Critical disability in surgical patients. Specialized secondary education of a medical profile Disability syndromes

Date: 01.07.2020

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 - a drop in vascular tone with a relative decrease in the volume of circulating blood.

The degree of impairment of consciousness Sopor - unconsciousness, preservation of protective movements in response to pain and sound stimuli. Moderate coma - unintelligibility, lack of protective movements. Deep coma - suppression of tendon reflexes, a drop in muscle tone. Terminal coma is an agonal state.

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

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

Physiology of respiration The process of respiration The process of respiration 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 violation of the transport of oxygen to the tissues and the removal of carbon dioxide from the body.

Indicators of blood gases in a healthy person Indicator Arterial blood Mixed blood р О 2 mm Hg. Art SaО 2,% рСО 2, mm Hg. st

Etiological classification ONE PRIMARY (pathology of stage 1 - oxygen delivery to the alveoli) Causes: mechanical asphyxia, spasm, swelling, vomit, pneumonia, pneumothorax. SECONDARY (stage 2 pathology - impaired oxygen transport from the alveoli to the tissues) Causes: microcirculation disorders, hypovolemia, LA thromboembolism, 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 (accidents on submarines, highlands). 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 - impaired airway patency, a decrease in the respiratory surface of the lungs, respiratory depression of central genesis); b) circulatory (against the background of acute and chronic circulatory failure); c) tissue (poisoning with potassium cyanide - the process of oxygen assimilation by tissues is disrupted); d) hemic (decrease in erythrocyte mass or hemoglobin in erythrocytes).

3. Hypoxemic syndrome - impaired 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. Major ARF syndromes

Clinical stages of ODN Stage I: Consciousness: preserved, anxiety, euphoria. Respiratory function: lack of air, respiratory rate per minute, mild acrocyanosis. Blood circulation: heart rate in min. BP-norm or slightly increased. The skin is pale and moist. Partial pressure of O 2 and CO 2 blood: p O 2 up to 70 mm Hg. р СО 2 up to 35 mm Hg

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

Stage III: Consciousness: absent, clonic-tonic convulsions, pupils are dilated, do not react to light. Respiratory function: tachypnea 40 or more per minute turns into bradypnea 8-10 per minute, spotted cyanosis. Blood circulation: heart rate more than 140 per minute. BP, atrial fibrillation. Partial pressure of О 2 and СО 2: р О 2 up to 50 mm Hg. р СО 2 to mm Hg Clinical stages of ARF

Emergency care for ARF 1. Restoring the patency of the airways. 2. Elimination of disorders of alveolar ventilation (local and general). 3. Elimination of violations of central hemodynamics. 4. Correction of the etiological factor of ARF. 5. Oxygen therapy 3-5 l / min. at stage I of ODN. 6. At II - III stages of ARF, tracheal intubation and artificial ventilation of the lungs are performed.

Treatment of OCH 1. Subcutaneous administration of 1-2 ml of morphine, preferably combined with the introduction of 0.5 ml of 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 i / v, i / m, no-spa 2.0 i / m, analgin 2.0 i / m. 4. In case of cardiac arrhythmias: lidocaine mg i / v, novocainamide 10% 10.0 i / v, obzidan 5 mg i / v. 5. With pulmonary edema: dopmin 40 mg IV on glucose, lasix 40 mg IV, aminophylline 2.4% 10.0 IV.

ETIOLOGY OF ARF 1. Traumatic, hemorrhagic, blood transfusion, bacterial, anaphylactic, cardiogenic, burn, operational shock; electrical injury, postpartum sepsis, etc. 2. Acute infarcted kidney. 3. Vascular abstraction. 4. Urological abstraction.

DIAGNOSIS 1. Decrease in urine output (less than 25 ml / h) with the appearance of protein, erythrocytes, leukocytes, cylinders, decrease in urine density to 1.005-1, Increase in azotemia (16.7-20.0 mmol / l). 3. Hyperkalemia. 4. Decrease in blood pressure. 5. Decrease in hemoglobin and erythrocytes.

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

Classification of OPF 1. Endogenous - the basis is 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 "hepatic odor" from the mouth 3. Icterus of the sclera and skin 4. Signs of hemorrhagic syndrome 5. The appearance of erythema patches in the form of stellate angiomas 6. Jaundice 7. Ascites 8. Splenomegaly

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

Principles of ARF treatment 1. Eliminate bleeding and hypovolemia. 2. Eliminate hypoxia. 3. Detoxification. 4. Normalization of energy metabolism. 5. The 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.

The main clinical characteristics of the assessment of the state of consciousness:

Clear consciousness - its complete safety, adequate reaction to the environment, full orientation, wakefulness.

Moderate stunning - moderate drowsiness, partial disorientation, delayed answers to questions (repetition is often required), slower command execution.

Deep stun - deep drowsiness, disorientation, limitation and difficulty in speech contact, the execution of only simple commands.

Stupor (unconsciousness, deep sleep) - almost complete lack of consciousness, preservation of purposeful, coordinated protective movements, opening eyes to pain and sound stimuli, episodically monosyllabic answers to questions, loss of control over pelvic functions.

Moderate coma (I) - lack of consciousness, chaotic uncoordinated movements in response to painful stimuli, lack of opening the eyes in response to stimuli.

Deep coma (II) - lack of consciousness and protective movements, impaired muscle tone, suppression of tendon reflexes, respiratory and cardiovascular disorders.

Extreme (terminal) coma (III) - agonal state, atony, areflexia, vital functions are supported by mechanical ventilation and cardiovascular drugs.

The clinic distinguishes 5 degrees of severity of the general condition of the patient:

Satisfactory state - clear consciousness. Vital functions (VF) are not impaired.

A state of moderate severity - clear consciousness or there is moderate stunning. LWF are slightly disturbed.

Severe condition - consciousness is impaired to deep stunning or stupor. Severe violations of the respiratory and / or cardiovascular systems.

The condition is extremely serious - moderate or deep coma, severe symptoms of damage to the respiratory and / or cardiovascular systems.

The terminal state is a transcendental coma with gross signs of damage to the trunk and impaired vital functions.

Types of disruption of the body's vital functions. Acute respiratory failure.

Acute respiratory failure (ARF) Is a syndrome based on disturbances in the external respiration system, in which the normal gas composition of arterial blood is not provided or its maintenance at a normal level is achieved due to excessive functional stress of this system.

Etiology.

Distinguish between pulmonary and extrapulmonary causes of ARF.

Extrapulmonary causes:

Violation of the central regulation of respiration: a) acute vascular disorders (acute disorders of cerebral circulation, cerebral edema); b) brain injury; c) intoxication with drugs acting on the respiratory center (narcotic drugs, barbiturates); d) infectious, inflammatory and neoplastic processes leading to damage to the brain stem; e) coma.

Damage to the musculoskeletal system of the chest and damage to the pleura: a) peripheral and central paralysis of the respiratory muscles; b) spontaneous pneumothorax; c) degenerative-dystrophic changes in the respiratory muscles; d) poliomyelitis, tetanus; e) spinal cord injury; f) the consequences of the action of organophosphorus compounds and muscle relaxants.

ODN in violation of oxygen transport with large blood loss, acute circulatory failure and poisoning (carbon monoxide).

Pulmonary causes:

Obstructive disorders: a) blockage of the airways by a foreign body, sputum, vomit; b) mechanical obstruction to air access when compressed from the outside (hanging, strangulation); c) allergic laryngo - and bronchospasm; d) tumor processes of the respiratory tract; e) violation of the act of swallowing, paralysis of the tongue with its retraction; f) edematous-inflammatory diseases of the bronchial tree.

Respiratory disorders: a) infiltration, destruction, dystrophy of the lung tissue; b) pneumosclerosis.

Reduction of the functioning pulmonary parenchyma: a) underdevelopment of the lungs; b) compression and atelectasis of the lung; c) a large amount of fluid in the pleural cavity; d) pulmonary embolism (PE).

ODN classification.

Etiological:

Primary ARF - associated with impaired oxygen delivery to the alveoli.

Secondary ARF - associated with impaired oxygen transport from the alveoli to the tissues.

Mixed ODN - a combination of arterial hypoxemia with hypercapnia.

Pathogenetic:

The ventilatory form of ODN occurs when the respiratory center of any etiology is affected, when impulse transmission in the neuromuscular apparatus is disturbed, chest and lung injuries, changes in normal breathing mechanics in pathology of the abdominal organs (for example, intestinal paresis).

The parenchymal form of ARF occurs with obstruction, restriction of the airways, as well as with impaired diffusion of gases and blood flow in the lungs.

ODN pathogenesis due to the development of oxygen starvation of the body as a result of disturbances in alveolar ventilation, diffusion of gases through the alveolar-capillary membranes and the uniformity of oxygen distribution throughout organs and systems.

Allocate three main syndromes ONE:

I .Hypoxia- a condition that develops as a result of reduced tissue oxygenation.

Taking into account etiological factors, hypoxic conditions are divided into 2 groups:

A). Hypoxia due to a reduced partial pressure of oxygen in the inhaled air (exogenous hypoxia), for example, in high altitude conditions.

B) Hypoxia in pathological processes that disrupt the supply of oxygen to tissues at its normal partial stress in the inhaled air:

Respiratory (respiratory) hypoxia - the basis is alveolar hypoventilation (impaired airway patency, chest trauma, inflammation and pulmonary edema, respiratory depression of central origin).

Circulatory hypoxia occurs against the background of acute or chronic circulatory failure.

Tissue hypoxia - a violation of the processes of oxygen assimilation at the tissue level (poisoning with potassium cyanide)

Hemic hypoxia - the basis is a significant decrease in erythrocyte mass or a decrease in the hemoglobin content in erythrocytes (acute blood loss, anemia).

II. Hypoxemia- violation of the processes of oxygenation of arterial blood in the lungs. This syndrome can occur as a result of hypoventilation of the alveoli of any etiology (for example, asphyxia), with a predominance of blood flow in the lungs over ventilation in case of airway obstruction, in violation of the diffusion capacity of the alveolar-capillary membrane in respiratory distress syndrome. An integral indicator of hypoxemia is the level of partial tension of oxygen in arterial blood (P a O 2 is normally 80-100 mm Hg).

III. Hypercapnia- a pathological syndrome characterized by an increased content of carbon dioxide in the blood or at the end of expiration in the exhaled air. Excessive accumulation of carbon dioxide in the body disrupts the dissociation of oxyhemoglobin, causing hypercatecholaminemia. Carbon dioxide is a natural stimulant of the respiratory center, therefore, at the initial stages, hypercapnia is accompanied by tachypnea, however, as its excessive accumulation in arterial blood, depression of the respiratory center develops. Clinically, this is manifested by bradypne and respiratory rhythm disturbances, tachycardia, increased bronchial secretion and blood pressure (BP). In the absence of proper treatment, a coma develops. An integral indicator of hypercapnia is the level of partial tension of carbon dioxide in arterial blood (Pa CO 2 is 35-45 mm Hg in the norm).

The clinical picture.

Shortness of breath, disturbance in the rhythm of breathing: tachypnoe, accompanied by a feeling of lack of air with the participation of auxiliary muscles in the act of breathing, with an increase in hypoxia - bradypne breathing, Cheyne-Stokes breathing, Biot, with the development of acidosis - breathing of Kussmaul.

Cyanosis: acrocyanosis against the background of pallor of the skin and their normal moisture, with an increase in cyanosis becomes diffuse, there may be "red" cyanosis against the background of increased sweating (evidence of hypercapnia), "marbling" of the skin, spotted cyanosis.

The clinic allocates three stages of ODN.

Ithe stage I am. The patient is conscious, restless, may be euphoric. Complaints about feeling short of breath. The skin is pale, moist, mild acrocyanosis. The number of breaths (RR) is 25-30 per minute, the number of heartbeats (HR) is 100-110 beats / min, blood pressure is within normal limits or slightly increased, P a O 2 70 mm Hg, P a CO 2 35 mmHg. (hypocapnia is compensatory in nature as a consequence of shortness of breath).

IIstage... Complaints of severe suffocation. Psychomotor agitation. Delirium, hallucinations, loss of consciousness are possible. The skin is cyanotic, sometimes in combination with hyperemia, profuse sweat. RR - 30 - 40 per minute, heart rate - 120-140 beats / min, arterial hypertension. R a O 2 decreases to 60 mm Hg, R a CO 2 increases to 50 mm Hg.

IIIstage... Consciousness is absent. Convulsions. Dilatation of the pupils with the absence of their response to light, spotted cyanosis. Bradypnoe (BH - 8-10 per minute). Falling blood pressure. Heart rate more than 140 beats / min, arrhythmias. R a O 2 decreases to 50 mm Hg, R a CO 2 increases to 80 - 90 mm Hg. and more.

1. Types of disorders of the body's vital functions. Shock, terminal conditions, acute respiratory, renal, cardiovascular failure in surgical patients.

Shock- an acutely emerging critical state of the body with progressive failure of the life support system, caused by acute insufficiency of blood circulation, microcirculation and tissue hypoxia.

In shock, the functions of the cardiovascular system, respiration, kidneys change, the processes of microcirculation and metabolism are disrupted. Shock is a polyetiological disease. Depending on the cause of the occurrence, the following types are distinguished.

1. Traumatic shock: a) as a result of mechanical injury (wounds, bone fractures, tissue compression, etc.); b) burn shock (thermal and chemical burns); c) when exposed to low temperatures - cold shock; d) as a result of electrical injury - electrical shock.

2. Hemorrhagic, or hypovolemic, shock: a) bleeding, acute blood loss; b) an acute violation of the water balance - dehydration of the body.

3. Septic (bacterial-toxic) shock (common purulent processes caused by gram-negative or gram-positive microflora).

4. Anaphylactic shock.

5. Cardiogenic shock (myocardial infarction, acute heart failure)

Varieties and manifestations of terminal conditions.

Pre-gonal states;

Clinical death.

In addition, grade III-IV shock has a number of features characteristic of terminal states.

Terminal conditions most often develop as a result of acute blood loss, traumatic and surgical shock, asphyxia, collapse, severe acute intoxication (sepsis, peritonitis), coronary circulation disorders, etc.

The preagonal state is characterized by a darkened, confused consciousness, pallor of the skin, pronounced acrocyanosis, and impaired blood circulation. Eye reflexes are preserved, breathing is weakened, the pulse is threadlike, blood pressure is not determined. Oxygen starvation and acidosis. In the brain tissue, the amount of free sugar decreases, and the content of lactic acid increases. Further development of the pathological process leads to agony.

Agony - there is no consciousness, areflexia, a sharp pallor of the skin, pronounced cyanosis. Pulse only on the carotid arteries, deaf heart sounds, bradycardia, breathing is arrhythmic, convulsive. Increasing acidosis, oxygen starvation of vital centers.

Clinical death. Breathing and cardiac activity are absent. Metabolic processes are kept at the lowest level. The body's vital activity is minimal. Clinical death lasts 5-6 minutes (V.A.Negovsky, 1969), but the body can still be revived. First of all, the cerebral cortex dies as a younger (phylogenetically) formation. Subcortical formations are more stable and viable.

Biological death develops if measures were not taken in time to revive the body. Irreversible processes develop. Reanimation techniques are useless.

A comprehensive technique for resuscitation of terminal conditions provides for:

Intra-arterial blood pressure;

Heart massage (direct and indirect);

Defibrillation of the heart;

Artificial ventilation of the lungs;

Assisted artificial circulation.

These activities can be carried out simultaneously, or selectively. It is important to know that if clinical death occurs, then a complex of therapeutic measures can lead to the revitalization of the body.

Acute Respiratory Failure (ARF)- a syndrome based on disturbances in the external respiration system, in which the normal gas composition of arterial blood is not provided or its maintenance at a normal level is achieved due to excessive functional stress of this system.

Etiology.

Distinguish between pulmonary and extrapulmonary causes of ARF.

Extrapulmonary causes:

1. Violation of the central regulation of respiration: a) acute vascular disorders (acute disorders of cerebral circulation, cerebral edema); b) brain injury; c) intoxication with drugs acting on the respiratory center (narcotic drugs, barbiturates); d) infectious, inflammatory and neoplastic processes leading to damage to the brain stem; e) coma.

2. Damage to the musculoskeletal system of the chest and damage to the pleura: a) peripheral and central paralysis of the respiratory muscles; b) spontaneous pneumothorax; c) degenerative-dystrophic changes in the respiratory muscles; d) poliomyelitis, tetanus; e) spinal cord injury; f) the consequences of the action of organophosphorus compounds and muscle relaxants.

3. ONE in violation of oxygen transport with large blood loss, acute circulatory failure and poisoning (carbon monoxide).

Pulmonary causes:

1. Obstructive disorders: a) blockage of the respiratory tract by a foreign body, sputum, vomit; b) mechanical obstruction to air access when compressed from the outside (hanging, strangulation); c) allergic laryngo - and bronchospasm; d) tumor processes of the respiratory tract; e) violation of the act of swallowing, paralysis of the tongue with its retraction; f) edematous-inflammatory diseases of the bronchial tree.

2. Respiratory disorders: a) infiltration, destruction, dystrophy of the lung tissue; b) pneumosclerosis.

3.Reduction of the functioning pulmonary parenchyma: a) underdevelopment of the lungs; b) compression and atelectasis of the lung; c) a large amount of fluid in the pleural cavity; d) pulmonary embolism (PE).

ODN classification.

1.Etiological:

Primary ARF - associated with impaired oxygen delivery to the alveoli.

Secondary ARF - associated with impaired oxygen transport from the alveoli to the tissues.

Mixed ODN - a combination of arterial hypoxemia with hypercapnia.

2.Pathogenetic:

The ventilation form of ODN occurs when the respiratory center of any etiology is affected, when impulse transmission in the neuromuscular apparatus is disturbed, chest and lung injuries, changes in the normal mechanics of respiration in pathology of the abdominal organs (for example, intestinal paresis).

The parenchymal form of ARF occurs with obstruction, restriction of the airways, as well as with impaired diffusion of gases and blood flow in the lungs.

The pathogenesis of ARF is due to the development of oxygen starvation of the body as a result of disturbances in alveolar ventilation, diffusion of gases through the alveolar-capillary membranes and uniformity of oxygen distribution throughout organs and systems.

There are three main ADF syndromes:

I. Hypoxia is a condition that develops as a result of decreased tissue oxygenation.

Taking into account etiological factors, hypoxic conditions are divided into 2 groups:

A). Hypoxia due to a reduced partial pressure of oxygen in the inhaled air (exogenous hypoxia), for example, in high altitude conditions.

B) Hypoxia in pathological processes that disrupt the supply of oxygen to tissues at its normal partial stress in the inhaled air:

Respiratory (respiratory) hypoxia - based on alveolar hypoventilation (impaired airway patency, chest trauma, inflammation and pulmonary edema, respiratory depression of central origin).

Circulatory hypoxia occurs against the background of acute or chronic circulatory failure.

Tissue hypoxia - a violation of the processes of oxygen assimilation at the tissue level (poisoning with potassium cyanide)

Hemic hypoxia - the basis is a significant decrease in erythrocyte mass or a decrease in the hemoglobin content in erythrocytes (acute blood loss, anemia).

II.Hypoxemia - violation of the processes of oxygenation of arterial blood in the lungs. This syndrome can occur as a result of hypoventilation of the alveoli of any etiology (for example, asphyxia), with a predominance of blood flow in the lungs over ventilation in case of airway obstruction, in violation of the diffusion capacity of the alveolar-capillary membrane in respiratory distress syndrome. An integral indicator of hypoxemia is the level of partial tension of oxygen in arterial blood (PaO2 is normally 80-100 mm Hg).

III.Hypercapnia is a pathological syndrome characterized by an increased content of carbon dioxide in the blood or at the end of expiration in the exhaled air. Excessive accumulation of carbon dioxide in the body disrupts the dissociation of oxyhemoglobin, causing hypercatecholaminemia. Carbon dioxide is a natural stimulant of the respiratory center, therefore, at the initial stages, hypercapnia is accompanied by tachypnea, however, as its excessive accumulation in arterial blood, depression of the respiratory center develops. Clinically, this is manifested by bradypne and respiratory rhythm disturbances, tachycardia, increased bronchial secretion and blood pressure (BP). In the absence of proper treatment, a coma develops. An integral indicator of hypercapnia is the level of partial tension of carbon dioxide in arterial blood (PaCO2 is 35-45 mm Hg in the norm).

The clinical picture.

In the clinic, there are three stages of ODN.

Stage I. The patient is conscious, restless, may be euphoric. Complaints about feeling short of breath. The skin is pale, moist, mild acrocyanosis. The number of breaths (RR) is 25-30 per minute, the number of heartbeats (HR) is 100-110 beats / min, blood pressure is within normal limits or slightly increased, PaO2 70 mm Hg, PaCO2 35 mm Hg. (hypocapnia is compensatory in nature as a consequence of shortness of breath).

Stage II. Complaints of severe suffocation. Psychomotor agitation. Delirium, hallucinations, loss of consciousness are possible. The skin is cyanotic, sometimes in combination with hyperemia, profuse sweat. RR - 30 - 40 per minute, heart rate - 120-140 beats / min, arterial hypertension. PaO2 decreases to 60 mm Hg, PaCO2 increases to 50 mm Hg.

Stage III. Consciousness is absent. Convulsions. Dilatation of the pupils with the absence of their response to light, spotted cyanosis. Bradypnoe (BH - 8-10 per minute). Falling blood pressure. Heart rate more than 140 beats / min, arrhythmias. PaO2 decreases to 50 mm Hg, PaCO2 increases to 80 - 90 mm Hg. and more.

Acute heart failure (AHF) Is a clinical syndrome resulting from primary heart disease or other diseases in which the heart does not provide sufficient blood circulation to organs and tissues in accordance with their metabolic needs.

OSN classification.

1.Acute left ventricular failure:

Interstitial pulmonary edema or cardiac asthma:

Alveolar pulmonary edema.

Acute right ventricular failure.

Acute biventricular insufficiency.

In terms of severity, the following stages of AHF are distinguished (Killip's classification):

Stage I - no signs of heart failure.

Stage II - mild AHF: there is shortness of breath, moist fine bubbling rales are heard in the lower parts of the lungs.

Stage III - severe AHF: severe shortness of breath, a significant amount of moist wheezing over the lungs.

Stage IV - a sharp drop in blood pressure (systolic blood pressure of 90 mm Hg or less) up to the development of cardiogenic shock. Severe cyanosis, cold skin, clammy sweat, oliguria, darkening of consciousness.

Etiology of acute left ventricular heart failure:

1. IHD: acute coronary syndrome (prolonged anginal attack, painless widespread myocardial ischemia), acute myocardial infarction (AMI).

2. Insufficiency of the mitral valve caused by the avulsion of the papillary muscle (with AMI) or the detachment of the mitral valve chord (with infective endocarditis or chest trauma).

3. Stenosis of the left atrioventricular orifice associated with a tumor in any of the heart chambers (most often - myxoma of the left atrium), thrombosis of the mitral valve prosthesis, mitral valve lesion in infective endocarditis.

4. Insufficiency of the aortic valve with rupture of the aortic valves, with dissecting aneurysm of the ascending aorta.

5. Acutely increased heart failure in patients with chronic heart failure (acquired or congenital heart defects, cardiomyopathy, postinfarction or atherosclerotic cardiosclerosis); this may be associated with a hypertensive crisis, arrhythmia paroxysm, fluid overload as a result of inadequate diuretic or excessive fluid therapy.

Etiology of acute right ventricular heart failure:

1. AMI of the right ventricle.

2.Pulmonary embolism (PE).

3.Stenotic process in the right atrioventricular orifice (as a result of a tumor or vegetative growths with infective endocarditis of the tricuspid valve).

4. Asthmatic status.

Etiology of acute biventricular heart failure:

1. AMI with damage to the right and left ventricles.

2. Rupture of the interventricular septum in AMI.

3. Paroxysmal tachycardia.

4. Acute myocarditis of severe course.

Pathogenesis. The main mechanisms of development:

Primary myocardial damage, leading to a decrease in myocardial contractility (coronary artery disease, myocarditis).

Left ventricular pressure overload (arterial hypertension, aortic valve stenosis).

Overload of the left ventricle volume (insufficiency of the aortic and mitral valves, defect of the interventricular septum).

Decreased filling of the ventricles of the heart (cardiomyopathy, hypertension, pericarditis).

High cardiac output (thyrotoxicosis, severe anemia, liver cirrhosis).

Acute left ventricular heart failure.

The main pathogenetic factor is a decrease in the contractility of the left ventricle with preserved or increased venous return, which leads to an increase in hydrostatic pressure in the system of the pulmonary circulation. With an increase in hydrostatic pressure in the pulmonary capillaries of more than 25 - 30 mm Hg. there is a transudation of the liquid part of the blood into the interstitial space of the lung tissue, which causes the development of interstitial edema. One of the important pathogenetic mechanisms is foaming with each inhalation of the fluid that has entered the alveoli, which rises upward, filling the bronchi of a larger caliber, i.e. alveolar pulmonary edema develops. So, from 100 ml of sweated plasma, 1 - 1.5 liters of foam are formed. Foam not only disrupts the airway, but also destroys the surfactant of the alveoli, which causes a decrease in lung compliance, increases hypoxia and edema.

Clinical picture:

Cardiac asthma (interstitial pulmonary edema) most often develops at night with a feeling of shortness of breath, dry cough. A patient in a forced orthopnea position. Cyanosis and pallor of the skin, cold clammy sweat. Tachypnea, moist rales in the lower parts of the lungs, muffled heart sounds, tachycardia, accent of the second tone over the pulmonary artery.

Alveolar pulmonary edema is characterized by the development of a sharp attack of suffocation, there is a cough with the release of foamy pink sputum, "bubbling" in the chest, acrocyanosis, profuse sweating, tachypnea. In the lungs, rales of various sizes. Tachycardia, accent of the second tone over the pulmonary artery.

Acute right ventricular heart failure is a consequence of a sharp increase in pressure in the pulmonary artery system. Given the low prevalence of isolated right ventricular MI and tricuspid valve infections, acute right ventricular failure is usually found in combination with left ventricular failure in clinical practice.

Clinical picture: gray cyanosis, tachypnoe, acute enlargement of the liver, pain in the right hypochondrium, swelling of the cervical veins, peripheral and cavity edema.

Acute biventricular heart failure: symptoms of left and right ventricular failure appear simultaneously.

Acute renal failure (ARF) - pathological clinical syndrome of various etiologies, characterized by a significant and rapid decrease in the glomerular filtration rate (GFR), which is based on an acute lesion of the nephron, followed by a violation of its main functions (urinary and urinary) and the occurrence of azotemia, a violation of the acid-base state and water-electrolyte metabolism ...

Classification opn.

1.According to the place of origin of the "damage":

Prerenal;

Renal;

Post-renal.

2.By etiology:

Shock kidney - traumatic, hemorrhagic, blood transfusion, septic, anaphylactic, cardiogenic, burn, operational shock, electrical trauma, termination of pregnancy, postpartum sepsis, severe gestosis, dehydration;

Toxic kidney - poisoning with exogenous poisons;

Severe infections;

Acute obstruction of the urinary tract;

Arenal condition.

3.Driver:

The initial period (the period of the initial action of the factors);

Period of oligo -, anuria (uremia);

Diuresis recovery period:

the phase of the initial diuresis (diuresis 500 ml / day);

phase of polyuria (diuresis more than 1800 ml / day);

recovery period.

4.By severity:

I degree - mild: increase in blood creatinine by 2-3 times;

II degree - moderate: blood creatinine increased by 4-5 times;

Grade III - severe: blood creatinine increased by more than 6 times.

The reasons for the development of prerenal ARF.

1.Decreased cardiac output:

Cardiogenic shock;

Pericardial tamponade;

Arrhythmias;

Congestive heart failure.

2.Reduction of vascular tone:

Anaphylactic, septic shock;

Irrational intake of antihypertensive drugs.

3.Reduction of extracellular fluid volume:

Blood loss, dehydration,

Profuse vomiting, diarrhea, polyuria.

The reasons for the development of the renal form of acute renal failure.

1.Acute tubular necrosis:

Ischemic;

Nephrotoxic;

Drug.

2.Internal obstruction:

Pathological cylinders, pigments;

Crystals.

3.Acute tubulo-interstitial nephritis:

Drug;

Infectious;

Acute pyelonephritis.

4.Cortical necrosis:

Obstetric;

Anaphylactic shock;

5. Glomerulonephritis.

6.Damage of renal vessels:

Traumatic;

Immunoinflammatory.

Reasons for the development of postrenal acute renal failure.

1. Damage to the ureters:

Obstruction (stone, blood clots);

Compression (swelling).

2. Damage to the bladder:

Stones, swelling, inflammatory obstruction, prostate adenoma;

Disruption of the innervation of the bladder; spinal cord injury.

3.Stricture of the urethra.

The pathogenesis is based on a violation of systemic hemodynamics and depletion of the vascular bed of the kidneys. Vasoconstriction is induced with redistribution of blood flow, ischemia of the renal cortex and a decrease in glomerular filtration. Renin - angiotensin - aldosterone system, production of ADH and catecholamines are activated, which leads to renal vasoconstriction, further decrease in glomerular filtration, sodium and water retention. If the disturbance of the blood supply to the kidneys lasts no more than 1-2 hours, their morphological structure is not significantly damaged and functional changes are of an incoming nature. If renal blood flow is not restored within 1-2 hours, severe morphological changes form in the kidneys. Clinically, this is manifested by a decrease in urine output (less than 25 ml / hour) and inhibition of the concentration ability of the kidneys (urine density decreases to 1005 - 1008). After 10-12 hours, azotemia and hyperkalemia increase in blood plasma.

Symptoms of severe hyperkalemia:

Arrhythmias, bradycardia, AV - blockade;

Paresthesia;

Muscle paralysis;

Depression of consciousness.

To oliguria, and especially anuria, symptoms of overhydration quickly join - peripheral and cavity edema, pulmonary edema, cerebral edema. The appearance of an excess of under-oxidized products in the body contributes to the development of metabolic acidosis, which in the initial stages of the disease is compensated for by respiratory alkalosis (shortness of breath). The accumulation of urea and creatinine in conditions of increased protein catabolism and disturbances in the water-electrolyte state increase metabolic acidosis (vomiting). ARF is characterized by hyperphosphatemia with hypocalcemia. In the polyuric phase, hypocalcemia can cause seizures. Severe intoxication is formed, manifested by headache, irritability, anxiety, and then depression of consciousness of varying severity. As acute renal failure progresses, anemia develops, which may be due to blood loss (hemorrhagic syndrome against a background of uremia), shortened life expectancy and hemolysis of erythrocytes, as well as a decrease in renal erythropoietin production. A significant suppression of the immune system contributes to the rapid addition of infectious complications.

2. Shock. Pathogenesis, clinical picture, diagnosis.

In shock, the functions of the cardiovascular system, respiration, kidneys change, the processes of microcirculation and metabolism are disrupted. Shock is a polyetiological disease.

In the development of traumatic shock, the main pathogenetic moments are the pain factor and blood loss (plasma loss), which lead to acute vascular insufficiency with microcirculation disorder and the development of tissue hypoxia.

At the heart of hemorrhagic shock is a decrease in the volume of circulating blood and, as a result, a circulatory disorder. A feature of the pathogenesis of septic shock is that impaired blood circulation under the influence of bacterial toxins leads to the opening of arteriovenous shunts, and blood bypasses the capillary bed, rushing from arterioles to venules. Cell nutrition is disrupted due to a decrease in capillary blood flow and the action of bacterial toxins directly on the cell, the supply of the latter with oxygen decreases.

1.Burn shock, its features, shock treatment.

Lasts 1-3 days

It occurs with deep burns of more than 15-20% of the body surface.

Consists of 2 phases: erectile and torpid

Erectile phase - the patient is agitated, groans, actively complains of pain, A / D is normal or increased.

Torpid phase - lethargy with preserved consciousness, A / D - a tendency to hypotension, CVP, BCC, diuresis decrease. T body N.

The end of the period of shock is evidenced by the restoration of diuresis

Septic shock is a condition of peripheral vascular collapse caused by endotoxins from gram-negative bacteria, less often by endotoxins from gram-positive bacteria.

Clinic. preceded by a progressive bacterial infection; begins with a sharp increase in body temperature to 3940 ° C, chills; intense sweating; shortness of breath, detoxification; a sharp drop in blood pressure, up to collapse and loss of consciousness.

Multiple organ failure syndrome develops: cardiovascular disorders: rhythm disturbances, myocardial ischemia, arterial hypotension; respiratory disorders: tachypnea, hypoxia, respiratory distress syndrome; neuropsychiatric disorders: agitation, convulsions, stupor, coma; renal dysfunction: oliguria, hyperazotemia, hypercreatininemia; renal function: jaundice, increased activity of plasma enzymes; changes in the hemogram: thrombocytopenia, anemia, leukocytosis, leukopenia, hypoproteinemia, acidosis; pronounced changes in the hemostasis system - the development of DIC syndrome.

There are 3 phases of the development of septic shock: Phase I - early, "warm": an increase in body temperature to 3840 ° C, chills; tachycardia; a decrease in systolic blood pressure (SAS) to 9585 mm Hg; a decrease in urine output to 30 ml / hour; the duration of the phase several hours and depends on the severity of the infection. Phase II - late or "cold": subnormal body temperature; cold, moist skin; hemorrhages; severe arterial hypotension (CAS decreases to 70 mm Hg); acrocyanosis, tachycardia, threadlike pulse; skin sensitivity disorder; oliguria, anuria. Phase III - irreversible septic shock: drop in blood pressure; anuria; coma; RDS

Hemotransfusion shock develops only during transfusion of incompatible blood through the AB0, "Rhesus" systems or other acquired systems. With a complete and high-quality conduct of all compatibility tests, this complication should not be in the doctor's practice!

Hemotransfusion shock develops only with "negligent attitude to duties" (Art. 172 of the Criminal Procedure Code of the Russian Federation). Patients with such complications rarely die immediately, so there is always an opportunity to save them. If you conceal an incompatible fatal blood transfusion, you will be held criminally liable under Article 103 of the Code of Criminal Procedure of the Russian Federation, and perhaps by a court decision, and on charges of a more serious CRIME.

Therapeutic measures for blood transfusion shock should be aimed at: arresting anaphylaxis, cardiovascular failure, eliminating hypovolemia, but the main task is to restore renal blood flow and urine output, because the maximum load on the kidneys is to eliminate the products of hemolysis of erythrocytes, which clog the renal tubules and form renal failure with the development of anuria. They are carried out in the following order

3. First aid for shock. Complex shock therapy.

In shock, first aid is the more effective, the earlier it is provided. It should be aimed at eliminating the causes of shock (relieving or reducing pain, stopping bleeding, taking measures to improve breathing and cardiac activity and prevent general cooling).

Pain reduction is achieved by giving the patient or injured limb a position in which there are fewer conditions for pain intensification, by the behavior of reliable immobilization of the injured part of the body, by giving painkillers.

In case of injury, the bleeding is stopped and the wound is bandaged, in case of bone fractures and extensive damage to soft tissues, splints are applied. The victim should be treated as carefully as possible.

To facilitate breathing, the clothes are unbuttoned (unbutton the collar, loosen the belt).

The patient is placed on his back, the head is somewhat lowered, the legs are raised upward by 20-30 cm. In this case, the blood flows towards the heart. At the same time, the volume of circulating blood also increases.

To protect from cooling, the patient is covered with blankets: he should not lose the heat of his body; other means of keeping warm are unacceptable due to the danger of further dilatation of the blood vessels.

In a state of shock, the patient becomes agitated, he is tormented by fear, so the person providing assistance must constantly be there, calm down and do everything to make the patient feel safe. It is extremely important to protect the patient from noise, for example, conversations of people around.

SHOCK TREATMENT

one . Provide an airway, if necessary, intubate and mechanically ventilate the lungs.

2. Position the patient with raised legs effectively in case of hypotension, especially if no medical equipment is available, however, it can impair ventilation, and in cardiogenic shock with stagnation of blood in the pulmonary circulation - also the work of the heart.

3. Place intravascular catheters:

1) up to peripheral veins 2 catheters of large diameter (preferably ≥ 1.8 mm [≤ 16 G]), which will allow effective infusion therapy → see below;

2) if necessary, the introduction of many drugs (including catecholamines → see below) a catheter in the vena cava; also allows monitoring of central venous pressure (CVP);

3) a catheter in an artery (usually a radial one) makes invasive monitoring of blood pressure in case of persistent shock or the need for long-term use of catecholamines. Catheterization of the vena cava and arteries should not delay treatment.

4 . Apply etiological treatment → see below and at the same time maintain circulatory system function and tissue oxygenation

1) if the patient is receiving antihypertensive drugs → cancel them;

2) in most types of shock, restoration of intravascular volume by intravascular infusion of solutions is of primary importance; the exception is cardiogenic shock with symptoms of blood stagnation in the pulmonary circulation. It has not been proven that colloidal solutions (6% or 10% hydroxyethyl starch [HES] solution, 4% gelatin solution, dextran, albumin solution) reduce mortality more effectively than crystalloid solutions (Ringer's solution, polyelectrolyte solution, 0.9% NaCl), although to correct hypovolemia, a smaller volume of colloid is needed than crystalloids. At the beginning, usually 1000 ml of crystalloids or 300-500 ml of colloids are injected for 30 minutes, and this strategy is repeated depending on the effect on blood pressure, CVP and diuresis, as well as side effects (symptoms of volume overload). For massive infusions, do not apply 0.9% NaCl exclusively, as infusion of large volumes of this solution (which is incorrectly called physiological) leads to hyperchloremic acidosis, hypernatremia and hyperosmolarity. Even with hypernatremia, do not apply 5% glucose to restore volemia in shock. Colloidal solutions reproduce the intravascular volume - they almost completely remain in the vessels (plasma-substituting agents - gelatin, 5% albumin solution), or remain in the vessels and lead to the transfer of water from the extravascular space to the intravascular [means that increase the plasma volume - hydroxyethylated starch [HES], 20% solution of albumin, dextran); crystalloid solutions equalize the deficiency of extracellular fluid (extra- and intravascular); glucose solutions increase the volume of total water in the body (external and intracellular fluid). Correction of a significant deficit of volemia can begin with the infusion of hypertonic solutions, for example, Special mixtures of crystalloids and colloids (so-called resuscitation in small volumes with the use between others .. 7 , 5% NaCl with 10% HES) as they increase the plasma volume better. In patients with severe sepsis or at increased risk of acute kidney injury, it is best not to use HES, especially those with a molecular weight ≥ 200 kDa and / or molar displacement> 0.4, albumin solution may be used instead (but not in patients after head injury);

3) if it is not possible to eliminate hypotension, despite the infusion of solutions → start a continuous intravenous infusion (preferably through a catheter in the vena cava) of catecholamines, vasoconstrictor, norepinephrine (adrenore, noradrenaline tartrate Agetan), usually 1-20 μg / min (more than 1-2 μg / kg / min) or epinephrine 0.05-0.5 μg / kg / min, or dopamine (dopamine Admeda, Dopamine-Darnitsa, Dopamine hydrochloride, dopamine-Health, Dopmin, at the moment is not drug of choice for septic shock) 3-30 mcg / kg / min and use invasive blood pressure monitoring. For anaphylactic shock, start with an injection of epinephrine 0.5 mg IM into the outer thigh;

4) in patients with low cardiac output, despite the corresponding flooding (or in hyperhydration), inject dobutamine (dobutamine Admed, dobutamine-Health) 2-20 μg / kg / min in a constant intravenous infusion; if hypotension coexists, a vasoconstrictor drug can be used at the same time;

5) simultaneously with the treatment described above, use oxygen therapy (maximally saturating hemoglobin with oxygen, its supply to tissues increases; an absolute indication is SaO 2<95%);

6) if, despite the above actions, SvO 2<70%, а гематокрит <30% → примените трансфузию эритроцитарной массы.

5 . The main method for correcting lactic acidosis is etiological treatment and treatment that maintains the function of the circulatory system; evaluate the indications for the introduction of NaHCO 3 i / v at pH<7,15 (7,20) или концентрации гидрокарбонатного иона <14 ммоль / л.

6. Monitor vital signs (blood pressure, pulse, respiration), state of consciousness, ECG, SaO 2, CVP, gas metrics (and possibly lactate concentration), natremia and potassium, kidney and liver function parameters; if necessary, cardiac output and pulmonary capillary wedge pressure.

7. Protect the patient from heat loss and provide a calm environment for the patient.

8. If the shock contains:

1) allow bleeding from the gastrointestinal tract and thromboembolic complications (in patients with active bleeding or a high risk of bleeding, do not use anticoagulant drugs, only mechanical methods);

2) correct hyperglycemia if> 10-11.1 mmol / L) constant intravenous infusion of short-acting insulin, however, avoid hypoglycemia; try to maintain a glycemic level between 6.7-7.8 mmol / L (120-140 mg / dL) to 10-11.1 mmol / L (180-200 mg / dL).

4. Fainting, collapse, shock. Anti-shock measures.

Fainting is an attack of short-term loss of consciousness caused by a temporary disturbance of cerebral blood flow.

Collapse (from Lat. Collapsus - fallen) is a life-threatening condition characterized by a drop in blood pressure and a deterioration in the blood supply to vital organs. In humans, it is manifested by severe weakness, pointed facial features, pallor, cold extremities. It occurs with infectious diseases, poisoning, large blood loss, overdose, side effects of certain drugs, etc.

Shock is an acutely emerging critical state of the body with progressive failure of the life support system, caused by acute insufficiency of blood circulation, microcirculation and tissue hypoxia.

The main anti-shock measures.

Traumatic shock is the body's response to painful irritations caused by mechanical, chemical or thermal injuries.

The frequency and severity of shock increases significantly during a nuclear war. Especially often it will be observed with combined radiation injuries, since the effect of ionizing radiation on the central nervous system disrupts its regular functions. This, in turn, leads to disruption of the activity of organs and systems, i.e. to metabolic disorders, a drop in blood pressure, which predisposes to shock.

Depending on the reasons that led to the shock, there are:

one). Traumatic shock caused by various injuries,

2). Burn shock that occurs after a burn injury

3). Operational shock caused by surgery with insufficient anesthesia

Topic 11. Wounds and wound process. Definition of the wound and symptoms of the wound. Types of wounds. The concept of single, multiple, combined and combined wounds. Phases of the course of the wound process. Types of wound healing. Principles of first aid for injuries. Primary surgical treatment of wounds, its types. Secondary surgical treatment. Closing the wound 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 course of the wound process. The use of proteolytic enzymes. Additional methods for treating purulent wounds.

Topic 12. General disabilities in a surgical patient. Clinical assessment of the general condition of patients. Types of general disorders of the body 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: pre-agony, agony, clinical death. Signs of biological death. First aid for cessation of breathing and blood circulation. Criteria for the effectiveness of revitalization. Monitoring control systems. Indications for discontinuing cardiopulmonary resuscitation.

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

Topic 13. Mechanical injury. Fractures and dislocations. Trauma concept. 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 diagnosis of traumatic injuries, first aid and treatment. Non-specific and specific prevention of infectious complications.

Mechanical injury. Types of mechanical injury: closed (subcutaneous) and open (wounds). Closed mechanical injuries of soft tissues: bruises, sprains and tears (subcutaneous), concussion and compression, prolonged compression syndrome. First aid and treatment of closed soft tissue injuries.

Types of mechanical damage to tendons, bones and joints. Tears of ligaments and tendons. Traumatic dislocations. Joint bruises, Hemarthrosis, First aid and treatment. Bone fractures. Classification. Clinical symptoms of fractures. Fundamentals 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 spinal cord injury. First aid "for fractures of the pelvic bones with or without injury to the pelvic organs. Transport immobilization - goals, objectives and principles. Types of transport immobilization. Standard splints. The principles of fracture treatment: reduction, immobilization, surgical treatment. The concept of plaster casts. Plaster cast. Basic rules for applying plaster casts The main types of plaster casts Instruments 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 hazards of head injuries that pose a threat to the life of patients. First aid tasks for head trauma. Measures for their implementation. Features of transportation of patients.

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

Damage to the abdomen with and 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 loss of abdominal organs into the wound. Features of gunshot wounds to the abdomen. Complications of traumatic abdominal injuries: acute anemia, peritonitis.

Features of treatment tactics on an outpatient basis.

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

Burns. Burn classification. Recognition of the depth of burns. Determination of the area of the burn. Predictive techniques 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 transplant. Antimicrobial therapy (sulfonamides, antibiotics, serums). Outpatient treatment of burns: indications, contraindications, methods. Reconstructive and plastic surgery of post-burn Cicatricial 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).

Cold injury. Types of cold injury: general - freezing and chills; local - frostbite. Prevention of cold injury in peacetime and wartime. Symptoms of freezing and chills, first aid for them and further treatment.

Classification of frostbite by degrees. The 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 trauma. Prevention of tetanus and purulent infection, nutrition and care.

Electric 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 Exposure to corrosive chemicals on fabric. Features of local manifestation. First aid for chemical burns of the skin, mouth, esophagus, stomach. Complications and consequences of burns of the esophagus.

Features of treatment tactics on an outpatient basis.

Topic 15. Fundamentals of purulent-septic surgery. General questions of surgical infection. Concept of surgical infection. Classification of surgical infection: acute and chronic purulent (aerobic), acute anaerobic, acute and chronic specific. The concept of a 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 treatment of a purulent focus and methods of postoperative management. General treatment for purulent diseases: rational antibiotic therapy, immunotherapy, complex infusion therapy, hormone and enzyme therapy, symptomatic therapy.

Acute aerobic surgical infection . The main pathogens. Infection routes. Pathogenesis of purulent inflammation. The staging of the development of pyoinflammatory diseases. Classification of acute purulent diseases. Local manifestations.

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

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

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 typical clinical signs are 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, near-wound 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. Potential complications. Purulent diseases of lymphatic and blood vessels.

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

Purulent surgery of cellular spaces . Phlegmon of the neck. Axillary and subpectoral phlegmon. Subfascial and intermuscular phlegmon of the extremities. Phlegmon of the foot. Suppurative mediastinitis. Purulent processes in the tissue of the retroperitoneal space and pelvis. Purulent paranephritis. Purulent and chronic acute paraproctitis. Causes, 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 lactational postpartum mastitis.

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

Purulent surgery of serous cavities. An understanding 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 operative).

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