Shock of unknown etiology according to ICD 10. Hemorrhagic shock - description, causes, symptoms (signs), treatment

Infectious-toxic shock is a nonspecific pathological condition caused by the influence of bacteria and the toxins they secrete. This process can be accompanied by various disorders - metabolic, neuroregulatory and hemodynamic. This condition of the human body is an emergency 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 this disease is severe infectious processes. Infectious-toxic shock in children is very often formed on the basis. The development of such a syndrome depends entirely on the causative agent of this disease, the state of the person’s immune system, the presence or absence of drug therapy, and the intensity of exposure to the bacterium.

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 progression of the underlying disease. The very first symptom is severe chills. A little later, increased sweating, intense headaches, convulsions, and episodes of loss of consciousness appear. In children, this syndrome manifests itself somewhat differently - frequent vomiting that has nothing to do with eating, diarrhea and a gradual increase in pain.

Diagnosis of infectious-toxic shock consists of detecting the pathogen in the patient's blood tests. Treatment of the disease is based on the use of medications and special solutions. Since this syndrome is a very serious condition, before the patient enters a medical facility, he must 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.

Etiology

The reasons for the progression of this condition are the combination of an acute infectious process and weakened human immunity. This syndrome is a common complication of the following diseases:

pneumonia (of any nature);

Other nonspecific factors in the development of infectious-toxic shock in children and adults are:

surgical intervention;
any violation of the integrity of the skin;
pathological labor activity;
complicated abortion;
allergic reactions;
or ;
substance abuse.

Another reason for this condition is the use of sanitary tampons by female representatives. This is due to the fact that when using such an item during menstruation, it can penetrate into the female body, which produces dangerous toxins. The disease often affects girls and women aged fifteen to thirty years. The mortality rate in this case is sixteen percent. In addition, there have been recorded cases of the occurrence of such a disorder due to the use of vaginal contraceptives.

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 disruption of blood circulation.

Varieties

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, we distinguish:

initial degree- in which blood pressure remains unchanged, but heart rate increases. It can reach one hundred and twenty beats per minute;
moderate severity– characterized by progression of symptoms from the cardiovascular system. Accompanied by a decrease in systolic blood pressure and increased heart rate;
severe degree– a significant drop in systolic tone (pressure reaches seventy millimeters of mercury). The shock index increases. Fever and a decrease in the volume of urine emitted are often observed;
complicated stage– characterized by the development of irreversible changes in internal organs and tissues. The patient's skin takes on an earthy tint. A comatose state is often observed.

Depending on the pathogen, there are:

streptococcal syndrome– occurs after childbirth, infection of wounds, cuts or burns of the skin, and is also a complication after infectious disorders, in particular pneumonia;
staphylococcal toxic shock– often develops after surgery and the use of hygienic tampons;
bacterial toxic shock– occurs for a reason and can complicate any stage of sepsis.

Symptoms

Symptoms of toxic shock are characterized by rapid onset and intensification. The main features are:

decrease in blood pressure, heart rate increases;
sudden increase in body temperature, even fever;
intense headaches;
bouts of vomiting that are not associated with food intake;
diarrhea;
stomach cramps;
severe muscle pain;
dizziness;
seizures;
episodes of short-term loss of consciousness;
tissue death - only in cases of infection due to a violation of the integrity of the skin.

In addition, there is a development of, and. A similar syndrome in young children is expressed by stronger signs of intoxication and constant jumps in blood pressure and pulse. Toxic shock syndrome from tampons is expressed by similar symptoms, which are accompanied by a rash on the skin of the feet and palms.

Complications

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 may develop:

impaired blood circulation, causing internal organs to not receive the proper amount of oxygen;
acute respiratory failure - formed due to severe damage to the lungs, especially if the syndrome was provoked by pneumonia;
impaired blood clotting and increased likelihood of blood clots, which can cause excessive hemorrhage;
renal failure or complete failure of the functioning of this organ. In such cases, treatment will consist of lifelong dialysis or transplant surgery.

Untimely emergency care and improper therapy lead to the death of the patient within two days after the expression of the first symptoms.

Diagnostics

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 must carefully study the person’s medical history, determine the intensity of symptoms, and also conduct an examination. If the cause of this condition is the use of tampons, then patients are required to be examined by a gynecologist.

Other diagnostic methods include:

conducting general and biochemical blood tests is the main way to identify the pathogen;
measuring the amount of urine emitted per day - with such an illness, the volume of daily urine will be much less than that of a healthy person;
instrumental examinations, which include CT, MRI, ultrasound, ECG, etc. - aimed at determining the extent of damage to internal organs.

An experienced specialist can easily determine infectious-toxic shock by the patient’s appearance.

Treatment

Before carrying out therapy in a medical facility, it is necessary to provide the patient with emergency first aid. Such events consist of several stages, which include:

ridding the victim of narrow and tight clothing;
ensuring a horizontal position so that the head is slightly elevated in relation to the entire body;
You need to put a heating pad under your feet;
allow fresh air to flow in.

These actions are limited to emergency care, which is not performed by a specialist.

After transporting the patient to a medical facility, intensive treatment of infectious-toxic shock with medications begins. Often, hormonal substances, antibiotics and glucocorticoids are used to actively destroy bacteria. The use of medications is individual and depends on the causative agent of the disease.

If the infection occurs due to the use of tampons or vaginal contraceptives, then treatment is to immediately remove them from the body. This may require curettage, and the cavity is treated with antiseptic drugs.

Prevention

Preventive measures against toxic shock syndrome consist of following several rules:

timely elimination of diseases that may cause the development of such a condition. In most cases in children and adults it is pneumonia;
always ensure the cleanliness of the skin, and if any damage to the integrity occurs, immediately treat the affected area with antiseptic substances;
take breaks from using tampons during menstruation. Alternate pads and tampons every two menstruation, and also change such hygiene products in a timely manner.

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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Stage 1 (compensated shock), when 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, moderate tachycardia up to 90-110 beats/min.
Stage 2 (decompensated shock) is characterized by an increase in cardiovascular disorders, and the body’s compensatory mechanisms fail. Blood loss is 25-40% of the bcc, impaired consciousness to the point of soporosis, acrocyanosis, cold extremities, blood pressure is sharply reduced, tachycardia 120-140 beats/min, pulse is weak, thread-like, shortness of breath, oliguria up to 20 ml/hour.
Stage 3 (irreversible shock) is a relative concept and largely depends on the resuscitation methods used. The patient's condition is extremely serious. Consciousness is sharply depressed to the point of complete loss, the skin is pale, the skin is “marbled”, systolic pressure is below 60, the pulse is determined only in the main vessels, sharp tachycardia up to 140-160 beats/min.
As a rapid diagnostic for assessing the severity of shock, the concept of shock index is used - SI - the ratio of heart rate to systolic pressure. For 1st degree shock, CI = 1 (100/100), 2nd degree shock - 1.5 (120/80), 3rd degree shock - 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 (decreased 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; blood loss of 50% of the bcc leads to a breakdown of the compensation mechanism; blood loss of 25% of the bcc is almost completely compensated by the body.
The relationship between the amount of blood loss and its clinical manifestations:
Blood loss is 10-15% of the volume of blood volume (450-500 ml), there is no hypovolemia, blood pressure is not reduced;
Blood loss 15-25% of blood volume (700-1300 ml), mild hypovolemia, blood pressure reduced by 10%, moderate tachycardia, pale skin, cold extremities;
Blood loss 25-35% of the bcc (1300-1800 ml), moderate severity of hypovolemia, blood pressure reduced to 100-90, tachycardia up to 120 beats/min, pale skin, cold sweat, oliguria;
Blood loss up to 50% of the volume of blood volume (2000-2500 ml), severe hypovolemia, blood pressure reduced to 60, thready pulse, absent or confused consciousness, severe pallor, cold sweat, anuria;
Blood loss of 60% of the blood volume is fatal.
The initial stage of hemorrhagic shock is characterized by a disorder of microcirculation due to centralization of blood circulation. The mechanism of centralization of blood circulation occurs due to an acute deficit of bcc due to blood loss, venous return to the heart decreases, venous return to the heart decreases, stroke volume of the heart decreases and blood pressure drops. 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 overall peripheral vascular resistance to blood flow increases.
In the early stages of shock, centralization of the circulation ensures blood flow in the coronary and cerebral vessels. The functional state of these organs is very important for maintaining the vital functions of the body.
If there is no replenishment of BCC and the sympathoadrenergic reaction is delayed over time, then the overall picture of shock reveals the negative aspects of vasoconstriction of the microvasculature - 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, red blood cells, hematocrit (red blood cell volume, the norm for men is 44-48%, for women 38-42%). Determining the blood volume in emergency situations is difficult and associated with loss of time.
Disseminated intravascular coagulation syndrome (DIC syndrome) 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 quantities of canned blood, sepsis, severe infectious diseases, etc.
The first stage of DIC syndrome is characterized by the predominance of hypercoagulation with simultaneous activation of anticoagulant systems in patients with blood loss and trauma.
The second stage of hypercoagulation is manifested by coagulopathic bleeding, the stop and treatment of which is very difficult.
The third stage is characterized by hypercoagulation syndrome, and the development of thrombotic complications or recurrent bleeding is possible.
Both coagulopathic bleeding and hypercoagulability 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 (microcirculation crisis) and metabolism (acidosis, accumulation of biologically active substances, hypoxia).

Peripheral circulatory failure NOS

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits 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. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Hemorrhagic shock - description, causes, symptoms (signs), treatment.

Short description

Hemorrhagic shock (a type of hypovolemic shock) is caused by uncompensated blood loss, a decrease in blood volume 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.

Causes

Pathogenesis. The patient’s adaptation 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 central venous pressure begins to fall and the venous return to the heart decreases. Small output syndrome occurs, leading to decreased 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, chloride and water by the kidneys, while increasing potassium losses and decreasing diuresis. The result of the release of epinephrine and norepinephrine is peripheral vasoconstriction. Less important organs (skin, muscles, intestines) are switched off from the bloodstream, and the blood supply to vital organs (brain, heart, lungs) is preserved, i.e. centralization of blood circulation occurs. Vasoconstriction leads to deep tissue hypoxia and the development of acidosis. Under these conditions, proteolytic enzymes of the pancreas enter the blood and stimulate the formation of kinins. The latter increase the permeability of the vascular wall, which promotes the passage of water and electrolytes into the interstitial space. As a result, red blood cell aggregation occurs in the capillaries, creating a springboard for the formation of blood clots. This process immediately precedes the irreversibility of shock.

Symptoms (signs)

Clinical picture. When hemorrhagic shock develops, there are 3 stages.

Compensated reversible shock. The volume of blood loss does not exceed 25% (700–1300 ml). Tachycardia is moderate, blood pressure is either unchanged or slightly reduced. The saphenous veins become empty and the central venous pressure decreases. A sign of peripheral vasoconstriction occurs: coldness of the extremities. The amount of urine excreted is reduced by half (at a normal rate of 1–1.2 ml/min).

Decompensated reversible shock. The volume of blood loss is 25–45% (1300–1800 ml). The pulse rate reaches 120–140 per minute. Systolic blood pressure drops below 100 mm Hg, and pulse pressure decreases. Severe shortness of breath occurs, partly compensating for metabolic acidosis through respiratory alkalosis, but can also be a sign of shock lung. Increased coldness of the extremities and acrocyanosis. Cold sweat appears. The rate of urine excretion 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 drops below 60 mm Hg. or not determined. There is no consciousness. Oligoanuria develops.

Treatment

TREATMENT. In hemorrhagic shock, vasopressor drugs (epinephrine, norepinephrine) are strictly contraindicated, since they aggravate peripheral vasoconstriction. To treat arterial hypotension that develops as a result of blood loss, the procedures listed below are performed sequentially.

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.). Fresh frozen plasma is transfused, and, if possible, albumin or protein. For moderate and severe shock, blood transfusion is performed.

Combating metabolic acidosis: infusion of 150–300 ml of 4% sodium bicarbonate solution.

GK simultaneously with the start of blood replacement (up to 0.7–1.5 g of hydrocortisone IV). Contraindicated in cases of suspected gastric bleeding.

Relieving spasm of peripheral vessels. Considering the presence (usually) of hypothermia - warming the patient.

Aprotinin-ED in 300–500 ml of 0.9% sodium chloride solution intravenously.

Inhalation of humidified oxygen.

Broad-spectrum antibiotics for wounds and septic diseases.

Maintaining diuresis (50–60 ml/h) Adequate infusion therapy (until the CVP reaches 120–150 mm water column) If infusion is ineffective, osmotic diuretics (mannitol 1–1.5 g/kg in 5% glucose solution in /in a stream), if there is no effect - furosemide 40-160 mg IM or IV.

Cardiac glycosides (contraindicated in case of conduction disorders [complete or partial AV block] and myocardial excitability [the occurrence of ectopic foci of excitation]). With the development of bradycardia - stimulants of b - adrenergic receptors (isoprenaline 0.005 g sublingually). If ventricular arrhythmias occur, lidocaine 0.1–0.2 g IV.

Hypovolemic shock

Upon diagnosis

Level of consciousness, respiratory efficiency and rate, blood pressure, heart rate, pulse, physical examination. Particular attention to the chest, abdomen, thighs, possible external bleeding

Laboratory tests: hemoglobin, red blood cells, blood group 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, pulmonary pulmonary arterial pressure, in women, gynecological examination

Laboratory tests: enzymes (AlAT, AST, a-amylase, CPK)

During treatment

Monitoring in accordance with clause 1.5. hourly diuresis, central venous pressure

In patients with insufficiency of cardiac contractile function, if possible, monitor central hemodynamic parameters (Swan-Hans catheter, Doppler ultrasonography), construct Frank-Starling curves

Three main goals: maximizing oxygen delivery, preventing further blood loss, replenishing blood volume and fluid-electrolyte disorders. All measures to ensure adequate ventilation, oxygen inhalation, tracheal intubation and mechanical ventilation. When using mechanical ventilation, be sure to use antibacterial filters Venous access - 2 large-diameter catheters, Trendelenburg position, in pregnant women - turn on the left side (preventing compression of the inferior vena cava by the uterus). Warming of transfused solutions

In case of injury or blood loss:

Initial bolus for an adult: 2 l of 0.9% sodium chloride solution (20 ml/kg); if there is no effect from the introduction of this amount of liquid, urgently transfuse blood of group I (0), if there is a temporary effect, you can wait for the results of group compatibility and transfuse blood of the same group. Approximate composition of transfusion media: packed red blood cells 0.6 l, fresh frozen plasma 0.4 l , 9% sodium chloride solution -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:

Stopping 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 involves taking into account the following provisions: In case of intrapleural or intra-abdominal bleeding - emergency tracotomy or laparotomy, respectively

Bleeding from the gastrointestinal tract - an attempt at endoscopic stop, if unsuccessful - laparotomy

Retroperitoneal bleeding is treated conservatively

As a temporary measure for massive ongoing blood loss - thoracotomy with aortic clamping

If you are dehydrated (high hemoglobin, hematocrit):

An initial bolus of 20 ml/kg of 0.9% sodium chloride solution can be repeated three or more times, assessing hemodynamics and diuresis after each administration

It is permissible to administer synthetic colloids - preparations based on dextran in a maximum dose of 1.5 g/kg, or hydroxyethyl starch - 2 g/kg. For hypoproteinemia - albumin in a single dose in adults ml in terms of 5% solution, to maintain the level of albumin in the blood plasma not less than 30 g/l

If the effect of infusion therapy is insufficient: catheterization of the central vein, control of central venous pressure. The intermediate goal of therapy is CVP >12 cm H2O. Art., diuresis more than 1 ml/kg, blood lactate level not more than 2 mmol/l

In the absence of response to infusion load - vasopressors:

Dopamine 2.µg/kg/min., as a continuous infusion. Norepinephrine at an initial rate of 1 mcg/min. (in adults) selecting the dose to achieve a systolic pressure of 90 mm Hg. Art.

For low cardiac output - inotropic drugs: dobutamine as a constant infusion 5-20 mcg/kg/min

A set of diagnostic and therapeutic measures for R57.1 Hypovolemic shock

Medical studies intended to monitor the effectiveness of treatment

Medicines prescribed

solution for local approx. 0.1%: bottle-drip. 30 ml;

concentrate for preparation. solution for infusion 5 mg/ml, 40 mg/ml: 5 ml amp. 5 or 10 pcs.

concentrate for preparation. solution for injection 50 mg/5 ml: amp. 5, 30 or 300 pcs.;

concentrate for preparation. solution for infusion 200 mg/5 ml: amp. 5 pieces.

solution for injection 0.5% (25 mg/5 ml), 4% (200 mg/5 ml): amp. 5 or 10 pcs.

lyophilization powder for preparation. solution for injection 15 units: amp., fl. 5 or 10 pcs.

solution for infusion 500 thousand KIE/50 ml: fl. 1 PC.

tab. 500 mcg: 50 pcs.;

solution for injection 4 mg/ml: amp. 25 pcs.;

solution for injection 4 mg/1 ml, 8 mg/2 ml: amp. 5, 10 or 25 pcs.

tab. 10 mg: 100 pcs.

tab. 4 mg, 8 mg, 10 mg: 60, 100 or 120 pcs.

powder for preparation. injection solution 25, 50 or 250 mg, in klmpl. with r-rit. in amp. 10 ml each

solution for infusion 1.5 g/100 ml: bottle. 200 ml or 400 ml

solution for infusion: fl. 200 ml or 400 ml

solution for infusion 10%: bottle. 250 ml or 500 ml

solution for infusion 60 mg/1 ml: vial. 100 ml, 200 ml or 400 ml

solution for infusion 6 g/100 ml: fl. 200 ml 1, 24 or 48 pcs, fl. 400 ml 1, 12 or 24 pcs., fl. 100 ml 1 or 48 pcs.

solution for infusion 10%: fl. or bottle 200, 250, 400 or 500 ml 1 or 10 pcs.

solution for infusion 10%: bottle. 200 ml 1, 24 or 40 pcs., bottle. 400 ml 1, 24 or 40 pcs.

solution for infusion 10%: fl. 200 ml 1, 24 or 28 pcs., fl. 400 ml 1, 12 or 15 pcs.

solution for infusion: 200 ml bottle. 1 or 28 pcs., 400 ml bottle. 1 or 15 pcs.

solution for infusion: 100 ml, 200 ml, 250 ml, 400 ml or 500 ml containers

solution for infusion 20%: fl. 50 ml or 100 ml 1 pc.

ICD code: R57.1

Hypovolemic shock

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Hemorrhagic shock

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 is caused by 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 conditions of sudden bleeding, an unreplaced volume of 0.5 liters is accompanied by acute tissue oxygen deficiency (hypoxia).

Most often, blood loss is observed during injuries, surgical interventions, and in 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 of nervous regulation of vascular tone;
the ability of the heart to work under hypoxic conditions;
blood clotting;
environmental conditions 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. In this case, 75% is in the 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 supplies 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 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.

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, and in the 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 and the severity of cardiac and vascular insufficiency. Depending on the stage of development of pathological changes, it is customary to distinguish the stages of hemorrhagic shock:

Compensation or the 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.
The second stage, or decompensation, - in accordance with the name, symptoms of oxygen deficiency in the brain and weak cardiac output appear. 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.
The third stage is irreversible - the patient’s condition is regarded 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. The pulse on the ulnar artery cannot be felt, but with sufficiently good skills it can be felt on the 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.

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:

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

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 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, limb immobilization 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 with warm blankets and 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:

checking the effectiveness of a pressure bandage, tourniquet, applying clamps to blood vessels for open wounds;
installation of systems for transfusion into 2 veins, if possible, puncture of the subclavian vein and its catheterization;
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;
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;
carrying out pain relief using injections of narcotic analgesics, Baralgin and antihistamines, Ketamine;
administration of corticosteroids to 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:

catheterization of the subclavian vein is carried out, a jet injection of Polyglyukin is added 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 test is good, blood transfusion is started; in the 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 death due to cardiac arrest.

The most severe complication is the development of disseminated intravascular coagulation syndrome. It disrupts the balance of formed elements, vascular permeability, and 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.

Peripheral circulatory failure NOS

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. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Hemorrhagic shock - description, causes, symptoms (signs), treatment.

Short description

Hemorrhagic shock (a type of hypovolemic shock) is caused by uncompensated blood loss, a decrease in blood volume 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.

Causes

Symptoms (signs)

Clinical picture. When hemorrhagic shock develops, there are 3 stages.

Treatment

Catheterization of the main vein (most often the subclavian or internal jugular according to Seldinger).

Combating metabolic acidosis: infusion of 150–300 ml of 4% sodium bicarbonate solution.

GK simultaneously with the start of blood replacement (up to 0.7–1.5 g of hydrocortisone IV). Contraindicated in cases of suspected gastric bleeding.

Relieving spasm of peripheral vessels. Considering the presence (usually) of hypothermia - warming the patient.

Aprotinin-ED in 300–500 ml of 0.9% sodium chloride solution intravenously.

Inhalation of humidified oxygen.

Broad-spectrum antibiotics for wounds and septic diseases.

Hemorrhagic shock is a consequence of acute blood loss

What it is?

A sharp disruption 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 sudden blood loss. In the International Classification of Diseases, 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 reduction in circulating blood volume due to dehydration.

Causes

They are divided into 3 main groups:

spontaneous bleeding - for example, nosebleeds;

Most often, obstetricians and gynecologists encounter hemorrhagic shock, because this condition is one of the main causes of maternal mortality. In gynecology, such shock results from:

tubal pregnancy;

Stages and symptoms

The clinical picture depends on the stage of shock, each of which is discussed in the table:

Hemorrhagic shock

The development of hemorrhagic shock usually results from hemorrhages exceeding 1000 ml, i.e., a loss of more than 20% of the blood volume or 15 ml of blood per 1 kg of body weight. Continued bleeding, in which blood loss exceeds 1500 ml (more than 30% of the total volume), is considered massive and poses an immediate threat to the woman’s life. The volume of circulating blood in women is not the same, depending on the constitution it is: for normostenics - 6.5% of body weight, for asthenics - 6.0%, for picnics - 5.5%, for muscular women of athletic build - 7%, therefore, the absolute numbers of BCC may vary, which must be taken into account in clinical practice.

ICD-10 code

Causes and pathogenesis of hemorrhagic shock

The causes of bleeding leading to shock in gynecological patients can be: disrupted ectopic pregnancy, ovarian rupture, spontaneous and induced abortion, frozen pregnancy, hydatidiform mole, dysfunctional uterine bleeding, submucous form of uterine fibroids, genital injuries.

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 first manifests itself as a violation of macrocirculation, i.e., systemic circulation, then microcirculatory disorders appear and, as a consequence, progressive disorganization develops metabolism, enzymatic shifts and proteolysis.

The macrocirculatory system consists of arteries, veins and the heart. The microcirculatory system includes arterioles, venules, capillaries and arteriovenous anastomoses. As is known, 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 by increasing 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, and tissue perfusion does not change.

Symptoms of hemorrhagic shock

Symptoms of hemorrhagic shock have the following stages:

Stage I - compensated shock;
Stage II - decompensated reversible shock;
Stage III - irreversible shock.

The stages of shock are determined based on an assessment of the complex of clinical manifestations of blood loss corresponding to pathophysiological changes in organs and tissues.

Stage 1 hemorrhagic shock (small output syndrome, or compensated shock) usually develops with blood loss approximately corresponding to 20% of the blood volume (from 15% to 25%). At this stage, compensation for the loss of bcc. carried out due to the hyperproduction of catecholamines. The clinical picture is dominated by symptoms indicating changes in cardiovascular activity of a functional nature: pallor of the skin, neglect 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 continue for quite a long time. If bleeding is not stopped, circulatory disorders further deepen, and the next stage of shock occurs.

Who to contact?

Treatment of hemorrhagic shock

Treatment of hemorrhagic shock is an extremely important task, for the solution of 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, and be carried out taking into account the cause that caused the bleeding and the patient’s health status that preceded it.

The complex of treatment measures includes the following:

Gynecological operations to stop bleeding.
Providing anesthesia care.
Directly removing the patient from a state of shock.

All of the above activities must be carried out in parallel, clearly and quickly.

Medicines

Medical Expert Editor

Portnov Alexey Alexandrovich

Education: Kyiv National Medical University named after. A.A. Bogomolets, specialty - "General Medicine"

ICD code 10 hemorrhagic shock

Hemorrhagic shock develops as a result of a decrease in blood volume during bleeding, which leads to a critical decrease in tissue blood flow and the development of tissue hypoxia.

SYNONYMS

Hypovolemic hemorrhagic shock.

O75.1 Shock during or after labor and delivery.

EPIDEMIOLOGY

Women around the world die every year from hemorrhages associated with childbirth. MS from obstetric hemorrhage and hemorrhagic shock in the Russian Federation for 2001–2005. is 63–107 live births or 15.8–23.1% in the structure of MS.

PREVENTION

The main cause of mortality in hemorrhagic shock in obstetrics is underestimation of the volume of blood loss, delayed and insufficiently vigorous treatment measures. In case of obstetric hemorrhage, timely provision of qualified assistance is necessary.

ETIOLOGY

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 the bcc or ³1.5% of body weight). The following conditions are considered life-threatening bleeding:

· loss of 100% of bcc within 24 hours or 50% of bcc in 3 hours;

· blood loss at a rate of 150 ml/min or 1.5 ml/(kg´min) for 20 minutes or longer;

· instantaneous blood loss of ³1500–2000 ml (25–35% of bcc).

The causes of massive bleeding during pregnancy and childbirth can be premature abruption of a normal or low-lying placenta, placenta previa, uterine rupture, and velamentous 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 placenta accreta, trauma to the birth canal, uterine inversion, and blood clotting disorders. A mnemonic designation for the causes of postpartum hemorrhage has been proposed - “4 T”: tone, tissue, trauma, thrombin.

PATHOGENESIS

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 sinocarotid 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, increased tone of venous vessels (increased venous return and preload), increased heart rate and force of heart contractions, and decreased 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, a slow movement of intercellular fluid into the vascular bed occurs (transcapillary replenishment). A decrease in blood flow in organs and tissues leads to changes in the CBS of arterial blood - 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 brain stem, 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 in case of severe gestosis, even “normal” systolic blood pressure figures. The continued release of stress hormones causes glycogenolysis and lipolysis (moderate hyperglycemia and hypokalemia). Hyperventilation is not enough to ensure normal arterial blood pH, resulting in acidosis. A further decrease in tissue blood flow leads to increased anaerobic metabolism with increased lactic acid secretion.

Progressive metabolic lactic acidosis lowers tissue pH and blocks vasoconstriction. The arterioles expand, and blood fills the microcirculatory bed. Cardiac output decreases, damage to endothelial cells and the development of disseminated intravascular coagulation are possible.

With blood loss of ³40% of bcc and a decrease in systolic blood pressure of ³50 mm Hg. CNS ischemia additionally stimulates the sympathetic nervous system, which leads to the formation of the so-called second plateau of blood pressure. Without vigorous intensive therapy, shock progresses to an irreversible stage (widespread cell damage, MODS, deterioration of myocardial contractility up to cardiac arrest).

After 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, their release of oxygen radicals, 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 liver damage with an increase in the activity of transaminases in the plasma. Spasm of the preglomerular arterioles of the kidneys, development of acute tubular necrosis and acute renal failure are possible. Due to a decrease in the release of glucose by the liver, disruption of the hepatic production of ketones and inhibition of peripheral lipolysis, the supply of energy substrates to the heart and brain is disrupted.

CLASSIFICATION

Obstetric hemorrhages are 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)

Hemorrhagic shock

ICD-10 code

Associated diseases

Titles

Description

Acute blood loss is the sudden release of blood from the vascular bed. The main clinical symptoms of the resulting decrease in blood volume (hypovolemia) are pallor of the skin and visible mucous membranes, tachycardia and arterial hypotension.

Symptoms

Stage 2 (decompensated shock) is characterized by an increase in cardiovascular disorders, and the body’s compensatory mechanisms fail. Blood loss is 25-40% of the bcc, impaired consciousness to the point of soporosis, acrocyanosis, cold extremities, blood pressure is sharply reduced, tachycardia beats/min, pulse is weak, thread-like, shortness of breath, oliguria up to 20 ml/hour.

Stage 3 (irreversible shock) is a relative concept and largely depends on the resuscitation methods used. The patient's condition is extremely serious. Consciousness is sharply depressed to the point of complete loss, the skin is pale, the skin is “marbled”, systolic pressure is below 60, the pulse is determined only in the main vessels, sharp tachycardia dpm.

As a rapid diagnostic for assessing the severity of shock, the concept of shock index is used - SI - the ratio of heart rate to systolic pressure. For 1st degree shock, CI = 1 (100/100), 2nd degree shock - 1.5 (120/80), 3rd degree shock - 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 (decreased 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; blood loss of 50% of the bcc leads to a breakdown of the compensation mechanism; blood loss of 25% of the bcc is almost completely compensated by the body.

The relationship between the amount of blood loss and its clinical manifestations:

Blood loss% of blood volume (ml), no hypovolemia, blood pressure not reduced;.

Blood loss% BCC (ml), mild hypovolemia, blood pressure reduced by 10%, moderate tachycardia, pale skin, cold extremities;.

Blood loss% BCC ml), moderate severity of hypovolemia, blood pressure reduced to, tachycardia to 120 beats/min, pale skin, cold sweat, oliguria;.

Blood loss up to 50% of blood volume ml), severe hypovolemia, blood pressure reduced to 60, thready pulse, absent or confused consciousness, severe pallor, cold sweat, anuria;.

Blood loss of 60% of the blood volume is fatal.

The initial stage of hemorrhagic shock is characterized by a disorder of microcirculation due to centralization of blood circulation. The mechanism of centralization of blood circulation occurs due to an acute deficit of bcc due to blood loss, venous return to the heart decreases, venous return to the heart decreases, stroke volume of the heart decreases and blood pressure drops. 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 overall peripheral vascular resistance to blood flow increases.

In the early stages of shock, centralization of the circulation ensures blood flow in the coronary and cerebral vessels. The functional state of these organs is very important for maintaining the vital functions of the body.

If there is no replenishment of BCC and the sympathoadrenergic reaction is delayed over time, then the overall picture of shock reveals the negative aspects of vasoconstriction of the microvasculature - 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, red blood cells, hematocrit (red blood cell volume, normal for men%, for women%). Determining the blood volume in emergency situations is difficult and associated with loss of time.

Disseminated intravascular coagulation syndrome (DIC syndrome) 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 quantities of canned blood, sepsis, severe infectious diseases, etc.

The first stage of DIC syndrome is characterized by the predominance of hypercoagulation with simultaneous activation of anticoagulant systems in patients with blood loss and trauma.

The second stage of hypercoagulation is manifested by coagulopathic bleeding, the stop and treatment of which is very difficult.

The third stage is characterized by hypercoagulation syndrome, and the development of thrombotic complications or recurrent bleeding is possible.

Both coagulopathic bleeding and hypercoagulability 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 (microcirculation crisis) and metabolism (acidosis, accumulation of biologically active substances, hypoxia).

Causes

With the slow loss of even large volumes of blood (mL), compensatory mechanisms have time to turn on, hemodynamic disturbances arise gradually and are not very serious. On the contrary, intense bleeding with loss of a smaller volume of blood leads to severe hemodynamic disturbances and, as a consequence, to hemorrhagic shock.

Treatment

1. Reduction or elimination of existing phenomena of acute respiratory failure (ARF), the cause of which may be aspiration of knocked out teeth, blood, vomit, cerebrospinal fluid from a fracture of the base of the skull. This complication is especially often observed in patients with confused or absent consciousness and, as a rule, is combined with retraction of the root of the tongue.

Treatment comes down to mechanical release of the mouth and oropharynx, aspiration of the contents using suction. Transportation can be carried out with an inserted airway or endotracheal tube and mechanical ventilation through them.

2, Carrying out pain relief with medications that do not depress breathing and blood circulation. Among 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 nitrous-oxygen analgesia, intravenous administration of subnarcotic doses of ketamine (calypsol, ketalar), but these are purely anesthetic treatments that require an anesthesiologist and the necessary equipment.

3, Reduction or elimination of hemodynamic disorders, primarily hypovolemia. In the first minutes after severe injury, the main cause of hypovolemia and hemodynamic disorders is blood loss. Prevention of cardiac arrest and all other serious disorders is the 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 case of 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 part of this complex and is aimed at replenishing blood volume.

In carrying out intensive care for acute blood loss, it is necessary to reliably provide continuous transfusion therapy with a rational combination of available funds. It is equally important to observe a certain stage in treatment, speed and adequacy of assistance in the most difficult situations.

As an example, the following procedure can be given:

Immediately upon admission, the patient’s blood pressure, pulse and respiration rates are measured, the bladder is catheterized and urine excreted is taken into account, all these data are recorded;

The central or peripheral vein is catheterized, infusion therapy is started, and CVP is measured. In case of collapse, without waiting for catheterization, a stream infusion of polyglucin is started by puncture of a peripheral vein;

A jet infusion of polyglucin restores central blood supply, and a jet infusion of saline restores diuresis;

The number of red blood cells in the blood and the hemoglobin content, hematocrit, as well as the approximate amount of blood loss and what is still possible in the coming hours are determined, and the required amount of donor blood is indicated;

The patient's blood group and Rh status are determined. After receiving this data and donated blood, tests are carried out for individual and Rh compatibility, a biological test and blood transfusions begin;

When the central venous pressure increases above 12 cm of water column, the infusion rate is limited to rare drops;

If surgical intervention is proposed, the question of the possibility of performing it is decided;

After blood circulation is normalized, water balance is maintained and hemoglobin, red blood cells, protein, etc. are normalized.

Continuous intravenous infusion is stopped after 3-4 hours of observation have proven: no new bleeding, stabilization of blood pressure, normal intensity of diuresis and no threat of heart failure.

Abstracts on medicine

Hemorrhagic shock and DIC syndrome

Hemorrhagic shock (HS) is the main and immediate cause of death in women in labor and childbirth, and continues to be the most dangerous manifestation of various diseases that determine death. GSH is a critical condition associated with acute blood loss, as a result of which a crisis of macro- and microcirculation develops, a syndrome of multiple organ and multisystem failure. The source of acute massive blood loss in obstetric practice can be:

Premature abruption 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, genitals);

Damage to vessels of parametric tissue with the formation of large hematomas.

Many women during pregnancy, against the background of late toxicosis of somatic diseases, are “ready” for shock due to severe initial hypovolemia and chronic circulatory failure. Hypovolemia in pregnant women is often observed with polyhydramnios, multiple pregnancies, vascular allergic lesions, circulatory failure, inflammatory kidney diseases

GSH leads to severe multiple organ disorders. As a result of hemorrhagic shock, the lungs are affected with the development of acute pulmonary failure of the “shock lung” type. With HS, renal blood flow sharply decreases, hypoxia of the renal tissue develops, and a “shock kidney” forms. The effect of HS on the liver is especially unfavorable, where morphological and functional changes cause the development of a “shock liver”. Dramatic changes during hemorrhagic shock also occur in the adenohypophysis, leading to its necrosis. Thus, with HS, multiple organ failure syndromes occur.

PATHOGENESIS. Acute blood loss, a decrease in blood volume, venous return and cardiac output lead to activation of the sympathetic-adrenal system, which leads to spasm of blood vessels, 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 background of a decrease in hydrostatic pressure. Cardiac output continues to decrease, persistent spasm of arterioles occurs, and the rheological properties of the blood change (erythrocyte aggregation “sludge” is a phenomenon).

Subsequently, peripheral vascular spasm becomes the cause of the development of microcirculation disorders and leads to irreversible shock, which is divided into the following phases:

Vasoconstriction phase with decreased capillary blood flow

Vasodilation phase with expansion of the vascular space and decrease in blood flow in the capillaries;

Disseminated intravascular coagulation (DIC) phase;

Irreversible shock phase.

In response to DIC, the fibrinolytic system is activated, clots are lysed and blood flow is disrupted.

CLINIC OF GSH is determined by the mechanisms leading to a deficiency of 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, pale skin, cold and damp, sharpening of facial features, tachycardia and weak pulse filling, decreased blood pressure, shortness of breath, cyanosis.

Based on the severity, they distinguish between compensated, decompensated, reversible and irreversible shock. There are 4 degrees of hemorrhagic shock.

1st degree of HS, BCC deficiency up to 15%. Blood pressure is above 100 mm Hg; central venous pressure (CVP) is within normal limits. Slight pallor of the skin and increased heart rate, beat/min, hemoglobin 90g/li more.

2nd degree GS. BCC deficit up to 30%. The condition is of moderate severity, weakness, dizziness, darkening of the eyes, nausea, lethargy, and pale skin are observed. Arterial hypotension (domm Hg), decreased central venous pressure (below 60 mmHg), tachycardia dpm, decreased diuresis, hemoglobin to 80 g/l or less.

3rd degree GS. BCC deficit is 30-40%. The condition is severe or very severe, lethargy, confusion, pale skin, cyanosis. Blood pressure below mmHg Tachycardia dpm, weak pulse filling. Oliguria.

4th degree GS Deficiency of blood volume more than 40%. Extreme degree of depression of all vital functions: consciousness is absent, blood pressure and central venous pressure, and pulse in the peripheral arteries are not determined. Breathing is shallow and frequent. Hyporeflexia. Anuria.

Diagnosis of HS is not difficult, but determining the degree of its severity, as well as the volume of blood loss, can cause certain difficulties.

Deciding on the severity of shock means determining the amount of intensive treatment.

It is difficult to determine the volume of blood loss. There are direct and indirect methods for assessing blood loss.

Direct methods for assessing blood loss: colorimetric, gravimetric, electrometric, gravitational - based on changes in hemoglobin and hematocrit.

Indirect methods: assessment of clinical signs, measurement of blood loss using graduated cylinders or visual method, determination of blood volume, hourly diuresis, composition and density of urine. The approximate volume of blood loss can be determined by calculating the Algover shock index (the ratio of the pulse rate to the level of systolic blood pressure).

Shock index Volume of blood loss (% of blood volume)

The severity of HS depends on individual tolerance to blood loss, premorbid background, obstetric pathology and method of delivery. Features of the development of HS in various obstetric pathologies are different.

GSH for placenta previa. Factors contributing to the development of shock with placenta previa are: arterial hypertension, iron deficiency anemia, reduced increase in blood volume at the onset of labor. Repeated bleeding during pregnancy or childbirth leads to activation of thromboplastin, a decrease in blood clotting ability and the development of hypocoagulation.

GSH for premature abruption 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, plasma loss, hyperviscosity, stasis and lysis of red blood cells, activation of endogenous thromboplastin, platelet consumption, and chronic disseminated intravascular coagulation occur. Chronic circulatory disorders are always observed with toxicosis in pregnant women, especially with a long course, against the background of somatic diseases, such as kidney and liver diseases, cardiovascular system, and anemia. When placental abruption occurs, extravasation occurs, releasing thromboplastins and biogenic amines in the process of cell destruction, which “trigger” the mechanism of disruption of the hemostasis system. Against this background, coagulopathic disorders quickly occur. GSH with premature abruption of a normally located placenta is especially difficult, accompanied by anuria, cerebral edema, respiratory failure, and a closed hematoma of the retroplacental space like compartment syndrome contributes to this. The lives of patients depend on the quick adoption of tactical decisions and measures.

GSH for hypotonic bleeding. Hypotonic bleeding and massive blood loss (1500 ml or more) are accompanied by instability of compensation. In this case, hemodynamic disturbances, symptoms of respiratory failure, and a syndrome with profuse bleeding due to the consumption of blood coagulation factors and a sharp activity of fibrinolysis develop. This leads to irreversible multiorgan changes.

GSH for uterine rupture. A special feature is the combination of hemorrhagic and traumatic shock, which contribute to the rapid development of disseminated intravascular coagulation syndrome, hypovolemia and respiratory failure.

DIC syndrome. It occurs in successive phases, which in practice cannot always be clearly distinguished. The following phases are distinguished: 1 - hypercoagulation; 2 - hypocoagulation (consumptive coagulopathy) without generalized activation of fibrin; 3. - hypocoagulation (consumptive coagulopathy with generalized activation of fibrinolysis - secondary fibrinolysis); 4 - complete non-coagulation, terminal degree of hypocoagulation. The central mechanism underlying bleeding in DIC syndrome is the inclusion of plasmatic blood coagulation factors, including fibrinogen, in 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, disruption of transcapillary exchange, hypoxia of vital organs during obstetric hemorrhage lead to disruption of the rheological properties of blood and its complete non-coagulation.

The main factors contributing to the development of DIC syndrome:

severe forms of late toxicosis of pregnancy

premature abruption of a normally located placenta

amniotic fluid embolism

extragenital pathology (diseases of the cardiovascular system, kidneys, liver).

Blood transfusion complications (incompatible transfusion).

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 (ischemia of the limbs, infarction pneumonia, thrombosis of the great vessels)

dysfunction of the central nervous system (disorientation, stupor, coma).

Impaired respiratory function (shortness of breath, cyanosis, tachycardia).

Clinical manifestations of DIC syndrome are varied and change in different phases. The duration of clinical manifestations is 7-9 hours or more. Laboratory diagnosis of the phases of DIC syndrome is important. The most informative and quickly performed tests are: determination of whole blood clotting time and thrombin time, thrombin test, spontaneous lysis of whole blood clot, platelet count, etc.

Clinical and laboratory data specific for each phase of DIC syndrome. Massive and rapid blood loss is associated with a decrease in the content of fibrinogen, platelets, other blood clotting factors and impaired fibrinolysis.

Hemorrhagic shock (a type of hypovolemic shock)- caused by uncompensated blood loss, a decrease in blood volume 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 degree (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.

Causes

Pathogenesis. The patient’s adaptation 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 central venous pressure begins to fall and the venous return to the heart decreases. Small output syndrome occurs, leading to decreased 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, chloride and water by the kidneys, while increasing potassium losses and decreasing diuresis. The result of the release of epinephrine and norepinephrine is peripheral vasoconstriction. Less important organs (skin, muscles, intestines) are switched off from the bloodstream, and the blood supply to vital organs (brain, heart, lungs) is preserved, i.e. centralization of blood circulation occurs. Vasoconstriction leads to deep tissue hypoxia and the development of acidosis. Under these conditions, proteolytic enzymes of the pancreas enter the blood and stimulate the formation of kinins. The latter increase the permeability of the vascular wall, which promotes the passage of water and electrolytes into the interstitial space. As a result, red blood cell aggregation occurs in the capillaries, creating a springboard for the formation of blood clots. This process immediately precedes the irreversibility of shock.

Symptoms (signs)

Clinical picture. When hemorrhagic shock develops, there are 3 stages.

Compensated reversible shock. The volume of blood loss does not exceed 25% (700-1300 ml). Tachycardia is moderate, blood pressure is either unchanged or slightly reduced. The saphenous veins become empty and the central venous pressure decreases. A sign of peripheral vasoconstriction occurs: coldness of the extremities. The amount of urine excreted is reduced by half (at a norm of 1-1.2 ml/min).

Decompensated reversible shock. The volume of blood loss is 25-45% (1300-1800 ml). The pulse rate reaches 120-140 per minute. Systolic blood pressure drops below 100 mm Hg, and pulse pressure decreases. Severe shortness of breath occurs, partly compensating for metabolic acidosis through respiratory alkalosis, but can also be a sign of shock lung. Increased coldness of the extremities and acrocyanosis. Cold sweat appears. The rate of urine output is below 20 ml/hour.

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 drops below 60 mm Hg. or not determined. There is no consciousness. Oligoanuria develops.

Treatment

TREATMENT. In hemorrhagic shock, vasopressor drugs (epinephrine, norepinephrine) are strictly contraindicated, since they aggravate peripheral vasoconstriction. To treat arterial hypotension that develops as a result of blood loss, the procedures listed below are performed sequentially.

Catheterization of the main vein (most often the subclavian or internal jugular according to Seldinger).

Combating metabolic acidosis: infusion of 150-300 ml of 4% sodium bicarbonate solution.

GK simultaneously with the start of blood replacement (up to 0.7-1.5 g of hydrocortisone IV). Contraindicated in cases of suspected gastric bleeding.

Relieving spasm of peripheral vessels. Considering the presence (usually) of hypothermia, warming the patient.

Aprotinin 30,000-60,000 units in 300-500 ml of 0.9% sodium chloride solution intravenously.

Inhalation of humidified oxygen.

Broad-spectrum antibiotics for wounds and septic diseases.

Maintain diuresis (50-60 ml/h) .. Adequate infusion therapy (until the central venous pressure reaches 120-150 mm water column).. If infusion is ineffective - osmotic diuretics (mannitol 1-1.5 g/kg in 5% p - glucose injection intravenously), if there is no effect - furosemide 40-160 mg intramuscularly or intravenously.

Cardiac glycosides (contraindicated in case of conduction disorders [complete or partial AV block] and myocardial excitability [the occurrence of ectopic foci of excitation]). With the development of bradycardia, b - adrenergic receptor stimulants (isoprenaline 0.005 g sublingually). If ventricular arrhythmias occur, lidocaine 0.1-0.2 g IV.

ICD-10 . R57.1 Hypovolemic shock