of the human body have this property to a more pronounced extent. Thus, the heart retains its viability for 1.5-2 hours after the onset of biological death. Kidneys, liver and some other organs remain viable for up to 3-4 hours. Muscle tissue, skin and some other tissues may well be viable up to 5-6 hours after the onset of biological death. Bone tissue, being the most inert tissue of the human body, retains its vitality for up to several days. Associated with the phenomenon of survivability of organs and tissues of the human body is the possibility of transplanting them, and the earlier the organs are removed for transplantation after the onset of biological death, the more viable they are, the greater the likelihood of their successful further functioning in another organism.

2. Clothes are removed from the corpse, placed on a gurney specially designed for this purpose on the back with the knees bent, the eyelids are closed, the lower jaw is tied up, covered with a sheet and taken to the sanitary room of the department for 2 hours (until cadaveric spots appear).

3. Only after this, the nurse writes down his last name, initials, medical history number on the deceased’s thigh and the corpse is taken to the morgue.

4. Things and valuables are transferred to the relatives or loved ones of the deceased against receipt, according to an inventory drawn up at the time of the patient’s death and certified by at least 3 signatures (nurse, nurse, doctor on duty).

5. All bedding from the bed of the deceased is sent for disinfection. The bed and bedside table are wiped with a 5% solution of chloramine B, the bedside table is soaked in a 5% solution of chloramine B.

6. During the day, it is not customary to place newly admitted patients on a bed where the patient recently died.

7. It is necessary to report the death of the patient to the hospital emergency department, to the relatives of the deceased, and in the absence of relatives, as well as in the case of sudden death, the cause of which is not clear enough - to the police department.

Types of depression of consciousness Fainting - generalized muscle weakness, inability to stand upright, loss of consciousness. Coma is a complete shutdown of consciousness with a total loss of perception of the environment and oneself. Collapse is a drop in vascular tone with a relative decrease in circulating blood volume.

Degrees of impairment of consciousness Stupor – unconsciousness, preservation of defensive movements in response to painful and sound stimuli. Moderate coma – inability to wake up, lack of defensive movements. Deep coma - suppression of tendon reflexes, loss of muscle tone. Terminal coma is an agonal state.

Assessment of the depth of impairment of consciousness (Glasgow scale) Clear consciousness 15 Stunning Stupor 9-12 Coma 4-8 Brain death 3

Emergency care for loss of consciousness Eliminate etiological factors. Place the patient in a horizontal position with the leg end raised. Ensure free breathing: unfasten the collar and belt. Give stimulants (ammonia, vinegar) to inhale. Rub the body, cover with warm heating pads. Inject 1% mezaton 1 ml IM or s/c 10% caffeine 1 ml. For severe hypotension and bradycardia, 0.1% atropine 0.5-1 ml.

Physiology of respiration The breathing process The breathing process is conventionally divided into 3 stages: The first stage includes the delivery of oxygen from the external environment to the alveoli. The second stage involves the diffusion of oxygen through the alveolar membrane of the acinus and its delivery to the tissues. The third stage includes the utilization of oxygen during the biological oxidation of substrates and the formation of energy in cells. If pathological changes occur at any of these stages, ARF may occur. With ARF of any etiology, there is a disruption in the transport of oxygen to tissues and the removal of carbon dioxide from the body.

Indicators of blood gases in a healthy person Indicator Arterial blood Mixed blood p O 2 mm Hg. st SaO 2, % pCO 2, mm Hg. st

Etiological classification of ARF PRIMARY (stage 1 pathology - oxygen delivery to the alveoli) Causes: mechanical asphyxia, spasm, tumor, vomit, pneumonia, pneumothorax. SECONDARY (stage 2 pathology - oxygen transport from the alveoli to the tissues is impaired) Causes: microcirculation disorders, hypovolemia, pulmonary embolism, cardiogenic pulmonary edema.

The main syndromes of ARF 1. Hypoxia is a condition that develops with a decrease in tissue oxygenation. Exogenous hypoxia - due to a decrease in the partial pressure of oxygen in the inhaled air (submarine accidents, high altitudes). Hypoxia due to pathological processes that disrupt the supply of oxygen to tissues at its partial pressure.

Hypoxia due to pathological processes is divided into: a) respiratory (alveolar hypoventilation - obstruction of the airways, reduction of the respiratory surface of the lungs, respiratory depression of central origin); b) circulatory (against the background of acute and chronic circulatory failure); c) tissue (potassium cyanide poisoning - the process of oxygen absorption by tissues is disrupted); d) hemic (decrease in red blood cell mass or hemoglobin in red blood cells).

3. Hypoxemic syndrome is a violation of oxygenation of arterial blood in the lungs. An integral indicator is a reduced level of partial oxygen tension in arterial blood, which occurs in a number of parenchymal lung diseases. Main syndromes of ARF

Clinical stages of ARF Stage I: Consciousness: preserved, anxiety, euphoria. Respiratory function: lack of air, respiratory rate per minute, mild acrocyanosis. Blood circulation: heart rate per minute. BP is normal or slightly elevated. The skin is pale and moist. Partial pressure of O 2 and CO 2 of blood: p O 2 up to 70 mm Hg. p CO 2 up to 35 mmHg.

Stage II: Consciousness: impaired, agitation, delirium. Respiratory function: severe suffocation, respiratory rate per minute. Cyanosis, sweating of the skin. Blood circulation: heart rate per minute. Blood pressure Partial pressure of O 2 and CO 2 of blood: p O 2 to 60 mm Hg. p CO 2 up to 50 mmHg. Clinical stages of ARF

Stage III: Consciousness: absent, clonic-tonic convulsions, pupils dilated, do not respond to light. Respiratory function: tachypnea 40 or more per minute turns into bradypnea 8-10 per minute, spotty cyanosis. Blood circulation: heart rate more than 140 per minute. Blood pressure, atrial fibrillation. Partial pressure of O 2 and CO 2: p O 2 up to 50 mmHg. p CO 2 to mmHg. Clinical stages of ARF

Emergency care for acute respiratory failure 1. Restoration of airway patency. 2. Elimination of alveolar ventilation disorders (local and general). 3. Elimination of central hemodynamic disorders. 4. Correction of the etiological factor of ARF. 5. Oxygen therapy 3-5 l/min. at stage I ARF. 6. At stages II – III of ARF, tracheal intubation and artificial ventilation are performed.

Treatment of AHF 1. Subcutaneous administration of 1-2 ml of morphine, preferably combined with the administration of 0.5 ml of a 0.1% solution of atropine sulfate; 2. Nitroglycerin under the tongue - 1 tablet or 1-2 drops of 1% solution on a piece of sugar; 3. Analgesics: baralgin 5.0 IV, IM, no-shpa 2.0 IM, analgin 2.0 IM. 4. For cardiac arrhythmias: lidocaine mg IV, procainamide 10% 10.0 IV, obzidan 5 mg IV. 5. For pulmonary edema: dopmin 40 mg IV on glucose, Lasix 40 mg IV, aminophylline 2.4% 10.0 IV.

ETIOLOGY OF AKI 1. Traumatic, hemorrhagic, blood transfusion, bacterial, anaphylactic, cardiogenic, burn, surgical shock; electrical trauma, postpartum sepsis, etc. 2. Acute infarction of the kidney. 3. Vascular abstraction. 4. Urological abstraction.

DIAGNOSIS 1. Decreased diuresis (less than 25 ml/h) with the appearance of protein, red blood cells, leukocytes, casts, decreased urine density to 1.005-1, increased azotemia (16.7-20.0 mmol/l). 3. Hyperkalemia. 4. Decrease in blood pressure. 5. Decrease in hemoglobin and red blood cells.

Prevention and treatment of acute renal failure 1. Sufficient pain relief for injuries. 2. Elimination of hypovolemia. 3. Elimination of water and electrolyte disturbances. 4. Correction of cardiodynamics and rheology. 5. Correction of respiratory function. 6. Correction of metabolic disorders. 7. Improving blood supply to the kidneys and eliminating foci of infection in them. 8. Antibacterial therapy. 9. Improving rheology and microcirculation in the kidneys. 10. Extracorporeal detoxification (hemodialysis). 11. Osmodiuretics (Manitol 20% 200.0 IV), saluretics (Lasix mg IV).

Classification of acute liver disease 1. Endogenous – it is based on massive necrosis of the liver, resulting from direct damage to its parenchyma; 2. Exogenous (portocaval) – the form develops in patients with liver cirrhosis. In this case, the metabolism of ammonia by the liver is disrupted; 3. Mixed form.

CLINICAL MANIFESTATIONS OF OPEN 1. Depression of consciousness up to coma 2. Specific “liver odor” from the mouth 3. Icterus of the sclera and skin 4. Signs of hemorrhagic syndrome 5. Appearance of areas of erythema in the form of stellate angiomas 6. Jaundice 7. Ascites 8. Splenomegaly

LABORATORY DIAGNOSTICS Study of liver functions (increased bilirubin, transaminases, decreased protein), kidneys (azotemia), acid-base balance (metabolic acidosis), water and electrolyte metabolism (hypokalemia, hyponatremia), blood coagulation system (hypocoagulation).

Principles of treatment for APE 1. Eliminate bleeding and hypovolemia. 2. Eliminate hypoxia. 3. Detoxification. 4. Normalization of energy metabolism. 5. Use of hepatotropic vitamins (B 1 and B 6), hepatoprotectors (essentiale). 6. Normalization of protein metabolism. 7. Normalization of water-electrolyte metabolism, acid-base balance. 8. Normalization of the blood coagulation system.

Topic 11. Wounds and wound process. Wound definition and wound symptoms. Types of wounds The concept of single, multiple, combined and combined wounds. Phases of the wound process. Types of wound healing. Principles of first aid for wounds. Primary surgical treatment of wounds, its types. Secondary surgical treatment. Wound closure using skin grafting.

Purulent wounds, primary and secondary. General and local signs of wound suppuration. Treatment of a purulent wound depending on the phase of the wound process. Application of proteolytic enzymes. Additional methods for treating purulent wounds.

Topic 12. General dysfunctions in a surgical patient. Clinical assessment of the general condition of patients. Types of general disorders of the body's vital functions in surgical patients: terminal conditions, shock, acute blood loss, acute respiratory failure, acute heart failure, dysfunction of the digestive tract, acute renal failure, hemorheological disorders, endogenous intoxication. Glasgow Coma Scale.

Types, symptoms and diagnosis of terminal conditions: preagonia, agony, clinical death. Signs of biological death. First aid for cessation of breathing and circulation. Criteria for the effectiveness of revival. Monitor control systems. Indications for stopping cardiopulmonary resuscitation.

Shock – causes, pathogenesis, clinical picture, diagnosis, phases and stages of surgical shock. First aid for shock. Complex therapy of shock. Criteria for the success of shock treatment. Prevention of surgical shock. The concept of shocks of other etiologies: hemorrhagic shock, cardiogenic shock, anaphylactic shock, septic shock. Intensive therapy of the consequences of acute and chronic blood loss. The concept of hypoventilation. Diagnosis of insufficiency of external respiration function. Equipment for artificial lung ventilation (ALV). Indications for the use and administration of mechanical ventilation. Tracheostomy, tracheostomy care. Diagnosis and intensive treatment of disorders of the motor-evacuation function of the digestive tract. Diagnosis of the main syndromes of water-electrolyte and acid-base balance disorders. Principles of drawing up a corrective program. Intensive therapy for disorders of the coagulation system. Diagnosis and intensive therapy of exogenous intoxications. Parenteral nutrition as a component of intensive care.

Topic 13. Mechanical injury. Fractures and dislocations. The concept of trauma. Types of injuries and classification of injuries. The concept of isolated, multiple, combined and combined injuries. Medical prevention of injuries. Complications and dangers of injuries: immediate, immediate and late. General principles of diagnosing traumatic injuries, providing first aid and treatment. Nonspecific and specific prevention of infectious complications.

Mechanical injury. Types of mechanical injuries: closed (subcutaneous) and open (wounds). Closed mechanical injuries of soft tissues: bruises, sprains and ruptures (subcutaneous), concussions and compression, long-term compartment syndrome. First aid and treatment of closed soft tissue injuries.

Types of mechanical damage to tendons, bones and joints. Ligament and tendon ruptures. Traumatic dislocations. Joint bruises, Hemarthrosis, First aid and treatment. Bone fractures. Classification. Clinical symptoms of fractures. Basics of X-ray diagnostics of dislocations and fractures. The concept of fracture healing. The process of callus formation. First aid for closed and open fractures. Complications of traumatic fractures: shock, fat embolism, acute blood loss, development of infection and their prevention. First aid for spinal fractures with and without damage to the spinal cord. First aid "for fractures of the pelvic bones with and without damage to the pelvic organs. Transport immobilization - goals, objectives and principles. Types of transport immobilization. Standard splints. Principles of treatment of fractures: reposition, immobilization, surgical treatment. The concept of plaster casts. Plaster. Basic rules for applying plaster casts. Main types of plaster casts. Tools and techniques for removing plaster casts. Complications in the treatment of fractures. The concept of orthopedics and prosthetics.

The concept of traumatic brain injury, classification. The main dangers of head injuries that pose a threat to the lives of patients. Objectives of first aid for head injury. Measures for their implementation. Features of transporting patients.

Types of chest injuries: open, closed, with and without damage to the bone base of the chest, with and without damage to internal organs, one- and two-sided. The concept of pneumothorax. Types of pneumothorax: open, closed, valve (tension) external and internal. First aid and transportation features for tension pneumothorax, hemoptysis, foreign bodies in the lungs, open and closed injuries to the lungs, heart and great vessels. Features of gunshot wounds to the chest, first aid, transportation of the victim.

Injuries to the abdomen with or without violation of the integrity of the abdominal wall, abdominal organs and retroperitoneal space. First aid tasks for abdominal trauma. Features of first aid and transportation in case of prolapse of abdominal organs into the wound. Features of gunshot wounds of the abdomen. Complications of traumatic abdominal injuries: acute anemia, peritonitis.

Features of treatment tactics in outpatient settings.

Topic 14. Thermal, chemical and radiation damage. Electrical injury. Combustiology is a branch of surgery that studies thermal injuries and their consequences.

Burns. Classification of burns. Recognizing the depth of burns. Determination of burn area. Prognostic methods for determining the severity of a burn.

First aid for burns. Primary surgical treatment of the burn surface: anesthesia, asepsis, surgical technique. Treatment methods for local treatment of burns: open, closed, mixed. Skin grafting. Antimicrobial therapy (sulfonamides, antibiotics, serums). Outpatient treatment of burns: indications, contraindications, methods. Reconstructive and plastic surgery of post-burn scar deformities.

Burn disease: 4 periods of its development and course. General principles of infusion therapy for various periods of burn disease, enteral nutrition and patient care.

Types of radiation burns. Features of first aid for radiation burns. Phases of local manifestations of radiation burns. Treatment of radiation burns (first aid and further treatment).

Injuries from cooling. Types of cold injury: general – freezing and chills; local – frostbite. Prevention of cold injury in peacetime and war. Symptoms of freezing and chills, first aid for them and further treatment.

Classification of frostbite by degree. Clinical course of frostbite: pre-reactive and reactive periods of the disease.

First aid for frostbite in the pre-reactive period. General and local treatment of frostbite during the reactive period, depending on the degree of damage. 0 "general complex therapy for victims of cold injury. Prevention of tetanus and purulent infection, nutrition and care features.

Electrical trauma. The effect of electric current on the human body. The concept of electropathology. Local and general action of electric current. First aid for electrical injury. Features of further examination and treatment of local and general pathology. Lightning strikes. Local and general manifestations. First aid.

Chemical burns. Impact of caustic chemicals on tissue. Features of local manifestation. First aid for chemical burns of the skin, mouth, esophagus, stomach. Complications and consequences of esophageal burns.

Features of treatment tactics in outpatient settings.

Topic 15. Fundamentals of purulent-septic surgery. General issues of surgical infection. The concept of surgical infection. Classification of surgical infections: acute and chronic purulent (aerobic), acute anaerobic, acute and chronic specific. The concept of mixed infection.

Local and general manifestations of purulent-septic diseases. Purulent-resorptive fever. Features of asepsis in purulent-septic surgery. Modern principles of prevention and treatment of purulent diseases. Local non-operative and surgical treatment. General principles of surgical techniques. Modern methods of treating purulent lesions and methods of postoperative management. General treatment for purulent diseases: rational antibacterial therapy, immunotherapy, complex infusion therapy, hormone and enzyme therapy, symptomatic therapy.

Acute aerobic surgical infection . Main pathogens. Routes of infection. Pathogenesis of purulent inflammation. Stages of development of purulent-inflammatory diseases. Classification of acute purulent diseases. Local manifestations.

Chronic aerobic surgical infection. Reasons for development. Features of manifestation. Complications: amyloidosis, wound exhaustion.

Acute anaerobic surgical infection. The concept of clostridial and non-clostridial anaerobic infection. Main pathogens. Conditions and factors contributing to the occurrence of anaerobic gangrene and phlegmon. Incubation period. Clinical forms. Comprehensive prevention and treatment of clostridial anaerobic infection. The use of hyperbaric oxygen therapy. Prevention of nosocomial spread of anaerobic infection.

The place of non-clostridial anaerobic infection in the general structure of surgical infection. Pathogens. Endogenous anaerobic infection. Frequency of anaerobic non-clostridial infection. The most characteristic clinical signs: local and general. Prevention and treatment (local and general) of anaerobic surgical infection.

Topic 16. Acute purulent nonspecific infection. Purulent surgery of the skin and subcutaneous tissue. Types of purulent skin diseases: acne, ostiofolliculitis, folliculitis, furuncle and furunculosis, carbuncle, hydradenitis, erysipelas, erysipeloid, periwound pyoderma. Clinic, features of the course and treatment. Types of purulent-inflammatory diseases of the subcutaneous tissue: abscess, cellulite, phlegmon. Clinic, diagnostics, local and general treatment. Possible complications. Purulent diseases of the lymphatic and blood vessels.

Purulent hand surgery. The concept of felon. Types of felon. Boils and carbuncles of the hand. Purulent tendovaginitis. Purulent inflammation of the palm. Purulent inflammation of the back of the hand. Special types of panaritium. Principles of diagnosis and treatment (local and general). Prevention of purulent diseases of the hand.

Purulent surgery of cellular spaces . Cellulitis of the neck. Axillary and subpectoral phlegmon. Subfascial and intermuscular phlegmon of the extremities. Phlegmons of the foot. Purulent mediastinitis. Purulent processes in the tissue of the retroperitoneum and pelvis. Purulent paranephritis. Purulent and chronic acute paraproctitis. Causes of occurrence, symptoms, diagnosis, principles of local and general treatment.

Purulent surgery of glandular organs. Purulent parotitis. Predisposing factors, clinical signs, methods of prevention and treatment.

Acute and chronic purulent mastitis. Symptoms, prevention, treatment of acute lactation postpartum mastitis.

Purulent diseases of other glandular organs (pancreatitis, prostatitis, etc.).

Purulent surgery of serous cavities. An idea of ​​the etiology, clinical manifestations and principles of treatment of purulent meningitis and brain abscesses. Acute purulent pleurisy and pleural empyema. Pericarditis. Purulent lung diseases: abscess and gangrene of the lung, chronic suppurative lung diseases. General understanding of the causes, symptoms, diagnosis and treatment (conservative and surgical).

Purulent diseases of the peritoneum and abdominal organs. Acute peritonitis. Classification. Etiology and pathogenesis. Symptomatology and diagnosis. General disorders in the body in acute peritonitis. Principles of treatment. First aid for acute surgical diseases of the abdominal organs.

Features of diagnostics and treatment tactics in outpatient settings.

Topic 17. Purulent surgery of bones and joints. General purulent surgical infection. Purulent bursitis. Purulent arthritis. Causes, clinical picture, principles of treatment. Osteomyelitis. Classification. The concept of exogenous (traumatic) and endogenous (hematogenous) osteomyelitis. Modern "idea of ​​the etiopathogenesis of hematogenous osteomyelitis. Symptoms of acute osteomyelitis. The concept of primary-chronic forms of osteomyelitis. Chronic recurrent osteomyelitis. Diagnosis of various forms of osteomyelitis. Principles of general and local (operative and non-operative) treatment of osteomyelitis.

Concept of sepsis. Types of sepsis. Etiopathogenesis. An idea of ​​the entrance gate, the role of macro- and microorganisms in the development of sepsis. Clinical forms of the course and clinical picture of sepsis. Diagnosis of sepsis. Treatment of sepsis: surgical sanitation of a purulent focus, general replacement and corrective therapy.

Features of diagnostics and treatment tactics in outpatient settings.

Topic 18. Acute and chronic specific infection. The concept of a specific infection. Main diseases: tetanus, anthrax, rabies, wound diphtheria. Tetanus is an acute specific anaerobic infection. Ways and conditions of penetration and development of tetanus infection.

Incubation period. Clinical manifestations. Prevention of tetanus: specific and nonspecific. The importance of early diagnosis of tetanus. Complex symptomatic treatment of tetanus. Anthrax and diphtheria of wounds: features of the clinical picture, treatment, isolation of the patient.

The concept of chronic specific infection. Surgical tuberculosis in children and adults. Forms of surgical tuberculosis. The most common forms of osteoarticular tuberculosis. Features of tuberculous sintered (cold) abscess Diagnosis and complex treatment of osteoarticular tuberculosis. Local treatment of edema abscesses and fistulas. Surgical forms of pulmonary tuberculosis. Tuberculous lymphadenitis.

Actinomycosis. Clinical picture, differential diagnosis, complex therapy.

The concept of surgical syphilis.

Features of diagnostics and treatment tactics in outpatient settings.

Topic 19. Fundamentals of surgery for circulatory disorders and necrosis. Necrosis. Circulatory disorders that can cause necrosis. Other factors leading to local (limited or widespread) tissue necrosis. Types of necrosis, local and general manifestations. Gangrene is dry and wet.

Arterial blood flow disorders: acute and chronic. General principles of clinical and instrumental diagnostics. Surgical and conservative treatment. First aid for acute thrombosis and arterial embolism.

Venous circulation disorders: acute and chronic. The concept of phlebothrombosis, phlebitis, thrombophlebitis. The concept of pulmonary embolism. Other peripheral venous diseases and their complications. Trophic ulcers, principles of surgical and non-operative treatment. First aid for acute thrombosis and thrombophlebitis, bleeding from varicose ulcers, pulmonary embolism.

Bedsores as a particular type of necrosis. Causes of occurrence. Dynamics of bedsore development. Prevention of bedsores: features of care for patients who stay in bed for a long time. Local treatment of bedsores. The significance and nature of general measures in the treatment of pressure ulcers.

Features of diagnostics and treatment tactics in outpatient settings.

Topic 20. Fundamentals of tumor surgery. The concept of benign and malignant tumors. Precancerous diseases. Features of the clinical picture and development of the disease in benign and malignant neoplasms. Clinical classification of tumors. Surgical treatment of benign tumors. Preventive examinations. Organization of oncology service. Principles of complex therapy of malignant tumors and the place of surgical methods in the treatment of tumors.

Features of diagnostics and treatment tactics in outpatient settings.