Unclear shock according to ICD 10. Hemorrhagic shock - description, causes, symptoms (signs), treatment

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.

Etiology

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:

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 abortive termination of pregnancy;
allergic reactions;
or ;
drug abuse.

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.

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, distinguish:

initial degree- in which blood pressure remains unchanged, but the heart rate increases. It can reach one hundred and twenty beats per minute;
degree of moderate severity- characterized by the 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 is increasing. Often there is a fever and a decrease in the volume of urine emitted;
complicated stage- characterized by the development of irreversible changes in internal organs and tissues. The patient's skin takes on an earthy hue. Often there is a coma.

Depending on the pathogen, there are:

streptococcal syndrome- occurs after labor, 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 surgical operations 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 aggravation. The main features are:

decrease in blood pressure, while the heart rate increases;
a sudden increase in body temperature, up to a fever;
intense headaches;
bouts of vomiting that are not associated with eating;
diarrhea;
stomach cramps;
severe muscle pain;
dizziness;
convulsions;
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 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.

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 can develop:

violation of blood circulation, which is why the internal organs do not receive the proper amount of oxygen;
acute respiratory failure - is formed due to severe damage to the lungs, especially if the onset of the syndrome was triggered by pneumonia;
violation of blood clotting and an increased likelihood of blood clots, which can cause profuse hemorrhages;
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 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:

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 ailment, 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 degree of damage to internal organs.

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

Treatment

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:

getting rid of the victim from narrow and tight clothing;
ensuring a horizontal position, so that the head is slightly raised in relation to the entire body;
under the feet you need to put a heating pad;
allow fresh air to flow in.

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.

Prevention

Preventive measures for toxic shock syndrome consist in following several rules:

timely elimination of diseases that can cause the development of such a condition. In most cases in children and adults, it is pneumonia;
always monitor the cleanliness of the skin, and in the event of any violation of integrity, immediately treat the affected area with antiseptic substances;
take breaks in the use of tampons during the course of menstruation. Alternate pads and tampons every two periods, and also change such a hygiene product 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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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 contact 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 - description, causes, symptoms (signs), treatment.

Short description

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.

Causes

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.

Symptoms (signs)

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

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.

hypovolemic shock

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 studies: 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

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

Medical studies provided for monitoring the effectiveness of treatment

Medications prescribed

rr d / local. approx. 0.1%: vial-drip 30 ml;

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

concentrate for preparation. r-ra d / in / in the input. 50 mg/5 ml: amp. 5, 30 or 300 pieces;

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

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

lyophilization. powder for preparation. r-ra d / in / in the input. 15 units: amp., vial. 5 or 10 pcs.

solution for infusions 500 thousand CIE / 50 ml: fl. 1 PC.

tab. 500 mcg: 50 pieces;

solution for injections. 4 mg/ml: amp. 25 pieces;

solution for injections. 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. solution for injections. 25, 50 or 250 mg, in clmpl. with r-rit. in amp. 10 ml

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

solution for infusions: fl. 200 ml or 400 ml

solution for infusions 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: vial. 200 ml 1, 24 or 48 pcs, vial. 400 ml 1, 12 or 24 pieces, vial 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 pieces, bottle 400 ml 1, 24 or 40 pcs.

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

solution for infusion: 200 ml bottle. 1 or 28 pieces, 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 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.

On what mechanisms does the severity of shock depend?

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

state of nervous regulation of vascular tone;
the ability of the heart to work in conditions of hypoxia;
blood clotting;
environmental conditions for additional oxygen supply;
the level of immunity.

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 the circulatory hypoxia of tissues, the blood becomes “acidified” with 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.

Causes

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:

rupture of the uterus and birth canal;
placenta previa;
in the normal position of the placenta, its early detachment is possible;
abortion;
hypotension of the uterus after childbirth.

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

Clinical manifestations

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:

Compensation or the first stage - blood loss is not more than 15-25% of the total volume, the patient is fully conscious, he adequately answers questions, on examination, pallor and coldness of the skin of the extremities, weak pulse, blood pressure at the lower limits of the norm attract attention , heart rate increased to 90-110 per minute.
The second stage, or decompensation, - in accordance with the name, symptoms of oxygen deficiency of the brain, weakness of cardiac output. Usually characteristic of acute blood loss from 25 to 40% of the total circulating blood volume. Disruption of adaptive mechanisms is accompanied by a violation of the patient's consciousness. In neurology, it is regarded as soporous, there is a retardation of thinking. There is pronounced cyanosis on the face and extremities, the hands and feet are cold, the body is covered with sticky sweat. Blood pressure (BP) drops sharply. Pulse of weak filling, characterized as "filamentous", frequency up to 140 per minute. Breathing is frequent and shallow. Urination is sharply limited (up to 20 ml per hour). This 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. Consciousness is absent, the skin is pale, with a marble tint, blood pressure is not determined or only the upper level can be measured within 40–60 mm Hg. Art. It is impossible to feel the pulse on the ulnar artery, with sufficiently good skills it is felt on the carotid arteries, heart sounds are deaf, tachycardia reaches 140–160 per minute.

How is the degree of blood loss determined?

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

the volume of circulating blood (CBV) - is determined by the laboratory;
shock index.

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 they have weak compensation mechanisms.

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.

How to provide assistance in 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 the maximum bent arm helps to stop bleeding from the vessels of the shoulder and forearm

Help with hemorrhagic shock cannot do without:

imposition of hemostatic dressings, tourniquet, immobilization of the limb in case of injuries of large vessels;
giving the victim a lying position, with a mild degree of shock, the victim may be in a euphoric state and inadequately assess his state of health, try to get up;
if possible, replenish the loss of fluid with the help of plentiful drinking;
warming with warm blankets, heating pads.

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:

checking the effectiveness of a pressure bandage, tourniquet, applying clamps to blood vessels with open wounds;
installation of systems for transfusion into 2 veins, if possible, puncture of the subclavian vein and its catheterization;
establishing a transfusion of fluid for the speedy reimbursement of BCC, in the absence of Reopoliglyukin or Poliglukin, 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 hardware breathing or using an Ambu manual bag;
conducting anesthesia with the help of injections of narcotic analgesics, Baralgin and antihistamines, Ketamine;
administration of corticosteroids to maintain blood pressure.

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:

Fundamentals of therapy for hemorrhagic shock

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

observance of continuity in the provision of care with the pre-hospital stage;
continuation of replacement transfusion with solutions;
measures to finally stop bleeding;
adequate use of medications depending on the severity of the victim;
antioxidant therapy - inhalation of a humidified oxygen-air mixture;
warming the patient.

Reopoliglyukin normalizes platelet aggregation, serves as a prevention of DIC

When a patient is admitted to the intensive care unit:

carry out catheterization of the subclavian vein, add a jet injection of Poliglukin to a drip infusion of saline;
blood pressure is constantly measured, the heart rate is noted on the heart monitor, the allocated amount of urine is recorded through the catheter from the bladder;
when catheterizing a vein, blood is taken for an urgent analysis to determine the degree of loss of BCC, anemia, blood type and Rh factor;
after the readiness of analyzes and diagnostics of the moderate stage of shock, donor blood is ordered, tests are made for individual sensitivity, Rh compatibility;
with a good biological sample, 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 assistance is also determined.

How much blood should be transfused?

When transfusing, 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 young children, the total volume is combined by half with the erythrocyte mass;
if the BCC is reduced by 35%, it is necessary to use both the erythrocyte mass and blood substitutes (1: 1);
the total volume of transfused fluids should be 15–20% higher than the defined blood loss;
if severe shock with a loss of 50% of blood is detected, then the total volume should be twice as large, and the ratio between red blood cells and blood substitutes is observed as 2:1.

An indication for stopping the continuous infusion of blood and blood substitutes is:

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

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.

What complications are possible with hemorrhagic shock?

The state of hemorrhagic shock is very transient, dangerously massive blood loss and death in cardiac arrest.

The most severe complication is the development of disseminated intravascular coagulation syndrome. It disrupts the balance of formed elements, vascular permeability, impairs microcirculation.
Tissue hypoxia most strongly 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, necrosis is possible.
Hepatic and renal tissues react with manifestations of organ failure, impaired synthesis of coagulation factors.
With obstetric massive bleeding, long-term consequences are a violation of the reproductive capabilities of a woman, the appearance of endocrine pathology.

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.

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.

Causes

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.

Symptoms (signs)

Clinical picture. With the development of hemorrhagic shock, 3 stages are distinguished.

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.

Treatment

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).

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

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 body.
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).

Descriptions of diseases

Titles

hemorrhagic shock.

Description

Hemorrhagic shock develops as a result of acute blood loss.
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.

Symptoms

Causes

The cause of acute blood loss can be trauma, spontaneous bleeding, surgery. Of great importance are the speed and volume of blood loss.
With a slow loss of even large volumes of blood (1000-1500 ml), 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.

Treatment

The principles of resuscitation and intensive care in patients with acute blood loss and in a state of hemorrhagic shock at the prehospital stage are as follows:
1. Reduction or elimination of the existing phenomena of acute respiratory failure (ARF), the cause of which may be the 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 puncture of 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 are determined, 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 rate of infusion is limited to rare drops;
If surgery is expected, decide on the possibility of its implementation;
After normalization of blood circulation, they maintain water balance and normalize 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.