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Infectious-toxic shock is a non-specific pathological condition caused by the influence of bacteria and the toxins they secrete. Such a process can be accompanied by various disorders - metabolic, neuroregulatory and hemodynamic. This condition of the human body is urgent and requires immediate treatment. The disease can affect absolutely anyone, regardless of gender and age group. In the international classification of diseases (ICD 10), toxic shock syndrome has its own code - A48.3.
The cause of such an ailment is a severe course of infectious processes. Infectious-toxic shock in children is very often formed on the basis of. The development of such a syndrome depends entirely on the causative agent of this disease, the state of the human immune system, the presence or absence of drug therapy, and the intensity of exposure to bacteria.
The characteristic symptoms of the disease are a combination of signs of acute circulatory failure and a massive inflammatory process. Often, the external expression develops quite quickly, especially in the first few days of the progression of the underlying disease. The very first symptom is severe chills. A little later, increased sweating, intense headaches, convulsions, episodes of loss of consciousness appear. In children, this syndrome manifests itself somewhat differently - frequent vomiting, which has nothing to do with eating food, diarrhea and a gradual increase in soreness.
Diagnosis of toxic shock consists of finding the pathogen in a patient's blood tests. Treatment of the disease is based on the use of drugs and special solutions. Since such a syndrome is a very serious condition, before the patient enters a medical facility, he needs to be given first aid. The prognosis of toxic shock syndrome is relatively favorable and depends on timely diagnosis and effective treatment tactics. However, the chance of death is forty percent.
The reasons for the progression of this condition is the combination of the course of an acute infectious process and weakened human immunity. This syndrome is a common complication of the following diseases:
Other nonspecific factors in the development of infectious-toxic shock in children and adults are:
Another reason for the occurrence of this condition is the use of hygienic tampons by female representatives. This is due to the fact that during the use of such an item during menstruation, it can penetrate into the female body, which produces dangerous toxins. Often the disease affects girls and women between the ages of fifteen and thirty. The mortality rate in this case is sixteen percent. In addition, cases of the appearance of such a disorder due to the use of vaginal contraceptives have been recorded.
The pathogenesis of infectious-toxic shock is the entry of a large amount of toxic substances into the circulatory system. This process entails the release of biologically active substances, which leads to a violation of blood circulation.
There is a classification of toxic shock syndrome depending on the degree of its development. This division is based on the severity of symptoms. Thus, distinguish:
Depending on the pathogen, there are:
Symptoms of toxic shock are characterized by rapid onset and aggravation. The main features are:
In addition, there is a development of , and . A similar syndrome in young children is expressed by stronger intoxication symptoms and constant jumps in blood pressure and pulse. Toxic shock syndrome from tampons is expressed by similar signs, which are accompanied by a rash on the skin of the feet and palms.
Quite often, people mistake the above symptoms for a cold or infection, which is why they are in no hurry to seek help from specialists. Without timely diagnosis and treatment, a number of irreversible complications of infectious-toxic shock can develop:
Untimely emergency care and improper therapy lead to the death of the patient within two days after the expression of the first symptoms.
Diagnostic measures for toxic shock syndrome are aimed at detecting the causative agent of the disease. Before performing laboratory and instrumental examinations of the patient, the doctor needs to carefully study the person’s medical history, determine the intensity of symptoms, and conduct an examination. If the cause of this condition was the use of tampons, then the patients must be examined by a gynecologist.
Other diagnostic methods include:
An experienced specialist can easily determine the infectious-toxic shock by the appearance of the patient.
Before the implementation of therapy in a medical institution, it is necessary to provide the patient with emergency first aid. Such activities consist of several stages, which include:
These actions are limited to emergency care, which is performed by a non-specialist.
After the patient is transported to a medical facility, intensive treatment of toxic shock with medications begins. Often, hormonal substances, antibiotics and glucocorticoids are used to actively destroy bacteria. The use of medicines is individual and depends on the causative agent of the disease.
If the infection has occurred due to the use of tampons or vaginal contraceptives, then the treatment consists in immediately removing them from the body. This may require scraping, and the cavity is treated with antiseptic preparations.
Preventive measures for toxic shock syndrome consist in following several rules:
The prognosis of the disease will be favorable only if first aid is provided in a timely manner, the cause of this condition is identified, and drug treatment is started.
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Hemorrhagic shock (a type of hypovolemic shock)- due to uncompensated blood loss, a decrease in BCC by 20% or more.
Code according to the international classification of diseases ICD-10:
Classification. Mild degree (loss of 20% of BCC). Moderate degree (loss of 20-40% of BCC). Severe (loss of more than 40% of BCC).
Compensatory mechanisms. secretion of ADH. secretion of aldosterone and renin. secretion of catecholamines.
Physiological reactions. Decreased diuresis. Vasoconstriction. Tachycardia.
Pathogenesis. Adaptation of the patient to blood loss is largely determined by changes in the capacity of the venous system (containing up to 75% of blood volume in a healthy person). However, the possibilities for mobilizing blood from the depot are limited: with a loss of more than 10% of the BCC, the CVP begins to fall and the venous return to the heart decreases. There is a syndrome of small ejection, leading to a decrease in perfusion of tissues and organs. In response, nonspecific compensatory endocrine changes appear. The release of ACTH, aldosterone and ADH leads to the retention of sodium, chlorides and water by the kidneys, while increasing potassium loss and reducing diuresis. The result of the release of epinephrine and norepinephrine is peripheral vasoconstriction. Less important organs (skin, muscles, intestines) are switched off from the blood flow, and the blood supply to vital organs (brain, heart, lungs) is preserved, i.e. circulation is centralized. Vasoconstriction leads to deep tissue hypoxia and the development of acidosis. Under these conditions, proteolytic enzymes of the pancreas enter the bloodstream and stimulate the formation of kinins. The latter increase the permeability of the vascular wall, which contributes to the transition of water and electrolytes into the interstitial space. As a result, aggregation of red blood cells occurs in the capillaries, creating a springboard for the formation of blood clots. This process immediately precedes the irreversibility of the shock.
Clinical picture. With the development of hemorrhagic shock, 3 stages are distinguished.
Compensated reversible shock. The volume of blood loss does not exceed 25% (700-1300 ml). Moderate tachycardia, blood pressure is either unchanged or slightly reduced. Saphenous veins become empty, CVP decreases. There is a sign of peripheral vasoconstriction: cold extremities. The amount of urine excreted is reduced by half (at a rate of 1-1.2 ml / min).
Decompensated reversible shock. The volume of blood loss is 25-45% (1300-1800 ml). The pulse rate reaches 120-140 per minute. Systolic blood pressure falls below 100 mm Hg, the value of pulse pressure decreases. Severe shortness of breath occurs, partly compensating for metabolic acidosis by respiratory alkalosis, but can also be a sign of a shock lung. Increased cold extremities, acrocyanosis. Cold sweat appears. The rate of urine output is below 20 ml/h.
Irreversible hemorrhagic shock. Its occurrence depends on the duration of circulatory decompensation (usually with arterial hypotension over 12 hours). The volume of blood loss exceeds 50% (2000-2500 ml). The pulse exceeds 140 per minute, systolic blood pressure falls below 60 mm Hg. or not defined. Consciousness is absent. oligoanuria develops.
TREATMENT. In hemorrhagic shock, vasopressor drugs (epinephrine, norepinephrine) are strictly contraindicated, since they aggravate peripheral vasoconstriction. For the treatment of arterial hypotension that has developed as a result of blood loss, the following procedures are sequentially performed.
Catheterization of the main vein (most often the subclavian or internal jugular according to Seldinger).
Jet intravenous administration of blood substitutes (polyglucin, gelatinol, rheopolyglucin, etc.). Transfuse fresh frozen plasma and, if possible, albumin or protein. With moderate shock and severe shock, blood transfusion is performed.
Fight against metabolic acidosis: infusion of 150-300 ml of 4% solution of sodium bicarbonate.
GC simultaneously with the beginning of blood replacement (up to 0.7-1.5 g of hydrocortisone IV). Contraindicated in case of suspected gastric bleeding.
Removal of spasm of peripheral vessels. Given the presence (as a rule) of hypothermia - warming the patient.
Aprotinin 30,000-60,000 IU in 300-500 ml of 0.9% solution of sodium chloride intravenously drip.
Humidified oxygen inhalation.
Broad-spectrum antibiotics in the presence of wounds, septic diseases.
Maintenance of diuresis (50-60 ml / h) .. Adequate infusion therapy (until CVP reaches 120-150 mm of water column) .. If the infusion is ineffective - osmotic diuretics (mannitol 1-1.5 g / kg in 5% r - re-glucose intravenously, in the absence of effect - furosemide 40-160 mg intramuscularly or intravenously.
Cardiac glycosides (contraindicated in conduction disorders [complete or partial AV block] and myocardial excitability [occurrence of ectopic foci of excitation]). With the development of bradycardia - stimulants of b-adrenergic receptors (isoprenaline 0.005 g sublingually). In the event of ventricular arrhythmias - lidocaine 0.1-0.2 g IV.
ICD-10 . R57.1 hypovolemic shock
Peripheral circulatory failure NOS
In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to apply to medical institutions of all departments, and causes of death.
ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170
The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.
With amendments and additions by WHO.
Processing and translation of changes © mkb-10.com
Hemorrhagic shock (a kind of hypovolemic shock) - due to uncompensated blood loss, a decrease in BCC by 20% or more.
Classification Mild (loss of 20% of BCC) Moderate (loss of 20–40% of BCC) Severe (loss of more than 40% of BCC).
Compensatory mechanisms Secretion of ADH Secretion of aldosterone and renin Secretion of catecholamines.
Physiological reactions Decreased diuresis Vasoconstriction Tachycardia.
Pathogenesis. Adaptation of the patient to blood loss is largely determined by changes in the capacity of the venous system (containing up to 75% of blood volume in a healthy person). However, the possibilities for mobilizing blood from the depot are limited: with a loss of more than 10% of the BCC, the CVP begins to fall and the venous return to the heart decreases. There is a syndrome of small ejection, leading to a decrease in perfusion of tissues and organs. In response, nonspecific compensatory endocrine changes appear. The release of ACTH, aldosterone and ADH leads to the retention of sodium, chlorides and water by the kidneys, while increasing potassium loss and reducing diuresis. The result of the release of epinephrine and norepinephrine is peripheral vasoconstriction. Less important organs (skin, muscles, intestines) are switched off from the blood flow, and the blood supply to vital organs (brain, heart, lungs) is preserved, i.e. circulation is centralized. Vasoconstriction leads to deep tissue hypoxia and the development of acidosis. Under these conditions, proteolytic enzymes of the pancreas enter the bloodstream and stimulate the formation of kinins. The latter increase the permeability of the vascular wall, which contributes to the transition of water and electrolytes into the interstitial space. As a result, aggregation of red blood cells occurs in the capillaries, creating a springboard for the formation of blood clots. This process immediately precedes the irreversibility of the shock.
clinical picture. With the development of hemorrhagic shock, 3 stages are distinguished.
Compensated reversible shock. The volume of blood loss does not exceed 25% (700-1300 ml). Moderate tachycardia, blood pressure is either unchanged or slightly reduced. Saphenous veins become empty, CVP decreases. There is a sign of peripheral vasoconstriction: cold extremities. The amount of urine excreted is reduced by half (at a rate of 1–1.2 ml / min).
Decompensated reversible shock. The volume of blood loss is 25–45% (1300–1800 ml). The pulse rate reaches 120-140 per minute. Systolic blood pressure falls below 100 mm Hg, the value of pulse pressure decreases. Severe shortness of breath occurs, partly compensating for metabolic acidosis by respiratory alkalosis, but can also be a sign of a shock lung. Increased cold extremities, acrocyanosis. Cold sweat appears. The rate of urine output is below 20 ml/h.
Irreversible hemorrhagic shock. Its occurrence depends on the duration of circulatory decompensation (usually with arterial hypotension over 12 hours). The volume of blood loss exceeds 50% (2000-2500 ml). The pulse exceeds 140 per minute, systolic blood pressure falls below 60 mm Hg. or not defined. Consciousness is absent. oligoanuria develops.
TREATMENT. In hemorrhagic shock, vasopressor drugs (epinephrine, norepinephrine) are strictly contraindicated, since they aggravate peripheral vasoconstriction. For the treatment of arterial hypotension that has developed as a result of blood loss, the following procedures are sequentially performed.
Catheterization of the main vein (most often the subclavian or internal jugular according to Seldinger).
Jet intravenous administration of blood substitutes (polyglucin, gelatinol, rheopolyglucin, etc.). Transfuse fresh frozen plasma and, if possible, albumin or protein. With moderate shock and severe shock, blood transfusion is performed.
Fight against metabolic acidosis: infusion of 150–300 ml of 4% solution of sodium bicarbonate.
GC simultaneously with the beginning of blood replacement (up to 0.7-1.5 g of hydrocortisone IV). Contraindicated in case of suspected gastric bleeding.
Removal of spasm of peripheral vessels. Given the presence (as a rule) of hypothermia - warming the patient.
Aprotinin-ED in 300-500 ml of 0.9% solution of sodium chloride intravenously drip.
Humidified oxygen inhalation.
Broad-spectrum antibiotics in the presence of wounds, septic diseases.
Maintenance of diuresis (50–60 ml/h) Adequate infusion therapy (until CVP reaches 120–150 mm of water column) / in a jet), in the absence of effect - furosemide 40-160 mg IM or IV.
Cardiac glycosides (contraindicated in conduction disorders [complete or partial AV block] and myocardial excitability [occurrence of ectopic foci of excitation]). With the development of bradycardia - stimulants b - adrenoreceptors (isoprenaline 0.005 g sublingually). If ventricular arrhythmias occur, lidocaine 0.1–0.2 g IV.
A sharp violation of the usual blood circulation causes a shock condition, which is called hemorrhagic. This is an acute reaction of the body, provoked by the inability to control vital systems as a result of a sudden loss of blood. In the International Classification of Diseases of the 10th revision (ICD-10), the condition is classified as one of the types of hypovolemic shock (code R57.1) - an emergency pathological condition caused by a sharp decrease in circulating blood volume due to dehydration.
They are divided into 3 main groups:
Most often, obstetrician-gynecologists meet with hemorrhagic shock, because this condition is one of the main causes of maternal death. In gynecology, this shock leads to:
The clinical picture depends on the stage of shock, each of which is discussed in the table:
The development of hemorrhagic shock usually leads to hemorrhages exceeding 1000 ml, i.e., the loss of more than 20% of BCC or 15 ml of blood per 1 kg of body weight. Ongoing bleeding, in which blood loss exceeds 1500 ml (more than 30% of BCC), is considered massive and poses an immediate threat to the life of a woman. The volume of circulating blood in women is not the same, depending on the constitution, it is: in normosthenics - 6.5% of body weight, in asthenics - 6.0%, in picnics - 5.5%, in muscular women of athletic build - 7%, therefore, the absolute numbers of BCC may vary, which must be taken into account in clinical practice.
The causes of bleeding leading to shock in gynecological patients can be: disturbed ectopic pregnancy, ovarian rupture, spontaneous and induced abortion, miscarriage, hydatidiform mole, dysfunctional uterine bleeding, submucosal form of uterine fibroids, genital trauma.
Whatever the cause of massive bleeding, the leading link in the pathogenesis of hemorrhagic shock is the disproportion between the reduced BCC and the capacity of the vascular bed, which is first manifested by a violation of macrocirculation, i.e., systemic circulation, then microcirculatory disorders appear and, as a result, progressive disorganization develops metabolism, enzymatic shifts and proteolysis.
The macrocirculation system is formed by arteries, veins and the heart. The microcirculation system includes arterioles, venules, capillaries and arteriovenous anastomoses. As you know, about 70% of the total bcc is in the veins, 15% - in the arteries, 12% - in the capillaries, 3% - in the chambers of the heart.
With blood loss not exceeding ml, i.e., about 10% of the BCC, compensation occurs due to an increase in the tone of the venous vessels, the receptors of which are most sensitive to hypovolemia. In this case, there is no significant change in arterial tone, heart rate, tissue perfusion does not change.
Symptoms of hemorrhagic shock have the following stages:
The stages of shock are determined on the basis of an assessment of the complex of clinical manifestations of blood loss, corresponding to pathophysiological changes in organs and tissues.
Stage 1 hemorrhagic shock (small ejection syndrome, or compensated shock) usually develops with blood loss approximately corresponding to 20% of the BCC (from 15% to 25%). In this stage, compensation for the loss of bcc. due to overproduction of catecholamines. The clinical picture is dominated by symptoms indicating a change in cardiovascular activity of a functional nature: pallor of the skin, desolation of the saphenous veins in the arms, moderate tachycardia up to 100 beats / min, moderate oliguria and venous hypotension. Arterial hypotension is absent or mild.
If the bleeding has stopped, then the compensated stage of shock can last quite a long time. With unchecked bleeding, further deepening of circulatory disorders occurs, and the next stage of shock occurs.
The treatment of hemorrhagic shock is an extremely responsible task, for which the gynecologist must join forces with the anesthesiologist-resuscitator, and, if necessary, involve a hematologist-coagulologist.
To ensure the success of therapy, it is necessary to be guided by the following rule: treatment should begin as early as possible, be comprehensive, be carried out taking into account the cause of the bleeding and the patient's state of health that preceded it.
The complex of therapeutic measures includes the following:
All of these activities should be carried out in parallel, clearly and quickly.
Portnov Alexey Alexandrovich
Education: Kyiv National Medical University. A.A. Bogomolets, specialty - "Medicine"
Hemorrhagic shock develops due to a decrease in BCC during bleeding, which leads to a critical decrease in tissue blood flow and the development of tissue hypoxia.
Hypovolemic hemorrhagic shock.
O75.1 Shock during or after labor and delivery.
Women die every year from childbirth-related bleeding. MS from obstetric bleeding and hemorrhagic shock in the Russian Federation for 2001–2005. is 63-107 live births or 15.8-23.1% in the MS structure.
The main cause of death in hemorrhagic shock in obstetrics is the underestimation of the volume of blood loss, belated and insufficiently vigorous therapeutic measures. With obstetric bleeding, timely provision of qualified assistance is necessary.
The causes of hemorrhagic shock in obstetrics are massive bleeding in the second half of pregnancy, during and after childbirth (loss of more than 1000 ml of blood, i.e. ³15% of BCC or ³1.5% of body weight). The following conditions are considered life-threatening bleeding:
Loss of 100% BCC within 24 hours or 50% BCC in 3 hours;
· blood loss at a rate of 150 ml/min or 1.5 ml/(kg´min) for 20 minutes or longer;
One-stage blood loss ³1500–2000 ml (25–35% of BCC).
The causes of massive bleeding during pregnancy and childbirth can be premature detachment of a normally or low-lying placenta, placenta previa, uterine rupture, membrane attachment of the umbilical cord. The causes of massive bleeding in the third stage of labor and the early postpartum period are hypotension and atony of the uterus, placental defects, tight attachment and accretion of the placenta, trauma to the birth canal, uterine inversion, and bleeding disorders. A mnemonic designation of the causes of postpartum hemorrhage is proposed - "4 T": tone, tissue, trauma, thrombin.
Blood loss of ³15% of the BCC leads to the activation of compensatory reactions, including stimulation of the sympathetic nervous system due to reflexes from the baroreceptors of the carotid sinus zone and large intrathoracic arteries, activation of the hypothalamic-pituitary-adrenal system with the release of catecholamines, angiotensin, vasopressin, and antidiuretic hormone. These changes contribute to spasm of arterioles, increase in venous vascular tone (increase in venous return and preload), increase in heart rate and heart rate, and decrease in excretion of sodium and water in the kidneys. Due to the fact that the hydrostatic pressure in the capillaries decreases more than in the interstitium, in the period 1-40 hours after blood loss, there is a slow movement of the intercellular fluid into the vascular bed (transcapillary replenishment). A decrease in blood flow in organs and tissues leads to changes in arterial blood acid-base balance - an increase in lactate concentration and an increase in base deficiency. In order to maintain normal pH, when acidemia affects the chemoreceptor of the respiratory center of the brainstem, minute ventilation increases, leading to a decrease in carbon dioxide tension in the blood.
With blood loss of ³30% of the BCC, decompensation occurs in the form of arterial hypotension - a decrease in systolic blood pressure less than 90 mm Hg. If the condition was preceded by hypertension, a level of 100 mm Hg should be considered decompensation, and with severe gestosis, even “normal” systolic blood pressure numbers. Continued release of stress hormones causes glycogenolysis, lipolysis (moderate hyperglycemia and hypokalemia). Hyperventilation is insufficient to maintain normal arterial blood pH, resulting in acidosis. A further decrease in tissue blood flow leads to an increase in anaerobic metabolism with an increase in the release of lactic acid.
Progressive metabolic lactic acidosis lowers tissue pH and blocks vasoconstriction. There is an expansion of arterioles, blood fills the microcirculatory bed. Cardiac output falls, damage to endothelial cells and the development of DIC are possible.
With blood loss ³40% of the BCC and a decrease in systolic blood pressure ³50 mm Hg. CNS ischemia additionally stimulates the sympathetic nervous system, which leads to the formation of the so-called second BP plateau. Without vigorous intensive care, shock passes into an irreversible stage (common cell damage, PON, worsening of myocardial contractility up to cardiac arrest).
After the restoration of cardiac output and tissue blood flow, more pronounced organ damage is possible than during the period of hypotension. Due to the activation of neutrophils, the release of oxygen radicals by them, the release of inflammatory mediators from ischemic tissues, damage to cell membranes occurs, an increase in the permeability of the pulmonary endothelium with the development of acute RDS, mosaic intralobular damage to the liver with an increase in plasma transaminase activity. Possible spasm of the preglomerular arterioles of the kidneys, the development of acute tubular necrosis and acute renal failure. Due to a decrease in the release of glucose by the liver, a violation of the hepatic production of ketones and inhibition of peripheral lipolysis, there is a violation of the supply of energy substrates to the heart and brain.
Obstetric bleeding is divided into four classes depending on the amount of blood loss (Table 53-3).
Table 53-3. Classification of bleeding and clinical stages of hemorrhagic shock during pregnancy (for a pregnant woman weighing 60 kg and with a circulating blood volume of 6000 ml)
Acute hemorrhage is a sudden release of blood from the vascular bed. The main clinical symptoms of the resulting decrease in BCC (hypovolemia) are pallor of the skin and visible mucous membranes, tachycardia and arterial hypotension.
Stage 2 (decompensated shock) is characterized by an increase in cardiovascular disorders, there is a breakdown of the compensatory mechanisms of the body. Blood loss is 25-40% of the BCC, impaired consciousness to soporous, acrocyanosis, cold extremities, blood pressure is sharply reduced, tachycardia beats / min, the pulse is weak, thready, shortness of breath, oliguria up to 20 ml / hour.
Stage 3 (irreversible shock) is a relative concept and largely depends on the methods of resuscitation used. The patient's condition is extremely serious. Consciousness is sharply depressed to complete loss, the skin is pale, "marbling" of the skin, systolic pressure is below 60, the pulse is determined only on the main vessels, a sharp tachycardia doud/min.
As an express diagnostic for assessing the severity of shock, the concept of a shock index is used - SI - the ratio of heart rate to systolic pressure. With shock of the 1st degree, SI = 1 (100/100), shock of the 2nd degree - 1.5 (120/80), shock of the 3rd degree - 2 (140/70).
Hemorrhagic shock is characterized by a general severe condition of the body, insufficient blood circulation, hypoxia, metabolic disorders and organ functions. The pathogenesis of shock is based on hypotension, hypoperfusion (decrease in gas exchange) and hypoxia of organs and tissues. The leading damaging factor is circulatory hypoxia.
A relatively rapid loss of 60% of the BCC is considered fatal for a person, a blood loss of 50% of the BCC leads to a breakdown in the compensation mechanism, and a blood loss of 25% of the BCC is almost completely compensated by the body.
The ratio of the amount of blood loss and its clinical manifestations:
Blood loss% BCC (ml), no hypovolemia, blood pressure is not reduced;
Blood loss% BCC (ml), mild hypovolemia, blood pressure reduced by 10%, moderate tachycardia, pallor of the skin, cold extremities;
Blood loss% BCC ml), moderate severity of hypovolemia, blood pressure reduced to, tachycardia up to 120 beats / min, pallor of the skin, cold sweat, oliguria;
Blood loss up to 50% of BCC ml), severe hypovolemia, blood pressure reduced to 60, thready pulse, consciousness is absent or confused, severe pallor, cold sweat, anuria;
Blood loss of 60% of the BCC is fatal.
The initial stage of hemorrhagic shock is characterized by a disorder of microcirculation due to the centralization of blood circulation. The mechanism of centralization of blood circulation occurs due to an acute deficiency of the BCC due to blood loss, the venous return to the heart decreases, the venous return to the heart decreases, the stroke volume of the heart decreases and blood pressure falls. As a result, the activity of the sympathetic nervous system increases, the maximum release of catecholamines (adrenaline and norepinephrine) occurs, the heart rate increases and the total peripheral vascular resistance to blood flow increases.
In the early stage of shock, the centralization of circulation provides blood flow in the coronary vessels and vessels of the brain. The functional state of these organs is very important for maintaining the vital activity of the organism.
If there is no replenishment of the BCC and the sympathoadrenergic reaction is delayed in time, then in the general picture of shock, the negative aspects of vasoconstriction of the microcirculatory bed appear - a decrease in perfusion and hypoxia of peripheral tissues, due to which centralization of blood circulation is achieved. In the absence of such a reaction, the body dies in the first minutes after blood loss from acute circulatory failure.
The main laboratory parameters for acute blood loss are hemoglobin, erythrocytes, hematocrit (the volume of erythrocytes, the norm for men%, for women%). The determination of BCC in emergency situations is difficult and is associated with a loss of time.
Disseminated intravascular coagulation syndrome (DIC) is a severe complication of hemorrhagic shock. The development of DIC-syndrome is facilitated by a violation of microcirculation as a result of massive blood loss, trauma, shock of various etiologies, transfusion of large amounts of canned blood, sepsis, severe infectious diseases, etc.
The first stage of DIC is characterized by the predominance of hypercoagulability with simultaneous activation of anticoagulant systems in patients with blood loss and trauma.
The second stage of hypercoagulability is manifested by coagulopathic bleeding, the stop and treatment of which is very difficult.
The third stage is characterized by a hypercoagulable syndrome, the development of thrombotic complications or repeated bleeding is possible.
Both coagulopathic bleeding and hypercoagulable syndrome serve as a manifestation of a general process in the body - thrombohemorrhagic syndrome, the expression of which in the vascular bed is DIC - syndrome. It develops against the background of severe circulatory disorders (crisis of microcirculation) and metabolism (acidosis, accumulation of biologically active substances, hypoxia).
With a slow loss of even large volumes of blood, compensatory mechanisms have time to turn on, hemodynamic disturbances occur gradually and are not very serious. On the contrary, intense bleeding with the loss of a smaller volume of blood leads to severe hemodynamic disturbances and, as a result, to hemorrhagic shock.
1, Reduction or elimination of existing phenomena of acute respiratory failure (ARF), the cause of which may be aspiration of broken teeth, blood, vomit, cerebrospinal fluid in case of a fracture of the skull base. Especially often this complication is observed in patients with confused or absent consciousness and, as a rule, is combined with the retraction of the root of the tongue.
Treatment is reduced to the mechanical release of the mouth and oropharynx, aspiration of the contents using suction. Transportation can be carried out with an inserted air duct or endotracheal tube and ventilation through them.
2. Carrying out anesthesia with medications that do not depress breathing and blood circulation. Of the central narcotic analgesics, devoid of the side effects of opiates, you can use lexir, fortral, tramal. Non-narcotic analgesics (analgin, baralgin) can be combined with antihistamines. There are options for performing oxygen-oxygen analgesia, intravenous administration of subnarcotic doses of ketamine (calypsol, ketalara), but these are purely anesthetic aids that require the presence of an anesthesiologist and the necessary equipment.
3, Reduction or elimination of hemodynamic disorders, primarily hypovolemia. In the first minutes after a severe injury, the main cause of hypovolemia and hemodynamic disorders is blood loss. Prevention of cardiac arrest and all other serious disorders - immediate and maximum possible elimination of hypovolemia. The main therapeutic measure should be massive and rapid infusion therapy. Of course, stopping external bleeding should precede infusion therapy.
Resuscitation in case of clinical death due to acute blood loss is carried out according to generally accepted rules.
The main task in acute blood loss and hemorrhagic shock at the hospital stage is to carry out a set of measures in a certain relationship and sequence. Transfusion therapy is only a part of this complex and is aimed at replenishing the BCC.
In carrying out intensive care for acute blood loss, it is necessary to reliably ensure continuous transfusion therapy with a rational combination of available funds. It is equally important to observe a certain stage in treatment, the speed and adequacy of assistance in the most difficult situation.
An example would be the following procedure:
Immediately upon admission to the patient, blood pressure, pulse rate and respiration are measured, the bladder is catheterized and the excreted urine is taken into account, all these data are recorded;
Catheterize the central or peripheral vein, start infusion therapy, measure CVP. In case of collapse, without waiting for catheterization, a jet infusion of polyglucin is started by puncturing a peripheral vein;
A jet infusion of polyglucin restores the central blood supply, and a jet infusion of saline restores diuresis;
The number of erythrocytes in the blood and the content of hemoglobin, hematocrit, as well as the approximate amount of blood loss and more possible in the coming hours, indicate the required amount of donor blood;
Determine the patient's blood type and Rh affiliation. After receiving these data and donated blood, tests are carried out for individual and Rh compatibility, a biological test, and blood transfusion is started;
With an increase in CVP in excess of 12 cm of the water column, the infusion rate is limited to rare drops;
If surgery is planned, decide on the possibility of its implementation;
After normalization of blood circulation, they maintain water balance and normalize the indicators of hemoglobin, erythrocytes, protein and ;.
Stop continuous IV infusion after a 3-4 hour observation proves: no new bleeding, stabilization of blood pressure, normal urine output and no threat of heart failure.
Hemorrhagic shock and DIC
Hemorrhagic shock (HS) is the main and immediate cause of death in parturient women and puerperas, and continues to be the most dangerous manifestation of various diseases that determine the lethal outcome. HS is a critical condition associated with acute blood loss, which results in a crisis of macro- and microcirculation, a syndrome of multiple organ and polysystemic insufficiency. The source of acute massive blood loss in obstetric practice can be:
Premature detachment of a normally located placenta
Bleeding in the afterbirth and early postpartum period
Damage to the soft tissues of the birth canal (ruptures of the body and cervix, vagina, genital organs);
Damage to the vessels of parametric fiber with the formation of large hematomas.
Many women during pregnancy against the background of late toxicosis of somatic diseases have a "readiness" for shock due to severe initial hypovolemia and chronic circulatory insufficiency. Hypovolemia of pregnant women is often observed with polyhydramnios, multiple pregnancies, vascular allergic lesions, circulatory failure, inflammatory diseases of the kidneys.
HS leads to severe multiple organ disorders. As a result of hemorrhagic shock, the lungs are affected with the development of acute pulmonary insufficiency of the "shock lung" type. With HSH, the renal blood flow sharply decreases, hypoxia of the renal tissue develops, and the formation of a "shock kidney" occurs. Especially unfavorable is the effect of HS on the liver, in which morphological and functional changes cause the development of a "shock liver". Sharp changes in hemorrhagic shock also occur in the adenohypophysis, leading to its necrosis. Thus, with HS, there are syndromes of multiple organ failure.
PATHOGENESIS. Acute blood loss, decreased BCC, venous return, and cardiac output lead to activation of the sympathetic-adrenal system, which leads to vasospasm, arterioles, and precapillary sphincters in various organs, including the brain and heart. There is a redistribution of blood in the vascular bed, autohemodilution (transition of fluid into the vascular bed) against the backdrop of a decrease in hydrostatic pressure. The cardiac output continues to decrease, a persistent spasm of arterioles occurs, the rheological properties of the blood change (erythrocyte sludge aggregation is a phenomenon).
In the future, peripheral vascular spasm becomes the cause of the development of microcirculation disorders and leads to irreversible shock, which is divided into the following phases:
Phase of vasoconstriction with reduced capillary blood flow
The phase of vasodilation with the expansion of the vascular space and a decrease in blood flow in the capillaries;
Phase of disseminated intravascular coagulation (DIC);
Phase of irreversible shock.
In response to DIC, the fibrinolytic system is activated; clots are lysed and blood flow is disturbed.
CLINIC GSH is determined by the mechanisms leading to a deficiency of the BCC, changes in the CBS of the blood and electrolyte balance, impaired peripheral circulation and DIC syndrome.
The symptom complex of clinical signs of HS includes: weakness, dizziness, thirst, nausea, dry mouth, darkening of the eyes, pallor of the skin, cold and wet, sharpening of facial features, tachycardia and weak filling of the pulse, decrease in blood pressure, shortness of breath, cyanosis.
The degree of severity distinguishes between compensated, decompensated, reversible and irreversible shock. There are 4 degrees of hemorrhagic shock.
1 degree GSH, BCC deficiency up to 15%. BP above 100 mm Hg central venous pressure (CVP) within normal limits. Slight pallor of the skin and increased heart rate doud / min, hemoglobin 90g / or more.
2 degree GSH. BCC deficit up to 30%. The state of moderate severity, weakness, dizziness, darkening in the eyes, nausea, lethargy, pallor of the skin are observed. Arterial hypotension domm Hg, decrease in CVP (below 60 mm water column), tachycardia doud / min, decrease in diuresis, hemoglobin to 80 g / l or less.
3 degree GSH. Deficiency of BCC 30-40%. The condition is severe or very severe, lethargy, confusion, pallor of the skin, cyanosis. BP low mmHg Tachycardia doud / min, weak filling of the pulse. Oliguria.
4 degree GSH Deficit of BCC more than 40%. The extreme degree of oppression of all vital functions: consciousness is absent, blood pressure and CVP, and the pulse on the peripheral arteries is not determined. Breathing shallow, frequent. Hyporeflexia. Anuria.
Diagnosis of HS is simple, but determining the degree of its severity, as well as the volume of blood loss, can cause certain difficulties.
Deciding the severity of shock means determining the amount of intensive treatment.
It is difficult to determine the amount of blood loss. There are direct and indirect methods for assessing blood loss.
Direct methods for assessing blood loss: colorimetric, gravimetric, electrometric, gravitational - by changes in hemoglobin and hematocrit.
Indirect methods: assessment of clinical signs, measurement of blood loss using graduated cylinders or a visual method, determination of BCC, hourly diuresis, composition and density of urine. Approximately the amount of blood loss can be determined by calculating the Algover shock index (the ratio of pulse rate to the level of systolic blood pressure).
Shock index Volume of blood loss (% CBV)
The severity of HSH depends on the individual tolerance of blood loss, premorbid background, obstetric pathology and method of delivery. Features of the development of HS in various obstetric pathologies are different.
GS with placenta previa. Factors contributing to the development of shock in placenta previa are: arterial hypertension, iron deficiency anemia, reduced increase in BCC by the onset of labor. Repeated bleeding during pregnancy or childbirth leads to the activation of thromboplastin, a decrease in blood coagulation and the development of hypocoagulation.
GSh with premature detachment of a normally located placenta. A feature of the development of HS in this pathology is the unfavorable background of chronic peripheral circulatory disorders. In this case, there is a loss of plasma, hyperviscosity, stasis and lysis of erythrocytes, activation of endogenous thromboplastin, platelet consumption, chronic DIC. Chronic circulatory disorders are always observed with toxicosis of pregnant women, especially with its prolonged course, against the background of somatic diseases, such as diseases of the kidneys and liver, cardiovascular system, anemia. With placental abruption, extravasation occurs, releasing thromboplastins and biogenic amines in the process of cell destruction, which “trigger” the mechanism of hemostasis system disruption. Against this background, coagulopathic disorders quickly occur. HS with premature detachment of a normally located placenta is especially difficult, accompanied by anuria, cerebral edema, respiratory failure, and a closed hematoma of the retroplacental space by the type of compression syndrome contributes to this. The lives of patients depend on the rapid adoption of tactical decisions and measures.
GSH in hypotonic bleeding. Hypotonic bleeding and massive blood loss (1500 ml or more) are accompanied by compensation instability. At the same time, hemodynamic disturbances, symptoms of respiratory failure, a syndrome with profuse bleeding due to the consumption of blood coagulation factors and a sharp activity of fibrinolysis develop. This leads to irreversible multiple organ changes.
GSH with uterine rupture. A feature is the combination of hemorrhagic and traumatic shock, which contribute to the rapid development of DIC, hypovolemia and respiratory failure.
ICE syndrome. It proceeds in the form of successive phases, which in practice can not always be clearly distinguished. The following phases are distinguished: 1 - hypercoagulability; 2 - hypocoagulation (consumption coagulopathy) without generalized fibrin activation; 3. - hypocoagulation (coagulopathy of consumption with generalized activation of fibrinolysis - secondary fibrinolysis); 4 - complete non-clotting, terminal degree of hypocoagulation. The central mechanism underlying bleeding in DIC is the incorporation of plasma coagulation factors, including fibrinogen, into microthrombi. Activation of plasma factors entails the consumption of the main blood anticoagulant (antithrombin 3) and a significant decrease in its activity. Blockade of microcirculation, impaired transcapillary metabolism, hypoxia of vital organs in obstetric bleeding lead to a violation of the rheological properties of blood and its complete non-clotting.
The main factors contributing to the development of DIC:
severe forms of late toxicosis of pregnant women
premature detachment of a normally located placenta
amniotic fluid embolism
extragenital pathology (diseases of the cardiovascular system, kidneys, liver).
Blood transfusion complications (transfusion of incompatible blood).
Ante- and intrapartum fetal death.
hemorrhagic manifestations (skin petechial hemorrhages at injection sites, in the sclera of the eyes, in the mucous membrane of the gastrointestinal tract, etc.).
profuse bleeding from the uterus
thrombotic manifestations (limb ischemia, infarct pneumonia, thrombosis of the main vessels)
dysfunction of the central nervous system (disorientation, stupor, coma).
Violation of the function of external respiration (dyspnea, cyanosis, tachycardia).
The clinical manifestations of the DIC syndrome are diverse and change in different phases. The duration of clinical manifestations is 7-9 hours or more. Important is the laboratory diagnosis of the phases of the DIC syndrome. The following tests are most informative and quickly performed: determination of whole blood clotting time and thrombin time, thrombin test, spontaneous lysis of a whole blood clot, platelet count, etc.
Clinical and laboratory data specific for each phase of DIC. Massive and rapid blood loss is associated with a decrease in the content of fibrinogen, platelets, other blood coagulation factors and impaired fibrinolysis.
Stage 1 (compensated shock), when the blood loss is 15-25% of the BCC, the patient's consciousness is preserved, the skin is pale, cold, blood pressure is moderately reduced, the pulse is weak filling, moderate tachycardia up to 90-110 beats / min.
Stage 2 (decompensated shock) is characterized by an increase in cardiovascular disorders, there is a breakdown of the compensatory mechanisms of the body. Blood loss is 25-40% of the BCC, impaired consciousness to soporous, acrocyanosis, cold extremities, blood pressure is sharply reduced, tachycardia is 120-140 beats / min, the pulse is weak, thready, shortness of breath, oliguria up to 20 ml / hour.
Stage 3 (irreversible shock) is a relative concept and largely depends on the methods of resuscitation used. The patient's condition is extremely serious. Consciousness is sharply depressed to complete loss, the skin is pale, "marbling" of the skin, systolic pressure is below 60, the pulse is determined only on the main vessels, a sharp tachycardia up to 140-160 beats / min.
As an express diagnostic for assessing the severity of shock, the concept of a shock index is used - SI - the ratio of heart rate to systolic pressure. With shock of the 1st degree, SI = 1 (100/100), shock of the 2nd degree - 1.5 (120/80), shock of the 3rd degree - 2 (140/70).
Hemorrhagic shock is characterized by a general severe condition of the body, insufficient blood circulation, hypoxia, metabolic disorders and organ functions. The pathogenesis of shock is based on hypotension, hypoperfusion (decrease in gas exchange) and hypoxia of organs and tissues. The leading damaging factor is circulatory hypoxia.
A relatively rapid loss of 60% of the BCC is considered fatal for a person, a blood loss of 50% of the BCC leads to a breakdown in the compensation mechanism, and a blood loss of 25% of the BCC is almost completely compensated by the body.
The ratio of the amount of blood loss and its clinical manifestations:
Blood loss 10-15% BCC (450-500 ml), no hypovolemia, blood pressure is not reduced;
Blood loss 15-25% of the BCC (700-1300 ml), mild hypovolemia, blood pressure reduced by 10%, moderate tachycardia, pallor of the skin, cold extremities;
Blood loss 25-35% of BCC (1300-1800 ml), moderate severity of hypovolemia, blood pressure reduced to 100-90, tachycardia up to 120 beats / min, pallor of the skin, cold sweat, oliguria;
Blood loss up to 50% of the BCC (2000-2500 ml), severe hypovolemia, blood pressure reduced to 60, thready pulse, consciousness is absent or confused, severe pallor, cold sweat, anuria;
Blood loss of 60% of the BCC is fatal.
The initial stage of hemorrhagic shock is characterized by a disorder of microcirculation due to the centralization of blood circulation. The mechanism of centralization of blood circulation occurs due to an acute deficiency of the BCC due to blood loss, the venous return to the heart decreases, the venous return to the heart decreases, the stroke volume of the heart decreases and blood pressure falls. As a result, the activity of the sympathetic nervous system increases, the maximum release of catecholamines (adrenaline and norepinephrine) occurs, the heart rate increases and the total peripheral vascular resistance to blood flow increases.
In the early stage of shock, the centralization of circulation provides blood flow in the coronary vessels and vessels of the brain. The functional state of these organs is very important for maintaining the vital activity of the organism.
If there is no replenishment of the BCC and the sympathoadrenergic reaction is delayed in time, then in the general picture of shock, the negative aspects of vasoconstriction of the microcirculatory bed appear - a decrease in perfusion and hypoxia of peripheral tissues, due to which centralization of blood circulation is achieved. In the absence of such a reaction, the body dies in the first minutes after blood loss from acute circulatory failure.
The main laboratory parameters for acute blood loss are hemoglobin, erythrocytes, hematocrit (the volume of erythrocytes, the norm for men is 44-48%, for women 38-42%). The determination of BCC in emergency situations is difficult and is associated with a loss of time.
Disseminated intravascular coagulation syndrome (DIC) is a severe complication of hemorrhagic shock. The development of DIC-syndrome is facilitated by a violation of microcirculation as a result of massive blood loss, trauma, shock of various etiologies, transfusion of large amounts of canned blood, sepsis, severe infectious diseases, etc.
The first stage of DIC is characterized by the predominance of hypercoagulability with simultaneous activation of anticoagulant systems in patients with blood loss and trauma.
The second stage of hypercoagulability is manifested by coagulopathic bleeding, the stop and treatment of which is very difficult.
The third stage is characterized by a hypercoagulable syndrome, the development of thrombotic complications or repeated bleeding is possible.
Both coagulopathic bleeding and hypercoagulable syndrome serve as a manifestation of a general process in the body - thrombohemorrhagic syndrome, the expression of which in the vascular bed is DIC - syndrome. It develops against the background of severe circulatory disorders (crisis of microcirculation) and metabolism (acidosis, accumulation of biologically active substances, hypoxia).
Peripheral circulatory failure NOS
In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to apply to medical institutions of all departments, and causes of death.
ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170
The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.
With amendments and additions by WHO.
Processing and translation of changes © mkb-10.com
Hemorrhagic shock (a kind of hypovolemic shock) - due to uncompensated blood loss, a decrease in BCC by 20% or more.
Classification Mild (loss of 20% of BCC) Moderate (loss of 20–40% of BCC) Severe (loss of more than 40% of BCC).
Compensatory mechanisms Secretion of ADH Secretion of aldosterone and renin Secretion of catecholamines.
Physiological reactions Decreased diuresis Vasoconstriction Tachycardia.
Pathogenesis. Adaptation of the patient to blood loss is largely determined by changes in the capacity of the venous system (containing up to 75% of blood volume in a healthy person). However, the possibilities for mobilizing blood from the depot are limited: with a loss of more than 10% of the BCC, the CVP begins to fall and the venous return to the heart decreases. There is a syndrome of small ejection, leading to a decrease in perfusion of tissues and organs. In response, nonspecific compensatory endocrine changes appear. The release of ACTH, aldosterone and ADH leads to the retention of sodium, chlorides and water by the kidneys, while increasing potassium loss and reducing diuresis. The result of the release of epinephrine and norepinephrine is peripheral vasoconstriction. Less important organs (skin, muscles, intestines) are switched off from the blood flow, and the blood supply to vital organs (brain, heart, lungs) is preserved, i.e. circulation is centralized. Vasoconstriction leads to deep tissue hypoxia and the development of acidosis. Under these conditions, proteolytic enzymes of the pancreas enter the bloodstream and stimulate the formation of kinins. The latter increase the permeability of the vascular wall, which contributes to the transition of water and electrolytes into the interstitial space. As a result, aggregation of red blood cells occurs in the capillaries, creating a springboard for the formation of blood clots. This process immediately precedes the irreversibility of the shock.
clinical picture. With the development of hemorrhagic shock, 3 stages are distinguished.
Compensated reversible shock. The volume of blood loss does not exceed 25% (700-1300 ml). Moderate tachycardia, blood pressure is either unchanged or slightly reduced. Saphenous veins become empty, CVP decreases. There is a sign of peripheral vasoconstriction: cold extremities. The amount of urine excreted is reduced by half (at a rate of 1–1.2 ml / min).
Decompensated reversible shock. The volume of blood loss is 25–45% (1300–1800 ml). The pulse rate reaches 120-140 per minute. Systolic blood pressure falls below 100 mm Hg, the value of pulse pressure decreases. Severe shortness of breath occurs, partly compensating for metabolic acidosis by respiratory alkalosis, but can also be a sign of a shock lung. Increased cold extremities, acrocyanosis. Cold sweat appears. The rate of urine output is below 20 ml/h.
Irreversible hemorrhagic shock. Its occurrence depends on the duration of circulatory decompensation (usually with arterial hypotension over 12 hours). The volume of blood loss exceeds 50% (2000-2500 ml). The pulse exceeds 140 per minute, systolic blood pressure falls below 60 mm Hg. or not defined. Consciousness is absent. oligoanuria develops.
TREATMENT. In hemorrhagic shock, vasopressor drugs (epinephrine, norepinephrine) are strictly contraindicated, since they aggravate peripheral vasoconstriction. For the treatment of arterial hypotension that has developed as a result of blood loss, the following procedures are sequentially performed.
Catheterization of the main vein (most often the subclavian or internal jugular according to Seldinger).
Jet intravenous administration of blood substitutes (polyglucin, gelatinol, rheopolyglucin, etc.). Transfuse fresh frozen plasma and, if possible, albumin or protein. With moderate shock and severe shock, blood transfusion is performed.
Fight against metabolic acidosis: infusion of 150–300 ml of 4% solution of sodium bicarbonate.
GC simultaneously with the beginning of blood replacement (up to 0.7-1.5 g of hydrocortisone IV). Contraindicated in case of suspected gastric bleeding.
Removal of spasm of peripheral vessels. Given the presence (as a rule) of hypothermia - warming the patient.
Aprotinin-ED in 300-500 ml of 0.9% solution of sodium chloride intravenously drip.
Humidified oxygen inhalation.
Broad-spectrum antibiotics in the presence of wounds, septic diseases.
Maintenance of diuresis (50–60 ml/h) Adequate infusion therapy (until CVP reaches 120–150 mm of water column) / in a jet), in the absence of effect - furosemide 40-160 mg IM or IV.
Cardiac glycosides (contraindicated in conduction disorders [complete or partial AV block] and myocardial excitability [occurrence of ectopic foci of excitation]). With the development of bradycardia - stimulants b - adrenoreceptors (isoprenaline 0.005 g sublingually). If ventricular arrhythmias occur, lidocaine 0.1–0.2 g IV.
When making a diagnosis
Level of consciousness, respiratory efficiency and frequency, blood pressure, heart rate, pulse, physical examination. Special attention to chest, abdomen, hips, possibility of external bleeding
Laboratory tests: hemoglobin, erythrocytes, blood type and Rh, coagulation parameters (platelets, APTT, PTT), electrolytes (Na, K, Cl, Ca), protein, leukocytes, blood count, urea, creatinine
Additional (according to indications)
R-graphy of the chest organs Ultrasound of the abdominal organs, gastric tube, laparocentesis, invasive blood pressure, PAWP, in women, gynecological examination
Laboratory studies: enzymes (AlAT, AsAT, a-amylase, CPK)
During treatment
Monitoring according to clause 1.5. hourly diuresis, CVP
In patients with insufficiency of the contractile function of the heart, if possible, control of indicators of central hemodynamics (Swan-Gans catheter, Doppler ultrasonography), construction of Frank-Starling curves
Three main goals: maximization of oxygen delivery, prevention of further blood loss, replenishment of BCC and fluid and electrolyte disorders. All measures to ensure adequate ventilation of the lungs, oxygen inhalation, tracheal intubation and mechanical ventilation. When using mechanical ventilation, it is mandatory to use antibacterial filters. Venous access - 2 large-diameter catheters, Trendelenburg position, in pregnant women - turning to the left side (preventing compression of the inferior vena cava by the uterus). Warming of transfused solutions
In case of trauma, blood loss:
Adult initial bolus: 2 L 0.9% sodium chloride solution (20 ml/kg); if there is no effect from the introduction of this amount of liquid - an urgent blood transfusion of group I (0), if there is a temporary effect - you can wait for the results of group compatibility and transfuse one-group blood. , 9% solution of sodium chloride -0.5 l,
(whole blood 1 l, 9% sodium chloride solution 0.5 l), the volume of transfusion is determined by hemodynamic parameters and the required level of hemoglobin (see.
Measures to prevent further blood loss:
Stop external bleeding. The fastest possible transportation to the operating room to stop internal bleeding. Indications for surgery are determined by the surgeon. A rational approach implies taking into account the following provisions: In case of intrapleural or intra-abdominal bleeding, an emergency tracotomy or laparotomy, respectively
Bleeding from the gastrointestinal tract - an attempt at endoscopic arrest, if unsuccessful - laparotomy
Retroperitoneal bleeding is treated conservatively
As a temporary measure for massive ongoing blood loss - thoracotomy with aortic clamping
With dehydration (high values of hemoglobin, hematocrit):
The initial bolus of 20 ml/kg 0.9% sodium chloride may be repeated 3 or more times with hemodynamic and urine output assessed after each administration.
It is acceptable to introduce synthetic colloids - preparations based on dextran at a maximum dose of 1.5 g / kg, or hydroxyethyl starch - 2 g / kg In case of hypoproteinemia - albumin in a single dose in adults ml in terms of 5% solution, to maintain the level of albumin in blood plasma not less than 30 g/l
With insufficient effect of infusion therapy: central vein catheterization, CVP control. The intermediate goal of therapy is CVP > 12 cm of water. Art., diuresis more than 1 ml/kg, blood lactate level not more than 2 mmol/l
If there is no response to the infusion load - vasopressors:
Dopamine 2, mcg / kg / min., as a continuous infusion. Norepinephrine at an initial rate of 1 µg/min. (in adults) adjusting the dose to achieve a systolic pressure of 90 mm Hg. Art.
With a small cardiac output - inotropic drugs: dobutamine in the form of a continuous infusion of 5-20 mcg / kg / min
solution for infusion 20%: fl. 50 ml or 100 ml 1 pc.
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A state of shock occurs when there is a sharp violation of the usual blood circulation. This is a severe stress reaction of an organism that has not managed to control vital systems. Hemorrhagic shock is caused by sudden blood loss. Since blood is the main fluid that supports cell metabolism, this kind of pathology refers to hypovolemic conditions (dehydration). In the ICD-10, it is regarded as "Hypovolemic shock" and is coded R57.1.
In conditions of sudden bleeding, an unsubstituted volume of 0.5 liters is accompanied by acute tissue oxygen deficiency (hypoxia).
Most often, blood loss is observed in injuries, surgical interventions, in obstetric practice during labor in women.
In the development of the pathogenesis of compensation for blood loss, the following are important:
It is clear that a person with chronic diseases is much less likely to suffer massive blood loss than a previously healthy person. The work of military doctors in the conditions of the Afghan war showed how difficult moderate blood loss is for healthy fighters in high mountains, where air oxygen saturation is reduced.
The rapid transport of the wounded with the help of armored personnel carriers and helicopters saved many soldiers
In humans, on average, about 5 liters of blood constantly circulates through the arterial and venous vessels. At the same time, 75% is in the venous system. Therefore, the subsequent reaction depends on the speed of adaptation of the veins.
The sudden loss of 1/10 of the circulating mass does not make it possible to quickly "replenish" stocks from the depot. Venous pressure drops, which leads to the maximum centralization of blood circulation to support the work of the heart, lungs and brain. Tissues such as muscles, skin, intestines are recognized by the body as “superfluous” and are turned off from the blood supply.
During a systolic contraction, the volume of blood expelled is insufficient for the tissues and internal organs, it feeds only the 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, 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 vasospasm in the periphery, and vascular resistance increases.
Due to circulatory tissue hypoxia, the blood is "acidified" by accumulated toxins - metabolic acidosis. It promotes an increase in the concentration of kinins, which destroy the vascular walls. The liquid part of the blood enters the interstitial space, and cellular elements accumulate in the vessels, all the conditions for increased thrombus formation are formed. There is a danger of irreversible disseminated intravascular coagulation (DIC).
The heart tries to compensate for the necessary output by increasing contractions (tachycardia), but they are not enough. Losses of potassium reduce the contractility of the myocardium, heart failure is formed. Blood pressure drops sharply.
The cause of hemorrhagic shock is acute bleeding.
Traumatic pain shock is not always accompanied by significant blood loss. It is more characteristic of a widespread surface of the lesion (extensive burns, combined fractures, crushing of tissues). But the combination with unstopped bleeding exacerbates the effect of damaging factors, aggravates the clinical course.
In pregnant women, urgent diagnosis of the cause of shock is important.
Hemorrhagic shock in obstetrics occurs during difficult childbirth, during pregnancy, in the postpartum period. Massive blood loss is caused by:
In such cases, bleeding is often combined with another pathology (injuries during labor, preeclampsia, concomitant chronic diseases of a woman).
The clinic of hemorrhagic shock is determined by the degree of impaired microcirculation, the severity of cardiac and vascular insufficiency. Depending on the stage of development of pathological changes, it is customary to distinguish between the stages of hemorrhagic shock:
In diagnosis, it is most convenient for a doctor to use objective signs of shock. For this, the following indicators are suitable:
Death occurs with a sharp decrease in BCC by 60% or more.
To ascertain the severity of the patient, there is a classification associated with minimal possibilities in determining hypovolemia by laboratory and clinical signs.
These indicators are not suitable for assessing the severity of shock in children. If in a newborn baby the total blood volume barely reaches 400 ml, then for him the 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.
The shock index is able to determine any medical worker. This is the ratio of the calculated heart rate to the systolic pressure. Depending on the coefficient obtained, the degree of shock is approximately judged:
Laboratory indicators in the diagnosis should indicate the severity of anemia. For this, the following are defined:
For the 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.
Control of diuresis is necessary in the diagnosis of kidney damage and filtration disorders.
First aid actions against the background of detected acute bleeding should be aimed at:
Applying a belt to the maximum bent arm helps to stop bleeding from the vessels of the shoulder and forearm
Help with hemorrhagic shock cannot do without:
An ambulance must be called to the scene. The life of the patient depends on the speed of action.
Hemorrhagic shock treatment starts in the ambulance
The algorithm of the doctor's actions is determined by the severity of the injury and the patient's condition:
The ambulance should ensure the fastest (with a sound signal) delivery of the patient to the hospital, inform by radio or telephone about the arrival of the victim for the readiness of the staff of the emergency department.
Video about the principles of first aid for acute blood loss:
In a hospital, shock therapy is provided by a set of measures aimed at counteracting the damaging mechanisms of pathogenesis. It is based on:
Reopoliglyukin normalizes platelet aggregation, serves as a prevention of DIC
When a patient is admitted to the intensive care unit:
If surgical intervention is necessary, the issue of its urgency is decided collectively by surgeons, and the possibility of anesthesia assistance is also determined.
When transfusing, doctors use the following rules:
An indication for stopping the continuous infusion of blood and blood substitutes is:
In the presence of 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.
The state of hemorrhagic shock is very transient, dangerously massive blood loss and death in cardiac arrest.
To combat hemorrhagic shock, it is necessary to maintain the constant readiness of medical personnel, to have a supply of funds and blood substitutes. The public needs to be reminded of the importance of donation and community involvement in care.