Can lead to the development of acute blood loss of the wound. Course of lectures on resuscitation and intensive care
Bleeding (haemorrhagia) - outflow of blood from blood vessels in case of damage or violation of the permeability of their wall.
The loss of blood poses an immediate threat to the life of the victim, and his fate depends on immediate measures to stop the bleeding.
Classification of bleeding
I. Depending on the cause of occurrence:
a) mechanical damage, rupture of blood vessels (haemorrhagia per rhexin);
b) arrosive bleeding (haemorrhagia per diabrosin);
c) diapedetic bleeding (haemorrhagia per diapedesin);
d) a violation of the chemical composition of the blood, a change in the coagulation and anticoagulation system of the blood.
II. Depending on the type of bleeding vessel:
a) arterial;
b) arteriovenous;
c) venous;
d) capillary;
e) parenchymal.
III. In relation to the external environment and clinical manifestations:
a) external;
b) internal;
c) hidden.
IV. By time of occurrence:
a) primary;
b) secondary.
Mechanical damage vessels can occur with open and closed injuries (ruptures, wounds), burns, frostbite.
Arrosive bleeding arise when the integrity of the vascular wall is violated due to the germination of the tumor and its decay, when the vessel is destroyed by spreading ulceration in the case of necrosis, destructive inflammation, etc.
Diapedetic bleeding arise due to increased permeability of small vessels (capillaries, venules, arterioles), observed in a number of diseases: beriberi C, hemorrhagic vasculitis (Schoenlein-Genoch disease), uremia, sepsis, scarlet fever, smallpox, phosphorus poisoning, etc. This state of the vessels is due to molecular, physical and chemical changes in their wall.
The possibility of bleeding is determined by the condition blood coagulation system. In violation of blood coagulation, massive blood loss is possible if even small vessels are damaged.
The diseases accompanied by disorders of the blood coagulation system include hemophilia and Werlhof's disease. At hemophilia(hereditary disease) there are defective specific coagulation factors in plasma: factor VIII (hemophilia A) or factor IX (hemophilia B). The disease is manifested by increased bleeding. The slightest injury can lead to massive bleeding that is difficult to stop. At Werlhof's disease(thrombocytopenic purpura) reduced platelet count in the blood.
Severe changes in the blood coagulation system are observed with disseminated intravascular coagulation syndrome(DIC). The formation of multiple clots and blood clots in the vessels leads to the depletion of blood clotting factors, which causes a violation of its coagulation, hypocoagulation and bleeding: tissue bleeding during surgery, gastrointestinal, uterine bleeding, hemorrhages in the skin, subcutaneous tissue at the injection site, at the site of palpation . The causes of DIC can be shock, sepsis, massive traumatic injuries, multiple fractures, traumatic toxicosis (crush syndrome), massive blood transfusions, massive bleeding, etc.
Disturbances in the blood coagulation system and, as a result, bleeding can be caused by the action of certain medicinal substances. The use of indirect anticoagulants (ethyl biscumacetate, acenocoumarol, phenindione, etc.), which disrupt the synthesis of blood coagulation factors VII, IX, X in the liver, as well as sodium heparin, which has a direct effect on the process of thrombosis, fibrinolytic drugs (streptokinase, streptodecase etc.), leads to a violation in the blood coagulation system. Drugs such as phenylbutazone, acetylsalicylic acid, can increase bleeding due to impaired platelet function.
Bleeding due to clotting disorders includes cholemic bleeding. It has long been observed that in patients with jaundice
blood clotting is disturbed and both spontaneous bleeding (hemorrhage into muscles, skin, internal organs, nosebleeds) and increased tissue bleeding during surgery and in the postoperative period can occur. The cause of changes in the blood coagulation system is a decrease in the synthesis of coagulation factors V, VII, IX, X, XIII in the liver due to impaired absorption of vitamin K.
To increase blood clotting, plasma transfusions, cryoprecipitate, and the introduction of vitamin K are used.
The nature of bleeding is determined by the type of damaged vessel.
For arterial bleeding blood of scarlet color beats with a pulsating jet. The larger the vessel, the stronger the jet and the greater the volume of blood lost per unit time.
For venous bleeding the outflow of blood is constant, only when the damaged vein is located next to a large artery, transmission pulsation is possible, as a result of which the blood stream will be intermittent. If large veins in the chest area are damaged, the impulse of the heart is transmitted to the blood stream or the suction effect of the chest is influenced (when inhaling, the bleeding slows down, while exhaling it intensifies). Only at high venous pressure, for example, when varicose veins of the esophagus rupture, does a jet flow of blood occur. If large veins of the neck or subclavian vein are damaged, severe complications and even death due to air embolism may develop. This is due to the negative pressure in these veins that occurs during inspiration, and the possible entry of air through the damaged vessel wall. Venous blood is dark in color.
capillary bleeding mixed, there is an outflow of arterial and venous blood. In this case, the entire wound surface bleeds, after removal of the outflowing blood, the surface is again covered with blood.
Parenchymal bleeding are observed when parenchymal organs are damaged: the liver, spleen, kidneys, lungs, etc. They are essentially capillary, but they are more massive, difficult to stop and more dangerous due to the anatomical features of the structure of the vessels of these organs.
For external bleeding blood is shed into the environment.
Internal bleeding can occur both in the cavity and in the tissue. Hemorrhages in tissue occur by impregnation of the latter with blood with the formation of swelling. The size of the hemorrhage
be different, depending on the caliber of the damaged vessel, the duration of bleeding, the state of the blood coagulation system. The blood poured into the tissue imbibes (impregnates) the interstitial cracks, coagulates and gradually resolves. Massive hemorrhages may be accompanied by tissue stratification with the formation of an artificial cavity filled with blood, - hematomas. The resulting hematoma can resolve, or a connective tissue capsule forms around it, and the hematoma turns into a cyst. With the penetration of microorganisms into the hematoma, the latter suppurates. Non-resorbed hematomas can germinate with connective tissue and calcify.
Bleeding is of particular importance. into the serous cavities- pleural, abdominal. Such bleeding is massive due to the fact that it rarely stops spontaneously. This is due to the fact that the blood that has poured into the serous cavities loses its ability to coagulate, and the walls of these cavities do not create a mechanical obstacle to the blood flowing from the vessels. In the pleural cavities, in addition, a suction effect is created due to the negative pressure. Blood clotting is disturbed due to the loss of fibrin from the blood, which is deposited on the serous cover, while the process of thrombus formation is disturbed.
To hidden include bleeding without clinical signs. As an example, clinically not manifested bleeding from gastric and duodenal ulcers can be cited. Such bleeding can be detected only by a laboratory method - a study of feces for occult blood. Undetected long-term occult bleeding can lead to the development of anemia.
Primarybleeding occurs immediately after damage to the vessel, secondary- after a certain period of time after the primary bleeding stops.
Factors that determine the volume of blood loss and the outcome of bleeding
The cause of death in blood loss is the loss of the functional properties of blood (transfer of oxygen, carbon dioxide, nutrients, metabolic products, detoxification function, etc.) and impaired blood circulation (acute vascular insufficiency - hemorrhagic shock). The outcome of bleeding is determined by a number of factors, but volume and rate of blood loss: rapid blood loss of about a third of the BCC is life-threatening, acute blood loss is absolutely fatal.
a loss of about half of the BCC. Under other unfavorable circumstances, the death of the patient may also occur with the loss of less than a third of the BCC.
The rate and volume of blood loss depend on the nature and type of the damaged vessel. The most rapid blood loss occurs when arteries are damaged, especially large ones. When arteries are injured, edge damage to the vessel is more dangerous than its complete transverse rupture, since in the latter case the damaged vessel contracts, the inner membrane is screwed inward, the possibility of thrombosis is greater and the probability of self-stopping of bleeding is higher. With marginal damage, the artery does not contract - it gapes, bleeding can continue for a long time. Naturally, in the latter case, the volume of blood loss may be higher. Arterial bleeding is more dangerous than venous, capillary or parenchymal bleeding. The volume of blood loss is also affected by disturbances in the coagulation and anticoagulation system of the blood.
Important in the outcome of blood loss general condition of the body. Healthy people tolerate blood loss more easily. Unfavorable conditions arise with traumatic shock, previous (initial) anemia, debilitating diseases, starvation, traumatic long-term operations, cardiac insufficiency, disorders in the blood coagulation system.
The outcome of blood loss depends on the rapid adaptation of the body to blood loss. Thus, other things being equal, blood loss is easier to tolerate and faster adapted to it by women and donors, since blood loss during menstruation or constant donation create favorable conditions for compensating various systems, primarily cardiovascular, for blood loss.
The reaction of the body to blood loss depends on the environmental conditions in which the victim is located. Hypothermia, like overheating, adversely affects the body's adaptability to blood loss.
Factors such as age and sex of the victims, also play a role in the outcome of blood loss. As already mentioned, women tolerate blood loss more easily than men. It is difficult for children and the elderly to tolerate blood loss. In children, this is due to the anatomical and physiological characteristics of the organism. So, for a newborn, the loss of even a few milliliters of blood is dangerous. In the elderly, due to age-related changes in the heart and blood vessels (atherosclerosis), the adaptation of the cardiovascular system to blood loss is much lower than in young people.
Localization of bleeding
Even with minor bleeding, there may be a danger to the life of the victim, which is determined by the role of the organ into which the hemorrhage occurred. So, a slight hemorrhage in the substance of the brain can be extremely dangerous due to damage to vital centers. Hemorrhages in the subdural, epidural, subarachnoid spaces of the skull, even small in volume, can lead to compression of the brain and disruption of its functions, although the volume of blood loss does not affect the state of blood circulation. Hemorrhages in the heart sac, which in themselves, given the small amount of blood loss, are not dangerous, can lead to the death of the victim due to compression and cardiac arrest due to his tamponade.
ACUTE BLOOD LOSS
The risk of blood loss is associated with the development of hemorrhagic shock, the severity of which is determined by the intensity, duration of bleeding and the amount of blood lost. A rapid loss of 30% of the BCC leads to acute anemia, cerebral hypoxia and may result in the death of the patient. With a slight but prolonged bleeding, the hemodynamics change little, and the patient can live even if the hemoglobin level drops to 20 g / l. A decrease in BCC will lead to a decrease in venous pressure and cardiac output. In response to this, catecholamines are released by the adrenal glands, which leads to vasospasm, as a result of which the vascular capacity decreases and thus hemodynamics is maintained at a safe level.
Acute blood loss due to a decrease in BCC can lead to hemorrhagic shock, the development of which is possible with blood loss equal to 20-30% of BCC. Shock is based on disorders of central and peripheral hemodynamics due to hypovolemia. With severe massive blood loss as a result of hemodynamic disorders, capillary paresis occurs, decentralization of blood flow, and shock can go into an irreversible stage. If arterial hypotension lasts more than 12 hours, complex therapy is ineffective, multiple organ failure occurs.
With an increase in blood loss, acidosis develops, sharp disturbances occur in the microcirculation system, and erythrocyte aggregation occurs in the capillaries. Oliguria (a decrease in the amount of urine) at first has a reflex character, in the stage of decompensation it
passes into anuria, which develops as a result of impaired renal blood flow.
Signs of blood loss: pallor and moisture of the skin, a haggard face, frequent and small pulse, increased respiration, in severe cases, Cheyne-Stokes breathing, lowering of CVP and blood pressure. Subjective symptoms: dizziness, dry mouth, thirst, nausea, darkening of the eyes, increasing weakness. However, with a slow flow of blood, the clinical manifestations may not correspond to the amount of blood lost.
It is important to determine the amount of blood loss, which, along with stopping bleeding, is of decisive importance for the choice of therapeutic tactics.
The content of erythrocytes, hemoglobin (Hb), hematocrit (Ht) must be determined immediately upon admission of the patient and the study should be repeated in the future. These indicators in the first hours with severe bleeding do not objectively reflect the amount of blood loss, since autohemodilution occurs later (it is most pronounced after 1.5-2 days). The most valuable indicators are Ht and relative blood density, which reflect the ratio between blood cells and plasma. With a relative density of 1.057-1.054, Hb 65-62 g/l, Ht 40-44, blood loss is up to 500 ml, with a relative density of 1.049-1.044, Hb 53-38 g/l, Ht 30-23 - more than 1000 ml.
A decrease in CVP in dynamics indicates an insufficient blood flow to the heart due to a decrease in BCC. CVP is measured in the superior or inferior vena cava using a catheter inserted into the cubital or great saphenous vein of the thigh. The most informative method for determining the amount of blood loss is to determine the deficiency of the BCC and its components: the volume of circulating plasma, the volume of formed elements - the globular volume. The research methodology is based on the introduction of a certain amount of indicators (Evans blue dye, radioisotopes, etc.) into the vascular bed. The volume of circulating plasma is determined by the concentration of the indicator diluted in the blood; taking into account the hematocrit, with the help of tables, BCC and globular volume are calculated. Proper indicators of BCC and its components are found according to the tables, which indicate the body weight and sex of patients. By the difference between due and actual indicators, the deficit of BCC, globular volume, volume of circulating plasma, that is, the amount of blood loss, is determined.
It should be borne in mind that it is necessary to judge the amount of blood loss primarily by clinical signs, as well as by the totality of laboratory data.
Depending on the volume of outflowing blood and the level of decrease in BCC, four degrees of severity of blood loss:
I - mild degree: loss of 500-700 ml of blood (decrease in BCC by 10-15%);
II - medium degree: loss of 1000-1500 ml of blood (decrease in BCC
by 15-20%);
III - severe degree: loss of 1500-2000 ml of blood (decrease in BCC
by 20-30%);
IV degree - massive blood loss: loss of more than 2000 ml of blood (decrease in BCC by more than 30%).
Clinical signs observed with blood loss, allow you to determine its degree. At the I degree of blood loss, there are no pronounced clinical signs. With the II degree of blood loss, the pulse is up to 100 per minute, the blood pressure drops to 90 mm Hg, the skin is pale, the extremities are cold to the touch. With severe blood loss (III degree), the patient's restless behavior, cyanosis, pallor of the skin and visible mucous membranes, increased respiration, and "cold" sweat are noted. The pulse reaches 120 per minute, blood pressure is lowered to 70 mm Hg. The amount of separated urine is reduced - oliguria. With massive blood loss (IV degree), the patient is inhibited, is in a state of stupor, there is a sharp pallor of the skin, acrocyanosis, anuria (cessation of urination). The pulse on the peripheral vessels is weak, threadlike or not detected at all, with a frequency of up to 130-140 per minute or more, blood pressure is lowered to 30 mm Hg. and below.
Timely started treatment can prevent the development of hemorrhagic shock, so it should be started as quickly as possible. In case of severe blood loss, they immediately begin to administer blood substitute fluids, the use of which is based on the fact that the loss of plasma and, consequently, a decrease in BCC are much more difficult for the body than the loss of red blood cells. Albumin, protein, dextran [cf. they say weight 50,000-70,000] are well kept in the bloodstream. If necessary, crystalloid solutions can be used, but it should be remembered that they quickly leave the vascular bed. Low molecular weight dextrans (dextran [cf. mol. weight 30,000-40,000]) replenish the volume of intravascular fluid, improve microcirculation and blood rheology. Transfusion of blood products is necessary when the hemoglobin level drops below 80 g / l and the hematocrit index is less than 30. In severe acute blood loss, treatment begins with a jet infusion into one, two or three veins and only after the SBP rises above 80 mm Hg. switch to drip.
To eliminate anemia, erythrocyte mass infusions are used, it is more expedient to administer it after the infusion of blood substitutes, as this improves capillary blood flow and reduces the deposition of blood cells.
Replenishment of blood loss
With a deficiency of BCC up to 15%, the volume of the infusion medium is 800-1000 ml (crystalloids 80% + colloids 20%) - 100% in relation to the deficit.
With blood loss of 15-25% of the BCC, the transfusion volume is 150% deficit - 1500-2300 ml, the ratio of crystalloids, colloids and plasma is 4:4:2.
With blood loss of 25-35% of the BCC, the replacement volume is 180-220% - 2700-4000 ml (crystalloids 30% + colloids 20%, plasma 30%, erythrocyte mass 20%).
With a BCC deficiency of more than 35%, the volume of transfusion is 220% - 4000-6000 ml (crystalloids 20% + colloids 30%, plasma 25%, erythrocyte mass - 25%).
Transfusions of blood products are indicated for blood loss exceeding 35-40% of the BCC, when both anemia and hypoproteinemia occur. Acidosis is corrected by the administration of sodium bicarbonate, trometamol (see. Blood transfusion). The use of drugs that increase vascular tone (vasoconstrictor agents) is contraindicated until the blood volume is fully restored, as they aggravate hypoxia. On the contrary, glucocorticoids improve myocardial function and reduce spasm of peripheral vessels. Oxygen therapy, hyperbaric oxygen therapy, used after bleeding has stopped, are shown.
EXTERNAL AND INTERNAL BLEEDING
external bleeding
The main sign of a wound is external bleeding. The color of the blood in this case is different: scarlet - with arterial bleeding, dark cherry - with venous bleeding. Bleeding not only from the aorta, but also from the femoral or axillary artery can lead to death within a few minutes after injury. Damage to large veins can also quickly cause death. If large veins of the neck and chest are damaged, such a dangerous complication as air embolism is possible. This complication develops as a result
air entering through a wound in a vein (into the right parts of the heart, and then into the pulmonary artery) and blockage of its large or small branches.
internal bleeding
With traumatic injury or the development of a pathological process in the area of the vessel, internal bleeding occurs. Recognizing such bleeding is more difficult than external bleeding. The clinical picture consists of general symptoms due to blood loss, and local signs, depending on the location of the source of bleeding. In acutely developed anemia (for example, a disturbed ectopic pregnancy or rupture of the spleen capsule in the presence of a subcapsular hematoma), pale skin and visible mucous membranes, darkening of the eyes, dizziness, thirst, drowsiness may occur. The pulse is frequent - 120-140 per minute, blood pressure is lowered. With slow bleeding, signs of blood loss develop gradually.
Bleeding into the lumen of hollow organs
If bleeding occurs into the lumen of hollow organs and blood flows out through natural openings, it is difficult to determine the source of such bleeding. Thus, the release of blood through the mouth may be due to bleeding from the lungs, trachea, pharynx, esophagus, stomach, duodenum. Therefore, the color and condition of the outflowing blood matter: foamy scarlet blood is a sign of pulmonary bleeding, vomiting of "coffee grounds" - gastric or duodenal. Black tarry stools (melena) are a sign of bleeding from the upper gastrointestinal tract, discharge of scarlet blood from the rectum - bleeding from the sigmoid or rectum. Hematuria is a sign of bleeding from the kidney or urinary tract.
Taking into account the expected localization of bleeding, special research methods are chosen to identify its source: gastric probing and digital examination of the rectum, endoscopic methods, for example, bronchoscopy - for lung diseases, esophagogastroduodeno-, sigmoidomano- and colonoscopy - for gastrointestinal bleeding, cystoscopy - for damage to the urinary system, etc. Ultrasound, x-ray and radioisotope research methods are of great importance, especially for determining hidden bleeding that occurs with minor
or unusual manifestations. The essence of the radioisotope method is that the radionuclide (usually a colloidal solution of gold) is administered intravenously, while together with the outflowing blood it accumulates in the tissues, cavity or lumen of the internal organs. An increase in radioactivity at the site of damage is detected by radiometry.
Bleeding into closed cavities
More difficult is the diagnosis of bleeding in closed body cavities: the cranial cavity, spinal canal, chest and abdominal cavities, pericardium, joint cavity. These bleedings are characterized by certain signs of fluid accumulation in the cavity and general symptoms of blood loss.
Hemoperitoneum
Accumulation of blood in the abdominal cavity - hemoperitoneum (haemoperitoneum)- associated with wound and closed trauma of the abdomen, damage to parenchymal organs (liver, spleen), mesenteric vessels, violation of ectopic pregnancy, rupture of the ovary, eruption or slipping of the ligature applied to the vessels of the mesentery or omentum, etc.
Against the background of blood loss, local signs are determined. The abdomen is limitedly involved in breathing, painful, soft, sometimes a slight muscular defense is determined, symptoms of peritoneal irritation are mild. In sloping areas of the abdomen, dullness of percussion sound is detected (with an accumulation of about 1000 ml of blood), percussion is painful, in women a protrusion of the posterior vaginal fornix can be observed, which is determined during vaginal examination. Patients with suspected hemoperitoneum need strict observation, determining the dynamics of hemoglobin and hematocrit levels; a rapid drop in these indicators confirms the presence of bleeding. It should be remembered that with simultaneous rupture of a hollow organ, local signs of bleeding will be masked by symptoms of developing peritonitis.
To clarify the diagnosis, puncture of the abdominal cavity using a "groping" catheter, laparoscopy, and puncture of the posterior vaginal fornix are of great importance. When the diagnosis is established, an emergency operation is indicated - laparotomy with a revision of the abdominal organs and stopping bleeding.
Hemothorax
Accumulation of blood in the pleural cavity - hemothorax (haemothorax)- due to bleeding due to trauma to the chest and lungs, including the operating room, a complication of a number of diseases of the lungs and pleura (tuberculosis, tumors, etc.). Significant bleeding is observed when the intercostal and internal thoracic arteries are damaged. There are small, medium and large (total) hemothorax. With a small hemothorax, blood usually fills only the sinuses of the pleural cavity, with an average it reaches the angle of the scapula, with a total hemothorax it occupies the entire pleural cavity. The blood in the pleural cavity, with the exception of cases of severe and massive bleeding, does not coagulate, since there are anticoagulant substances in the blood flowing from the lung.
The clinical picture of hemothorax depends on the intensity of bleeding, compression and displacement of the lungs and mediastinum. In severe cases, the patient's anxiety, chest pain, shortness of breath, pallor and cyanosis of the skin, cough, sometimes with blood, increased heart rate and lowering blood pressure are noted. During percussion, a dull sound is determined, voice trembling and breathing are weakened. The degree of anemia depends on the amount of blood loss. Due to aseptic inflammation of the pleura (hemopleurisy), serous fluid also enters the pleural cavity. When a hemothorax is infected from a damaged bronchus or lung, a severe complication develops - purulent pleurisy. The diagnosis of hemothorax is confirmed by X-ray data and pleural puncture. Treatment of small and medium hemothorax is carried out by pleural punctures, with the development of a large hemothorax, an emergency thoracotomy with ligation of the vessel or suturing of the lung wound is indicated.
Hemopericardium
Most common cause of hemopericardium (haemopericardium)- accumulation of blood in the pericardial sac - bleeding in case of injury and closed injuries of the heart and pericardium, less often - with rupture of an aneurysm of the heart, myocardial abscesses, sepsis, etc. The accumulation of 400-500 ml of blood in the pericardium threatens the life of the patient. The patient's anxiety, pain in the region of the heart, frightened facial expression, shortness of breath, tachycardia, frequent weak filling of the pulse are noted. BP is lowered. Displacement or disappearance of a cardiac impulse, expansion of the boundaries of cardiac dullness, deafness of heart sounds are revealed. With an increase in the amount of blood in the pericardium, a dangerous complication occurs - cardiac tamponade.
If hemopericardium is suspected, a diagnostic puncture is performed. With the slow development of hemopericardium, a small accumulation of blood, conservative treatment is possible (rest, cold, pericardial puncture); in severe cases, an emergency operation is performed and the causes of bleeding are eliminated.
Accumulation of blood in the cranial cavity
Accumulation of blood in the cranial cavity (haemocranion), observed more often due to trauma, leads to the appearance of cerebral and focal neurological symptoms.
Hemarthrosis
Hemarthrosis (haemarthrosis)- accumulation of blood in the joint cavity due to bleeding that occurred during closed or open joint injuries (fractures, dislocations, etc.), hemophilia, scurvy and a number of other diseases. With significant bleeding, the functions of the joint are limited, its contours are smoothed, fluctuation is determined, and if the knee joint is damaged, the patella ballots. To clarify the diagnosis and exclude bone damage, an X-ray examination is performed.
Joint puncture is both diagnostic and therapeutic manipulation.
interstitial bleeding
Interstitial bleeding causes hematomas, sometimes of considerable size. For example, with a fracture of the femur, the amount of blood released can exceed 500 ml. The most dangerous are hematomas that form during rupture and crushing of large main vessels. In cases where the hematoma communicates with the lumen of the artery, the so-called pulsating hematoma develops, and later, with the formation of a capsule, a false aneurysm is formed. Along with the general symptoms of acute anemia, two main features are characteristic of a pulsating hematoma: a pulsation over the swelling, synchronous with heart contractions, and a blowing systolic murmur when auscultated. The limb in case of damage to the main artery is in a state of ischemia, pale, cold to the touch, there are violations of sensitivity, the pulse in the distal parts of the artery is not determined. In such cases, an emergency operation is indicated to restore the blood supply to the limb.
Interstitial bleeding can lead to impregnation (imbibition) of tissues with blood. This type of internal bleeding is called hemorrhage. Hemorrhage can occur in the muscles, fatty tissue, brain, heart, kidney, etc.
Hemorrhages are not significant in volume, but can lead to serious consequences (for example, hemorrhage into the substance of the brain).
INFLUENCE OF BLOOD LOSS ON THE ORGANISM. PROTECTIVE COMPENSATOR REACTIONS
Developed posthemorrhagic hypovolemia leads to circulatory disorders in the body. As a result, protective and compensatory processes are activated, aimed at restoring the correspondence between the BCC and the capacity of the vascular bed, thereby the body ensures the maintenance of blood circulation by adaptive reactions. These reactions include three main mechanisms.
1. Reducing the volume of the vascular bed by increasing the tone of the veins (venospasm) and peripheral arterioles (arteriolospasm).
2. Compensation for the lost part of the BCC due to autohemodilution due to the movement of the intercellular fluid into the bloodstream and the release of blood from the depot.
3. Compensatory reaction of life support organs (heart, lungs, brain).
Veno- and arteriolospasm is based on the reflex reaction of baro- and chemoreceptors of vessels, stimulation of the sympathetic-adrenal system. An increase in the tone of the veins compensates for the loss of BCC up to 10-15%. Vessels of the skin, kidneys, liver, abdominal cavity undergo vasoconstriction, while the vessels of the brain, heart, lungs remain unchanged, which ensures the maintenance of blood circulation in these vital organs (centralization of blood circulation).
The movement of tissue fluid into the vascular bed occurs quickly. So, within a few hours, a liquid transition in a volume of up to 10-15% of the BCC is possible, and up to 5-7 liters of liquid can move in 1.5-2 days. The influx of tissue fluid does not allow to fully restore the lost blood, since it does not contain formed elements and is characterized by a low protein content. Hemodilution occurs (dilution, blood thinning).
developed tachycardia, due to the influence of the sympathetic-adrenal system, allows you to maintain the minute volume of the heart
ca at a normal level. Hyperventilation provides adequate gas exchange, which is very important in conditions of hypoxia caused by a low level of hemoglobin in the blood and circulatory disorders.
Activation due to hypovolemia of the secretion of the pituitary antidiuretic hormone and aldosterone causes an increase in reabsorption in the kidneys and a delay in the body of sodium and chlorine ions. developed oliguria reduces the excretion of fluid from the body, thereby maintaining the level of volemia.
Such a compensatory reaction cannot last for a long time, the developed state of vascular resistance leads to a breakdown in compensation. Hypoxia of the liver, kidneys, subcutaneous tissue causes serious metabolic disorders.
The progression of disorders in the body is due to slugging (gluing) of erythrocytes in the capillaries due to their spasm and slowing of blood flow, as well as increasing tissue hypoxia. In metabolism, anaerobic processes prevail over aerobic ones, and tissue acidosis increases. Such disorders of tissue metabolism and microcirculation lead to multiple organ failure: glomerular filtration decreases or stops in the kidneys and oliguria or anuria develops, necrotic processes occur in the liver, the contractility of the heart decreases due to myocardial damage, interstitial edema develops in the lungs with impaired gas exchange through the lungs. capillary membrane ("shock lung").
Thus, even with stopped bleeding, blood loss leads to serious changes in all vital systems of the body, which makes it necessary to use a wide variety of means and methods of treatment, the main among which is the replacement of blood loss, and the earlier it is performed, the better for the patient.
STOP BLEEDING
Bleeding from small arteries and veins, as well as from capillaries, in most cases stops spontaneously. Rarely there is an independent stop of bleeding from large vessels.
One of the important defense systems of the body is the blood coagulation system. Spontaneous hemostasis in some cases, it allows the body to cope with bleeding on its own.
Hemostasis- a complex biochemical and biophysical process in which a blood vessel and surrounding tissues, thrombosis,
bocytes and plasma factors of the blood coagulation and anticoagulation system.
The contraction of the smooth muscle cells of the vessel leads to vasoconstriction, in the area of damage to the vessels, the disturbed endothelium creates a surface, a place for the formation of a thrombus. Changes in hemodynamics, slowing of blood flow make the process of thrombosis possible, and the thromboplastin of the damaged vessel and surrounding tissues (tissue thromboplastin) takes part in the process of blood clotting. Changes in the electrical potential of the damaged vessel, exposure of collagen, accumulation of active biochemical substances (glycoproteins, von Willebrand factor, calcium ions, thrombospandin, etc.) ensure adhesion (sticking) of platelets to the exposed collagen of the vessel wall. Adhering platelets create conditions for platelet aggregation - a complex biochemical process involving epinephrine, ADP, thrombin with the formation of arachidonic acid, prostaglandins, thromboxane and other substances. Aggregated platelets, together with thrombin and fibrin, form a platelet clot - a surface for subsequent thrombosis with the participation of the blood coagulation system.
In the 1st phase, clotting occurs with the participation of plasma factors (VIII, IX, XI, XII Hageman factor) and blood platelets - blood thromboplastin is formed. The latter, together with tissue thromboplastin, in the presence of Ca 2 + ions, converts prothrombin into thrombin (2nd phase of coagulation), and thrombin, in the presence of factor XIII, converts fibrinogen into fibrin polymer (3rd phase). The process of clot formation ends with the retraction of the latter with the formation of a thrombus. This ensures hemostasis, and bleeding from small vessels reliably stops. The whole process of thrombus formation occurs very quickly - within 3-5 minutes, and processes such as platelet adhesion, the transition of prothrombin to thrombin, and the formation of fibrin take a few seconds.
Continued bleeding, if the body has not coped with it on its own, is an indication for a temporary stop of bleeding.
Methods for temporarily stopping bleeding
Tourniquet application
The most reliable method is the application of a tourniquet, but it is used mainly in the limbs.
Rice. 28.Applying a tourniquet: a - preparation for applying a tourniquet; b - the beginning of the overlay; c - fixation of the first round; d - final view after applying the tourniquet.
The hemostatic tourniquet is a rubber band 1.5 m long, ending with a metal chain on one side and a hook on the other. With established arterial bleeding, a tourniquet is applied proximal to the injury site.
The intended area of application of the tourniquet is wrapped with a soft material (towel, sheet, etc.), i.e. create a soft pad. The tourniquet is stretched, applied closer to the chain or hook, and 2-3 rounds are made with a tourniquet, subsequent turns are applied, stretching the tourniquet. Then the hook is attached to the chain (Fig. 28). Be sure to indicate the time of application of the tourniquet, since compression of the artery by it for longer than 2 hours on the lower limb and 1.5 hours on the upper one is fraught with the development of necrosis of the limb. The control of the correct application of the tourniquet is the cessation of bleeding, the disappearance of the pulsation of the peripherally located arteries and light
Rice. 29.The imposition of an army tourniquet.
"waxy" pallor of the skin of the limb. If the transportation of the wounded takes more than 1.5-2 hours, the tourniquet should be periodically removed for a short time (10-15 minutes) until the arterial blood flow is restored. In this case, the damaged vessel is pressed down with a tupfer in the wound or the artery is pressed with fingers. Then the tourniquet is applied again, slightly above or below the place where it was located.
Subsequently, if necessary, the procedure for removing the tourniquet is repeated: in winter - after 30 minutes, in summer - after 50-60 minutes.
To stop bleeding, a special military tourniquet or an impromptu twist can be used (Fig. 29).
The application of a tourniquet on the neck (with bleeding from the carotid artery) with a bar or through the armpit on the healthy side is rarely resorted to. You can use the Cramer splint applied to the healthy half of the neck, which serves as a frame (Fig. 30). A tourniquet is pulled over it, which presses down on the gauze roller and squeezes the vessels on one side. In the absence of a tire, you can use the opposite hand as a frame - it is placed on the head and bandaged. The imposition of a tourniquet to compress the abdominal aorta is dangerous because injury to the internal organs can occur.
Rice. thirty.The imposition of a tourniquet on the neck.
Tourniquet application for bleeding from the femoral and axillary arteries is shown in Fig. 31.
After applying the tourniquet, the limb is immobilized with a transport splint; in the cold season, the limb is wrapped to prevent frostbite. Then, after the introduction of analgesics, the victim with a tourniquet is quickly transported to the clinic in the supine position.
Rough and prolonged compression of tissues with a tourniquet can lead to paresis and paralysis of the limb due to both traumatic damage to the nerve trunks and ischemic neuritis that develops as a result of oxygen starvation. The lack of oxygen in the tissues located distally to the applied tourniquet creates favorable conditions for the development of anaerobic gas infection, i.e. for bacterial growth,
multiplying without oxygen. Given the risk of developing severe complications, it is better to temporarily stop bleeding by applying a pneumatic cuff to the proximal part of the limb. In this case, the pressure in the cuff should be slightly higher than the blood pressure.
Finger artery pressure
Finger pressing of the artery for a long time, if performed correctly, leads to the cessation of bleeding, but it is short-lived, since it is difficult to continue pressing the vessel for more than 15-20 minutes. The artery is pressed in those areas where the arteries are located superficially and near the bone: carotid artery - transverse process C IV, subclavian - rib I, humerus - the area of the inner surface of the humerus, femoral artery - pubic bone (Fig. 32, 33) . The pressing of the brachial and femoral arteries is good, worse - the carotid.
Rice. 32.Places of pressure of arteries for a temporary stop of bleeding.
Rice. 33.Finger pressure on the carotid (a), facial (b), temporal (c), subclavian (d), brachial (e), axillary (f), femoral (g) arteries to temporarily stop bleeding.
It is even more difficult to press the subclavian artery due to its location (behind the collarbone). Therefore, in case of bleeding from the subclavian and axillary arteries, it is better to fix the arm by moving it as far back as possible. This causes compression of the subclavian artery between the clavicle and the first rib. Finger pressing of the artery is especially important in preparation for the application of a tourniquet or its change, and also as a technique for amputation of a limb.
Flexion of the limb at the joint
Flexion of the limb in the joint is effective provided that the arm bent to failure is fixed in the elbow joint in case of bleeding from the vascular
Rice. 34.Temporary stop of bleeding from the arteries by maximum flexion: a - from the femoral artery; b - from the popliteal; in - from the shoulder and elbow.
dov of the forearm or hand, and the legs - in the knee joint with bleeding from the vessels of the lower leg or foot. In case of high injuries of the femoral artery that are inaccessible to the application of a tourniquet, the thigh should be fixed to the stomach with maximum flexion of the limb in the knee and hip joints (Fig. 34).
Wound tamponade and pressure dressing
Wound tamponade and application of a pressure bandage with immobilization under the condition of an elevated position of the limb are a good method for temporarily stopping bleeding from veins and small arteries, from soft tissues covering the bones of the skull, elbow and knee joints. For tight tamponade, a gauze pad is inserted into the wound, filling it tightly, and then fixed with a pressure bandage. Tight tamponade is contraindicated for injuries in the area of the popliteal fossa, since in these cases gangrene of the limb often develops. Pressure with a weight (sandbag) or in combination with cooling (ice pack) is used for interstitial bleeding, and is also often used as a method of preventing postoperative hematomas.
Pressing the vessel in the wound with fingers
Pressing the vessel in the wound with fingers is carried out in emergency situations, sometimes during surgery. For this purpose, the doctor quickly puts on a sterile glove or treats the hand with alcohol, iodine and presses or compresses the vessel in the wound, stopping the bleeding.
Applying a hemostat
In case of bleeding from damaged deeply located vessels of the proximal parts of the limb, abdominal cavity, chest, when the methods of temporary stopping of bleeding listed above cannot be applied, a hemostatic clamp is applied to the bleeding vessel in the wound. To avoid injury to nearby formations (nerves), you must first try to stop the bleeding by pressing the vessel with your fingers, and then apply a clamp directly to the bleeding vessel, after draining the wound from the blood.
Temporary vascular bypass
Temporary shunting of a vessel is a way to restore blood circulation in case of damage to large arterial vessels. A densely elastic tube is inserted into both ends of the damaged artery, and the ends of the vessel are fixed on the tube with ligatures. This temporary shunt restores arterial circulation. The shunt can function from several hours to several days, until the possibility of a final stop of bleeding appears.
Methods for the final stop of bleeding
Methods for the final stop of bleeding are divided into four groups: 1) mechanical, 2) physical, 3) chemical and biological, 4) combined.
Mechanical Methods Ligation of a vessel in a wound
Bandaging a vessel in a wound is the most reliable way to stop bleeding. For its implementation, the central and peripheral ends of the bleeding vessel are isolated, captured with hemostatic clamps and tied up (Fig. 35).
Vessel ligation throughout
Ligation of the vessel throughout is used if it is impossible to detect the ends of the bleeding vessel in the wound (for example, when the external and internal carotid arteries are injured), as well as in secondary blood vessels.
Rice. 35.Methods for the final stop of bleeding from the vessel: a - ligation; b - electrocoagulation; c - ligation and crossing of the vessel at a distance; d - ligation of the vessel throughout; e - chipping of the vessel.
inflows, when the arrosated vessel is located in the thickness of the inflammatory infiltrate. In such cases, focusing on topographic anatomical data, they find, expose and tie up the vessel outside the wound. However, this method does not guarantee the cessation of bleeding from the peripheral end of the damaged artery and collaterals.
If it is impossible to isolate the ends of the vessel, the vessel is ligated along with the surrounding soft tissues. If the vessel is captured by the clamp, but it is not possible to bandage it, it is necessary to leave the clamp in the wound for a long time - up to 8-12 days, until reliable thrombosis of the vessel occurs.
Torsion of the vessel
Damaged vessels of small caliber can be grasped with a hemostatic forceps and rotational movements can be used to twist the vessel.
Tamponade of the wound
Sometimes, in the presence of small wounds and damage to small-caliber vessels, tamponade of the wound can be performed. Tampons are used dry or moistened with an antiseptic solution. Typical examples of stopping bleeding are anterior and posterior nasal tamponade in epistaxis, uterine tamponade in uterine bleeding.
clipping
For bleeding from vessels that are difficult or impossible to bandage, clipping is used - clamping the vessels with silver metal clips. After the final stop of the internal
For ripple bleeding, a part of the organ is removed (for example, gastric resection with a bleeding ulcer) or the entire organ (splenectomy in case of rupture of the spleen). Sometimes special sutures are applied, for example, to the edge of a damaged liver.
Artificial vascular embolization
At present, methods of artificial vascular embolization have been developed and introduced to stop pulmonary, gastrointestinal bleeding and bleeding from bronchial arteries, cerebral vessels. Under X-ray control, a catheter is inserted into the bleeding vessel, and emboli are placed along it, closing the lumen of the vessel, thereby stopping the bleeding. Balls made of synthetic polymeric materials (silicone, polystyrene), gelatin are used as emboli. Thrombus formation occurs at the site of embolization.
Vascular suture
The main indication for the imposition of a vascular suture is the need to restore the patency of the main arteries. The vascular suture must be highly airtight and meet the following requirements: it must not interfere with the blood flow (no narrowing or turbulence), there must be as little suture material as possible in the lumen of the vessel. There are manual and mechanical seams (Fig. 36).
Rice. 36.Vascular sutures. a - single nodal (according to Carrel): b - single U-shaped; in - continuous twisting; g - continuous U-shaped; d - mechanical.
Manual vascular suture is applied using atraumatic needles. An end-to-end connection is ideal. A circular vascular suture can be applied using tantalum staples, Donetsk rings. The mechanical seam is quite perfect and does not narrow the lumen of the vessel.
A lateral vascular suture is applied with a tangential injury to the vessel. After application, the suture is strengthened with the help of fascia or muscle.
Patches made from biological material
If there is a large defect in the wall resulting from injury or surgery (for example, after removal of the tumor), patches from biological material (fascia, vein walls, muscles) are used. More often, an autovein is chosen (a large saphenous vein of the thigh or a superficial vein of the forearm).
transplants
As grafts in vascular surgery, auto- and allografts of arteries or veins are used, prostheses made of synthetic materials are widely used. Reconstruction is performed by end-to-end anastomoses or by graft suturing.
Physical Methods
Thermal methods of stopping bleeding are based on the ability of high temperatures to coagulate proteins and on the ability of low temperatures to cause vasospasm. These methods are of great importance for combating bleeding during surgery. In case of diffuse bleeding from a bone wound, wipes soaked in hot isotonic sodium chloride solution are applied to it. Applying an ice pack for subcutaneous hematomas, swallowing pieces of ice for gastric bleeding are widely used in surgery.
Diathermocoagulation
Diathermocoagulation, based on the use of high frequency alternating current, is the main thermal method for stopping bleeding. It is widely used for bleeding from damaged vessels of subcutaneous fat and muscle, from small vessels of the brain. The main condition for the use of diathermocoagulation is the dryness of the wound, and when it is carried out, tissues should not be brought to charring, since this in itself can cause bleeding.
Laser
A laser (electron radiation focused in the form of a beam) is used to stop bleeding in patients with gastric bleeding (ulcer), in people with increased bleeding (hemophilia), and during oncological operations.
Cryosurgery
Cryosurgery - surgical methods of treatment with local application of cold during operations on richly vascularized organs (brain, liver, kidneys), especially when removing tumors. Local tissue freezing can be performed without any damage to healthy cells surrounding the area of cryonecrosis.
Chemical and biological methods
Hemostatic agents are divided into resorptive and local agents. Resorptive action develops when a substance enters the blood, local action develops when it comes into direct contact with bleeding tissues.
Substances of general resorptive action
Hemostatic substances of general resorptive action are widely used for internal bleeding. The most effective direct transfusion of blood products, plasma, platelet mass, fibrinogen, prothrombin complex, antihemophilic globulin, cryoprecipitate, etc. These drugs are effective for bleeding associated with congenital or secondary deficiency of certain blood coagulation factors in a number of diseases (pernicious anemia, leukemia, hemophilia and etc.).
Fibrinogen is obtained from donor plasma. It is used for hypo-, afibrinogenemia, profuse bleeding of a different nature, with a substitution purpose.
Currently widely used fibrinolysis inhibitors, having the ability to lower the fibrinolytic activity of the blood. Bleeding associated with an increase in the latter is observed during operations on the lungs, heart, prostate gland, with cirrhosis of the liver, septic conditions, transfusion of large doses of blood. Both biological antifibrinolytic drugs (for example, aprotinin) and synthetic ones (aminocaproic acid, aminomethylbenzoic acid) are used.
Etamzilat- drugs that accelerate the formation of thromboplastin, they normalize the permeability of the vascular wall, improve microcirculation. Rutoside, ascorbic acid are used as agents that normalize the permeability of the vascular wall.
menadione sodium bisulfite - a synthetic water-soluble analogue of vitamin K. As a therapeutic agent, it is used for bleeding associated with a decrease in the content of prothrombin in the blood. It is indicated for acute hepatitis and obstructive jaundice, parenchymal and capillary bleeding after injuries and surgical interventions, gastrointestinal bleeding, peptic ulcer, hemorrhoidal and prolonged nosebleeds.
The process of converting prothrombin to thrombin requires a very small amount of calcium ions, which are usually already present in the blood. Therefore, the use of calcium preparations as a hemostatic agent is advisable only in the case of transfusion of massive doses of citrated blood, because when calcium interacts with citrate, the latter loses its anticoagulant properties.
Substances of local action
Local hemostatic agents are widely used. With parenchymal bleeding from a liver wound, a kind of biological tampon is used - muscle tissue or omentum in the form of a free flap or flap on a leg. Of particular importance in surgery is the use of a fibrin film, a biological antiseptic swab, and a hemostatic collagen sponge. Hemostatic and gelatin sponges, a biological antiseptic tampon are used to stop capillary and parenchymal bleeding from bones, muscles, parenchymal organs, for tamponade of the sinuses of the dura mater.
Thrombin - a drug obtained from the blood plasma of donors, promotes the transition of fibrinogen to fibrin. The drug is effective in capillary and parenchymal bleeding of various origins. Before use, it is dissolved in isotonic sodium chloride solution. Sterile gauze wipes or a hemostatic sponge are impregnated with a solution of the drug, which are applied to the bleeding surface. The use of thrombin is contraindicated for bleeding from large vessels, since the development of widespread thrombosis with a fatal outcome is possible.
Combined Methods
To enhance the effect of hemostasis, various methods of stopping bleeding are sometimes combined. The most common are wrapping with muscle tissue or lubricating the vascular suture with glue, the simultaneous use of various types of sutures, biological swabs, etc., for parenchymal bleeding.
For the treatment of patients with DIC, it is important to eliminate the cause that caused it, restore the bcc, take measures to eliminate renal failure, as well as normalize hemostasis - the introduction of sodium heparin and (stream) native or fresh frozen plasma, platelet mass; if necessary apply IVL.
To stop bleeding caused by the action of drugs, native or fresh frozen plasma is used, with an overdose of indirect anticoagulants - menadione sodium bisulfite (vitamin K), with an overdose of sodium heparin - protamine sulfate, for inactivation of fibrinolytic drugs - aminocaproic acid, aprotinin.
To stop bleeding in patients with hemophilia, cryoprecipitate, antihemophilic plasma, native plasma, native donor plasma, freshly citrated blood, direct blood transfusions are used.
SECONDARY BLEEDING
Secondary bleeding may be early(in the first 3 days) and late- after a long period of time after injury (from 3 to several days, weeks). The division into early and late is determined by the causes of secondary bleeding (as a rule, they differ in the time of manifestation). The cause of early secondary bleeding is a violation of the rules for the final stop of bleeding: insufficient control of hemostasis during surgery or surgical treatment of the wound, loosely tied ligatures on the vessels. An increase in blood pressure after surgery (if the patient or wounded person is operated on under reduced pressure), shock, hemorrhagic anemia, controlled arterial hypotension, when blood clots can be pushed out of large or small vessels, slipping of ligatures can lead to bleeding.
The cause of both early and late secondary bleeding can be disorders in the coagulation or anticoagulation system of the blood (hemophilia, sepsis, cholemia, etc.), careless change of
viscous, tampons, drainages, in which the separation of a blood clot and the appearance of bleeding are possible.
The main causes of secondary bleeding are purulent-inflammatory complications in the wound, the development of necrosis, which can lead to melting of blood clots. The cause of late bleeding can also be bedsores of blood vessels with pressure on them from bone or metal fragments, drainage. The resulting necrosis of the vessel wall can lead to its rupture and bleeding.
Secondary bleeding, as well as primary, can be arterial, venous, capillary, parenchymal, as well as external and internal.
The severity of the patient's condition is determined by the volume of blood loss, depends on the caliber and nature of the damage to the vessel. Secondary bleeding is more severe in terms of its effect on the body than primary ones, since it occurs against the background of a condition after a previous blood loss (due to primary bleeding or surgery). Therefore, in secondary bleeding, the severity of the patient's condition does not correspond to the volume of blood loss.
The clinical picture of secondary bleeding consists of general and local symptoms, as with primary bleeding. With external bleeding, first of all, wetting of the bandage is observed: bright red blood - with arterial bleeding, dark - with venous bleeding. Bleeding into a wound closed with sutures leads to the formation of a hematoma, which is accompanied by the appearance of pain, a feeling of fullness in the wound, and swelling.
For internal secondary bleeding, first of all, general signs of blood loss are characteristic: increasing weakness, pallor of the skin, an increase in the frequency and decrease in the filling of the pulse, and a decrease in blood pressure. According to laboratory studies, there is a decrease in the concentration of hemoglobin and hematocrit. Local symptoms are determined by the localization of the hemorrhage: hemoperitoneum, hemothorax, hemopericardium. With bleeding into the gastrointestinal tract, hematemesis or vomiting of “coffee grounds”, blood-stained stools, and melena are possible.
Stop secondary bleeding
The principles of stopping secondary bleeding are the same as for primary bleeding. If secondary bleeding is detected, urgent measures are taken to temporarily stop it using the same
methods and means, as in the case of primary bleeding - the application of a tourniquet, finger pressure of the vessel, pressure bandage, tamponing. With massive bleeding from the wound, it is temporarily stopped by one of the methods, and then the sutures are removed and a thorough revision of the wound is carried out. A clamp is applied to the bleeding vessel, then ligated. In case of capillary bleeding in the wound, it is tightly packed with a gauze swab or a hemostatic sponge.
Ligation of a bleeding vessel in a purulent wound is unreliable due to the likelihood of recurrence of bleeding due to the progression of the purulent-necrotic process. In such situations, apply ligation of the vessel throughout within healthy tissues. To do this, the vessel is exposed from the additional reserve more proximal, outside the place of its damage, and a ligature is applied. With the final stop of secondary bleeding, the general condition of the patient should be taken into account and it should be done after the patient is removed from hemorrhagic shock. For this purpose, transfusion of blood, anti-shock blood substitutes is carried out.
With established secondary bleeding into the abdominal, pleural cavities, gastrointestinal tract, when a temporary stop is impossible due to the anatomical features of the location of the bleeding vessel, despite the severity of the patient's condition, the presence of shock, an emergency operation is indicated - relaparotomy, rethoracotomy. Surgical intervention to stop bleeding and anti-shock measures are carried out simultaneously.
During the operation, the source of bleeding is determined and its final stop is carried out - ligation, stitching, ligation of the vessel along with surrounding tissues, suturing the bleeding parenchyma of the organ - the liver, ovary, etc. The blood that has poured into the serous cavities, if it is not contaminated with the contents of the gastrointestinal a path and since bleeding there has passed no more than 24 h, collect, filter and pour in to the patient (blood reinfusion). After the final stop of bleeding, replenishment of blood loss and antishock therapy are continued.
Mechanical methods are combined with chemical and biological means to stop bleeding. If the cause of bleeding was a violation of the activity of the blood coagulation or anticoagulation system, special factors are used to increase the blood coagulation system or reduce the activity of the anticoagulant system: plasma cryoprecipitate, antihemophilic factor, fibrinogen, platelet mass, aminocaproic acid, etc.
Preventionsecondary bleeding are the following highlights.
1. Careful final stop of primary bleeding in case of vascular damage and during any surgical intervention. Before suturing the wound, the area of surgical intervention must be carefully examined (checking hemostasis). If there is no confidence in the complete stop of bleeding, additional methods are carried out - ligation, electrocoagulation of the vessel, the use of a hemostatic sponge. Only with complete hemostasis, the operation is completed by suturing the wound.
2. Careful primary surgical treatment of wounds, removal of foreign bodies - free-lying bone fragments, metal foreign bodies (shell fragments, bullets, shots, etc.).
3. Prevention of purulent complications from the wound: scrupulous observance of the rules of asepsis and antisepsis during surgery, antibiotic therapy.
4. Drainage of wounds, cavities, taking into account the topography of the vessels, in order to prevent the formation of bedsores in their walls, erosion.
5. Study before each planned operation of the state of the patient's blood coagulation and anticoagulation system: clotting time, bleeding time, prothrombin level, platelet count. If these indicators change, as well as patients with an unfavorable history of increased bleeding or suffering from blood diseases, jaundice, a detailed coagulogram is necessary. In case of disturbances in the state of the blood coagulation system, purposeful preoperative preparation is carried out to normalize or improve its condition. Monitoring the state of hemocoagulation in these patients, who are threatened in terms of secondary bleeding, is carried out systematically in the postoperative period.
Bleeding is the process of bleeding from damaged blood vessels, which is a direct complication of combat wounds and the main cause of death of the wounded on the battlefield and during the evacuation stages. In the Great Patriotic War, among the wounded who died on the battlefield, those who died from bleeding accounted for 50%, and in the military area they accounted for 30% of all deaths. In Afghanistan, 46% of the wounded died from bleeding and shock in the medical institutions of the military district (omedb, garrison hospital).
Bleeding is classified according to the time of occurrence, the nature and size of the damaged blood vessels, and the site of bleeding.
Distinguish primary and secondary bleeding. Primary bleeding occurs immediately after the injury or in the next few hours after it (weakening of the pressure bandage, the release of a blood clot from the wound of the vessel when the patient is shifted, displacement of bone fragments, increased blood pressure). Secondary bleeding is divided into early and late. Early secondary bleeding occurs before thrombus organization. They appear on the 3-5th day after the injury and are associated with the release of a loose thrombus obturating it from the wound (unsatisfactory immobilization, shocks during transportation, manipulations in the wound during dressings).
Late secondary bleeding occurs after the organization (germination by granulation tissue) of the thrombus. They are associated with the infectious process in the wound, melting of the thrombus, hematoma suppuration, sequestration of the bruised vessel wall. Secondary bleeding most often occurs during the 2nd week after injury. They are preceded by the appearance of pain in the wound and an increase in body temperature without disturbing the outflow from the wound, a short-term sudden wetting of the dressing with blood (the so-called signal bleeding), and the detection of vascular noises during auscultation of the wound circumference. Secondary bleeding can stop on its own; but threatened with relapse.
Classification of bleeding
By causal factor: trauma, injury, pathological process. According to the timing of occurrence: primary, secondary, single, repeated, early, later.
By type of damaged vessel: arterial, venous, arteriovenous capillary (parenchymal).
According to the place of outpouring of blood: external, internal, interstitial, combined. According to the state of hemostasis: ongoing, stopped. Depending on the place of bleeding, bleeding is distinguished external, internal and interstitial. Internal (occult) bleeding can occur in the anatomical cavities of the body and internal organs (lung, stomach, intestine, bladder). Interstitial bleeding, even with closed fractures, sometimes causes very large blood loss.
11.2. Definition and classification of blood loss
The clinical signs of bleeding depend on the amount of blood lost.
bloodslingerfromerya - this is a state of the body that occurs after bleeding and is characterized by the development of a number of adaptive and pathological reactions.
With all the variety of bleeding, their consequence - blood loss - has common features. It is necessary to know the signs of blood loss, which allow to differentiate the symptoms caused by the actual loss of blood from other manifestations (consequences of trauma, disease process, etc.). Features of each individual type of blood loss are considered in private sections of surgery.
Blood loss is classified both in terms of magnitude and severity of the upcoming changes in the body. Distinguish between the amount of blood loss and the severity of post-hemorrhagic disorders, assessed primarily by the depth of developing hypovolemia, due to the amount of lost circulating blood volume (BCV).
The amount of blood loss is considered from the standpoint of reducing the amount of fluid that fills the bloodstream; loss of red blood cells that carry oxygen; loss of plasma, which is of decisive importance in tissue metabolism.
Primary in the pathogenesis and thanatogenesis of blood loss is a decrease in the volume of blood filling the vascular bed, which leads to a violation of hemodynamics. Another factor is also important - a change in the oxygen regime of the body. Hemodynamic and anemic factors lead to the inclusion of the protective mechanisms of the body, due to which compensation for blood loss can occur. Compensation becomes a consequence of the movement of extracellular fluid into the vascular bed (hemodilution); increased lymph flow; regulation of vascular tone, known as “circulatory centralization”; increase in heart rate; increasing oxygen extraction in tissues. Compensation for blood loss is carried out the easier, the less blood is lost and the slower it expires. At the same time, in violation of compensation and even more so in decompensation, blood loss turns into hemorrhagic shock, which was determined by the main causative factor.
The so-called threshold of death is determined not by the amount of bleeding, but by the number of red blood cells remaining in circulation. This critical reserve is equal to 30% of the erythrocyte volume and only 70% of the plasma volume. The body can survive the loss of 2/3 of the volume of red blood cells, but will not tolerate the loss of 1/3 of the plasma volume. Such consideration of blood loss allows more complete consideration of compensatory processes in the body.
Blood loss is a common and evolutionarily oldest damage to the human body that occurs in response to the loss of blood from the vessels and is characterized by the development of a number of compensatory and pathological reactions.
Classification of blood loss
The state of the body that occurs after bleeding depends on the development of these adaptive and pathological reactions, the ratio of which is determined by the volume of blood lost. The increased interest in the problem of blood loss is due to the fact that almost all surgical specialists encounter it quite often. In addition, the mortality rates for blood loss remain high to date. Blood loss of more than 30% of circulating blood volume (CBV) in less than 2 hours is considered massive and life-threatening. The severity of blood loss is determined by its type, the speed of development, the volume of lost blood, the degree of hypovolemia and the possible development of shock, which is most convincingly presented in the classification of P. G. Bryusov (1998), (Table 1).
Classification of blood loss
1. Traumatic, wound, operating)
2. pathological (diseases, pathological processes)
3. artificial (exfusion, therapeutic bloodletting)
By the speed of development
1. acute (> 7% BCC per hour)
2. subacute (5-7% BCC per hour)
3. chronic (‹ 5% BCC per hour)
By volume
1. Small (0.5 - 10% bcc or 0.5 l)
2. Medium (11 - 20% BCC or 0.5 - 1 l)
3. Large (21 - 40% BCC or 1-2 liters)
4. Massive (41 - 70% BCC or 2-3.5 liters)
5. Fatal (> 70% BCC or more than 3.5 L)
According to the degree of hypovolemia and the possibility of developing shock:
1. Mild (deficit of BCC 10–20%, deficiency of GO less than 30%, no shock)
2. Moderate (deficiency of BCC 21–30%, deficiency of GO 30–45%, shock develops with prolonged hypovolemia)
3. Severe (deficit of BCC 31–40%, deficiency of GO 46–60%, shock is inevitable)
4. Extremely severe (deficit of BCC over 40%, deficit of GO over 60%, shock, terminal state).
Abroad, the most widely used classification of blood loss, proposed by the American College of Surgeons in 1982, according to which there are 4 classes of bleeding (Table 2).
Table 2.
Acute blood loss leads to the release of catecholamines by the adrenal glands, causing spasm of peripheral vessels and, accordingly, a decrease in the volume of the vascular bed, which partially compensates for the resulting deficiency of BCC. Redistribution of organ blood flow (centralization of blood circulation) allows you to temporarily maintain blood flow in vital organs and ensure life support in critical conditions. However, later this compensatory mechanism can cause the development of severe complications of acute blood loss. A critical condition, called shock, inevitably develops with a loss of 30% of BCC, and the so-called "death threshold" is determined not by the amount of bleeding, but by the number of red blood cells remaining in circulation. For erythrocytes, this reserve is 30% of the globular volume (GO), for plasma only 70%.
In other words, the body can survive the loss of 2/3 of the circulating red blood cells, but will not tolerate the loss of 1/3 of the plasma volume. This is due to the peculiarities of compensatory mechanisms that develop in response to blood loss and are clinically manifested by hypovolemic shock. Shock is understood as a syndrome based on inadequate capillary perfusion with reduced oxygenation and impaired oxygen consumption by organs and tissues. It (shock) is based on peripheral circulatory-metabolic syndrome.
Shock is a consequence of a significant decrease in BCC (i.e., the ratio of BCC to the capacity of the vascular bed) and a deterioration in the pumping function of the heart, which can manifest itself with hypovolemia of any origin (sepsis, trauma, burns, etc.).
A specific cause of hypovolemic shock due to loss of whole blood can be:
1. gastrointestinal bleeding;
2. intrathoracic bleeding;
3. intra-abdominal bleeding;
4. uterine bleeding;
5. bleeding into the retroperitoneal space;
6. ruptured aortic aneurysms;
7. injury, etc.
Pathogenesis
The loss of BCC disrupts the performance of the heart muscle, which is determined by:
1. Cardiac minute volume (MOV): MOV = SV x HR, (SV - stroke volume of the heart, HR - heart rate);
2. filling pressure of the cavities of the heart (preload);
3. the function of the heart valves;
4. total peripheral vascular resistance (OPVR) - afterload.
With insufficient contractility of the heart muscle, part of the blood remains in the cavities of the heart after each contraction, and this leads to an increase in preload. Part of the blood stagnates in the heart, which is called heart failure. In acute blood loss, leading to the development of BCC deficiency, the filling pressure in the heart cavities initially decreases, as a result of which the SV, MOS and BP decrease. Since the level of blood pressure is largely determined by the minute volume of the heart (MOV) and total peripheral vascular resistance (OPVR), to maintain it at the proper level with a decrease in BCC, compensatory mechanisms are activated to increase heart rate and OPSS. Compensatory changes that occur in response to acute blood loss include neuroendocrine changes, metabolic disorders, changes in the cardiovascular and respiratory systems. Activation of all links of coagulation causes the possibility of the development of disseminated intravascular coagulation (DIC). In the order of physiological protection, the body responds to its most frequent damage by hemodilution, which improves blood fluidity and reduces its viscosity, mobilization of erythrocytes from the depot, a sharp decrease in the need for both BCC and oxygen delivery, an increase in respiratory rate, cardiac output, return and utilization of oxygen. in tissues.
Neuroendocrine shifts are realized by activation of the sympathoadrenal system in the form of an increased release of catecholamines (adrenaline, norepinephrine) by the adrenal medulla. Catecholamines interact with a- and b-adrenergic receptors. Stimulation of adrenergic receptors in peripheral vessels causes vasoconstriction. Stimulation of p1-adrenergic receptors located in the myocardium has positive ionotropic and chronotropic effects, stimulation of p2-adrenergic receptors located in blood vessels causes slight dilatation of arterioles and constriction of veins. The release of catecholamines during shock leads not only to a decrease in the capacity of the vascular bed, but also to the redistribution of intravascular fluid from peripheral to central vessels, which contributes to the maintenance of blood pressure. The hypothalamus-pituitary-adrenal system is activated, adrenocorticotopic and antidiuretic hormones, cortisol, aldosterone are released into the blood, resulting in an increase in the osmotic pressure of the blood plasma, leading to an increase in the reabsorption of sodium and water, a decrease in diuresis and an increase in the volume of intravascular fluid. There are metabolic disorders. Developed blood flow disorders and hypoxemia lead to the accumulation of lactic and pyruvic acids. With a lack or absence of oxygen, pyruvic acid is reduced to lactic acid (anaerobic glycolysis), the accumulation of which leads to metabolic acidosis. Amino acids and free fatty acids also accumulate in tissues and exacerbate acidosis. The lack of oxygen and acidosis impair the permeability of cell membranes, as a result of which potassium leaves the cell, and sodium and water enter the cells, causing them to swell.
Changes in the cardiovascular and respiratory systems in shock are very significant. The release of catecholamines in the early stages of shock increases TPVR, myocardial contractility and heart rate - the goal of centralization of blood circulation. However, the resulting tachycardia very soon reduces the time of diastolic filling of the ventricles and, consequently, the coronary blood flow. Myocardial cells begin to suffer from acidosis. In the event of a prolonged shock, respiratory compensation mechanisms become untenable. Hypoxia and acidosis lead to increased excitability of cardiomyocytes, arrhythmias. Humoral shifts are manifested by the release of mediators other than catecholamines (histamine, serotonin, prostaglandins, nitric oxide, tumor necrotizing factor, interleukins, leukotrienes), which cause vasodilation and an increase in the permeability of the vascular wall, followed by the release of the liquid part of the blood into the interstitial space and a decrease in perfusion pressure. . This exacerbates the shortage of O2 in the tissues of the body, caused by a decrease in its delivery due to microthrombosis and an acute loss of O2 carriers - erythrocytes.
Changes that have a phase character develop in the microcirculatory bed:
1. 1 phase - ischemic anoxia or contraction of pre- and post-capillary sphincters;
2. 2nd phase - capillary stasis or expansion of precapillary venules;
3. Phase 3 - paralysis of peripheral vessels or expansion of pre- and post-capillary sphincters ...
Crisis processes in the capillary reduce the delivery of oxygen to the tissues. The balance between the delivery of oxygen and the need for it is maintained as long as the necessary tissue oxygen extraction is provided. If the start of intensive therapy is delayed, oxygen delivery to cardiomyocytes is disrupted, myocardial acidosis increases, which is clinically manifested by hypotension, tachycardia, and shortness of breath. A decrease in tissue perfusion develops into global ischemia with subsequent reperfusion tissue damage due to increased production of cytokines by macrophages, activation of lipid peroxidation, release of oxides by neutrophils, and further microcirculation disorders. Subsequent microthrombosis forms a violation of the specific functions of organs and there is a risk of developing multiple organ failure. Ischemia changes the permeability of the intestinal mucosa, which is especially sensitive to ischemic-reperfusion mediator effects, which causes the dislocation of bacteria and cytokines into the circulation system and the occurrence of such systemic processes as sepsis, respiratory distress syndrome, multiple organ failure. Their appearance corresponds to a certain time interval or stage of shock, which can be initial, reversible (reversible shock stage) and irreversible. To a large extent, the irreversibility of the shock is determined by the number of microthrombi formed in the capillaron and the temporary factor of the microcirculation crisis. As for the dislocation of bacteria and toxins due to intestinal ischemia and impaired permeability of its wall, this situation is not so unambiguous today and requires additional research. Nevertheless, shock can be defined as a condition in which the oxygen consumption of the tissues is inadequate to their needs for the functioning of aerobic metabolism.
clinical picture.
With the development of hemorrhagic shock, 3 stages are distinguished.
1. Compensated reversible shock. The volume of blood loss does not exceed 25% (700-1300 ml). Moderate tachycardia, blood pressure is either unchanged or slightly reduced. Saphenous veins become empty, CVP decreases. There are signs of peripheral vasoconstriction: cold extremities. The amount of urine excreted is reduced by half (at a rate of 1–1.2 ml / min). Decompensated reversible shock. The volume of blood loss is 25–45% (1300–1800 ml). The pulse rate reaches 120-140 per minute. Systolic blood pressure falls below 100 mm Hg, the value of pulse pressure decreases. Severe shortness of breath occurs, partly compensating for metabolic acidosis by respiratory alkalosis, but can also be a sign of a shock lung. Increased cold extremities, acrocyanosis. Cold sweat appears. The rate of urine output is below 20 ml/h.
2. Irreversible hemorrhagic shock. Its occurrence depends on the duration of circulatory decompensation (usually with arterial hypotension over 12 hours). The volume of blood loss exceeds 50% (2000-2500 ml). The pulse exceeds 140 per minute, systolic blood pressure falls below 60 mm Hg. or not defined. Consciousness is absent. oligoanuria develops.
Diagnostics
Diagnosis is based on the assessment of clinical and laboratory signs. In conditions of acute blood loss, it is extremely important to determine its volume, for which it is necessary to use one of the existing methods, which are divided into three groups: clinical, empirical and laboratory. Clinical methods allow to estimate the amount of blood loss based on clinical symptoms and hemodynamic parameters. The level of blood pressure and pulse rate before the start of replacement therapy largely reflect the magnitude of the BCC deficit. The ratio of pulse rate to systolic blood pressure allows you to calculate the Algover shock index. Its value, depending on the deficit of the BCC, is presented in Table 3.
Table 3. Assessment based on the Algover shock index
The capillary refill test, or "white spot" symptom, measures capillary perfusion. It is carried out by pressing on the fingernail, forehead skin or earlobe. Normally, the color is restored after 2 s, with a positive test - after 3 or more seconds. Central venous pressure (CVP) is an indicator of the filling pressure of the right ventricle, reflects its pumping function. Normal CVP ranges from 6 to 12 cm of water column. A decrease in CVP indicates hypovolemia. With a deficiency of BCC in 1 liter, the CVP decreases by 7 cm of water. Art. The dependence of the CVP value on the BCC deficit is presented in Table 4.
Table 4 Assessment of circulating blood volume deficit based on central venous pressure
Hourly diuresis reflects the level of tissue perfusion or the degree of filling of the vascular bed. Normally, 0.5-1 ml / kg of urine is excreted per hour. A decrease in diuresis less than 0.5 ml/kg/h indicates insufficient blood supply to the kidneys due to a deficiency of BCC.
Empirical methods for assessing the volume of blood loss are most often used in trauma and polytrauma. They use the average statistical values of blood loss established for a particular type of damage. In the same way, it is possible to roughly estimate the blood loss during various surgical interventions.
Average blood loss (l)
1. Hemothorax - 1.5–2.0
2. Fracture of one rib - 0.2–0.3
3. Abdominal injury - up to 2.0
4. Fracture of the pelvic bones (retroperitoneal hematoma) - 2.0–4.0
5. Hip fracture - 1.0–1.5
6. Shoulder/shin fracture - 0.5–1.0
7. Fracture of the bones of the forearm - 0.2–0.5
8. Fracture of the spine - 0.5–1.5
9. Scalped wound the size of a palm - 0.5
Operational blood loss
1. Laparotomy - 0.5–1.0
2. Thoracotomy - 0.7–1.0
3. Amputation of the lower leg - 0.7–1.0
4. Osteosynthesis of large bones - 0.5–1.0
5. Resection of the stomach - 0.4–0.8
6. Gastrectomy - 0.8–1.4
7. Resection of the colon - 0.8–1.5
8. Cesarean section - 0.5–0.6
Laboratory methods include the determination of hematocrit (Ht), hemoglobin concentration (Hb), relative density (p) or blood viscosity.
They are divided into:
1. calculation (use of mathematical formulas);
2. hardware (electrophysiological impedance methods);
3. indicator (the use of dyes, thermodilution, dextrans, radioisotopes).
Among the calculation methods, the Moore formula is most widely used:
KVP \u003d BCCd x Htd-Htf / Htd
Where KVP is blood loss (ml);
BCCd - the proper volume of circulating blood (ml).
Normally, in women, BCCd averages 60 ml / kg, in men - 70 ml / kg, in pregnant women - 75 ml / kg;
№d - proper hematocrit (for women - 42%, for men - 45%);
Nf is the patient's actual hematocrit. In this formula, instead of hematocrit, you can use the hemoglobin indicator, taking 150 g / l as its proper level.
You can also use the value of blood density, but this technique is applicable only for small blood loss.
One of the first hardware methods for determining BCC was a method based on measuring the basic resistance of the body using a reopletismograph (it was used in the countries of the "post-Soviet space").
Modern indicator methods provide for the establishment of BCC by changing the concentration of the substances used and are conventionally divided into several groups:
1. determination of the plasma volume, and then the total blood volume through Ht;
2. determination of the volume of erythrocytes and, according to it, the entire volume of blood through Ht;
3. simultaneous determination of the volume of erythrocytes and blood plasma.
Evans dye (T-1824), dextrans (polyglucin), human albumin labeled with iodine (131I) or chromium chloride (51CrCl3) are used as an indicator. But, unfortunately, all methods for determining blood loss give a high error (sometimes up to a liter), and therefore can only serve as a guideline for treatment. However, the determination of VO2 should be considered the simplest diagnostic criterion for detecting shock.
The strategic principle of transfusion therapy for acute blood loss is the restoration of organ blood flow (perfusion) by achieving the required BCC. Maintaining the level of coagulation factors in quantities sufficient for hemostasis, on the one hand, and to resist excessive disseminated coagulation, on the other. Replenishment of the number of circulating red blood cells (oxygen carriers) to a level that provides the minimum sufficient oxygen consumption in tissues. However, most experts consider hypovolemia to be the most acute problem of blood loss, and, accordingly, the replenishment of BCC, which is a critical factor for maintaining stable hemodynamics, is in first place in the treatment regimens. The pathogenetic role of a decrease in BCC in the development of severe homeostasis disorders predetermines the importance of timely and adequate correction of volemic disorders on treatment outcomes in patients with acute massive blood loss. The ultimate goal of all efforts by the resuscitator is to maintain adequate tissue oxygen consumption to maintain metabolism.
General principles for the treatment of acute blood loss are as follows:
1. Stop bleeding, fight pain.
2. Ensuring adequate gas exchange.
3. Replenishment of the BCC deficit.
4. Treatment of organ dysfunction and prevention of multiple organ failure:
Treatment of heart failure;
Prevention of renal failure;
Correction of metabolic acidosis;
Stabilization of metabolic processes in the cell;
Treatment and prevention of DIC.
5. Early prevention of infection.
Stop bleeding and control pain.
With any bleeding, it is important to eliminate its source as soon as possible. With external bleeding - pressing the vessel, pressure bandage, tourniquet, ligature or clamp on the bleeding vessel. With internal bleeding - urgent surgical intervention, carried out in parallel with therapeutic measures to remove the patient from shock.
Table No. 5 presents data on the nature of the infusion therapy for acute blood loss.
| Min. | Medium | Means. | Heavy. | Arrays | |
| BP sys. | 100–90 | 90–70 | 70–60 | ‹60 | ‹60 |
| heart rate | 100–110 | 110–130 | 130–140 | ›140 | ›140 |
| Algover index | 1–1,5 | 1,5–2,0 | 2,0–2,5 | ›2.5 | ›2.5 |
| The volume of blood flow.ml. | Up to 500 | 500–1000 | 1000–1500 | 1500–2500 | ›2500 ml |
| V krovop. (ml/kg) | 8–10 | 10–20 | 20–30 | 30–35 | ›35 |
| % loss of bcc | | 10–20
|
20–40
|
›40 |
>fifty |
|
| V infusion (in % of loss) | 100 | 130 | 150 | 200 | 250 |
| Hemotr. (% of V infusion) | - | 50–60 | 30–40 | 35–40 | 35–40 |
| Colloids (%V infusion) | 50 | 20–25 | 30–35 | 30 | 30 |
| Crystalloids (%V infusion) | 50 | 20–25 | 30–55 | 30 | 30 |
1. Infusion starts with crystalloids, then colloids. Hemotransfusion - with a decrease in Hb less than 70 g / l, Ht less than 25%.
2. Infusion rate for massive blood loss up to 500 ml/min!!! (catheterization of the second central vein, infusion of solutions under pressure).
3. Correction of volemia (stabilization of hemodynamic parameters).
4. Normalization of globular volume (Hb, Ht).
5. Correction of violations of water-salt metabolism
The fight against pain, protection from mental stress is carried out by intravenous (in / in) administration of analgesics: 1-2 ml of a 1% solution of morphine hydrochloride, 1-2 ml of a 1-2% solution of promedol, and sodium hydroxybutyrate (20-40 mg /kg of body weight), sibazon (5–10 mg), it is possible to use subnarcotic doses of calypsol and sedation with propofol. The dose of narcotic analgesics should be reduced by 50% due to the possible respiratory depression, nausea and vomiting that occurs with intravenous administration of these drugs. In addition, it should be remembered that their introduction is possible only after the exclusion of damage to internal organs. Ensuring adequate gas exchange is aimed at both the utilization of oxygen by tissues and the removal of carbon dioxide. All patients are shown prophylactic administration of oxygen through a nasal catheter at a rate of at least 4 l/min.
When respiratory failure occurs, the main objectives of treatment are:
1. ensuring airway patency;
2. prevention of aspiration of stomach contents;
3. release of the respiratory tract from sputum;
4. lung ventilation;
5. restoration of tissue oxygenation.
Developed hypoxemia may be due to:
1. hypoventilation (usually in combination with hypercapnia);
2. mismatch between ventilation of the lungs and their perfusion (disappears when breathing pure oxygen);
3. Intrapulmonary blood shunting (protected by breathing pure oxygen) caused by adult respiratory distress syndrome (PaO2 ‹ 60–70 mm Hg FiO2 > 50%, bilateral pulmonary infiltrates, normal ventricular filling pressure), pulmonary edema, severe pneumonia ;
4. violation of the diffusion of gases through the alveolo-capillary membrane (disappears when breathing pure oxygen).
Lung ventilation after tracheal intubation is carried out in specially selected modes that create conditions for optimal gas exchange and do not disturb central hemodynamics.
Replenishment of the BCC deficit
First of all, with acute blood loss, the patient should create an improved Trendelburg position to increase venous return. Infusion is carried out simultaneously in 2-3 peripheral or 1-2 central veins. The rate of replenishment of blood loss is determined by the value of blood pressure. As a rule, at first, the infusion is carried out by stream or fast drip (up to 250-300 ml / min). After stabilization of blood pressure at a safe level, the infusion is carried out by drip. Infusion therapy begins with the introduction of crystalloids. And in the last decade there has been a return to the consideration of the possibility of using hypertonic solutions of NaCI.
Hypertonic solutions of sodium chloride (2.5-7.5%), due to the high osmotic gradient, provide rapid mobilization of fluid from the interstitium into the bloodstream. However, their short duration of action (1–2 hours) and relatively small injection volumes (no more than 4 ml/kg of body weight) determine their predominant use at the prehospital stage of treatment of acute blood loss. Colloidal solutions of antishock action are divided into natural (albumin, plasma) and artificial (dextrans, hydroxyethyl starches). Albumin and plasma protein fraction effectively increase the volume of intravascular fluid, because. have high oncotic pressure. However, they easily penetrate the walls of the pulmonary capillaries and the basement membranes of the glomeruli of the kidneys into the extracellular space, which can lead to edema of the interstitial tissue of the lungs (adult respiratory distress syndrome) or kidneys (acute renal failure). The volume of diffusion of dextrans is limited, because they cause damage to the epithelium of the renal tubules ("dextran kidney"), adversely affect the blood coagulation system and immunocomponent cells. Therefore, today "drugs of the first choice" are solutions of hydroxyethyl starch. Hydroxyethyl starch is a natural polysaccharide derived from amylopectin starch and consisting of high molecular weight polarized glucose residues. The feedstock for the production of HES is starch from potato and tapioca tubers, grains of various varieties of corn, wheat, and rice.
HES from potato and corn, along with linear amylase chains, contains a fraction of branched amylopectin. Hydroxylation of starch prevents its rapid enzymatic cleavage, increases the ability to retain water and increase colloid osmotic pressure. In transfusion therapy, 3%, 6% and 10% HES solutions are used. The introduction of HES solutions causes isovolemic (up to 100% with a 6% solution) or even initially hypervolemic (up to 145% of the injected volume of a 10% solution of the drug) volume-replacing effect, which lasts for at least 4 hours.
In addition, HES solutions have the following properties that are not available in other colloidal plasma-substituting preparations:
1. prevent the development of increased capillary permeability syndrome by closing the pores in their walls;
2. modulate the action of circulating adhesive molecules or inflammatory mediators, which, circulating in the blood during critical conditions, increase secondary tissue damage by binding to neutrophils or endotheliocytes;
3. do not affect the expression of surface blood antigens, i.e. do not disrupt immune responses;
4. do not cause activation of the complement system (consists of 9 serum proteins C1 - C9), associated with generalized inflammatory processes that disrupt the functions of many internal organs.
It should be noted that in recent years there have been separate randomized trials of a high level of evidence (A, B) indicating the ability of starches to cause renal dysfunction and preferring albumin and even gelatin preparations.
At the same time, since the end of the 70s of the XX century, perfluorocarbon compounds (PFOS) began to be actively studied, which form the basis of a new generation of plasma expanders with the function of O2 transfer, one of which is perftoran. The use of the latter in acute blood loss makes it possible to influence the reserves of three levels of O2 exchange, and the simultaneous use of oxygen therapy makes it possible to increase the reserves of ventilation.
Table 6. The share of perftoran use depending on the level of blood replacement
| Blood replacement level | The amount of blood loss | Total transfusion volume (% of volume of blood loss) | Dose of perftoran |
| I | To 10 | 200–300 | not shown |
| II | 11–20 | 200 | 2–4 ml/kg body weight |
| III | 21–40 | 180 | 4–7 ml/kg body weight |
| IV | 41–70 | 170 | 7–10 ml/kg body weight |
| V | 71–100 | 150 | 10–15 ml/kg body weight |
Clinically, the degree of hypovolemia reduction reflects the following signs:
1. increased blood pressure;
2. decrease in heart rate;
3. warming and pinking of the skin; - increase in pulse pressure; - diuresis over 0.5 ml/kg/h.
Thus, summing up the above, we emphasize that the indications for blood transfusion are: - blood loss of more than 20% of the due BCC, - anemia, in which the hemoglobin content is less than 75 g / l, and the hematocrit number is less than 0.25.
Treatment of organ dysfunction and prevention of multiple organ failure
One of the most important tasks is the treatment of heart failure. If the victim was healthy before the accident, then in order to normalize cardiac activity, he usually quickly and effectively replenishes the BCC deficiency. If the victim has a history of chronic diseases of the heart or blood vessels, then hypovolemia and hypoxia aggravate the course of the underlying disease, therefore, special treatment is carried out. First of all, it is necessary to achieve an increase in preload, which is achieved by increasing the BCC, and then to increase myocardial contractility. Most often, vasoactive and inotropic agents are not prescribed, but if hypotension becomes persistent, not amenable to infusion therapy, then these drugs can be used. Moreover, their application is possible only after the full compensation of the BCC. Of the vasoactive agents, the first-line drug for maintaining the activity of the heart and kidneys is dopamine, 400 mg of which is diluted in 250 ml of isotonic solution.
The infusion rate is chosen depending on the desired effect:
1. 2–5 µg/kg/min (“renal” dose) dilates mesenteric and renal vessels without increasing heart rate or blood pressure;
2. 5-10 mcg/kg/min gives a pronounced ionotropic effect, mild vasodilation due to stimulation of β2-adrenergic receptors or moderate tachycardia;
3. 10–20 mcg/kg/min leads to a further increase in the ionotropic effect, severe tachycardia.
More than 20 mcg / kg / min - a sharp tachycardia with a threat of tachyarrhythmias, narrowing of the veins and arteries due to stimulation of a1_ adrenoreceptors and deterioration in tissue perfusion. Due to arterial hypotension and shock, as a rule, acute renal failure (ARF) develops. In order to prevent the development of the oliguric form of acute renal failure, it is necessary to control hourly diuresis (normal in adults is 0.51 ml / kg / h, in children - more than 1 ml / kg / h).
Measurement of the concentration of sodium and creatine in urine and plasma (with acute renal failure, plasma creatine exceeds 150 μmol / l, glomerular filtration rate is below 30 ml / min).
Infusion of dopamine in the "renal" dose. Currently, there are no randomized multicenter trials in the literature demonstrating the effectiveness of the use of "renal doses" of sympathomimetics.
Stimulation of diuresis against the background of the restoration of BCC (CVP more than 30–40 cm of water column) and satisfactory cardiac output (furosemide, IV at the initial dose of 40 mg with an increase if necessary by 5–6 times).
Normalization of hemodynamics and compensation of circulating blood volume (BCV) should be carried out under the control of DZLK (pulmonary capillary wedge pressure), CO (cardiac output) and OPSS. In shock, the first two indicators progressively decrease and the last increases. Methods for determining these criteria and their norms are well described in the literature, but, unfortunately, they are routinely used in clinics abroad and rarely in our country.
Shock is usually accompanied by severe metabolic acidosis. Under its influence, myocardial contractility decreases, cardiac output decreases, which contributes to a further decrease in blood pressure. The reactions of the heart and peripheral vessels to endo- and exogenous catecholamines are reduced. O2 inhalation, mechanical ventilation, infusion therapy restore physiological compensatory mechanisms and in most cases eliminate acidosis. Sodium bicarbonate is administered in severe metabolic acidosis (pH of venous blood below 7.25), having calculated it according to the generally accepted formula, after determining the indicators of acid-base balance.
The bolus can be given immediately with 44-88 mEq (50-100 ml 7.5% HCO3), the rest over the next 4-36 hours. It should be remembered that excessive administration of sodium bicarbonate creates prerequisites for the development of metabolic alkalosis, hypokalemia, and arrhythmias. A sharp increase in plasma osmolarity is possible, up to the development of a hyperosmolar coma. In shock, accompanied by a critical deterioration in hemodynamics, stabilization of metabolic processes in the cell is necessary. Treatment and prevention of DIC, as well as early prevention of infections, is carried out, guided by generally accepted schemes.
Justified, from our point of view, is the pathophysiological approach to solving the problem of indications for blood transfusions, based on the assessment of oxygen transport and consumption. Oxygen transport is a derivative of cardiac output and blood oxygen capacity. Oxygen consumption depends on the delivery and ability of the tissue to take oxygen from the blood.
When replenishing hypovolemia with colloid and crystalloid solutions, the number of erythrocytes is reduced and the oxygen capacity of the blood is reduced. Due to the activation of the sympathetic nervous system, cardiac output rises compensatory (sometimes exceeding normal values by 1.5–2 times), microcirculation “opens up” and the affinity of hemoglobin for oxygen decreases, tissues take relatively more oxygen from the blood (the oxygen extraction coefficient increases). This allows you to maintain normal oxygen consumption with a low oxygen capacity of the blood.
In healthy people, normovolemic hemodilution with a hemoglobin level of 30 g/l and a hematocrit of 17%, although accompanied by a decrease in oxygen transport, does not decrease oxygen consumption by tissues, the blood lactate level does not increase, which confirms the sufficiency of oxygen supply to the body and the maintenance of metabolic processes at sufficient level. In acute isovolemic anemia up to hemoglobin (50 g / l), in patients at rest, tissue hypoxia is not observed before surgery. Oxygen consumption does not decrease, and even slightly increases, the level of blood lactate does not increase. In normovolemia, oxygen consumption does not suffer at a delivery level of 330 ml/min/m2, at lower delivery there is a dependence of consumption on oxygen delivery, which corresponds to approximately a hemoglobin level of 45 g/l with normal cardiac output.
Increasing the oxygen capacity of blood by transfusing canned blood and its components has its negative sides. Firstly, an increase in hematocrit leads to an increase in blood viscosity and a deterioration in microcirculation, which creates an additional load on the myocardium. Secondly, a low content of 2,3-DPG in erythrocytes of donor blood is accompanied by an increase in the affinity of oxygen for hemoglobin, a shift in the dissociation curve of oxyhemoglobin to the left, and, as a result, a deterioration in tissue oxygenation. Thirdly, transfused blood always contains microclots, which can "clog" the capillaries of the lungs and dramatically increase the pulmonary shunt, impairing blood oxygenation. In addition, transfused erythrocytes begin to fully participate in oxygen transport only 12-24 hours after blood transfusion.
Our analysis of the literature showed that the choice of means for the correction of blood loss and posthemorrhagic anemia is not a settled issue. This is mainly due to the lack of informative criteria for assessing the optimality of certain methods of compensating transport and oxygen consumption. The current trend towards a decrease in blood transfusions is due, first of all, to the possibility of complications associated with blood transfusions, limitation of donation, refusal of patients from blood transfusions for any reason. At the same time, the number of critical conditions associated with blood loss of various origins is increasing. This fact dictates the need for further development of methods and means of substitution therapy.
An integral indicator that allows an objective assessment of the adequacy of tissue oxygenation is the saturation of hemoglobin with oxygen in mixed venous blood (SvO2). A decrease in this indicator to less than 60% over a short period of time leads to the appearance of metabolic signs of tissue oxygen debt (lactic acidosis, etc.). Therefore, an increase in the content of lactate in the blood can be a biochemical marker of the degree of activation of anaerobic metabolism and characterize the effectiveness of the therapy.
What is blood loss is best known in surgery and obstetrics, since they most often encounter a similar problem, which is complicated by the fact that there was no single tactic in the treatment of these conditions. Every patient needs individual selection optimal combinations of therapeutic agents, because blood transfusion therapy is based on the transfusion of donor blood components that are compatible with the patient's blood. Sometimes it can be very difficult to restore homeostasis, since the body reacts to acute blood loss with a violation of the rheological properties of blood, hypoxia and coagulopathy. These disorders can lead to uncontrolled reactions that threaten to end in death.
Hemorrhage acute and chronic
The amount of blood in an adult is approximately 7% of its weight, in newborns and infants this figure is twice as high (14-15%). It also increases quite significantly (on average by 30-35%) during pregnancy. Approximately 80-82% takes part in blood circulation and is called volume of circulating blood(OTsK), and 18-20% is in reserve in the depositing authorities. The volume of circulating blood is noticeably higher in people with developed muscles and not burdened with excess weight. In full, oddly enough, this indicator decreases, so the dependence of BCC on weight can be considered conditional. BCC also decreases with age (after 60 years) by 1-2% per year, during menstruation in women and, of course, during childbirth, but these changes are considered physiological and, in general, do not affect the general condition of a person. Another question is if the volume of circulating blood decreases as a result of pathological processes:
- Acute blood loss caused by traumatic impact and damage to a vessel of large diameter (or several with a smaller lumen);
- Acute gastrointestinal bleeding associated with human diseases of ulcerative etiology and being their complication;
- Blood loss during operations (even planned ones), resulting from a surgeon's mistake;
- Bleeding during childbirth, resulting in massive blood loss, is one of the most severe complications in obstetrics, leading to maternal death;
- Gynecological bleeding (uterine rupture, ectopic pregnancy, etc.).
Blood loss from the body can be divided into two types: acute and chronic, and chronic is better tolerated by patients and does not carry such a danger to human life.
Chronic (hidden) blood loss is usually caused by persistent but minor bleeding(tumors, hemorrhoids), in which compensatory mechanisms that protect the body have time to turn on, which does not occur with acute blood loss. With a hidden regular loss of blood, as a rule, the BCC does not suffer, but the number of blood cells and the level of hemoglobin drops markedly. This is due to the fact that replenishing the volume of blood is not so difficult, it is enough to drink a certain amount of liquid, but the body does not have time to produce new formed elements and synthesize hemoglobin.
Physiology and not so
The loss of blood associated with menstruation is a physiological process for a woman, it does not have a negative effect on the body and does not affect her health, if it does not exceed permissible values. The average blood loss during menstruation ranges from 50-80 ml, but can reach up to 100-110 ml, which is also considered the norm. If a woman loses more blood than this, then one should think about it, because a monthly blood loss of approximately 150 ml is considered abundant and in one way or another will lead to and in general can be a sign of many gynecological diseases.
Childbirth is a natural process and physiological blood loss will definitely take place, where values of about 400 ml are considered acceptable. However, everything happens in obstetrics, and it should be said that obstetric bleeding is quite complex and can become uncontrollable very quickly.
At this stage, all the classic signs of hemorrhagic shock are clearly and clearly manifested:
- Cold extremities;
- Paleness of the skin;
- acrocyanosis;
- Dyspnea;
- Muffled heart sounds (insufficient diastolic filling of the heart chambers and deterioration of the contractile function of the myocardium);
- Development of acute renal failure;
- Acidosis.
Distinguishing decompensated hemorrhagic shock from irreversible is difficult because they are very similar. Irreversibility is a matter of time, and if decompensation, despite treatment, continues for more than half a day, then the prognosis is very unfavorable. Progressive organ failure, when the function of the main organs (liver, heart, kidneys, lungs) suffers, leads to the irreversibility of shock.
What is infusion therapy?
Infusion therapy does not mean replacing lost blood with donor blood. The slogan “a drop for a drop”, which provides for a complete replacement, and sometimes even with a vengeance, has long gone into oblivion. - a serious operation involving the transplantation of foreign tissue, which the patient's body may not accept. Transfusion reactions and complications are even more difficult to deal with than acute blood loss, so whole blood is not transfused. In modern transfusiology, the issue of infusion therapy is solved differently: blood components are transfused, mainly fresh frozen plasma, and its preparations (albumin). The rest of the treatment is supplemented by the addition of colloidal plasma substitutes and crystalloids.
The task of infusion therapy in acute blood loss:
- Restoration of the normal volume of circulating blood;
- Replenishment of the number of red blood cells, as they carry oxygen;
- Maintaining the level of clotting factors, since the hemostasis system has already responded to acute blood loss.
It makes no sense for us to dwell on what the tactics of a doctor should be, since for this you need to have certain knowledge and qualifications. However, in conclusion, I would also like to note that infusion therapy provides for various ways of its implementation. Puncture catheterization requires special care for the patient, so you need to be very attentive to the slightest complaints of the patient, since complications can also occur here.
Acute bleeding. What to do?
As a rule, first aid in case of bleeding caused by injuries is provided by people who are nearby at that moment. Sometimes they are just passers-by. And sometimes a person has to do it himself if trouble has caught him far from home: on a fishing or hunting trip, for example. The very first thing to do - try with the available improvised means or by finger pressing the vessel. However, when using a tourniquet, it should be remembered that it should not be applied for more than 2 hours, so a note is placed under it indicating the time of application.
In addition to stopping bleeding, first aid also consists in carrying out transport immobilization if fractures occur, and making sure that the patient falls into the hands of professionals as soon as possible, that is, it is necessary to call a medical team and wait for her arrival.
Emergency care is provided by medical professionals, and it consists of:
- Stop the bleeding;
- Assess the degree of hemorrhagic shock, if any;
- Compensate the volume of circulating blood by infusion of blood substitutes and colloidal solutions;
- Carry out resuscitation in case of cardiac and respiratory arrest;
- Transport the patient to the hospital.
The faster the patient gets to the hospital, the more chances he has for life, although it is difficult to treat acute blood loss even in hospital conditions, since it never leaves time for reflection, but requires quick and clear action. And, unfortunately, he never warns of his arrival.
Video: acute massive blood loss - lecture by A.I. Vorobyov
