What is second degree hemorrhagic shock? Emergency conditions, shocks. Hypovolemic (hemorrhagic) shock. Urgent Care

A state of shock occurs when there is a sudden disruption of the usual blood circulation. This is a severe stress reaction of the body, which has failed to manage vital systems. Hemorrhagic shock causes sudden blood loss. Since blood is the main fluid that supports metabolism in cells, this type of pathology refers to hypovolemic conditions (dehydration). In ICD-10 it is regarded as “Hypovolemic shock” and is coded R57.1.

In the origin of hemorrhagic shock, it is important to exclude the slow loss of blood, even of a significant volume. It has been established that hemodynamic disturbances with a gradual loss of up to 1.5 liters do not lead to serious consequences. This is due to the inclusion of compensation mechanisms.

In conditions sudden bleeding an unsubstituted volume of 0.5 liters is accompanied by acute tissue oxygen deficiency (hypoxia).

Most often, blood loss occurs due to injuries, surgical interventions, V obstetric practice during labor in women.

What mechanisms determine the severity of shock?

In the development of pathogenesis, compensation for blood loss is important:

• state nervous regulation vascular tone;
• the ability of the heart to work under hypoxic conditions;
• blood clotting;
• conditions environment for additional oxygen supply;
• level of immunity.

It is clear that a person with chronic diseases has a much lower chance of suffering massive blood loss than a previously healthy person. The work of military doctors during the Afghan war showed how severe moderate blood loss is for healthy soldiers in high altitude conditions, where air oxygen saturation is reduced.

Rapid transportation of the wounded using armored personnel carriers and helicopters saved many soldiers

On average, a person constantly circulates about 5 liters of blood through arterial and venous vessels. At the same time, 75% is in venous system. Therefore, the subsequent reaction depends on the speed of adaptation of the veins.

A sudden loss of 1/10 of the circulating mass does not make it possible to quickly “replenish” reserves from the depot. Venous pressure drops, which leads to maximum centralization of blood circulation to support the work of the heart, lungs and brain. Tissues such as muscles, skin, and intestines are recognized by the body as “superfluous” and are turned off from the blood supply.

During systolic contraction, the ejected volume of blood is insufficient for tissues and internal organs; it only nourishes coronary arteries. In response, endocrine protection is activated in the form of increased secretion of adrenocorticotropic and antidiuretic hormones, aldosterone, and renin. This allows you to retain fluid in the body and stop the urinary function of the kidneys.

At the same time, the concentration of sodium and chlorides increases, but potassium is lost.

Increased synthesis of catecholamines is accompanied by vascular spasm in the periphery, and vascular resistance increases.

Due to circulatory hypoxia of tissues, “acidification” of the blood occurs with accumulated toxins - metabolic acidosis. It promotes an increase in the concentration of kinins, which destroy vascular walls. The liquid part of the blood enters the interstitial space, and cellular elements accumulate in the vessels, creating all the conditions for increased thrombus formation. There is a risk of irreversible disseminated intravascular coagulation (DIC syndrome).

The heart tries to compensate for the necessary output by increasing contractions (tachycardia), but there are not enough of them. Potassium loss reduces myocardial contractility and heart failure develops. Blood pressure drops sharply.

Replenishment of circulating blood volume can prevent general disorders microcirculation. The patient’s life depends on the speed and completeness of emergency measures.

Causes

The cause of hemorrhagic shock is acute bleeding.

Traumatic pain shock is not always accompanied by significant blood loss. It is more characterized by a widespread lesion surface (extensive burns, combined fractures, tissue crushing). But the combination with uncontrolled bleeding aggravates the effect of damaging factors and aggravates the clinical course.

In pregnant women, urgent diagnosis of the cause of shock is important

Hemorrhagic shock in obstetrics occurs during difficult labor, during pregnancy, postpartum period. Massive blood loss is caused by:

• ruptures of the uterus and birth canal;
• placenta previa;
• with the normal position of the placenta, its premature detachment is possible;
• abortion;
• uterine hypotension after childbirth.

In such cases, bleeding is often combined with another pathology (trauma during labor, gestosis, concomitant chronic diseases of the woman).

Clinical manifestations

The clinical picture of hemorrhagic shock is determined by the degree of impaired microcirculation, the severity of cardiac and vascular insufficiency. Depending on the stage of development pathological changes It is customary to distinguish the stages of hemorrhagic shock:

1. Compensation or first stage- blood loss is no more than 15–25% of the total volume, the patient is fully conscious, he answers questions adequately; upon examination, attention is drawn to pallor and coldness of the skin of the extremities, weak pulse, blood pressure at the lower limits of normal, heart rate increased to 90–110 per minute.
2. Second stage, or decompensation, - according to the name, symptoms appear oxygen deficiency brain, weakness cardiac output. Typically, acute blood loss ranges from 25 to 40% of the total circulating blood volume. The failure of adaptive mechanisms is accompanied by a disturbance in the patient’s consciousness. In neurology it is regarded as soporous, there is inhibition of thinking. There is pronounced cyanosis on the face and limbs, the hands and feet are cold, the body is covered with sticky sweat. Blood pressure (BP) drops sharply. The pulse is weakly filled, characterized as “thread-like”, frequency up to 140 per minute. Breathing is frequent and shallow. Urinary excretion is sharply limited (up to 20 ml per hour). Such a reduction in the filtration function of the kidneys is called oliguria.
3. The third stage is irreversible- the patient’s condition is assessed as extremely serious, requiring resuscitation measures. There is no consciousness, the skin is pale, with a marbled tint, blood pressure is not determined or only the upper level can be measured within 40–60 mm Hg. Art. It is impossible to palpate the pulse on the ulnar artery, but with sufficiently good skills it can be felt on carotid arteries, heart sounds are muffled, tachycardia reaches 140–160 per minute.

How is the degree of blood loss determined?

In diagnosis, it is most convenient for the doctor to use objective signs of shock. The following indicators are suitable for this:

• circulating blood volume (CBV) - determined in the laboratory;
• shock index.

It has been proven that the body can completely restore the loss of ¼ of the blood volume on its own. And with the rapid disappearance of half the volume, compensatory reactions fail. Recovery is only possible with the help of treatment.

Death occurs with a sharp decrease in blood volume by 60% or more.

To state the severity of the patient, there is a classification associated with minimal capabilities in determining hypovolemia based on laboratory and clinical signs.

The given indicators are not suitable for assessing the severity of shock in children. If a newborn baby’s total blood volume barely reaches 400 ml, then for him a loss of 50 ml is quite similar to 1 liter in an adult. In addition, children suffer from hypovolemia much more severely, since their compensation mechanisms are poorly expressed.

Any medical professional can determine the shock index. This is the ratio of the calculated heart rate to the systolic pressure. Depending on the obtained coefficient, the degree of shock is roughly judged:

• 1.0 - light;
• 1.5 - medium-heavy;
• 2.0 - heavy.

Laboratory values ​​in diagnosis should indicate the severity of anemia. For this purpose the following are determined:

• hemoglobin,
• number of red blood cells,
• hematocrit

For timely choice of treatment tactics and recognition of a severe complication in the form of disseminated intravascular coagulation syndrome, the patient is determined by coagulogram parameters.

Monitoring diuresis is necessary in the diagnosis of kidney damage and filtration disorders.

How to provide assistance at the prehospital stage?

First aid actions against the background of the detected acute bleeding should be aimed at:

• measures to stop bleeding;
• prevention of hypovolemia (dehydration).

Applying a belt to a maximally bent arm helps stop bleeding from the vessels of the shoulder and forearm

Help for hemorrhagic shock cannot be done without:

• application of hemostatic dressings, tourniquets, immobilization of the limb for injuries of large vessels;
• placing the victim in a lying position; with a mild degree of shock, the victim may be in a euphoric state and inadequately assess his well-being and try to get up;
• if possible, replenish fluid loss by drinking plenty of fluids;
• warming up warm blankets, heating pads.

An ambulance must be called to the scene of the incident. The patient’s life depends on the speed of action.

Treatment of hemorrhagic shock begins in an ambulance

The doctor’s algorithm of action is determined by the severity of the injury and the patient’s condition:

1. checking the effectiveness of a pressure bandage, tourniquet, applying clamps to blood vessels for open wounds;
2. installation of systems for transfusion into 2 veins, puncture if possible subclavian vein and its catheterization;
3. establishing a fluid transfusion to quickly restore the volume of blood volume; in the absence of Reopoliglyukin or Poliglyukin, a normal saline solution will do for the duration of transportation;
4. ensuring free breathing by fixing the tongue, installing an air duct, if necessary, intubation and transfer to mechanical breathing or using a hand-held Ambu bag;
5. carrying out pain relief using injections of narcotic analgesics, Baralgin and antihistamines, Ketamine;
6. administration of corticosteroids for support blood pressure.

The ambulance must ensure the fastest possible (with a sound signal) delivery of the patient to the hospital, inform by radio or telephone about the arrival of the victim so that the reception staff is ready.

Video about the principles of first aid for acute blood loss:

Basics of therapy for hemorrhagic shock

In a hospital setting, shock therapy is provided by a set of measures aimed at counteracting the damaging mechanisms of pathogenesis. It is based on:

• maintaining continuity of care with the prehospital stage;
• continuation of replacement transfusion with solutions;
• measures to completely stop bleeding;
• adequate use of medications depending on the severity of the injury;
• antioxidant therapy - inhalation of a humidified oxygen-air mixture;
• warming the patient.

Reopolyglucin normalizes platelet aggregation and serves as a prevention of DIC syndrome

When a patient is admitted to the intensive care unit:

• carry out, add a jet injection of Polyglucin to the drip infusion of saline solution;
• Blood pressure is constantly measured, the heart rate is noted on the cardiac monitor, and the amount of urine excreted through the catheter from the bladder is recorded;
• during vein catheterization, blood is taken for urgent analysis to determine the degree of loss of blood volume, anemia, blood type and Rh factor;
• after the tests and diagnosis of the moderate stage of shock are ready, donor blood is ordered, tests are performed for individual sensitivity and Rh compatibility;
• if the biological sample is good, blood transfusion is started, early stages transfusion of plasma, albumin or protein (protein solutions) is indicated;
• in order to eliminate metabolic acidosis an infusion of sodium bicarbonate is necessary.

If surgical intervention is necessary, the issue of its urgency is decided collectively by surgeons, and the possibility of anesthesia is also determined

How much blood should be transfused?

During blood transfusion, doctors use the following rules:

• for blood loss of 25% of the bcc, compensation is possible only with blood substitutes, and not with blood;
• for newborns and small children, the total volume is half combined with the erythrocyte mass;
• if the BCC is reduced by 35%, it is necessary to use both red blood cells and blood substitutes (1:1);
• the total volume of transfused fluids should be 15–20% higher than the specified blood loss;
• if severe shock is detected with a loss of 50% of blood, then the total volume should be twice as large, and the ratio between red blood cells and blood substitutes should be maintained as 2:1.

Indications for stopping the continuous infusion of blood and blood substitutes are:

• no new signs of bleeding within three to four hours of observation;
• restoration of stable blood pressure numbers;
• presence of constant diuresis;
• compensation of cardiac activity.

If there are wounds, antibiotics are prescribed to prevent infection.

Cardiac glycosides and osmotic diuretics such as Mannitol are used very carefully when blood pressure is stabilized and there are no contraindications based on ECG results.

What complications are possible with hemorrhagic shock?

The state of hemorrhagic shock is very transient, dangerous due to massive blood loss and fatal during cardiac arrest.

• The most severe complication is the development of disseminated intravascular coagulation syndrome. It upsets the balance shaped elements, vascular permeability, impairs microcirculation.
• Tissue hypoxia most affects the lungs, brain, and heart. This is manifested by respiratory and heart failure, mental disorders. In the lungs, the formation of a “shock lung” with hemorrhagic areas and necrosis is possible.
• Liver and kidney tissues react with manifestations of organ failure, impaired synthesis of coagulation factors.
• In case of obstetric massive bleeding, long-term consequences are considered to be a violation of a woman’s reproductive capabilities and the appearance of endocrine pathology.

To combat hemorrhagic shock, it is necessary to maintain constant readiness of medical personnel and have a supply of drugs and blood substitutes. The public has to be reminded of the importance of donation and community participation in providing assistance.

Hemorrhagic shock is a medical emergency.

Hemorrhagic shock is a life-threatening condition that develops when acute blood loss in a volume of more than 500 ml. In case of hemorrhagic shock, the emergency care algorithm should include measures to stop bleeding and transport the person to a surgical hospital.

In everyday life, hemorrhagic shock most often develops for several reasons:

• injury to a large vessel, vein or artery, which is accompanied by heavy bleeding without providing adequate medical care;
• uterine bleeding;
• gastrointestinal bleeding.

Important! The survival of patients with hemorrhagic shock depends on the time, how long this shock lasts and the action of the cause that caused it.

Establishing the cause is closely related to further tactics of action. Bleeding from a large vessel is not difficult to diagnose; it is important to determine which vessel is affected - a vein or an artery. Causes associated with chronic diseases of the stomach and intestines are also diagnosable.

The most dangerous bleeding from the female genital organs. Due to rapid blood loss, brain hypoxia increases and changes in consciousness occur. A person in the first stage of shock does not assess his condition and is either euphoric or aggressive. Moving into the second stage, loss of consciousness gradually occurs.

How can you help?

Actions pursue two goals, regardless of the reason that caused them:

• this is to replenish lost blood volume
• final stop of bleeding.

None of these two points can be accomplished without medical qualifications, so at the pre-medical stage it is important not to aggravate the situation, but to contribute to a successful outcome.

Bleeding from a vessel

First first aid in case of hemorrhagic shock, it should include a mandatory call for an ambulance resuscitation team and a temporary stop of bleeding, if possible.

How to understand what to do

We determine the affected vessel by its appearance.

Emergency care algorithm

You can learn more about actions depending on the type of bleeding by clicking on the links below:

If the patient is conscious and the bleeding has already been stopped, then it is necessary to start watering him off with warm water until the ambulance arrives.

Important! When calling an ambulance, you should clearly describe the nature of the bleeding, its duration, and the patient’s condition. This is necessary so that the dispatcher understands the seriousness of the situation and dispatches a resuscitation team to the call.

Internal bleeding

Internal bleeding is the most dangerous because there are no visible signs of blood loss

Internal bleeding occurs when organs are injured or diseased. Most often occurs in the abdominal or chest area, as well as in organs, less often in large muscles.

Uterine bleeding

The clinical picture and diagnosis of bleeding from the female genital organs often causes difficulty in identifying, especially if a woman tries to hide the fact of blood loss. This happens after criminal abortions, those performed outside a medical institution.

Regardless of whether there is pregnancy or not, and how much blood loss, you need to urgently contact an ambulance.

Symptoms

Primary symptoms:

• thirst,
• inappropriate behavior
• dizziness.

With further ongoing bleeding, the clinical picture of hemorrhagic shock begins to increase:

• cyanosis of the extremities appears,
• cold sweat,
• state of stupefaction,
• pressure drop,
• loss of consciousness.

First aid algorithm

You can read more about what to do and how to quickly help a victim in case of uterine bleeding.

Parenchymal bleeding

Parenchymal organs - lungs, kidneys, liver and spleen. The symptoms of this type of bleeding are vague. Signs of parenchymal bleeding depend on the damaged organ.

Symptoms

For lung damage:

• coughing up blood appears
• the patient begins to choke as swelling of this organ develops.

If the focus of blood loss is in the pleural area, then:

• breathing quickens,
• the skin and mucous membranes turn pale or blue.
• rapid pulse,
• decrease in blood pressure.

If the liver and kidneys are damaged, the patient is concerned about:

• acute pain in the area where the organ is located,
• swelling and increase in organ size,
• symptoms of acute blood loss, including hypovolemic shock.

Emergency care algorithm

Gastrointestinal bleeding

Heavy bleeding digestive tract usually caused by a previous stomach ulcer.

Symptoms

Guess ulcer bleeding It is possible in the case when the pain in the epigastric region that tormented the patient suddenly disappears. This may be followed by vomiting of coagulated blood – the color of “coffee grounds”.

First aid algorithm

If you do not provide first aid to the patient, hemorrhagic shock increases very quickly. Therefore, you definitely need to start by calling an ambulance. When specialists arrive, tell them about your ulcer history so that the doctor can quickly determine the tactics of action.

For more information about what to do in case of gastrointestinal bleeding for a person without medical training, read the link:

It is impossible to provide emergency care for hemorrhagic shock at home. The only thing you should try to do is call specialists quickly and try to stop the bleeding.

Shock is a general nonspecific reaction of the body to an excessive (in strength or duration) damaging effect. In the case of hemorrhagic shock, such an effect may be acute, timely uncompensated blood loss, leading to hypovolemia. Typically, for the development of hemorrhagic shock, a decrease in blood volume by more than 15–20% is necessary.

SYNONYMS

Hypovolemic shock.

CLASSIFICATION

By volume of blood loss:

• mild degree - decrease in blood volume by 20%;
• moderate degree - decrease in blood volume by 35–40%;
• severe degree - decrease in blood volume by more than 40%.

In this case, the rate of blood loss is crucial.

According to the Algover shock index (the quotient of heart rate divided by systolic blood pressure, normally it is less than 1)

• Mild shock - index 1.0–1.1.
• Average degree - index 1.5.
• Severe degree - index 2.
• Extreme severity - index 2.5.

According to clinical signs (according to G.Ya. Ryabov).

• Compensated hemorrhagic shock - moderate tachycardia, arterial hypotension is mild or absent. Venous hypotension and moderate shortness of breath are detected with physical activity, oliguria, cold extremities. In terms of the volume of blood loss, this stage corresponds to the mild degree of the first classification.
• Decompensated reversible hemorrhagic shock - heart rate 120–140 beats per minute, systolic blood pressure below 100 mm Hg, low pulse pressure, low central venous pressure, shortness of breath at rest, severe oliguria (less than 20 ml per hour), pallor, cyanosis, cold sweat, restless behavior. The volume of blood loss usually corresponds to the average degree of the first classification.
• Irreversible hemorrhagic shock. Persistent prolonged hypotension, systolic blood pressure below 60 mm Hg, heart rate above 140 beats per minute, negative central venous pressure, severe shortness of breath, anuria, lack of consciousness. The volume of blood loss is more than 40% of the total blood volume.

ETIOLOGY

The main etiological factor in the development of hemorrhagic shock is timely unreplenished blood loss exceeding 15–20% of the total volume. In gynecological practice, this condition is most often caused by an interrupted ectopic pregnancy, especially rupture fallopian tube; The closer to the uterus there is a violation of the integrity of the tube, the higher the volume of hemoperitoneum. However, other pathological conditions can also lead to the development of massive bleeding, such as:

• ovarian apoplexy;
• oncological diseases;
• septic processes associated with massive tissue necrosis and vascular erosion;
• genital injuries.

Contributing factors are:

• initial hypovolemia caused by heart failure, fever, etc.;
• iatrogenic hypovolemia resulting from the use of diuretics, ganglion blockers, resulting from epi and epidural anesthesia;
• incorrect assessment of the volume and rate of blood loss, tactical errors during replenishment, inadequate assessment of the state of the hemostatic system and delayed correction of its violations, untimely choice of means to stop bleeding, complications that arose during the provision of medical care.

DEVELOPMENT MECHANISM

The triggering mechanism of hemorrhagic shock is acute irreversible blood loss, leading to a decrease in blood volume by 15–20% or more, i.e. causing hypovolemia, parallel to which there is a decrease in venous return and cardiac output. In response to a diverse deficit of BCC, the sympathoadrenal system is activated, leading to spasm of capacitive vessels (arterioles and precapillaries) in all organs and systems, with the exception of the brain and heart, i.e. Centralization of blood circulation occurs, which is compensatory in nature. At the same time, autohemodilution processes begin to develop due to the movement of fluid from the interstitium to the vascular sector and the delay in the excretion of water from the body by increasing the reabsorption of it and sodium in the renal tubules. However, these mechanisms cannot guarantee long-term hemodynamic stabilization. In conditions of ongoing bleeding and inadequate replacement of blood loss, their depletion occurs within 30–40 minutes. Following the crisis of macrocirculation is a crisis of microcirculatory processes, which, due to its irreversibility, is more pronounced and life-threatening. Hemostasiological disorders, occurring in the form of blood disseminated intravascular coagulation syndrome, begin to play a decisive role in this. As a result of vasoconstriction and lack of perfusion pressure, blood flow stops in most metabolic vessels, which are capillaries. Platelet-fibrin thrombi quickly form in them, involving the red blood cells remaining in the capillaries in thrombus formation, which are relatively quickly destroyed, supplying new portions of activators of the coagulation process. This process ends with the formation of significant acidosis, causing a sharp increase in permeability cell membranes and vascular wall. The inversion of the potassium-sodium pump occurs, the movement of fluid first into the interstitium and then into the cells, their massive death in all organs and tissues, including vital ones, especially those with increased hydrophilicity, such as the brain and lungs. These changes are total in nature, have no exceptions and cannot stop on their own even with the restoration of central hemodynamics through active infusion therapy. Time is lost, the shock becomes irreversible, and the death of the body becomes almost inevitable.

CLINICAL PICTURE

The severity of clinical manifestations depends on the stages of development of hemorrhagic shock, the criteria of which are set out in clinical classification given in the corresponding section. It should be added to this that it is very short-sighted and dangerous to rely on the patient’s subjective feelings in assessing the condition. It must be remembered that significant clinical manifestations of hemorrhagic shock can be detected only when it enters the second, already decompensated stage, when the leading symptom becomes persistent arterial hypotension as a sign of hypovolemia and heart failure, indicating the impossibility of independent compensation of hemodynamics due to centralization of the blood circulation. In the absence of adequate assistance, especially infusion-transfusion therapy, in the conditions of ongoing bleeding, shock progresses towards its irreversibility, with inevitable rapidity the emphasis in pathogenetic processes shifts and clinical signs from macrocirculatory to microcirculatory problems, which leads to the development of multiple organ and multisystem failure with the corresponding symptom complex. In addition to the above, it is important to understand that constructing a concept of care based only on clinical diagnosis and prognosis without conducting appropriate laboratory and instrumental studies leads to disorientation of medical staff and a delay in the entire diagnostic and treatment process.

DIFFERENTIAL DIAGNOSTIC MEASURES

It should be remembered that if doubts arise regarding the type of shock, the main differential diagnostic criterion that rejects its hemorrhagic nature is the proven absence of ongoing bleeding and unreplenished blood loss. However, it is necessary to keep in mind the possibility of a combination of different types of shock in one patient, as well as the simultaneous or sequential additional action of several shockogenic factors (anaphylaxis, dehydration, trauma, excessive painful stimulus, septic agent) against the background of hemorrhagic shock, which undoubtedly leads to worsening its course and consequences.

The logic of the diagnostic process when hemorrhagic shock is suspected, first of all, involves determining the volume of blood loss and confirming or denying the fact of ongoing bleeding and the degree of its intensity. At the same time, there is often an underestimation of the volume of blood loss and, as a consequence, a delay in the start of infusion-transfusion therapy, late diagnosis of hemorrhagic shock, often in its already decompensated stage.

Some assistance in diagnosing the presence of hemorrhagic shock and its stage is provided by:

• the maximum possible clarification of the amount of irretrievably lost blood and its correlation with the calculated BCC (in percentage) and the volume of infusion therapy performed;
• determination of the state of central nervous activity, its mental and reflex components;
• assessment of the condition of the skin: its color, temperature and color, the nature of the filling of the central and peripheral vessels, capillary blood flow;
• auscultatory and radiological assessment of the activity of the respiratory and circulatory organs;
• monitoring of basic vital indicators: blood pressure, heart rate, respiratory rate, blood oxygen saturation;
• calculating the shock index (see section “Classification”);
• CVP measurement;
• control of minute and hourly diuresis;
• measurement of hemoglobin concentration and its correspondence to the hematocrit indicator. It should be noted that in case of acute blood loss, the hematocrit value may be more indicative of the volume of infusion therapy than the volume of blood lost;
• study of the hemostasis system for the presence and intensity of development of blood disseminated intravascular coagulation syndrome, the form and stage of its course. It is fundamental to determine, by qualitative or quantitative method, the presence in the blood of soluble complexes of fibrin monomers and/or fibrin degradation products (Ddimer), as well as the number of platelets;
• monitoring of acid-base status, electrolyte and gas composition blood, preferably with a comparison of arterial and venous blood parameters;
• electrocardiographic monitoring, if possible, echocardiography;
• study of biochemical blood parameters.

The synthetic and final diagnostic result of the above is an objective assessment of severity general condition patients, the formation of a structural diagnosis and the determination of strategies and tactics for providing medical care.

EMERGENCY MEASURES AND TREATMENT

• The main and most urgent measure for the treatment and prevention of progression of hemorrhagic shock should be considered the search for the source of bleeding and its elimination. In gynecological practice in the best possible way This is accomplished by surgical intervention.
• The second fundamental action that decides the issue of preserving the patient’s life is the speed of restoration of blood volume. The infusion rate is determined by the most accessible indicators - blood pressure, heart rate, central venous pressure and minute diuresis. Moreover, in the case of ongoing bleeding, it should advance the rate of blood flow by approximately 20%.
• Such a speed of solution administration can be achieved only if there is reliable access to the central venous vessels using a large-diameter catheter. Therefore, catheterization of the subclavian or jugular vein is included in the range of emergency measures.
• We should not forget about the simultaneous catheterization of preferably two peripheral vessels, necessary for long-term, strictly dosed administration of drugs, as well as the installation of a catheter in the bladder.
• In patients in critical condition, close to terminal, they begin intra-arterial injection of solutions.
• All of these measures are taken in order to maintain optimal tissue oxygen consumption and maintain metabolism in them, for which prolonged artificial ventilation with precise maneuvering of the composition of the gas mixture and adequate pain relief, as well as warming the patient, is very important.
• The priority in infusion therapy for hemorrhagic shock today undoubtedly belongs to HES solutions of 10% concentration. It is these solutions that make it possible to quickly and for a fairly long period of time (up to 4 hours) provide compensation for the volume of blood volume due to an increase in oncotic pressure. Infusion therapy for shock should begin with their rapid administration. Typically, up to 1.5 liters of HES are used per day, alternating with crystalloid (mostly glucose-free) and other colloid solutions (dextrans, gelatins), the ratio of which in the overall infusion program should be 1:1. To date, hypertonic 7–7.5% sodium chloride solution has not lost its importance as a starting component in the treatment of massive blood loss, infusion of 150–200 ml (6 ml/kg) with the subsequent administration of HES and crystalloids can effectively stabilize or even restore systolic blood pressure and cardiac output. Not long ago, the official hypertensive version of HES, HyperHaes©, appeared. Its administration in an amount of 1 liter is also very active and quickly affects blood pressure and volumetric parameters of the heart, but just as when using conventional HES, further infusion of a sufficient volume of liquid is necessary. All solutions must be heated to 30–35 °C.
• The fight against hemorrhagic shock and its consequences also implies, depending on hemostasiological parameters and the presence of blood disseminated intravascular coagulation syndrome, permanent correction of the hemostatic system by transfusion of FFP and suppression of fibrinolytic and proteolytic activity of the blood (for details, see the section “Blood disseminated intravascular coagulation syndrome” of this manual). It is important to remember that the earlier the decision is made on plasma replacement therapy and the more intensively it is carried out under the guise of fibrinolysis inhibitors, the faster and with less costs and consequences it is possible to transfer disturbances in the hemostatic system from acute form into chronic. You should also try to avoid technical errors when thawing and administering plasma (plasma is poured in a stream into the central vein and heated to 30 ° C, after each dose of plasma 10 ml of a 10% calcium chloride solution is administered to neutralize sodium citrate).
• Regarding the administration of red blood cells or suspension, it should be borne in mind that this is not the primary measure to combat shock, because critical decline oxygen carrier concentration usually occurs when blood loss exceeds 40% of the blood volume. Transfusion of red blood cells is started, as a rule, after stopping the bleeding, replenishing the volume of lost blood and obtaining relatively reliable results of the study, first of all, the gas composition of the blood, confirming the extremely low partial pressure of oxygen. It is unacceptable to focus only on the quantitative assessment of hemoglobin and hematocrit. If a decision is made on transfusion, it is necessary to limit the number of injected red blood cells to the minimum possible, postponing their further transfusion until a period further removed from the blood loss, when it will be possible to objectively judge the composition of the blood in the central and peripheral sectors. An immutable fact is strict adherence to all rules for blood transfusion and technical requirements, including the need to dilute red blood cells isotonic solution sodium chloride in a 1:1 ratio and the introduction after each dose of 10 ml of a 10% calcium chloride solution to neutralize sodium citrate.
• On average, with a loss of about 35–40% of the bcc, the volume of all infusion therapy, including blood components (1–1.5 liters of FFP and about 600 ml of red blood cells), subject to normalization of diuresis, per day is 250–300% of the final established volume irrevocably lost blood.
• An important issue, especially in gynecological practice, is the question of reinfusion of blood poured into abdominal cavity. Considering it from modern pathophysiological positions, we can conclude that it is impossible to reinfuse blood by filtering it through gauze. This blood can be returned to the patient only in the form of red blood cells washed in a special apparatus or using special filters.
• To compensate for acute adrenal insufficiency after the start of active infusion therapy, administration of prednisolone 90–120 mg or equivalent doses of hydrocortisone, dexamethasone or methylprednisolone is indicated. The use of these drugs must be repeated periodically until hemodynamic stabilization is achieved.
• Considering the problems with the perfusion of renal tissue that arise during shock, it is necessary, subject to adequate replenishment of blood loss and insufficient minute and hourly diuresis (less than 50–60 ml/hour), for each liter of transfused fluid, 10–20 mg of furosemide should be administered intravenously.
• The use of vasopressors, such as epinephrine, phenylephrine and their analogues, is contraindicated, especially before replenishment of blood volume. On the other hand, the permanent use of dopamine as an agonist of dopamine receptors through a perfusor in a renal dose of 2–3 μg/(kgxmin) after replenishment of the main part of the volume of circulating blood allows to improve renal and mesenteric blood flow, and also helps to normalize systemic hemodynamics.
• Correction of the acid-base state of the blood, protein and electrolyte metabolism, without a doubt, remains necessary component therapy throughout the entire period of treatment of hemorrhagic shock. The important thing is that this requires reliable laboratory data, otherwise, instead of helping the patient, harm can be caused to already extremely stressed organs and systems. Particular attention should be paid to calcium and potassium deficiency, as well as excess sodium, which can lead to the rapid development of cerebral edema. However, the use of 4% sodium bicarbonate solution in an amount of 2 ml/kg will reduce metabolic acidosis until laboratory data are obtained.

Criteria for the effectiveness of assistance:

• stabilization of blood pressure and heart rate at levels that are not life-threatening and ensure adequate perfusion of organs and tissues, i.e. Blood pressure not lower than 100/60 mm Hg. and heart rate 100/min;
• CVP not lower than 4–6 mm water column;
• minute diuresis of at least 1 ml and hourly diuresis of at least 60 ml;
• blood oxygen saturation is not lower than 94–96%;
• the hemoglobin concentration of venous blood is not lower than 60 g/l;
• venous blood hematocrit is not lower than 20%;
• the concentration of total blood plasma protein is not lower than 50 g/l;
• stable isocoagulation of venous blood with a tendency to hypercoagulation;
• absence of sudden changes in the acid-base state and electrolyte composition of the blood;
• absence of acute myocardial nutritional disorders.

BIBLIOGRAPHY
Anesthesiology and resuscitation: textbook / Ed. O.A. Valley. - M.: GEOTARMEDIA, 2002. - 552 p.
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Hemorrhagic shock in medicine refers to extensive blood loss, an unexpected release of blood from the blood vessels. This phenomenon usually develops quite rapidly and can lead to serious consequences, even a tragic outcome. What are the signs to use to diagnose hemorrhagic shock, and what kind of help can those around them provide to a person with sudden bleeding?

Causes of hemorrhagic shock

Root causes of hemorrhagic shock - various damages, injuries, operations, etc.

For your information. According to medical statistics, hemorrhagic shock in obstetrics ranks first in frequency of occurrence.

Excessive acute blood loss occurs in expectant mothers in the following cases:

• rupture of the fallopian tube - consequences of ectopic pregnancy;
• uterine rupture;
• some types of uterine bleeding;
• so-called acute fatty liver of pregnancy.

The consequences of this condition can be:

• development of cancer of the female genital organs;
• sepsis accompanied by tissue necrosis;
• ovarian apoplexy.

Hemorrhagic shock is also considered as a result of delayed or incorrectly selected therapy for such conditions/diseases as:

• cholera;
• diabetes;
• peritonitis;
• sepsis;
• cancer;
• osteomyelitis;
• prolonged stay in an environment with elevated air temperatures;
• pathology that provokes dehydration of the body, etc.

The following are considered indirect causes of shock:

• Incorrect assessment of bleeding characteristics - volume or speed.
• Incorrectly chosen method of replenishing lost blood.
• Incorrect/delayed error correction during blood transfusion.
• Late/incorrect choice of medications that can stop blood loss.

What determines the severity of the development of shock?

The basis for disruption of the body's vital functions during hemorrhagic shock is a sharp decrease in blood volumes distributed through the vessels. A decrease in the amount of blood provokes a spasm in these same vessels. The result is a transition tissue fluid into the blood vessels, which contributes to blood thinning and disruption of its microcirculation in organs.

The lack of timely assistance threatens global failures of microcircular processes and jeopardizes human health and even life.

The intensity of blood loss depends on a number of determining factors:

• body endurance;
• immunity strength;
• state nervous systems s (it is directly involved in the control of vascular tone);
• heart pathologies, etc.

Hemorrhagic shock (HS) is a complex of changes that occur in response to pathological blood loss and is characterized by the development of small output syndrome, tissue hypoperfusion, multisystem and multiple organ failure. Obstetric hemorrhagic shock is one of the causes of maternal mortality (2-3rd place in the structure of causes of maternal mortality).

Hemorrhagic shock develops when blood loss is more than 1% of body weight (1000-1500 ml). Against the background of extragenital pathology, gestosis, weakness of labor, and with inadequate pain relief during labor, symptoms of shock may appear with less blood loss (800-1000 ml).

Etiology. The cause of hemorrhagic shock is bleeding, which can be caused by premature detachment of a normally located and presenting placenta, uterine rupture, partial tight attachment or placenta accreta, hypotension and atony of the uterus, amniotic fluid embolism. Severe uterine bleeding is also possible if there is a dead fetus in the uterus.

Pathogenesis. In obstetrics, the pathogenesis of HS is similar to that of traumatic shock due to the presence of a pain factor during childbirth with inadequate pain relief and various manipulations ( obstetric forceps, manual examination of the uterus, suturing ruptures of the birth canal), with premature abruption of a normally located placenta. Birth trauma and blood loss are two factors that determine the development of obstetric shock.

The pathogenesis of HS is based on changes in macro- and microhemodynamics caused by hypovolemia, hypoperfusion, anemic and circulatory hypoxia with the development of dystrophic changes in vital organs. Disorders of hemodynamics and tissue metabolism depend on the amount of blood loss and the intensity of bleeding.

Initially, with acute blood loss (700-1300 ml, 15-25% of bcc), in response to a decrease in bcc and cardiac output, compensatory reactions develop, consisting of activation of the sympathetic-adrenal system with the release of catecholamines, which leads to tachycardia, increased tone of capacitive vessels (venules ), increased venous return. With continued blood loss, arteriolar resistance increases. Vasoconstriction of arterioles and precapillary sphincters contributes to the centralization of blood flow. As a result, blood circulation in the skin, intestines, and liver is reduced and optimal blood flow is ensured in the brain and heart muscle.

At the same time with vascular changes water retention in the body and an influx of interstitial fluid into the vascular bed due to increased secretion are observed antidiuretic hormone and aldosterone. The changes that occur increase blood volume, and systolic blood pressure may remain above the critical level. However, compensatory reactions to stabilize macrohemodynamics occur to the detriment of the state of microcirculation, especially in organs that are not vital. Vasoconstriction helps to increase the aggregation ability of erythrocytes, blood viscosity, and the appearance pathological forms red blood cells, the development of hypercoagulation (increased fibrinogen concentration, increased blood clotting rate). Changes in the intravascular microcirculation, along with vasoconstriction, lead to a progressive decrease in blood flow velocity and impaired tissue perfusion.

These disorders can be compensated independently if the bleeding is stopped in a timely manner.

With continued bleeding (blood loss 1300-1800 ml, 25-45% of blood volume), macro- and microhemodynamic disturbances worsen. Progressive hypovolemia stimulates the opening of arteriovenous shunts. In this case, blood circulates from arterioles through arteriovenous anastomoses, bypassing capillaries, aggravating tissue hypoxia, which promotes local dilation of blood vessels, which further reduces the speed of blood flow and leads to a sharp drop in venous return to the heart. Low blood flow velocity in the microvasculature creates conditions for the formation of cellular aggregates and their sedimentation in the vessels. Fibrin is formed on erythrocyte and platelet aggregates, which initially dissolves due to the activation of fibrinolysis. Instead of dissolved fibrin, new fibrin is deposited, which causes a decrease in its content in the blood (hypofibrinogenemia). Aggregates of red blood cells, enveloped in proteins, stick together, forming large cellular conglomerates, which excludes a significant number of red blood cells from the bloodstream. In erythrocyte aggregates, hemolysis of erythrocytes simultaneously occurs. The developing process of red blood sequestration, or sludge phenomenon (the appearance of immobile pathologically altered red blood cells and red blood cell aggregates in the vessels), leads to blood separation and the appearance of plasmatic capillaries free of red blood cells.

At this stage of HS, a clear picture of disseminated intravascular coagulation (DIC) develops. The level of clotting factors in the bloodstream decreases. The decrease is due to both coagulopathy of loss due to the loss of coagulation factors during bleeding, and the consumption of procoagulants in the process of activation of intravascular coagulation and activation of fibrinolysis, characteristic of DIC syndrome (consumption coagulopathy). With a progressive decrease in blood volume as a result of blood sequestration and prolonged arteriolospasm, the microcirculation disorder becomes generalized. Low cardiac output is not able to compensate for a significant decrease in blood volume. As a result, blood pressure begins to decrease. Hypotension is a cardinal symptom indicating circulatory decompensation.

Vital in tissues important organs with circulatory decompensation, metabolic acidosis develops due to anaerobic glycolysis, under conditions of which electrolyte balance is disturbed, leading to intracellular edema, lipid peroxidation and lysosomal enzymes are simultaneously activated with membrane destruction and cell death. The general circulation system receives a large number of acidic metabolites and aggressive polypeptides of high concentration with toxic properties. The resulting polypeptides primarily have a depressing effect on the myocardium, additionally leading to a decrease in cardiac output.

The presented circulatory and metabolic disorders do not disappear on their own even after the bleeding has stopped. To normalize organ blood flow, it is necessary to carry out timely treatment. In the absence of adequate therapy or with continued bleeding (2000-2500 ml or more, over 50% of the volume), hemodynamic and metabolic disorders progress. Under the influence of local hypoxia, arterioles and precapillary sphincters lose their tone and stop responding even to high concentrations of endogenous catecholamines. Atony and dilatation of blood vessels lead to capillary stasis, intravascular coagulation and the movement of fluid from the vascular and extracellular sectors to the cellular sector, which contributes to irreversible dystrophic changes in all organs. Capillary stasis, vascular atony, intracellular edema are characteristic signs of the irreversibility of the process in hemorrhagic shock.

Different organs are affected differently in HS. First of all, blood circulation is disrupted in the lungs (shock lung), in the kidneys (shock kidney), in the liver (centrilobular necrosis), in the pituitary gland, with the subsequent possible development of Sheehan syndrome. As microcirculation is disrupted, placental blood flow changes. The extensive microvasculature of the placenta becomes clogged with cellular aggregates. As a result of vascular blockade, the perfusion reserve of the placenta is reduced, leading to a decrease in fetoplacental blood flow and fetal hypoxia. Subsequently, structural damage to the myometrium occurs, which is based first on swelling of myocytes and then on their destruction. The most characteristic sign of a shock uterus is the absence contractile activity in response to the administration of uterotonics (oxytocin, prostaglandins). The final stage of shock uterus syndrome is Couveler's uterus. With HS, the functions of the cardiovascular and nervous systems are preserved longer than others. Loss of consciousness in patients in a state of shock occurs when blood pressure is below 60 mmHg. Art., i.e. already in a terminal state.

Clinical picture. By clinical course Depending on the volume of blood loss, 3 stages of shock are distinguished: I - mild, II - moderate, III - severe.

The peculiarity of obstetric bleeding is its suddenness and severity. At the same time, the stages of development of HS are not always clearly defined. The most pronounced clinical manifestations of shock are observed with premature abruption of a normally located placenta, with uterine rupture during childbirth, during which a preagonal state can occur very quickly, already in the first 10 minutes. At the same time, with prolonged bleeding against the background of uterine hypotension, if it is repeated in small portions, it can be difficult to determine the line when the body moves from the stage of relative compensation to the phase of decompensation. The relative well-being of the mother in labor disorients the doctor, and he may suddenly find himself confronted with a critical deficiency of blood volume. To objectively assess the severity of the condition when heavy bleeding should be considered next complex clinical and laboratory data:

Coloring of the skin and mucous membranes, respiratory and pulse rate, blood pressure (BP) and central venous pressure (CVP), shock index (ratio of blood pressure to pulse) Algover (not always informative for gestosis);

Minute diuresis, relative density of urine;

Indicators clinical analysis blood: hematocrit, number of red blood cells, hemoglobin content, indicator of the acid-base state and gas composition of the blood, state of water-electrolyte and protein metabolism;

Hemostasis indicators: blood clotting time according to Lee-White, number and aggregation of erythrocytes, concentration of fibrinogen, antithrombin III, content of fibrin/fibrinogen degradation products, paracoagulation tests.

With the development of GS for early detection changes and prevent the development of complications, it is necessary to carry out continuous monitoring of vital important functions sick. Changes in the presented indicators depending on the amount of blood loss and the severity of shock are presented in table. 24.1.

Table 24.1

In the mild (I) stage of shock, blood loss is compensated by changes in cardiovascular activity; in obstetric hemorrhages, this stage is short-lived and is often not diagnosed.

The middle (II) stage of shock is characterized by worsening circulatory and metabolic disorders. Generalized spasm of peripheral vessels is evidenced by the delayed disappearance of the spot when pressing on the nail bed, cold extremities. The first priority is to reduce blood pressure to a critical level (80 mm Hg). Symptoms appear indicating dysfunction of vital organs: severe shortness of breath as evidence of a shock lung, dullness of heart sounds with the appearance of changes on the ECG (decrease in the ST segment\\ flattening of tooth 7), oliguria associated with a disorder of renal blood flow and a decrease in hydrostatic pressure. Visible signs of bleeding disorders appear: blood flowing from the uterus loses its ability to clot, vomiting of coffee grounds, bloody discharge from the mucous membranes, hemorrhages on the skin of the hands, abdomen, face, at injection sites, subcutaneous hemorrhages, ecchymosis may appear; In operated patients, bleeding from the surgical wound is possible.

Heavy GS ( Stage III) develops with severe blood loss (35-40%), is characterized severe course, consciousness is impaired. When the period of circulatory decompensation continues for more than 12 hours, shock becomes irreversible, despite treatment. The blood loss is massive (more than 50-60% of the blood volume).

In the absence of treatment effect, terminal conditions develop:

Preagonal state, when the pulse is determined only in the carotid, femoral arteries or by the number of heart contractions, blood pressure is not determined, breathing is shallow, rapid, consciousness is confused;

Agonal state - consciousness is lost, pulse and blood pressure are not determined, severe respiratory distress;

Clinical death - cardiac and respiratory arrest for 5-7 minutes.

Treatment should be comprehensive and consist of stopping bleeding, compensating for blood loss and treating its consequences, and correcting hemostasis.

Stopping bleeding during HS should include a set of effective methods. In case of hypotonic bleeding and ineffectiveness of the measures taken ( external massage uterus, administration of uterotonic agents, manual examination of the uterus with gentle external-internal massage) with blood loss of 1000-1200 ml, the question of removing the uterus should be raised in a timely manner, without resorting to re-examination. In case of progressive premature detachment a normally located and previa placenta, in the absence of conditions for delivery through the birth canal, a caesarean section is immediately started. If there are signs of disseminated intravascular coagulation, Kuveler's uterus requires hysterectomy. In case of uterine rupture, urgent transection with its removal or suturing of the rupture is indicated.

In case of massive blood loss, emergency operations should be performed under combined endotracheal anesthesia. In case of bleeding accompanied by a clinical picture of coagulopathy, for complete surgical hemostasis, it is advisable to simultaneously perform ligation of the internal iliac arteries and hysterectomy. After the operation, it is necessary to adhere to the tactics artificial ventilation lungs against the background of therapeutic anesthesia and under the control of acid-base status and blood gases.

Simultaneously with stopping bleeding, therapy for massive blood loss should include compensation for blood loss and a set of measures aimed at maintaining systemic hemodynamics, microcirculation, adequate gas exchange, compensation for metabolic acidosis, protein and water-electrolyte metabolism, restoration of adequate diuresis, prevention of shock kidney, creation of antihypoxic protection of the brain , adequate pain relief.

Elimination of the consequences of blood loss is carried out by infusion therapy (IT). When carrying out IT, the speed, volume and composition of injected solutions are important.

The rate of infusions for decompensated shock should be high (the rate of infusions should not lag behind the rate of blood loss). Depending on the amount of blood loss and the severity of the condition, women puncture one or two peripheral veins or catheterize the central vein. In terminal conditions, the radial or posterior tibial artery and intra-arterial injection of solutions is carried out. Critical blood pressure (80 mm Hg) must be achieved as quickly as possible. For this purpose, a jet infusion of initially colloidal and then crystalloid solutions (up to 200 ml/min) is used, sometimes into two or three veins. Jet infusion of fluid must be carried out until blood pressure rises to 100 mm Hg, and CVP to 50-70 mm Hg. In the first 1-2 hours of treatment, blood loss should be compensated by an average of 70%. At the same time, at the beginning of treatment, glucocorticoid hormones (up to 1.5 g of hydrocortisone) are prescribed. In case of development of critical arterial hypotension, dopamine (from 1.0 to 5 mcg/min) or Dobutrex, Dopackard is administered, while cardiac output increases, systemic vasodilation occurs and peripheral resistance decreases, and renal blood flow significantly improves.

The volume of infusions in the first stages of intensive care depends on the amount of blood loss, the initial pathology (obesity, extragenital pathology, anemia, gestosis, etc.). The volume of infusions is determined by the following indicators: blood pressure level, pulse rate, central venous pressure level, blood concentration parameters (Hb, Ht, number of red blood cells), diuresis, blood clotting time (according to Lee-White).

When carrying out infusions, systolic blood pressure should not be lower than 90-100 mmHg, CVP should not be less than 30 mmHg. and no more than 100 mm water column, hemoglobin level not less than 75 g/l, hematocrit - 25%, number of red blood cells - 2.5-1012/l, blood clotting time according to Lee-White 6-10 minutes. Diuresis is of particular importance for monitoring IT, since it can be determined in any conditions and it quite accurately reflects organ blood flow and the degree of hypovolemia. Diuresis should be at least 30 ml/hour. On initial stages shock oliguria may occur functional character, caused by a deficiency of bcc. Correction of hypovolemia should eliminate this oliguria. After restoration of the bcc, it is possible to administer small doses of Lasix (10-20 ml). In the absence of treatment effect, it is necessary to exclude other causes of oliguria, in particular ligation of the ureter during hysterectomy to stop bleeding.

In the absence of the possibility of monitoring hemodynamic and blood concentration parameters, one should adhere to next rule: the volume of infusions depends on the amount of blood loss (blood loss up to 0.8% of body weight can be replaced by 80-100%, with blood loss of more than 0.8% of body weight, the volume of infusions exceeds the volume of blood loss). This is largely necessary to compensate for the deficiency of the extracellular sector and prevent cellular dehydration. The longer the period of bleeding and especially arterial hypotension, the greater the volume of “overtransfusions”. The approximate volume of infusions depending on blood loss is as follows: with blood loss of 0.6-0.8% of body weight - 80-100% of blood loss; 0.8-1.0% - 130-150%; 1.0-1.5% - 150-180%; 1.5-2.0% - 180-200%; over 2.0% - 220-250%.

The inclusion of blood components (plasma, red blood cells) and plasma substitutes is important for carrying out adequate IT.

Plasma plays an important role in the treatment of HS. Currently, fresh frozen plasma is used. It is especially advisable to use it in cases of impaired blood clotting ability. Fresh frozen plasma is administered at a rate of at least 15 ml/kg body weight per day. After warming the plasma to 37 °C, it is administered intravenously. Fresh frozen plasma contains all coagulation and fibrinolysis factors in a natural ratio. Plasma transfusion requires consideration of group affiliation. Other blood products may include albumin and platelet mass.

Platelet mass is transfused to stop bleeding caused by thrombocytopenia or to maintain the platelet count at the level of 50-70-109/l.

The indication for transfusion of blood components is a decrease in the level of hemoglobin (up to 80 g/l or less), the number of red blood cells (less than 2.5-109/l), and hematocrit (less than 0.25). For this purpose, red blood cell mass, a suspension of red blood cells in a suspension solution, or a concentrated suspension of washed red blood cells are used. For blood transfusions, preference should be given to red blood cells, the shelf life of which should not exceed 3 days.

Washed native or thawed red blood cells are transfused in cases where there is sensitization of the recipient to plasma factors. In these cases, transfusion of washed red blood cells is the prevention of complications: plasma protein syndrome, homologous blood or hemolytic syndrome causing acute renal failure.

Blood substitutes are of great importance in the treatment of HS: polyglucin, rheopolyglucin, gelatinol, as well as drugs of a new class - solutions of hydroxyethyl starch (6 and 10% HAES-sterile, ONKONAS).

Polyglucin is the main plasma substitute in the treatment of hypovolemic shock, since it is a hyperosmolar and hyperoncotic solution, thereby steadily increasing blood volume and stabilizing the macrocirculatory system. It lingers in the vascular bed for a long time (1 g of polyglucin binds 20-25 ml of water). The volume of daily infusions should not exceed 1500 ml due to the risk of hypocoagulation.

Reopolyglucin quickly increases the central nervous system, increases blood pressure, and improves not only macro- but also microcirculation. This is the most effective hemodilutant, capable of quickly restoring capillary blood flow, disaggregating stagnant red blood cells and platelets Single dose drug 500-800 ml/day. It should be used with caution in case of kidney damage. A dose of 1200 ml can cause hypo-coagulation due to a decrease in the number of platelets and the concentration of plasma factor VIII.

Gelatinol quickly increases the total blood volume, but is also quickly eliminated from the body: after 2 hours, only 20% of the transfused volume remains. Mainly used as a rheological agent. The amount of the administered drug can reach 2 liters.

Reogluman is a hyperosmolar and hyperoncotic solution with pronounced detoxification and diuretic effects. Reogluman effectively, but briefly eliminates hypovolemia, reduces blood viscosity, and relieves agglutination of blood cells. The use of reogluman can cause anaphylactoid reactions. The solution is contraindicated for hemorrhagic diathesis, circulatory failure, anuria and significant dehydration.

Solutions of hydroxyethyl starch, not having the ability to carry oxygen, nevertheless improve the gas transport function of the blood, due to an increase in blood volume, cardiac output, and erythrocyte circulation rate. At the same time, starch solutions improve the rheological properties of blood and restore blood flow in microvessels. Its advantages are the absence of anaphylactogenic properties, minimal effect on the coagulation properties of blood, and longer circulation in the bloodstream.

To normalize water-salt metabolism and the acid-base state (ABS) of blood and tissues, crystalloid solutions (solutions of glucose, Ringer, Hartmann, lactosol, halosol, etc.) must be included in the complex of infusion therapy. To correct concomitant metabolic acidosis, sodium bicarbonate is additionally used at a dose of 2 ml/kg body weight under the control of CBS.

The ratio of colloids to crystalloids depends on blood loss. For relatively minor bleeding, the ratio is 1:1, for massive bleeding - 2:1.

To correct hemostasis, transfusion of fresh frozen plasma is used. In its absence, for health reasons, it is advisable to use warm donated blood. The indication for direct blood transfusion is severe blood loss, accompanied by persistent arterial hypotension and increased bleeding (coagulopathic bleeding). The volume of direct transfusion is 300-400 ml from one donor within 10-15 minutes. At the same time, it is necessary to use inhibitors of proteolytic proteases, which regulate the relationship between the blood coagulation, fibrinolysis and kininogenesis systems and increase the body's adaptive capabilities in overcoming a critical lack of oxygen. It is recommended to use Contrical at a dose of 40,000-50,000 units. To neutralize plasmin in conditions of hemocoagulation disorders, it is advisable to use transamic acid preparations. Transamine at a dose of 500-750 mg inhibits plasmin and plasminogen receptors, preventing their fixation to fibrin, which prevents fibrinogen degradation.

Mechanical ventilation is indicated for increasing hypercapnia (increased PCO up to 60 mm Hg), the presence of symptoms of respiratory failure (hypnea, shortness of breath, cyanosis, tachycardia).

When treating HS, a mistake can be not only insufficient, but also excessive administration of solutions, which contributes to the development of severe conditions: pulmonary edema, “dextran kidney”, hypo- and hyperosmolar syndrome, uncontrolled dilatation of microcirculatory vessels.

Cessation of bleeding and stabilization of blood pressure levels in postpartum women do not fully guarantee a favorable outcome, especially in cases of severe obstetric hemorrhage. It is noted that irreversible changes in vital organs are formed not only during the period of acute circulatory disorders, but also subsequently with improper management of the post-resuscitation period.

In the post-resuscitation period, 4 stages should be distinguished: I - a period of unstable functions observed in the first 6-10 hours of treatment; II - period of relative stabilization of the main functions of the body (10-12 hours after treatment); III - period of repeated deterioration of the condition - begins from the end of the first - beginning of the second day of treatment; IV - period of improvement or progression of complications that began in stage III.

In stage I of the post-resuscitation period, the main task is to maintain systemic hemodynamics and adequate gas exchange. To maintain systemic hemodynamics in order to prevent critical arterial hypotension, it is necessary to administer solutions of hydroxyethyl starch (6 and 10% HAES - sterile, ONKONAS). Additional correction of globular blood volume is carried out by introducing red blood cells (no more than 3 days of storage). A hemoglobin level of at least 80 g/l and a hematocrit of at least 25% can be considered sufficient.

Considering the possibility of developing hypoglycemia in the post-resuscitation period, it is advisable to include solutions of concentrated carbohydrates (10 and 20%).

In stage I, it is also necessary to continue correction of hemostasis using replacement therapy (fresh frozen plasma) along with the administration of proteolysis inhibitors.

The specified infusion-transfusion program is implemented against the background of glucocorticoid therapy (hydrocortisone at least 10 mg/kg/hour) and the administration of proteolysis inhibitors at a dose of at least 10,000 units/hour.

In stage II of the post-resuscitation period (period of stabilization of functions), it is necessary to continue the normalization of microcirculation (desag-regants, heparin), correction of hypovolemia and anemia (protein preparations, red blood cells), elimination of disturbances in water-electrolyte metabolism, provision of the body’s energy needs (parenteral nutrition, glucose , fat emulsions, amino acids), oxygenation under the control of CBS, correction of immunity, desensitizing therapy.

In order to prevent purulent-septic complications in the post-resuscitation period, antibiotic therapy is carried out wide range actions.

Against the background of IT, when microcirculation is restored, under-oxidized metabolic products and various toxins enter the bloodstream, the circulation of which leads to insufficiency of the functions of vital organs. To prevent this in stage II of the post-resuscitation period, discrete plasmapheresis is indicated no later than 12 hours after surgical hemostasis. In this case, at least 70% of the bcc is exfused with adequate replacement with donor fresh frozen plasma. Plasmapheresis allows you to stop the violation of hemocoagulation potential and eliminate endotoxemia.

If stage III develops (the stage of repeated deterioration of the patient’s condition), which is characterized by the formation of multiple organ failure, then treatment is ineffective without the use of extracorporeal detoxification methods. It is necessary to use gentle detoxification methods, which include plasmapheresis, hemofiltration, hemodiafiltration and hemodialysis. When shock lung has developed, spontaneous arteriovenous or forced venovenous hemofiltration should be considered the method of choice.

With the development of renal and hepatic failure, a combination of discrete plasmapheresis and hemofiltration is performed; in acute renal failure accompanied by hyperkalemia (potassium level above 6 mmol/l), hemodialysis.

Infusion therapy in the post-resuscitation period should be carried out for at least 6-7 days, depending on the condition of the postpartum woman.

Therapy in stages III and IV of the post-resuscitation period is carried out in specialized departments.

You can note following errors in the treatment of HS: insufficient assessment of blood loss in the early stages, late diagnosis of HS; delayed implementation of measures aimed at ensuring local hemostasis; delayed replacement of blood loss, inadequate in volume and injected agents; irrational ratio between the volume of administered concentrated blood and plasma substitutes; untimely use of steroid hormones and tonics.

Women who have suffered massive blood loss may experience disability after 3-10 years. At the same time, chronic diseases of internal organs and endocrine disorders develop.