Acute internal blood loss. Classification of acute blood loss
Blood loss is called the process, the development of which occurs as a result bleeding... It is characterized by a combination of adaptive and pathological reactions of the body to a decrease in blood volume in the body, as well as a lack of oxygen (), which was caused by a decrease in the transport of this substance by blood.
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^ LECTURE: TOPIC: ACUTE BLOOD LOSS.
Kligunenko Elena Nikolaevna, Doctor of Medical Sciences, Laureate of the State Prize in Science and Technology, Professor, Head of the Department of Anesthesiology, Intensive Care and Medicine of Emergency Conditions, FPO, Dnipropetrovsk State Medical Academy
Under blood loss understand the state of the body that occurs after bleeding and is characterized by the development of a number of adaptive and pathological reactions. The increased interest in the problem of blood loss is due to the fact that almost all surgical specialists meet with it quite often. In addition, the mortality rates for blood loss remain high to date.
The severity of the course of blood loss is determined by its type, rapidity of development, the volume of lost blood, the degree of hypovolemia and possible development shock, which is most fully reflected in the classification of P.G. Bryusov, which is widely used in our country (Table 1).
^ Table 1.
Classification of blood loss (A.G. Bryusov, 1998).
Abroad is widespread classification blood loss, developed by the American College of Surgeons in 1982, according to which 4 classes of bleeding are distinguished (Table 2)
^ Table 2.
Bleeding classification by the American College of Surgeons
(P. L. Marino, 1998)
Class I - corresponds to a loss of 15% of the circulating blood volume (BCC) or less. In this case, there are no clinical symptoms or there is only orthostatic tachycardia (heart rate increases by 20 or more beats / min when moving from a horizontal position to a vertical one).
Class II - corresponds to a loss of 20 to 25% BCC. Its main clinical sign is orthostatic hypotension or a decrease in blood pressure when moving from a horizontal position to a vertical position by 15 mm Hg or more. Art. Diuresis is saved.
^ Class III - Corresponds to the loss of 30 to 40% BCC. It is manifested by hypotension in the supine position, oliguria (urine less than 400 ml / day).
Class IV - loss of more than 40% of the BCC. It is characterized by collapse (extremely low blood pressure) and impaired consciousness up to coma.
Thus, shock inevitably develops with a loss of 30% of the BCC, and the so-called "death threshold" is determined not by the volume of fatal bleeding, but by the number of red blood cells remaining in the circulation. For erythrocytes, this reserve is 30% of the globular volume, for plasma - only 70%. In other words, the body can survive with a loss of 2/3 of circulating red blood cells, but will not tolerate a loss of 1/3 of plasma volume. This is due to the specificity of compensatory mechanisms developing in response to blood loss and clinically manifested by hypovolemic shock.
Under shock understand the syndrome complex, which is based on inadequate capillary perfusion with reduced oxygenation and impaired metabolism of tissues and organs, and under hypovolemic shock, in particular, they understand acute cardiovascular insufficiency resulting from a significant deficiency of the BCC.
Shock is a consequence of a decrease in the effective BCC (i.e., the ratio of the BCC to the capacity of the vascular bed) or a consequence of a deterioration in the pumping function of the heart, which can occur with hypovolemia of any genesis, sepsis, trauma and burns, heart failure, or a decrease in sympathetic tone. A specific cause of hypovolemic shock with loss of whole blood may be:
gastrointestinal bleeding;
intrathoracic bleeding;
intra-abdominal bleeding;
uterine bleeding;
bleeding into the retroperitoneal space;
rupture of the aortic aneurysm;
injury.
cardiac output (MOC):
MOS \u003d UOS HR,
where: UOS - stroke volume of the heart, and heart rate - heart rate);
heart rate;
pressure of filling the cavities of the heart (preload);
the function of the heart valves;
total peripheral vascular resistance (OPSR) - afterload.
In acute blood loss, causing a deficiency of the BCC, the filling pressure in the cardiac cavities initially decreases, as a result of which the UOS, MOS and blood pressure (HELL). Since the level of blood pressure is determined by cardiac output and vascular tone (OPSS), then to maintain it at the proper level with a decrease in BCC, compensatory mechanisms are activated aimed at increasing heart rate and OPSS. The compensatory changes that occur in response to acute blood loss include: neuro-endocrine shifts, metabolic disorders, changes in the cardiovascular and respiratory systems.
^ Neuro-endocrine shifts n are activated by the sympathetic-adrenal system in the form increased emission catecholamines (adrenaline, norepinephrine) by the adrenal medulla. Catecholamines interact with ± - and I-adrenergic receptors. Stimulation of the ± -adrenergic receptors of peripheral vessels causes vasoconstriction, and their blockade causes vasodilation. Beta 1 - adrenergic receptors are localized in the myocardium, I 2 - adrenergic receptors - in the wall blood vessels... Stimulation of I 1 -adrenergic receptors has a positive inotropic and chronotropic effect. Stimulation of I 2 -adrenergic receptors causes slight dilation of arterioles and constriction of veins.
The release of catecholamines during shock causes a decrease in the capacity of the vascular bed, redistribution of intravascular fluid from peripheral vessels to central ones, which contributes to the maintenance of blood pressure. At the same time, the pituitary-hypothalamus-adrenal glands system is activated, which is manifested by a massive release of ACTH, cortisol, aldosterone, antidiuretic hormone into the blood, which results in an increase in the osmotic pressure of blood plasma, an increase in the reabsorption of sodium chloride and water, a decrease in urine output and an increase in the volume of intravascular fluid.
^ Metabolic disorders. In conditions of normal blood flow, cells use glucose, which is converted into pyruvic acid and further into ATP. With a lack or absence of oxygen, pyruvic acid is reduced to lactic acid (anaerobic glycolysis), the accumulation of the latter leads to metabolic acidosis. Amino acids and free fatty acids, which normally oxidize to produce energy, accumulate in tissues during shock and aggravate acidosis. Lack of oxygen and acidosis disrupt the function of cell membranes, as a result of which potassium is released into the extracellular space, and sodium and water enter the cells, causing them to swell.
^ Changes in the cardiovascular and respiratory systems when shocked are very significant. The release of catecholamines in the early stages of shock increases the systemic vascular resistance, myocardial contractility and heart rate. Tachycardia decreases diastolic ventricular filling time and therefore coronary blood flow. Myocardial cells begin to suffer from acidosis, which is initially compensated for by hyperventilation. In the event of prolonged shock, respirators and non-compensation mechanisms fail. Acidosis and hypoxia lead to suppression of heart function, increased excitability of cardiomyocytes, arrhythmias.
Humoral shifts nthey are caused by the release of vasoactive mediators (histamine, serotonin, prostaglandins, nitric oxide, necrotizing factor tumor, interleukins, leukotrienes), which cause vasodillation and an increase in the permeability of the vascular wall, followed by the release of the liquid part of blood into the interstitial space and a decrease in perfusion pressure. This aggravates the lack of O 2 in the tissues of the body caused by a decrease in the delivery of O 2 to them due to an acute loss of the main carriers of O 2 erythrocytes.
^ Capillary endothelial changes are manifested by hypoxic swelling of its cells and adhesion (adhesion) of activated polymorphonuclear leukocytes to them, which triggers a cascade of phase changes in blood flow in the microvasculature.
^ 1 phase - ischemic anoxia or contraction of the pre- and postcapillary sphincters - is completely reversible;
2nd phase - capillary stasis or expansion of precapillary sphincters with spasm of postcapillary venules - is partially reversible;
3 phase - paralysis of peripheral vessels or expansion of the pre- and postcapillary sphincters - is completely irreversible.
1 - initial;
2 - stage of reversible shock;
3 - stage of irreversible shock.
The clinical picture is determined by the stage of shock.
1st stage - characterized by pallor of mucous membranes and skin. psychomotor agitation, cold extremities, slightly increased or normal blood pressure, rapid pulse and respiration, increased central venous pressure, maintaining normal urine output.
Stage 2 - manifested by lethargy, pale gray skin covered with cold sticky sweat, thirst, shortness of breath, decreased arterial and central venous pressure, tachycardia, hypothermia, oliguria.
Stage 3 - characterized by adynamia, turning into a coma; pale, earthy and marbled skin, progressive respiratory distress, hypotension, tachycardia, anuria.
Diagnostics based on an assessment of clinical and laboratory signs. In conditions of acute blood loss, it is extremely important to determine its value for which it is necessary to use one of existing methods, which are divided into 3 groups: clinical, empirical and laboratory. The latter can be direct and indirect.
2. Sharp (within an hour).
3. Subacute (within 24 hours).
4. Chronic (within weeks, months, years).
By the time of occurrence.
1. Primary.
2. Secondary.
Pathological classification.
1. Bleeding resulting from mechanical destruction of the walls of blood vessels, as well as thermal injuries.
2. Arrosive bleeding resulting from the destruction of the vessel wall by a pathological process (disintegration of a tumor, bedsore, purulent fusion, etc.).
3. Diapedetic bleeding (in violation of the permeability of blood vessels).
2. Clinic of acute blood loss
Blood performs a number of important functions in the body, which mainly boil down to maintaining homeostasis. Due to the transport function of blood in the body, a constant exchange of gases, plastic and energy materials becomes possible, hormonal regulation is carried out, etc. The buffer function of the blood is to maintain acid-base balance, electrolyte and osmotic balances. Immune function is also aimed at maintaining homeostasis. Finally, due to the delicate balance between the coagulation and anti-coagulation systems, the blood is kept fluid.
Bleeding clinicconsists of local (due to the outflow of blood into the external environment or into tissues and organs) and general signs of blood loss.
Symptoms of acute blood loss- It is a unifying clinical sign for all types of bleeding. The severity of these symptoms and the body's response to blood loss depend on many factors (see below). Such a volume of blood loss is considered fatal when a person loses half of all circulating blood. But this is not an absolute statement. The second important factor determining the body's response to blood loss is its rate, that is, the rate at which a person loses blood. With bleeding from a large arterial trunk, death can occur with less blood loss. This is due to the fact that the compensatory reactions of the body do not have time to work at the proper level, for example, in case of chronic blood loss in volume. General clinical manifestations of acute blood loss are the same for all bleeding. Complaints of dizziness, weakness, thirst, flashing of flies before the eyes, drowsiness are observed. The skin is pale, with a high rate of bleeding can be observed cold sweat... Orthostatic collapse, development of fainting conditions are not uncommon. When objective research tachycardia, a decrease in blood pressure, a pulse of small filling are revealed. With the development of hemorrhagic shock, diuresis decreases. In the analysis of red blood, there is a decrease in hemoglobin, hematocrit and the number of erythrocytes. But a change in these indicators is observed only with the development of hemodilution and in the first hours after blood loss are of little information. The severity of clinical manifestations of blood loss depends on the rate of bleeding.
There are several severity of acute blood loss.
1. With a deficiency of circulating blood volume (BCC) 5-10%. The general condition is relatively satisfactory, there is an increase in the pulse, but it is sufficient filling. Blood pressure (BP) is normal. When examining blood, hemoglobin is more than 80 g / l. On capillaroscopy, the state of microcirculation is satisfactory: against a pink background, rapid blood flow, at least 3-4 loops.
2. With a deficit of BCC up to 15%. General state moderate... Tachycardia up to 110 per minute is noted. Systolic blood pressure drops to 80 mm Hg. Art. In the analysis of red blood, a decrease in hemoglobin from 80 to 60 g / l. With capillaroscopy, rapid blood flow is detected, but against a pale background.
3. With a deficit of BCC up to 30%. General grave condition of the patient. The pulse is threadlike, with a frequency of 120 in 1 min. Blood pressure drops to 60 mm Hg. Art. With capillaroscopy, pale background, slowing blood flow, 1-2 loops.
4. With a BCC deficit of more than 30%. The patient is in a very serious, often agonal state. Pulse and blood pressure at peripheral arteries absent.
3. The clinical picture of various types of bleeding
It is possible to clearly determine from which vessel blood is flowing only when external bleeding... As a rule, with external bleeding, diagnosis is not difficult. If the arteries are damaged, blood is poured into the external environment in a strong pulsating stream. Crimson blood. This is a very dangerous condition, since arterial bleeding quickly leads to critical anemization of the patient.
Venous bleedingusually characterized by a persistent bleeding of a dark color. But sometimes (when large venous trunks are injured) there may be diagnostic errors, since transmission pulsation of the blood is possible. Venous bleeding is dangerous for the possible development of air embolism (with low central venous pressure (CVP)). When capillary bleedingthere is a constant outflow of blood from the entire surface of the damaged tissue (like dew). Capillary bleeding, which occurs when trauma to the parenchymal organs (kidneys, liver, spleen, lungs), is especially severe. This is due to the structural features of the capillary network in these organs. Bleeding in this case is very difficult to stop, and with surgery on these organs, it turns into a serious problem.
3. artificial (exfusion, curative bloodletting)
By the speed of development
1.Acute (›7% BCC per hour)
2. subacute (5-7% of the blood volume per hour)
3.chronic (\u003c5% 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 liters)
By the degree of hypovolemia and the possibility of developing shock:
1. Mild (BCC deficit 10–20%, HO deficit less than 30%, no shock)
2. Moderate (BCC deficit 21-30%, GO deficit 30-45%, shock develops with prolonged hypovolemia)
3. Severe (BCC deficit 31-40%, HO deficit 46-60%, shock is inevitable)
4. Extremely severe (BCC deficit over 40%, HO deficit over 60%, shock, terminal state).
Abroad, the most widespread classification of blood loss, proposed by the American College of Surgeons in 1982, according to which 4 classes of bleeding are distinguished (Table 2).
Table 2.
Acute blood loss leads to the release of catecholamines by the adrenal glands, which cause spasm of peripheral vessels and, accordingly, a decrease in the volume of the vascular bed, which partially compensates for the resulting deficiency of the BCC. Redistribution of organ blood flow (centralization of blood circulation) allows you to temporarily maintain blood flow in vital organs and ensure the maintenance of life in critical conditions. However, subsequently, 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 the BCC, and the so-called "death threshold" is determined not by the volume of bleeding, but by the number of erythrocytes remaining in the circulation. For erythrocytes, this reserve is 30% of the globular volume (GO), for plasma only 70%.
In other words, the body can survive with a loss of 2/3 of circulating red blood cells, but will not tolerate a loss of 1/3 of plasma volume. This is due to the peculiarities of compensatory mechanisms developing in response to blood loss and 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 the BCC (i.e., the ratio of the BCC to the capacity of the vascular bed) and a deterioration in the pumping function of the heart, which can manifest itself in hypovolemia of any genesis (sepsis, trauma, burns, etc.).
A specific cause of hypovolemic shock due to loss of whole blood may be:
1.gastrointestinal bleeding;
2. intrathoracic bleeding;
3. intra-abdominal bleeding;
5. bleeding into the retroperitoneal space;
6. ruptures of aortic aneurysms;
7.trauma, etc.
Pathogenesis
Loss of BCC disrupts the performance of the heart muscle, which is determined by:
1. cardiac output (MOC): MOC \u003d UOS x heart rate, (UOS - stroke volume of the heart, heart rate - heart rate);
2. pressure of filling the cavities of the heart (preload);
3. the function of the heart valves;
4. total peripheral vascular resistance (OPSR) - afterload.
With insufficient contractility of the heart muscle, a part of the blood remains in the cavities of the heart after each contraction, and this leads to an increase in preload. Some 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 cardiac cavities initially decreases, as a result of which the VOS, MOS and blood pressure decrease. Since the level of blood pressure is largely determined by the minute volume of the heart (MOS) and the total peripheral vascular resistance (OPSR), then to maintain it at the proper level with a decrease in the BCC, compensatory mechanisms are activated aimed at increasing the heart rate and OPSS. Compensatory changes that occur in response to acute blood loss include neuroendocrine shifts, metabolic disturbances, and changes in the cardiovascular and respiratory systems. Activation of all coagulation links leads to the development of disseminated intravascular coagulation (DIC syndrome). As a physiological defense, the body responds to its most frequent damage by hemodilution, which improves blood flow 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 the respiratory rate, cardiac output, return and utilization of oxygen in the 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 peripheral vascular adrenergic receptors causes vasoconstriction. Stimulation of p1 - adrenergic receptors localized in the myocardium has positive ionotropic and chronotropic effects, stimulation of p2-adrenergic receptors located in blood vessels causes slight dilation 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 vessels to central ones, which contributes to the maintenance of blood pressure. The hypothalamus - pituitary adrenal gland system is activated, adrenocorticotopic and antidiuretic hormones, cortisol, aldosterone are released into the blood, which results in an increase in the osmotic pressure of blood plasma, leading to an increase in sodium and water reabsorption, a decrease in urine output and an increase in the volume of intravascular fluid. Metabolic disorders are observed. The developed disorders of blood flow 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 worsen acidosis. Lack of oxygen and acidosis disrupt 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 during shock are very significant. The release of catecholamines in the early stages of shock increases the systemic vascular resistance, myocardial contractility and heart rate - the goal is the 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 prolonged shock, respiratory compensation mechanisms fail. Hypoxia and acidosis lead to increased excitability of cardiomyocytes, arrhythmias. Humoral changes are manifested by the release of other, in addition to catecholamines, mediators (histamine, serotonin, prostaglandins, nitric oxide, tumor necrotizing factor, interleukins, leukotrienes), which cause vasodilation and an increase in the permeability of the vascular wall with the subsequent release of the fluid part of the blood into the interstitial space ... This aggravates the lack of O2 in the tissues of the body, caused by a decrease in its delivery due to microthrombus formation and an acute loss of O2 carriers - erythrocytes.
In the microvasculature, phase changes develop:
1. Phase 1 - ischemic anoxia or contraction of the pre- and postcapillary sphincters;
2. Phase 2 - capillary stasis or expansion of precapillary venules;
3.3 phase - paralysis of peripheral vessels or expansion of pre- and postcapillary sphincters ...
Crisis processes in the capillary reduce the delivery of oxygen to the tissues. The balance between oxygen delivery and demand is maintained as long as the required tissue oxygen extraction is provided. With a delay in the initiation of intensive therapy, oxygen delivery to cardiomyocytes is disrupted, myocardial acidosis increases, which is clinically manifested by hypotension, tachycardia, shortness of breath. A decrease in tissue perfusion develops into global ischemia with subsequent reperfusion damage to tissues due to increased production of cytokines by macrophages, activation of lipid peroxidation, release of oxides by neutrophils, and further disturbances of microcirculation. Subsequent microthrombosis forms a violation of 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 ischemia-reperfusion-mediator effects, which causes the dislocation of bacteria and cytokines into the circulation system and the emergence 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 (stage of reversible shock) and irreversible. To a large extent, the irreversibility of shock is determined by the number of microthrombi formed in the capillary 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 position is not so unambiguous today and requires additional research. Yet shock can be defined as a condition in which the oxygen consumption of tissues is inadequate to their needs for the functioning of aerobic metabolism.
The 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). Tachycardia is moderate, blood pressure is either not changed, or slightly decreased. Run out saphenous veins, CVP decreases. There are signs of peripheral vasoconstriction: cold extremities. The amount of excreted urine 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 drops below 100 mm Hg, the value of pulse pressure decreases. Severe dyspnea occurs, partly compensating for metabolic acidosis by respiratory alkalosis, but can also be a sign of shock lung. Cooling of the extremities, acrocyanosis intensifies. Cold sweat appears. Urine flow rate 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, the systolic blood pressure falls below 60 mm Hg. or not defined. There is no consciousness. Oligoanuria develops.
Diagnostics
Diagnosis is based on an 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 assessing the amount of blood loss based on clinical symptoms and hemodynamic parameters. Blood pressure and pulse rate before the start of replacement therapy largely reflect the amount of BCC deficiency. The ratio of pulse rate to systolic blood pressure allows you to calculate the Algover shock index. Its value depending on the BCC deficit is presented in Table 3.
Table 3. Assessment based on the Algover shock index
The capillary filling test, or "white spot" symptom, evaluates capillary perfusion. It is performed 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 and reflects its pumping function. Normally, CVP ranges from 6 to 12 cm of water column. A decrease in CVP indicates hypovolemia. With a deficiency of BCC in 1 liter, CVP decreases by 7 cm of water. Art. The dependence of the CVP value on the BCC deficiency is presented in Table 4.
Table 4. Assessment of circulating blood volume deficit based on the value of central venous pressure
Hourly urine output reflects the level of tissue perfusion or the degree of filling of the vascular bed. Normally, 0.5-1 ml / kg of urine is released per hour. A decrease in urine output of less than 0.5 ml / kg / h indicates insufficient blood supply to the kidneys due to a deficiency of the BCC.
Empirical methods for assessing the volume of blood loss are most often used in trauma and polytrauma. They use the average statistical values \u200b\u200bof blood loss established for a particular type of injury. In the same way, you can roughly assess 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 trauma - up to 2.0
4. Fracture of the pelvic bones (retroperitoneal hematoma) - 2.0-4.0
5. Hip fracture - 1.0-1.5
6. Fracture of the shoulder / lower leg - 0.5-1.0
7. Fracture of the forearm bones - 0.2-0.5
8. Fracture of the spine - 0.5-1.5
9. Scalped wound the size of a palm - 0.5
Operating 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. Gastric resection - 0.4-0.8
6. Gastrectomy - 0.8-1.4
7. Colon resection - 0.8-1.5
8. Cesarean section – 0,5–0,6
Laboratory methods provide for the determination of hematocrit number (Ht), hemoglobin concentration (Hb), relative density (p) or blood viscosity.
They are classified into:
1.calculated (using mathematical formulas);
2. hardware (electrophysiological impedance methods);
3. indicator (use of dyes, thermodilution, dextrans, radioisotopes).
Among the calculation methods, the Moore formula is most widespread:
KVP \u003d BCCd x Htd-Htf / Htd
Where KVP - blood loss (ml);
BCCd - the proper volume of circulating blood (ml).
Normally, in women, the BCC is on average 60 ml / kg, in men - 70 ml / kg, in pregnant women - 75 ml / kg;
Nd - proper hematocrit (for women - 42%, for men - 45%);
№f - 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 blood density value, but this technique is applicable only for small blood loss.
One of the first hardware methods for determining the BCC was a method based on the measurement of the basic body resistance using a rheoplethysmograph (found application in the countries of the "post-Soviet space").
Modern indicator methods provide for the establishment of the BCC by changing the concentration of the substances used and are conditionally 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 on it the total volume of blood through Ht;
3. Simultaneous determination of the volume of erythrocytes and blood plasma.
As an indicator, Evans' dye (T-1824), dextrans (polyglucin), human albumin labeled with iodine (131I) or chromium chloride (51CrCl3) are used. 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, VO2 measurements should be considered the simplest diagnostic test for 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 erythrocytes (oxygen carriers) to a level that ensures the minimum sufficient oxygen consumption in the tissues. However, most experts consider hypovolemia to be the most acute problem of blood loss, and, accordingly, in the first place in the therapy regimens, they put the replenishment of the BCC, which is a critical factor for maintaining stable hemodynamics. The pathogenetic role of a decrease in BCC in the development of severe disorders of homeostasis predetermines the importance of timely and adequate correction of volemic disorders on the outcomes of treatment in patients with acute massive blood loss. The ultimate goal of all efforts of the resuscitator is to maintain adequate tissue oxygen consumption to maintain metabolism.
General principles treatment of acute blood loss is as follows:
1. Stopping bleeding, fighting pain.
2. Ensuring adequate gas exchange.
3. Replenishment of the BCC deficit.
4. Treatment of organ dysfunction and prevention of multiple organ failure:
Heart failure treatment;
Prevention of renal failure;
Correction of metabolic acidosis;
Stabilization metabolic processes in a cage;
Treatment and prevention of DIC syndrome.
5. Early prevention of infection.
Stopping bleeding and managing pain.
For any bleeding, it is important to eliminate the source as soon as possible. For external bleeding - pressing the vessel, pressing bandage, tourniquet, ligature or clamp on the bleeding vessel. With internal bleeding - urgent surgery, carried out in parallel with therapeutic measures to remove the patient from shock.
Table 5 presents data on the nature of the infusion therapy for acute blood loss.
| Minimum | Average | Means. | Heavy. | Arrays | |
| AD sis. | 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 |
| Blood flow, ml. | Up to 500 | 500–1000 | 1000–1500 | 1500–2500 | ›2500 ml |
| V blood. (ml / kg) | 8–10 | 10–20 | 20–30 | 30–35 | ›35 |
| % BCC loss | \u003cten | 10–20 | 20–40 | ›40 | \u003efifty |
| V infusion (in% of loss) | 100 | 130 | 150 | 200 | 250 |
| Gemotr. (% 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. Blood transfusion - with a decrease in Hb less than 70 g / l, Ht less than 25%.
2. The infusion rate for massive blood loss is 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 syndrome, protection from mental stress is carried out by intravenous (iv) administration of analgesics: 1-2 ml of 1% morphine hydrochloride solution, 1-2 ml of 1-2% solution of promedol, as well as sodium oxybutyrate (20-40 mg / kg body weight), sibazone (5–10 mg), it is possible to use sub-drug doses of calypsol and sedation with propofol. The dose of narcotic analgesics should be reduced by 50% because of the possible respiratory depression, nausea and vomiting that occur with intravenous administration of these drugs. In addition, it should be remembered that their introduction is possible only after excluding damage 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 preventive 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.providing passability respiratory tract;
2. prevention of aspiration of stomach contents;
3. the release of the respiratory tract from phlegm;
4. ventilation of the lungs;
5. restoration of tissue oxygenation.
The developed hypoxemia may be due to:
1.hypoventilation (usually in combination with hypercapnia);
2.the mismatch between ventilation of the lungs and their perfusion (disappears with breathing pure oxygen);
3. intrapulmonary blood shunting (guarded when breathing pure oxygen) caused by adult respiratory distress syndrome (PaO2 \u003c60-70 mm Hg FiO2\u003e 50%, bilateral pulmonary infiltrates, normal pressure filling the ventricles), pulmonary edema, severe pneumonia;
4. violation of the diffusion of gases through the alveolo - capillary membrane (disappears when breathing pure oxygen).
Ventilation of the lungs, carried out after tracheal intubation, is carried out in specially selected modes that create conditions for optimal gas exchange and do not violate central hemodynamics.
Replenishment of the BCC deficit
First of all, in case of acute blood loss, the patient should create an improved Trendeleburg position to increase venous return. Infusion is carried out simultaneously in 2-3 peripheral or 1-2 central veins. The rate of blood loss replacement is determined by the value of blood pressure. As a rule, the first infusion is carried out in a stream or quickly 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 NaCl solutions.
Hypertonic sodium chloride solutions (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 h) and relatively small volumes of administration (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 anti-shock action are subdivided into natural (albumin, plasma) and artificial (dextrans, hydroxy-ethyl starches). Plasma albumin and protein fraction effectively increase the volume of intravascular fluid, because have high oncotic pressure. However, they readily 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 diffusion volume 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 first choice" are solutions of hydroxyethyl starch. Hydroxyethyl starch is a natural polysaccharide derived from amylopectin starch and composed of high molecular weight polarized glucose residues. The starting material for HES production is starch from potato and tapioca tubers, grain different varieties corn, wheat, rice.
HES from potatoes and corn, along with linear amylase chains, contains a branched amylopectin fraction. Hydroxylation of starch prevents its rapid enzymatic degradation, increases the ability to retain water and increase colloidal osmotic pressure. In transfusion therapy, 3%, 6% and 10% HES solutions are used. The introduction of HES solutions causes isovolemic (up to 100% when administered with a 6% solution) or even initially hypervolemic (up to 145% of the injected volume of a 10% drug solution) volume-replacing effect, which lasts for at least 4 hours.
In addition, HES solutions have the following properties that are absent in other colloidal plasma replacing drugs:
1. Prevent the development of the syndrome of increased capillary permeability by closing the pores in their walls;
2. modulate the action of circulating adhesive molecules or inflammatory mediators, which, circulating in the blood in critical conditions, increase secondary tissue damage by binding to neutrophils or endothelial cells;
3. do not affect the expression of blood surface antigens, that is, 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, separate randomized studies have appeared. high level 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), which form the basis of a new generation of plasma substitutes with the O2 transfer function, began to be actively studied, one of which is perfluoran. The use of the latter in acute blood loss makes it possible to influence the reserves of the three levels of O2 metabolism, and the simultaneous use of oxygen therapy can also increase the ventilation reserves.
Table 6. The share of perfluorane use depending on the level of blood substitution
| Blood replacement rate | The amount of blood loss | Total transfusion volume (% of blood loss) | Perftoran dose |
| 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 decrease in hypovolemia reflects the following symptoms:
1.increase in blood pressure;
2. decrease in heart rate;
3. warming and pinking of the skin; -increased 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 proper 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, it will usually quickly and effectively compensate for the BCC deficit. If the victim has a history of chronic heart or vascular diseases, then hypovolemia and hypoxia aggravate the course of the underlying disease, therefore they carry out special treatment... First of all, it is necessary to achieve an increase in preload, which is achieved by increasing the BCC, and then to enhance myocardial contractility. Most often, vasoactive and inotropic drugs are not prescribed, but if the hypotension becomes persistent, not amenable to infusion therapy, then these drugs can be used. Moreover, their use is possible only after full reimbursement of the BCC. Of the vasoactive drugs, 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 selected depending on the desired effect:
1. 2-5 mcg / kg / min ("renal" dose) dilates the mesenteric and renal vessels without increasing heart rate and blood pressure;
2. 5-10 μg / kg / min gives a pronounced ionotropic effect, mild vasodilation due to stimulation of β2 - adrenergic receptors, or moderate tachycardia;
3. 10–20 μg / kg / min leads to a further enhancement of the ionotropic effect, pronounced tachycardia.
More than 20 μg / kg / min - a sharp tachycardia with a threat of tachyarrhythmias, narrowing of veins and arteries due to stimulation of a1_ adrenergic receptors and impairment of tissue perfusion. Acute renal failure (ARF) usually develops as a result of arterial hypotension and shock. In order to prevent the development of the oliguric form of acute renal failure, it is necessary to control the hourly urine output (normally in adults it 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, the glomerular filtration rate is below 30 ml / min).
Dopamine infusion at a "renal" dose. Currently, there are no randomized multicenter studies in the literature demonstrating the effectiveness of the use of "renal doses" of sympathomimetics.
Stimulation of diuresis against the background of restoration of the BCC (CVP more than 30-40 cm of water column) and satisfactory cardiac output (furosemide, i.v. in an initial dose of 40 mg, with an increase of 5-6 times if necessary).
Normalization of hemodynamics and replacement of the circulating blood volume (BCC) should be carried out under the control of DZLK (pulmonary capillary jamming pressure), SV (cardiac output) and OPSS. In case of shock, the first two indicators progressively decrease and the last one rises. The 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 case of severe metabolic acidosis (venous blood pH is below 7.25), calculating it according to the generally accepted formula, after determining the acid base balance.
Bolus can be administered immediately 44–88 meq (50–100 ml of 7.5% HCO3), the rest within the next 4–36 hours. It should be remembered that the excessive introduction of sodium bicarbonate creates the prerequisites for the development of metabolic alkalosis, hypokalemia, arrhythmias. A sharp increase in plasma osmolarity is possible, up to the development of hyperosmolar coma. In shock, accompanied by a critical deterioration of hemodynamics, it is necessary to stabilize metabolic processes in the cell. Treatment and prevention of disseminated intravascular coagulation, as well as early prevention infections are carried out in accordance with generally accepted schemes.
Justified, from our point of view, is the pathophysiological approach to solving the problem of indications for blood transfusion, 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 hypovolemia is replenished with colloidal 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 increases compensatory (sometimes exceeding normal values \u200b\u200bby 1.5–2 times), microcirculation "opens" 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 at a low oxygen capacity of the blood.
Have healthy people normovolemic hemodilution with a hemoglobin level of 30 g / l and a hematocrit of 17%, although it is accompanied by a decrease in oxygen transport, oxygen consumption by tissues does not decrease, the level of blood lactate does not increase, which confirms the sufficiency of oxygen supply to the body and the maintenance of metabolic processes at a sufficient level. In acute isovolemic anemia up to hemoglobin (50 g / l), in patients at rest, tissue hypoxia is not observed before the operation. Oxygen consumption does not decrease, and even slightly increases, the level of blood lactate does not increase. With normovolemia, oxygen consumption does not suffer at a delivery level of 330 ml / min / m2; with a lower delivery, there is a dependence of consumption on oxygen delivery, which corresponds approximately to a hemoglobin level of 45 g / l with normal cardiac output.
An increase in the oxygen capacity of blood by transfusion of preserved blood and its components has its negative aspects. First, an increase in hematocrit leads to an increase in blood viscosity and a deterioration in microcirculation, creates an additional load on the myocardium. Secondly, the low content of 2,3-DPG in erythrocytes donated blood accompanied by an increase in the affinity of oxygen to hemoglobin, a shift in the oxyhemoglobin dissociation curve to the left and, as a result, a deterioration in tissue oxygenation. Thirdly, in the transfused blood there are always microclots that can "clog" the capillaries of the lungs and dramatically increase the pulmonary shunt, impairing blood oxygenation. In addition, the 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 correcting blood loss and posthemorrhagic anemia is not a settled issue. This is mainly due to the lack of informative criteria for evaluating the optimality of certain methods of compensation for transport and oxygen consumption. Modern trend to 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 transfusion 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 less than 60% within a short period of time leads to the appearance of metabolic signs of tissue oxygen debt (lactic acidosis, etc.). Therefore, an increase in blood lactate content can be a biochemical marker of the degree of activation of anaerobic metabolism and characterize the effectiveness of the therapy.
Acute blood loss causes a deep restructuring of blood circulation in the body and puts into action the most complex mechanisms for compensating for disturbed homeostasis. Clinical and pathological changes, regardless of the localization of the source of bleeding, are characterized by general manifestations. The starting link in the development of these disorders is an increasing decrease in the BCC (circulating blood volume). Acute blood loss is dangerous primarily by the development of circulatory and hemodynamic disorders that pose an immediate threat to life. In other words, in acute, especially massive, blood loss, the human body suffers not so much from a decrease in the number of erythrocytes and hemoglobin, but from a decrease in the BCC and hypovolemia.
Every person reacts differently to losing the same blood volume. If blood loss in a healthy adult reaches 10% of the BCC, which is an average of 500 ml, it does not lead to pronounced changes in hemodynamics. In chronic inflammatory processes, violations of the water-electrolyte balance, intoxication, hypoproteinemia, the same blood loss should be replenished with plasma substitutes and blood.
The nature and dynamics of the clinical manifestations of acute blood loss depend on various factors: the volume and rate of blood loss, age, initial state of the body, the presence of a chronic disease, the season (in the hot season, blood loss is worse tolerated), etc. Children and the elderly are more difficult to tolerate acute blood loss , as well as pregnant women suffering from toxicosis. The body's response to acute blood loss is determined in each individual case by the degree of self-regulation of functional systems on the basis of the "golden rule of the norm" formulated by academician L. K. Anokhin, according to which any deviation of any factor from the vital level serves as an impetus for the immediate mobilization of numerous apparatus of the corresponding functional systems that restore this important adaptive result again (Wagner E.A. et al., 1986).
V.A.Klimansky and L.A. Rudaev (1984) distinguish three degrees of blood loss:
Acute blood loss of 25% of the BCC is compensated for by a healthy body as a result of the inclusion of self-regulation mechanisms: hemodilution, blood redistribution and other factors.
The unification of various organs into functional systems with a beneficial result for the body always occurs according to the principle of self-regulation. Self-regulation is the main principle of the duration of functional systems.
Acute blood loss of 30% BCC leads to severe circulatory disorders, which, with timely assistance, consisting in stopping bleeding and intensive infusion-transfusion therapy, can normalize the patient's condition.
Deep circulatory disorders develop with acute blood loss of 40% of the volume of the BCC and more, are characterized by clinical picture hemorrhagic shock.
The condition of patients with acute blood loss can be different. Most patients with mechanical trauma in the presence of associated injuries are admitted in serious condition and need urgent treatment.
When assessing the general condition of patients with acute blood loss, one should take into account the anatomical localization of the injury. The degree and nature of clinical manifestations depend on which tissues and organs are damaged. Severe closed injuries of the limbs, chest wall, back and lumbar region may be accompanied by extensive hemorrhages into the subcutaneous tissue. Internal injuries are associated with bleeding in serous cavities and the lumen of the hollow organs.
The consequence of chest trauma can be hemothorax, often reaching a volume of 1–2 liters. With fractures of long bones, back bruises and fractures of the pelvic bones in the muscles, in the subcutaneous fatty tissue, in the retroperitoneal space, hematomas are formed. Closed damage to the liver and spleen, as a rule, are accompanied by massive internal blood loss.
The initial state can largely determine the resistance to blood loss. The statement that blood loss not exceeding 10-15% of the BCC is safe is valid only for people with a normal initial state. If hypovolemia has already taken place at the time of blood loss, then even slight bleeding can cause serious consequences.
Cachexia, purulent intoxication, prolonged bed rest, previous minor bleeding - all this creates a dangerous background against which new bleeding entails more severe consequences than usual. The elderly are characterized by chronic hypovolemia in combination with poor adaptive capacity of the vascular bed due to morphological changes in the walls of blood vessels. This increases the danger of even a small amount of blood loss due to disturbances in the functioning of functional self-regulation systems, in particular, the so-called "internal link of self-regulation".
Good known symptoms The triads of acute massive blood loss — low blood pressure, rapid, threadlike pulse, and cold, moist skin — are the main, but not the only, signs of a critical condition. Confusion, dry mouth and thirst, dilated pupils, and increased breathing are often observed. However, it should be borne in mind that when assessing the severity of a patient's condition with massive blood loss clinical signs it may appear to varying degrees, and some may even be absent. Determination of the clinical picture in acute blood loss should be comprehensive and include an assessment of the state of the central nervous system, skin and mucous membranes, determination of blood pressure, pulse rate, volume of blood loss, hematocrit value, hemoglobin content, number of erythrocytes, platelets, fibrinogen, blood clotting, hourly (minute ) diuresis.
Changes in the central nervous system (CNS) depend on the initial state of the patient and the amount of blood loss. With moderate blood loss (no more than 25% of the BCC) in a practically healthy person who does not suffer from a chronic somatic disease, consciousness may be clear. In some cases, patients are agitated.
With a large blood loss (30-40% of the BCC), consciousness is preserved, in a number of patients drowsiness and indifference to the environment are observed. Most often, patients complain of thirst.
Massive blood loss (over 40% of the BCC) is accompanied by significant depression of the central nervous system: weakness, apathy, and the development of hypoxic coma is possible. If the patients are conscious, they are drowsy and constantly ask for a drink.
Skin color, moisture and temperature are simple but important indicators of the patient's condition and, in particular, the nature of peripheral blood flow. Warm pink skin indicates normal peripheral circulation, even if blood pressure is low. Cold pale skin, pale nails suggest a pronounced peripheral arterial and venous spasm. Such a violation or partial cessation of blood supply to the skin, subcutaneous adipose tissue in response to a decrease in BCC is a consequence of the restructuring of blood circulation in order to maintain blood flow in vital organs - "centralization" of blood circulation. The skin is cold to the touch, may be damp or dry. The peripheral veins in the arms and legs are narrowed. After pressing on the nail, the capillaries of the nail bed are slowly filled with blood, which indicates a violation of microcirculation.
With deep circulatory disorders - hemorrhagic shock and "decentralization" of blood circulation - the skin becomes marbled or bluish-grayish. Its temperature is dropping. After pressing on the nail, the capillaries of the nail bed fill up very slowly.
Heart rate. A decrease in the BCC and a decrease in venous return of blood to the heart lead to excitation of the sympathetic-adrenal system and, at the same time, to inhibition of the vagal center, which is accompanied by tachycardia.
Stimulation of the alpha receptors of the sympathetic nervous system leads to arterial vasoconstriction of the vessels of the skin and kidneys. Vasoconstriction allows blood flow to vital organs (“centralization” of circulation), such as the heart and brain, that cannot tolerate inadequate blood flow for more than a few minutes. If peripheral vasoconstriction is excessive or prolonged, then the violation of tissue perfusion leads to the release of lysosomal enzymes and vasoactive substances, which themselves significantly aggravate circulatory disorders.
With massive blood loss, the pulse rate usually rises to 120–130 beats per minute, and sometimes to large values \u200b\u200bdue to stimulation of the sympathetic nervous system. This ensures that cardiac output is maintained while the volume of blood is reduced. However, if the heart rate exceeds 150 per minute, then cardiac output decreases, the duration of diastole decreases, coronary blood flow and ventricular filling decrease.
Tachycardia is an uneconomical mode of operation of the heart. An increase in heart rate up to 120–130 per minute or more in acute blood loss is a reason for concern and indicates an uncompensated BCC deficiency, ongoing vascular spasm and insufficient infusion therapy. Taking into account arterial and central venous pressure, skin color and temperature, hourly diuresis, it is necessary to establish whether tachycardia is a consequence of hypovolemia and insufficiently replenished BCC. If this is the case, then the source of bleeding should be sought, eliminated, and infusion-transfusion therapy should be intensified.
Therefore, a change in heart rate in acute blood loss is an important clinical sign. Its greatest value is manifested during dynamic observation, then this indicator reflects the clinic and the result of treatment.
In acute blood loss, a compensatory decrease in the capacity of the vascular bed is provided by vasoconstriction of arterioles and narrowing of large veins. Venous vasoconstriction is one of the most important compensatory mechanisms that allows patients to tolerate a BCC deficit of up to 25% without developing arterial hypotension.
In patients with acute blood loss or severe trauma, if narcotic analgesics, especially morphine, are administered to relieve pain, blood pressure suddenly drops. This is most often observed in patients with unstable hypovolemia, when blood pressure is maintained at a relatively normal level by vasoconstriction, which is reduced or removed by narcotic analgesics and vasodilators. They not only affect the vasoconstriction of arterioles, but also promote venous dilatation and can increase the vascular capacity to 1–2 liters or more, causing relative hypovolemia. Therefore, before introducing narcotic analgesics, a patient with trauma and blood loss needs to restore the BCC and normalize hemodynamics. A decrease in blood pressure in response to the administration of narcotic analgesics indicates persistent hypovolemia.
The functional state of self-regulation mechanisms can mutually affect the ability to compensate for hypovolemia.
The reaction to acute blood loss occurs very quickly - a few minutes after the onset of bleeding, signs of sympathetic-adrenal activation develop. The content of catecholamines, pituitary and adrenal hormones is increased, and many clinical symptoms hemorrhagic shock are signs of increased activation of the sympathetic-adrenal system in response to blood loss.
Blood pressure is an integral indicator of systemic blood flow. Its level depends on the BCC, peripheral vascular resistance and heart function. With the centralization of blood circulation, spasm of peripheral vessels and an increase in cardiac output can compensate for a decrease in BCC, blood pressure can be normal or even elevated, that is, normal blood pressure is maintained by cardiac output and vascular resistance. With a decrease in cardiac output due to a decrease in vascular volume, blood pressure remains normal as long as a high peripheral vascular resistance remains, which compensates for the decrease in cardiac output. Moderate hypovolemia (15–20% BCC), especially in the supine position, may not be accompanied by a decrease in blood pressure.
Blood pressure can remain normal until the decrease in cardiac output or loss of blood volume is so great that the adaptive mechanisms of homeostasis can no longer compensate for the reduced volume. As the BCC deficiency increases, progressive arterial hypotension develops. It is more correct to consider the level of arterial pressure in acute blood loss as an indicator of the organism's compensatory capabilities. Blood pressure reflects the state of blood flow in large vessels, but not hemodynamics in general. In addition, low blood pressure does not necessarily indicate insufficient tissue blood flow.
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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 medical institutions of the military district (medb, garrison hospital).
Hemorrhages are classified according to the time of their onset, the nature and caliber of the damaged blood vessels and the place of bleeding.
Distinguish primary and secondary bleeding. Primary bleeding occurs immediately after injury or in the next few hours after it (weakening of the pressing bandage, release of blood coagulum from the wound of the vessel during the transfer of the wounded, displacement of bone fragments, increased blood pressure). Among secondary bleeding, early and late are distinguished. Early secondary bleeding occurs before a thrombus is organized. They appear on the 3-5th day after injury and are associated with the emergence of a loose clotting clot from the wound (unsatisfactory immobilization, tremors during transportation, manipulations in the wound during dressing).
Late secondary bleeding occurs after the organization (growth of granulation tissue) thrombus. They are associated with an infectious process in a wound, melting of a blood clot, suppuration of a hematoma, sequestration of a 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 blotting of the bandage with blood (the so-called signal bleeding), and the detection of vascular murmurs during auscultation of the wound circumference. Secondary bleeding can stop on its own; but they threaten to relapse.
Classification of bleeding
By causal factor: trauma, injury, pathological process. By the timing of occurrence: primary, secondary, single, repeated, early, later.
By type of damaged vessel: arterial, venous, arteriovenous capillary (parenchymal).
At the site of blood effusion: external, internal, interstitial, combined. According to the state of hemostasis: continuing, stopped. Depending on the place of bleeding, bleeding is distinguished external, internal and interstitial. Internal (latent) bleeding can occur in anatomical body cavities and internal organs (lung, stomach, intestine, bladder). Intra-tissue 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.
Bloodsuckerfromerra - this is a state of the organism that arises 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, allowing to differentiate the symptoms caused by the actual loss of blood, with other manifestations (consequences of trauma, disease process, etc.). The peculiarities of each separate type of blood loss are considered in the private sections of surgery.
Blood loss is classified both by size and by the 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 caused by the amount of lost circulating blood volume (BCC).
The amount of blood loss is considered from the standpoint of reducing the amount of fluid filling the bloodstream; loss of red blood cells, which are oxygen carriers; loss of plasma, which is of decisive importance in tissue metabolism.
The primary factor 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 activation of the body's defense mechanisms, due to which compensation of blood loss can occur. Compensation results from the movement of extracellular fluid into the vascular bed (hemodilution); increased lymph flow; regulation of vascular tone, known as “centralization of blood circulation”; increased heart rate; increasing the extraction of oxygen in tissues. Compensation of blood loss is carried out the easier, the less blood is lost and the slower it flows. At the same time, in case of violation of compensation and even more in case of decompensation, blood loss turns into hemorrhagic shock, which is determined by the main causal factor.
The so-called death threshold is not determined by the amount of bleeding, but by the number of red blood cells remaining in the circulation. This critical reserve is equal to 30% of the volume of red blood cells and only 70% of the volume of plasma. The body can survive with a loss of 2/3 of the volume of red blood cells, but will not tolerate the loss of 1/3 of the volume of plasma. This consideration of blood loss makes it possible to more fully take into account the compensatory processes in the body.
Is an irreversible loss of blood in a short time. It occurs due to bleeding from damaged vessels. Affects the state of all organs and systems. The loss of a significant volume of blood is accompanied by the development of hemorrhagic shock, which poses a threat to the patient's life. Trauma and some diseases can cause acute blood loss. Manifested by pallor, tachycardia, decreased blood pressure, shortness of breath, euphoria, or depression of consciousness. Treatment - elimination of the source of bleeding, infusion of blood and blood substitutes.
ICD-10
D62 Acute post-hemorrhagic anemia
General information
Acute blood loss is a condition in which the body quickly and irreversibly loses a certain amount of blood as a result of bleeding. It is the most common injury to the human body throughout history. It occurs with injuries (both open and closed) and destruction of the vessel wall in some diseases (for example, ulcerative processes in the gastrointestinal tract). The loss of a large volume of blood is life-threatening due to a sharp decrease in the BCC and the subsequent development of hypoxia, hypoxemia, hypotension, insufficient blood supply to internal organs and metabolic acidosis. In severe cases, the development of DIC syndrome is also possible.
The greater the volume of blood loss and the faster the blood is poured out, the more severe the patient's condition and the worse the prognosis. In addition, factors such as age, general condition of the body, intoxication, chronic diseases and even the season (in the warm season, blood loss is more difficult to tolerate) affect the body's response. The loss of 500 ml (10% BCC) in a healthy adult does not lead to significant hemodynamic disturbances and does not require special correction. With a loss of similar volume by a patient suffering from chronic disease, it is necessary to replenish the BCC with the use of blood, blood and plasma substitutes. This condition is most difficult for the elderly, children and pregnant women suffering from toxicosis.
Causes
The most common causes are injuries: wounds of soft tissues and internal organs, multiple fractures or damage to large bones (for example, a severe fracture of the pelvis). In addition, acute blood loss can occur as a result of blunt trauma with rupture of an organ. Especially dangerous are wounds with damage to large vessels, as well as injuries and ruptures of parenchymal organs. Among the diseases that can cause blood loss are stomach and duodenal ulcers, Mallory-Weiss syndrome, cirrhosis of the liver, accompanied by varicose veins of the esophagus, malignant tumors Gastrointestinal tract and organs chest, gangrene of the lung, pulmonary infarction and other diseases in which the destruction of the vessel wall is possible.
Pathogenesis
In acute blood loss of a mild degree, the receptors of the veins are irritated, as a result of which a persistent and total venous spasm occurs. There are no significant hemodynamic disturbances. Replenishment of the BCC in healthy people occurs within 2-3 days due to the activation of hematopoiesis. If more than 1 liter is lost, not only the venous receptors are irritated, but also the alpha receptors of the arteries. This causes excitation of the sympathetic nervous system and stimulates the neurohumoral response - the release of a large amount of catecholamines by the adrenal cortex. At the same time, the amount of adrenaline exceeds the norm by 50-100 times, the amount of norepinephrine - 5-10 times.
Under the influence of catecholamines, first the capillaries, and then the larger vessels, spasm. The contractile function of the myocardium is stimulated, tachycardia occurs. The liver and spleen contract, ejecting blood from the depot into the vascular bed. Arteriovenous shunts open in the lungs. All of the above makes it possible to provide vital organs with the necessary amount of blood for 2-3 hours, maintain blood pressure and hemoglobin levels. Subsequently, the neuro-reflex mechanisms are depleted, vasodilation comes to replace angiospasm. The blood flow in all vessels decreases, and erythrocyte stasis occurs. Metabolic processes in tissues are even more disturbed, metabolic acidosis develops. All of the above forms a picture of hypovolemia and hemorrhagic shock.
The severity of hemorrhagic shock is determined taking into account the pulse, blood pressure, urine output and laboratory parameters (hematocrit and hemoglobin content in the blood). Under the influence of aldosterone, arteriovenous shunts are opened in the kidneys, as a result the blood is "dumped" without passing through the juxtaglomerular apparatus, which leads to a sharp decrease in urine output up to anuria. Due to hormonal changes, plasma does not leave the vessels into the interstitial tissues, which, along with the deterioration of microcirculation, further aggravates tissue metabolism disorders, aggravates acidosis and provokes the development of multiple organ failure.
The listed violations cannot be completely stopped even with immediate replacement of blood loss. After the restoration of the BCC, a decrease in blood pressure persists for 3-6 hours, impaired blood flow in the lungs - within 1-2 hours, impaired blood flow in the kidneys - within 3-9 hours. Microcirculation in tissues is restored only in 4-7 days, and complete elimination of the consequences takes many weeks.
Classification
There are several systematizations of acute blood loss. The following classification is most widely used in clinical practice:
- Mild degree - loss of up to 1 liter (10-20% BCC).
- The average degree is a loss of up to 1.5 liters (20-30% BCC).
- Severe - loss of up to 2 liters (40% BCC).
- Massive blood loss - loss of more than 2 liters (more than 40% of the BCC).
In addition, there is a supermassive or fatal blood loss, in which the patient loses over 50% of the BCC. With such acute blood loss, even in the case of immediate volume replacement, in the vast majority of cases, irreversible changes in homeostasis develop.
Symptoms of acute blood loss
Symptoms of this condition include sudden weakness, increased heart rate, decreased blood pressure, pallor, thirst, dizziness, lightheadedness, and fainting. In severe cases, shortness of breath, intermittent breathing, cold sweats, loss of consciousness and marbled skin are possible. In case of traumatic injury, a bleeding wound is found or signs of severe closed damage skeleton or internal organs.
Diagnostics
Along with clinical signs, there are laboratory indicators that allow assessing the amount of blood loss. The number of erythrocytes decreases below 3x10¹² / l, hematocrit - below 0.35. However, the listed figures only indirectly indicate the degree of acute blood loss, since the test results reflect the real course of events with some "lag", that is, with massive blood loss in the first hours, the tests may remain normal. This is especially common in children.
Considering the above, as well as the nonspecificity of signs of acute blood loss (especially mild or moderate), it is necessary to pay special attention to external signs. With external bleeding, establishing the fact of blood loss is not difficult. With anesthesiologists and resuscitators. Treatment tactics depend on the amount of blood lost and the patient's condition. With a loss of up to 500 ml, special measures are not required, the restoration of the BCC occurs independently. With a loss of up to 1 liter, the issue of volume replenishment is resolved differentially. With tachycardia no more than 100 beats / min, normal blood pressure and diuresis, infusions are not indicated, in case of violation of these indicators, plasma substitutes are transfused: saline, glucose and dextran. Decrease in blood pressure below 90 mm Hg. Art is an indication for drip infusion of colloidal solutions. With a decrease in blood pressure below 70 mm Hg. Art. produce jet transfusions.
With an average degree (up to 1.5 liters), transfusion of plasma substitutes is required in a volume that is 2-3 times higher than the amount of BCC loss. In addition, transfusion of 500-1000 ml of blood is recommended. In severe cases, transfusion of blood and plasma substitutes is necessary in a volume that is 3-4 times higher than the amount of BCC loss. With massive blood loss, it is required to transfuse 2-3 volumes of blood and several volumes of plasma substitutes.
Criteria for adequate recovery of BCC: pulse no more than 90 beats / min, stable blood pressure 100/70 mm Hg. Art., hemoglobin 110 g / l, CVP 4-6 cm. water. Art. and diuresis more than 60 ml / h. At the same time, one of the most important indicators is diuresis. Recovery of urine flow within 12 hours from the onset of blood loss is one of the primary tasks, since otherwise the renal tubules become necrotic and irreversible renal failure develops. To normalize diuresis use infusion therapy in combination with stimulation with furosemide and euphyllin.
Bleeding (haemorragia: syn. hemorrhage) - in vivo bleeding from a blood vessel in case of damage or violation of the permeability of its wall.
Classification of bleeding
Depending on the symptom underlying the classification, the following types of bleeding are distinguished:
I. Due to the occurrence:
one). Mechanical bleeding (h. per rhexin) - bleeding caused by a violation of the integrity of blood vessels during trauma, including combat damage or surgery.
2). Arrosive bleeding (h. per diabrosin) - bleeding that occurs when the integrity of the vessel wall is violated due to the growth of the tumor and its decay, with the destruction of the vessel by continuing ulceration with necrosis, a destructive process.
3). Diapedetic bleeding (h. per diapedesin) - bleeding that occurs without violating the integrity of the vascular wall, due to an increase in the permeability of small vessels caused by molecular and physicochemical changes in their wall, with a number of diseases (sepsis, scarlet fever, scurvy, hemorrhagic vasculitis, phosphorus poisoning and etc.).
The possibility of bleeding is determined by the state of the blood coagulation system. In this connection, they distinguish:
- fibrinolytic bleeding (h. fibrinolytica) - due to blood clotting disorders caused by an increase in its fibrinolytic activity;
- cholemic bleeding (h. cholaemica) - due to a decrease in blood clotting in cholemia.
II. By the type of bleeding vessel (anatomical classification):
one). Arterial bleeding (h. arterialis)- bleeding from a damaged artery.
2). Venous bleeding (h. venosa)- bleeding from a damaged vein.
3). Capillary bleeding (h.capillaris) - bleeding from capillaries, in which blood oozes evenly over the entire surface of damaged tissues.
4). Parenchymal bleeding (h. parenchymatosa) -capillary bleeding from the parenchyma of any internal organ.
5). Mixed bleeding (h. mixta) - bleeding occurring simultaneously from arteries, veins and capillaries.
III. In relation to the external environment and taking into account clinical manifestations:
one). External bleeding (h. extema) - bleeding from a wound or ulcer directly to the surface of the body.
2). Internal bleeding (h.intema) - bleeding into tissues, organs or body cavities.
3). Hidden bleeding (h. occuta) - bleeding without pronounced clinical manifestations.
In turn, internal bleeding can be divided into:
a) Internal cavity bleeding (h. cavalis) - bleeding into the abdominal, pleural or pericardial cavity, as well as into the joint cavity.
b) Intra-tissue bleeding (h. interstitialis) - bleeding into the thickness of tissues with their diffuse imbibition, stratification and hematoma formation.
The accumulation of blood poured out of a vessel in the tissues or cavities of the body is called hemorrhage (haemorragia).
Ecchymosis (ecchymosis) - extensive hemorrhage in the skin or mucous membrane.
Petechia (petechia, syn. hemorrhage point) - a spot on the skin or mucous membrane with a diameter of 1-2 mm, caused by capillary bleeding.
Vibices (vibices, syn. purple linear spots) - hemorrhagic spots in the form of stripes.
Bruise (suffusio, syn. bruise) - hemorrhage in the thickness of the skin or mucous membrane.
Hematoma (haematoma, syn. bloody tumor) - a limited accumulation of blood in the tissues with the formation of a cavity in them containing liquid or clotted blood.
Bleeding is always a serious threat to the victim's life. This is due to the fact that a sufficient volume of circulating blood (BCC) is a necessary condition for blood circulation. In turn, the adequacy of blood circulation is a necessary condition for maintaining the vital activity of the human body, since its violation leads to the loss of all those diverse and complex functions that blood performs.
A certain amount of blood circulates in the human bloodstream, depending on the person's body weight and age (on average, from 2.5 to 5 liters). One of the main tasks of surgery is to stop bleeding.
Bleeding is the flow of blood from blood vessels when their integrity or permeability is violated.
Hemorrhage is the outflow of blood from damaged vessels into the tissue or cavity of the body.
Bleeding of any origin requires urgent action to stop it.
shock bleeding vessel ligation
Classification of bleeding
I. Due to the occurrence:
- 1. Traumatic - occur when mechanical damage blood vessel as a result of injury.
- 2. Pathological - arise as a result of any disease (non-traumatic).
- a) arrosin bleeding - occurs as a result of erosion of the vascular wall of any pathological process.
For example: ulcer, suppuration, tumor decay.
b) neurotrophic bleeding - develops as a result of malnutrition of the vascular wall or metabolic disorders in it.
For example: bedsores, measles, rubella, scarlet fever, scurvy - vitamin C deficiency and others.
c) hypocoagulant bleeding - caused by impaired blood coagulation processes.
For example: hemophilia, Werlhof's disease, cirrhosis of the liver, disseminated intravascular coagulation syndrome, overdose of anticoagulants.
II. By the type of a bleeding vessel:
- 1. Arterial bleeding - the outflow of blood from a damaged artery - is characterized by a massive release of bright red blood in the form of a fountain, it flows out quickly, in a pulsating stream. The blood color is bright red due to oxygen saturation. If large arteries or the aorta are damaged, most of the circulating blood can flow out within a few minutes, blood loss will be incompatible with life.
- 2. Venous bleeding - bleeding from a damaged vein - is characterized by a slow flow of blood of dark cherry color. It is characterized by a continuous flow of blood stream from the damaged vessel due to low pressure in the veins and is not threatening to the victim's life. The exception is the large veins of the chest and abdominal cavity. Injuries to the large veins in the neck and chest are dangerous due to the potential for air embolism.
- 3. Capillary bleeding - the outflow of blood from the smallest blood vessels - capillaries. Such bleeding is observed with shallow cuts and abrasions of the skin, muscles, mucous membranes, bones. This bleeding usually stops on its own. Its duration increases significantly with reduced blood clotting.
- 4. Parenchymal - bleeding with damage to the parenchymal organs - liver, spleen, kidneys and lung. These bleeding are similar to capillary, but more dangerous than them, since the vessels of these organs do not collapse due to anatomical structure the stroma of the organ, profuse bleeding occurs, in which urgent help is needed.
- 5. Mixed bleeding - this bleeding combines the symptoms of two or more of the above.
III. In connection with the external environment.
- 1. External bleeding - blood is poured directly into the external environment, onto the surface of the human body through a defect in his skin.
- 2. Internal bleeding - the most diverse in nature and complex in the diagnostic and tactical terms. Blood is poured into the lumen of hollow organs, into tissues or into the internal cavities of the body. They are dangerous by compression of vital organs. Internal bleeding is divided into:
- a) obvious internal bleeding - blood is poured into the internal cavities and then out into the external environment. For example: bleeding into the lumen of the gastrointestinal tract, pulmonary, uterine, urological bleeding.
- b) latent internal bleeding - blood is poured into closed cavities that have no communication with the external environment. Bleeding in some cavities has received special names:
- - into the pleural cavity - hemothorax (hemotoraks);
- - in abdominal cavity - hemoperitoneum (hemoperitoneum);
- - into the pericardial cavity - hemopericardium;
- - into the joint cavity - hemarthrosis (hemartrosis).
A feature of bleeding into serous cavities is that fibrin is deposited on the serous integument, so the outflowing blood becomes defibrinated and usually does not clot.
Latent bleeding is characterized by the absence of obvious signs of bleeding. They can be interstitial, intestinal, intraosseous, or hemorrhages can permeate tissues (hemorrhagic infiltration takes place), or form accumulations of spilled blood in the form of a hematoma. They can be identified by special research methods.
The blood accumulated between the tissues forms artificial cavities, which are called hematomas - intermuscular hematomas, retroperitoneal hematomas, mediastinal hematomas. Very often in clinical practice, there are subcutaneous hematomas - bruises that do not entail any serious consequences.
IV. By the time of occurrence:
- 1. Primary bleeding - begins immediately after exposure to a traumatic factor.
- 2. Secondary bleeding - occurs after a certain period of time after stopping the primary bleeding and are divided into:
- a) secondary early bleeding - occur from several hours to 4-5 days after stopping the primary bleeding, as a result of slipping of the ligature from the vessel or washing out of a blood clot due to an increase in blood pressure.
- b) late secondary bleeding - develops in a purulent wound as a result of erosion (arrosion) by pus of a thrombus or vascular wall after more than five days.
V. By duration:
- 1. Acute bleeding - bleeding is observed for a short period of time.
- 2. Chronic bleeding - prolonged, persistent bleeding, usually in small portions.
VI. By clinical manifestation and localization:
- - hemoptysis - hematopoietic;
- - bloody vomiting - hematemesis;
- - uterine bleeding - metrorrhagia;
- - bleeding into the urinary cavity system - hematuria;
- - bleeding into the abdominal cavity - hemoperitoneum;
- - bleeding into the lumen of the gastrointestinal tract - tarry stools - chalky;
- - nosebleeds - epistoxis.
VII. According to the severity of blood loss:
- 1. I degree - mild - blood loss is 500 - 700 ml. blood (BCC decreases by 10-12%);
- 2. II degree - medium - blood loss is 1000-1500 ml. blood (BCC decreases by 15-20%);
- 3. III degree - severe - blood loss is 1500-2000 ml. blood (BCC decreases by 20-30%);
- 4. IV degree - blood loss is more than 2000 ml. blood (BCC decreases by more than 30%).
- 3. Clinical manifestations of bleeding
The manifestation of symptoms and their severity depend on the intensity of bleeding, the magnitude and rate of blood loss.
Subjective symptoms appear with significant blood loss, but they can also be with a relatively small blood loss, which occurred quickly, simultaneously.
Affected people complain about: increasing general weakness, dizziness, tinnitus, darkening in the eyes and flashing "flies" before the eyes, headache and pain in the heart, dry mouth, thirst, choking, nausea.
Such complaints of the victim are the result of circulatory disorders of the brain and internal organs.
Objective symptoms can be detected when examining the victim: drowsiness and lethargy, sometimes there is some excitement, pallor of the skin and mucous membranes, frequent pulse of weak filling, rapid breathing (shortness of breath), in severe cases, Cheyne-Stokes breathing, decreased arterial and venous pressure, loss consciousness. Local symptoms vary. With external bleeding, local symptoms are bright and easily identified. With internal bleeding, they are less pronounced and sometimes difficult to determine.
There are three degrees of blood loss:
Mild blood loss - heart rate - 90-100 beats per minute, blood pressure - 110/70 mm. rt. Art., indicators of hemoglobin and hematocrit remain unchanged, the BCC decreases by 20%.
The average degree of blood loss is pulse up to 120 - 130 beats per minute, blood pressure 90/60 mm. rt. Art., Ht-0.23.
Severe blood loss - there is a sharp pallor of the mucous membranes and skin, cyanosis of the lips, severe shortness of breath, very weak pulse, heart rate - 140-160 beats per minute, the hemoglobin level decreases to 60 g / l or more, the hemotacritis index is up to 20%, BCC decreases by 30-40%.
The body can independently compensate for the loss of blood no more than 25% of the BCC due to protective reactions, provided that the bleeding is stopped.
To assess the severity of the victim's condition and the amount of blood loss, the Altgover shock index is used - the ratio of pulse to systolic pressure (PS / BP). Normally, it is 0.5.
For example:
I degree - PS / HELL \u003d 100/100 \u003d 1 \u003d 1 liter. (BCC deficit 20%).
II degree - PS / HELL \u003d 120/80 \u003d 1.5 \u003d 1.5 liters. (BCC deficit is 30%).
III degree - PS / HELL \u003d 140/70 \u003d 2 \u003d 2L. (BCC deficit is 40%).
In addition to the severity of blood loss, clinical manifestations depend on:
- - gender (women tolerate blood loss more easily than men);
- - age (the clinic is less pronounced in middle-aged people than in children and the elderly);
- - from the initial condition of the victim (the condition worsens with initial anemia, debilitating diseases, starvation, traumatic long-term operations).
- 4. Possible complications bleeding
The most frequent complications bleeding are:
- 1. Acute anemia, which develops with blood loss from 1 to 1.5 liters.
- 2. Hemorrhagic shock, in which there are severe violations of microcirculation, respiration and multiple organ failure develops. Hemorrhagic shock requires emergency resuscitation and intensive care.
- 3. Compression of organs and tissues with outpouring blood - compression of the brain, cardiac tamponade.
- 4. Air embolismwhich can endanger the victim's life.
- 5. Coagulopathic complications - a violation in the blood coagulation system.
The outcome of bleeding is the more favorable, the earlier it is stopped.
5. The concept of hemostasis. Ways to temporarily and permanently stop bleeding
Stopping bleeding - hemostasis.
Temporary (preliminary) and final methods are used to stop bleeding.
I. Ways to temporarily stop bleeding.
Temporary stopping of bleeding is carried out in the order of emergency care to the victim at the prehospital stage and is carried out in the period necessary for taking measures to finally stop bleeding.
It is carried out with bleeding from arteries and large veins. With bleeding from small arteries, veins and capillaries, measures to temporarily stop bleeding can lead to a final one.
Temporary stopping of external bleeding is possible in the following ways:
- 1. Giving the damaged part of the body an elevated position;
- 2. Pressing the bleeding vessel in the wound with a finger;
- 3. Pressing the damaged artery above the bleeding site (over);
- 4. Pressing the bleeding vessel in the wound using a pressure bandage;
- 5. Compression of the artery by fixing the limb in the position of maximum flexion or overextension of it in the joint;
- 6. Compression of the artery by applying a tourniquet;
- 7. Applying a hemostatic forceps in the wound;
- 8. Tight packing of the wound or cavity with a dressing material.
II. Methods for the final stop of bleeding.
The final stop of bleeding is carried out by a doctor in a hospital. Almost all injured persons are subject to surgical treatment... With external bleeding, primary surgical debridement wounds.
For internal and latent external bleeding, more complex operations are performed: thoracotomy - opening pleural cavity, laparotomy - opening the abdominal cavity.
Methods for permanent control of bleeding:
With external bleeding, mainly mechanical methods of stopping are used, with internal bleeding - if no surgical intervention is performed, - physical, chemical, biological and combined.
Mechanical methods:
- 1. Bandaging the vessel in the wound. To do this, a hemostatic clamp is applied to the bleeding vessel, after which the vessel is tied up.
- 2. Ligation of the vessel along the length (Gunther's method) is used when it is impossible to find the ends of the vessel in the wound, as well as in case of secondary bleeding, when the arrosive vessel is in the inflammatory infiltrate. For this purpose, an incision is made above the site of injury, based on topographic anatomical data, an artery is detected and ligated.
- 3. Twisting the vessel, previously captured by the hemostatic clamp, then suturing and bandaging together with the surrounding tissues.
- 4. Clipping of bleeding vessels with metal braces. It is used in cases where the bleeding vessel is difficult or impossible to bandage. This method is widely used in laparoscopic and thoracoscopic operations, neurosurgery.
- 5. Artificial vascular embolization. It is used for pulmonary, gastrointestinal and cerebral bleeding.
- 6. The vascular suture can be made manually or mechanically.
- 7. Sealing of vessels. This method of hemostasis is used for bleeding from the vessels of the cancellous bone. Vascular filling is performed with a sterile paste, which is rubbed into the bleeding surface of the cancellous bone. The paste consists of 5 parts of paraffin, 5 parts of wax and 1 part of petroleum jelly.
Physical methods:
- 1. Application of hot saline solution. In case of diffuse bleeding from a bone wound, parenchymal organ, wipes moistened with hot (750C) isotonic sodium chloride solution are applied.
- 2. Local application cold. Under the influence of cold, a spasm of small blood vessels occurs, blood flow to the wound decreases, which contributes to vascular thrombosis and stops bleeding. Ice packs are applied to postoperative wound, subcutaneous hematomas, abdominal areas with gastrointestinal bleeding and give the patient pieces of ice for swallowing.
- 3. Diathermocoagulation. It is used to stop bleeding from damaged vessels of the subcutaneous fatty tissue, muscles, small vessels, parenchymal organs.
- 4. Laser photocoagulation. Focused in the form of a beam of quantum waves of electrons, laser radiation cuts tissue and simultaneously coagulates small vessels of parenchymal organs.
- 5. Cryosurgery. It is used in operations with extensive circulation. The method consists in local tissue freezing and promotes hemostasis.
Chemical methods:
The method is based on the use of vasoconstrictor and blood coagulation increasing agents.
- - Vasoconstrictor drugs - adrenaline, dopanin, pituitrin.
- - Drugs that increase blood clotting include: calcium chloride 10% -10 ml., Epsilon - aminocaproic acid, calcium gluconate, hydrogen peroxide 3%.
- - Means that reduce the permeability of the vascular wall: rutin, ascorbic acid, ascorutin, dicinone, etamsylate.
Biological methods:
- 1. Thomponade of a bleeding wound with the patient's own tissues.
- 2. Intravenous administration hemostatic agents of biological origin.
Used: transfusion of whole blood, plasma, platelet mass, fibrinogen, antihemophilic plasma, use of fibrinolysis inhibitors (contrikal, vicasol).