Septic shock with cardiac complications. Septic shock in intensive care

Septic shock is a systemic pathological response to severe infection. It is characterized by fever, tachycardia, tachypnea, and leukocytosis when identifying the source of primary infection. In this case, microbiological blood testing often reveals bacteremia. In some patients with sepsis syndrome, bacteremia is not detected. When arterial hypotension and multiple systemic failure become components of the sepsis syndrome, the development of septic shock is stated.

Causes and pathogenesis of the development of septic shock:

The incidence of sepsis and septic shock has been steadily increasing since the 1930s and is likely to continue to increase.
The reasons for this are:

1. Increasing use of invasive devices for intensive care, that is, intravascular catheters, etc.

2. Widespread use of cytotoxic and immunosuppressive drugs (for malignant diseases and transplantations), which cause acquired immunodeficiency.

3. Increase in life expectancy of patients with diabetes mellitus and malignant tumors, who have a high level of predisposition to sepsis.

Bacterial infection is the most common cause of septic shock. In sepsis, the primary foci of infection are often localized in the lungs, abdominal organs, peritoneum, and also in the urinary tract. Bacteremia is detected in 40-60% of patients in a state of septic shock. In 10-30% of patients in a state of septic shock, it is impossible to isolate the culture of bacteria whose action causes septic shock. It can be assumed that septic shock without bacteremia is the result of a pathological immune reaction in response to stimulation by antigens of bacterial origin. Apparently, this reaction persists after pathogenic bacteria are eliminated from the body by the action of antibiotics and other elements of therapy, that is, its endogenization occurs.
The endogenization of sepsis may be based on numerous, mutually reinforcing and realized through the release and action of cytokines, interactions of cells and molecules of innate immune systems and, accordingly, immunocompetent cells.

Sepsis, systemic inflammatory response, and septic shock are consequences of an excessive response to stimulation of cells that carry out innate immune responses by bacterial antigens. An excessive reaction of cells of the innate immune system and a secondary reaction of T-lymphocytes and B-cells cause hypercytokinemia. Hypercytokinemia is a pathological increase in the blood levels of agents of autoparacrine regulation of cells that carry out innate immune reactions and acquired immune reactions.

With hypercytokinemia in the blood serum, the content of primary proinflammatory cytokines, tumor necrosis factor-alpha and interleukin-1 increases abnormally. As a result of hypercytokinemia and systemic transformation of neutrophils, endothelial cells, mononuclear phagocytes and mast cells into cellular effectors of inflammation, an inflammatory process devoid of protective significance occurs in many organs and tissues. Inflammation is accompanied by alteration of the structural and functional elements of effector organs.

A critical deficiency of effectors causes multiple systemic failure.

Symptoms and signs of septic shock:

The development of a systemic inflammatory response is indicated by the presence of two or more of the following signs:

Body temperature is higher than 38 o C, or below 36 o C.

Respiratory rate above 20/minute. Respiratory alkalosis with carbon dioxide tension in arterial blood below 32 mmHg. Art.

Tachycardia with a heart rate greater than 90/minute.

Neutrophilia when the content of polymorphonuclear leukocytes in the blood increases to a level above 12x10 9 / l, or neutropenia when the content of neutrophils in the blood is below 4x10 9 / l.

A shift in the leukocyte formula, in which band neutrophils make up more than 10% of the total number of polymorphonuclear leukocytes.

Sepsis is indicated by two or more signs of a systemic inflammatory reaction when the presence of pathogenic microorganisms in the internal environment is confirmed by bacteriological and other studies.

Course of septic shock

In septic shock, hypercytokinemia increases the activity of nitric oxide synthetase in endothelial and other cells. As a result, the resistance of resistive vessels and venules decreases. A decrease in the tone of these microvessels reduces overall peripheral vascular resistance. During septic shock, some of the body's cells suffer from ischemia caused by peripheral circulatory disorders. Peripheral circulation disorders in sepsis and septic shock are consequences of systemic activation of endothelial cells, polymorphonuclear neutrophils and mononuclear phagocytes.

Inflammation of this origin is purely pathological in nature and occurs in all organs and tissues. A critical drop in the number of structural and functional elements of most effector organs is the main link in the pathogenesis of the so-called multiple system failure.

According to traditional and correct ideas, sepsis and a systemic inflammatory response are caused by the pathogenic action of gram-negative microorganisms.

In the occurrence of a systemic pathological reaction to invasion into the internal environment and blood of gram-negative microorganisms, the decisive role is played by:

Endotoxin (lipid A, lipopolysaccharide, LPS). This heat-stable lipopolysaccharide forms the outer coating of gram-negative bacteria. Endotoxin, acting on neutrophils, causes the release of endogenous pyrogens by polymorphonuclear leukocytes.

LPS-binding protein (LPBP), traces of which are determined in plasma under physiological conditions. This protein forms a molecular complex with endotoxin that circulates in the blood.

Cell surface receptor of mononuclear phagocytes and endothelial cells. Its specific element is a molecular complex consisting of LPS and LPSSB (LPS-LPSSB).

Currently, the frequency of sepsis caused by invasion of gram-positive bacteria into the internal environment is increasing. The induction of sepsis by Gram-positive bacteria is usually not associated with their release of endotoxin. Peptidoglycan precursors and other wall components of Gram-positive bacteria are known to trigger the release of tumor necrosis factor-alpha and interleukin-1 by immune cells. Peptidoglycan and other components of the walls of gram-positive bacteria activate the complement system through the alternative pathway. Activation of the complement system at the whole body level causes systemic pathogenic inflammation and contributes to endotoxicosis in sepsis and the systemic inflammatory response.

It was previously thought that septic shock was always caused by endotoxin (a lipopolysaccharide of bacterial origin) released by gram-negative bacteria. It is now generally accepted that less than 50% of cases of septic shock are caused by Gram-positive pathogens.

Disorders of peripheral circulation during septic shock, adhesion of activated polymorphonuclear leukocytes to activated endothelial cells - all this leads to the release of neutrophils into the interstitium and inflammatory alteration of cells and tissues. At the same time, endotoxin, tumor necrosis factor-alpha, and interleukin-1 increase the formation and release of tissue coagulation factor by endothelial cells. As a result, mechanisms of external hemostasis are activated, which causes fibrin deposition and disseminated intravascular coagulation.

Arterial hypotension in septic shock is mainly a consequence of a decrease in total peripheral vascular resistance. Hypercytokinemia and an increase in the concentration of nitric oxide in the blood during septic shock causes dilatation of arterioles. At the same time, through tachycardia, the minute volume of blood circulation increases compensatoryly. Arterial hypotension in septic shock occurs despite a compensatory increase in cardiac output. Total pulmonary vascular resistance increases during septic shock, which can be partly attributed to the adhesion of activated neutrophils to activated endothelial cells of the pulmonary microvessels.

The following main links in the pathogenesis of peripheral circulatory disorders in septic shock are distinguished:

1) increased permeability of the microvascular wall;

2) an increase in microvascular resistance, which is enhanced by cell adhesion in their lumen;

3) low response of microvessels to vasodilating influences;

4) arteriolo-venular shunting;

5) drop in blood fluidity.

Hypovolemia is one of the factors of arterial hypotension in septic shock.

The following causes of hypovolemia (a drop in cardiac preload) in patients in a state of septic shock are identified:

1) dilatation of capacitive vessels;

2) loss of the liquid part of the blood plasma in the interstitium due to a pathological increase in capillary permeability.

It can be assumed that in most patients in a state of septic shock, the drop in oxygen consumption by the body is mainly due to primary disorders of tissue respiration. In septic shock, moderate lactic acidosis develops with normal oxygen tension in the mixed venous blood.

Lactic acidosis in septic shock is considered to be a consequence of decreased pyruvate dehydrogenase activity and secondary accumulation of lactate, rather than a decrease in blood flow in the periphery.

Peripheral circulatory disorders in sepsis are systemic in nature and develop with arterial normotension, which is supported by an increase in minute volume of blood circulation. Systemic microcirculation disorders manifest themselves as a decrease in pH in the gastric mucosa and a decrease in oxygen saturation of blood hemoglobin in the hepatic veins. Hypoergosis of intestinal barrier cells, the action of immunosuppressive links in the pathogenesis of septic shock - all this reduces the protective potential of the intestinal wall, which is another cause of endotoxemia in septic shock.

Diagnosis of septic shock

Septic shock - sepsis (systemic inflammatory reaction syndrome plus bacteremia) in combination with a decrease in blood pressure. less than 90 mm Hg. Art. in the absence of visible reasons for arterial hypotension (dehydration, bleeding). Presence of signs of tissue hypoperfusion despite infusion therapy. Perfusion disorders include acidosis, oliguria, and acute disturbances of consciousness. In patients receiving inotropic agents, perfusion abnormalities may persist in the absence of arterial hypotension.
Refractory septic shock - septic shock lasting more than one hour, refractory to fluid therapy.

Treatment of septic shock:

1. Infusion therapy

Catheterization of two veins.
300-500 ml of crystalloid solution IV as a bolus, then 500 ml of crystalloid solution IV drip over 15 minutes. Assess for venous hypertension and the presence of cardiac decompensation.
In the presence of heart failure, catheterization is advisable a. pulmonalis with a Swan-Ganz catheter to assess volume status: optimal PCWP = 12 mm Hg. Art. in the absence of AMI and 14-18 mm Hg. Art. in the presence of AMI;
if after an infusion bolus the PCWP value exceeds 22 mmHg. Art., then progression of heart failure should be assumed and active crystalloid infusion should be stopped.
If, despite high values of filling pressure of the left ventricle, arterial hypotension persists - dopamine 1-3-5 or more mcg/kg/min, dobutamine 5-20 mcg/kg/min.
Sodium bicarbonate in a calculated dose to correct metabolic acidosis.

2. Therapy for hypoxemia/ARDS - oxygen therapy, mechanical ventilation using PEEP.

3. Therapy for reduced contractile ability of the myocardium - strophanthin K 0.5 mg 1-2 times a day intravenously in 10-20 ml of 5-20% glucose solution or saline; digoxin 0.25 mg 3 times a day per os for 7-10 days, then 0.25-0.125 mg per day; dobutamine 5-20 mcg/kg/min i.v.

4. DIC therapy

5. Therapy for acute renal failure.

6. Empirical antibiotic therapy (the localization of the source of the septic process and the expected range of possible microorganisms are taken into account).

7. Surgical drainage of foci of infection.

8. Drugs whose effectiveness has not been confirmed:

Naloxone.
Corticosteroids.

In this article we will talk about severe pathology. We will review the pathophysiology of septic shock, clinical guidelines for it, and its treatment.

Features of the disease

Septic shock is the terminal phase of a generalized (extended to all organs) septic process (blood poisoning), which is characterized by the active development of pathological processes in the body that practically do not respond to intensive resuscitation therapy.

Basic:

critical decrease in blood pressure (hypotension);
severe disruption of the blood supply to the most important organs and tissues (hypoperfusion);
partial and complete failure of several organs to function simultaneously (multiple organ dysfunction).

Considering the commonality of internal and external manifestations, septic shock is considered in medicine as successive stages of a single organism-wide pathological process. Another name for the disease is bacterial toxic shock, septic infectious toxic shock. The state of septic shock develops in almost 60% of cases of severe sepsis. As a result of such serious disorders in the functioning of body systems, deaths from septic shock are common.

According to ICD-10, septic shock has code A41.9.

The development of shock is more often observed when the body is attacked by gram-negative flora (Klebsiella, Escherichia coli, Proteus), and anaerobes. Gram-positive microorganisms (staphylococci, diphtheria bacteria, clostridia) cause the critical phase of sepsis in 5% of cases. But the difference between these pathogens is the release of toxins (exotoxins), which cause severe poisoning and tissue damage (for example, necrosis of muscle and kidney tissue).
But not only bacteria, but also protozoa, fungi, rickettsia and viruses can cause a state of septic shock.

This video talks about septic shock:

Stages

Conventionally, in a state of shock during sepsis, three phases are distinguished:

warm (hyperdynamic);
cold (hypodynamic);
irreversible.

Manifestations during different phases of septic shock Table No. 1

Stages (phases) of septic shock	Manifestations, characteristics of the condition
Warm	It has been proven that in case of shock caused by gram-positive flora, the course and prognosis are more favorable for the patient. Characterized by the following conditions: short duration (from 20 to 180 minutes); (“red hyperthermia”) against a background of high temperature; hands and feet are hot and covered with sweat. systolic (upper) blood pressure drops to 80 - 90 mmHg. Art., remaining at this level for about 0.5 - 2 hours, diastolic is not determined. at up to 130 beats per minute, pulse filling remains satisfactory; Cardiac output increases with the warm form of shock; central venous pressure is reduced.; excitement develops.
Cold shock phase	The course of “cold shock,” most often provoked by gram-negative organisms, is more severe and more difficult to respond to therapy, lasting from 2 hours to a day. This form is observed at the stage of centralization of blood circulation due to vascular spasm (outflow of blood from the liver, kidneys, peripheral vessels to the brain and heart). The “cold phase” is characterized by: decreased temperature in the arms and legs, pronounced whiteness and moisture in the skin (“white hyperthermia”); hypodynamic syndrome (organic damage to brain cells due to oxygen deficiency); deterioration of cardiac activity due to damage to heart tissue by bacterial poison; blood pressure is initially normal or falls moderately, then there is a sharp drop to critical levels, sometimes with short-term rises; , reaches 150 beats per minute, shortness of breath up to 60 breaths per minute; venous pressure is normal or increased; complete cessation of urine output (); disturbance of consciousness.
Irreversible phase	Severe organ failure of several organs and systems is observed (respiratory and, with depression of consciousness up to coma), a critical drop in blood pressure. Functions cannot be restored even with resuscitation measures. The comatose state leads to the death of the patient.

Immediate and competent treatment of shock in sepsis, carried out from the beginning of the “warm phase”, often stops the development of pathological processes, otherwise septic shock goes into the “cold phase”.

Unfortunately, due to its short duration, the hyperdynamic phase is often overlooked by physicians.

Causes

The causes of septic shock are similar to the causes of severe sepsis and the inability to stop the progression of the septic process during treatment.

Symptoms

The complex of symptoms during the development of septic shock is “inherited” from the previous stage - severe sepsis, differing in even greater severity and further increase.
The development of a shock state during sepsis is preceded by severe chills against the background of significant fluctuations in body temperature: from sharp hyperthermia, when it rises to 39 - 41 ° C, lasting up to 3 days, and a critical decrease in the range of 1 - 4 degrees to (up to 38.5) , normal 36 – 37 or falling below 36 – 35 C.

The main sign of shock is an abnormal drop in blood pressure without previous bleeding or not corresponding in severity, which cannot be raised to the minimum norm, despite intensive medical measures.

General symptoms:

In all patients, at the early stage of shock (often before the pressure drops), signs of damage to the central nervous system are observed:

euphoria, overexcitation, loss of orientation;
delusions, auditory hallucinations;
further - apathy and numbness (stupor) with a reaction only to strong painful stimuli.

Increasing severity of manifestations of severe sepsis are expressed in the following:

tachycardia up to 120 – 150 beats/min;
the shock index rises to 1.5 or more when the norm is 0.5.

It is a value equal to the heart rate divided by the systolic blood pressure. Such an increase in the index indicates the rapid development of hypovolemia - a decrease in circulating blood volume (CBV) - the amount of blood in the vessels and organs.

breathing is uneven, shallow and rapid (tachypne), 30–60 respiratory cycles per minute, indicating the development of acute acidosis (increased acidity of tissues and body fluids) and a state of “shock” lung (tissue damage preceding edema);
cold sticky sweat;
redness of the skin in a short “warm phase”, then a sharp pallor of the skin in the “cold stage” with a transition to marbling (whiteness) with a subcutaneous vascular pattern, the limbs become cold;
bluish coloration of lips, mucous membranes, nail plates;
sharpness of facial features;
frequent yawning if the patient is conscious, as a sign of oxygen deficiency;
increased thirst (decreased amount of urine) and subsequent anuria (stopping urination), which indicates severe kidney damage;
in half of the patients - vomiting, which, as the condition progresses, becomes like coffee, due to tissue necrosis and bleeding in the esophagus and stomach;
pain in the muscles, abdomen, chest, lower back, associated with circulatory disorders and hemorrhages in tissues and mucous membranes, as well as an increase in acute renal failure;
strong;
yellowness of the skin and mucous membranes becomes more pronounced as liver failure worsens;
hemorrhages under the skin in the form of pinpoint, cobweb-like petechiae on the face, chest, abdomen, folds of the arms and legs.

Diagnosis and treatment of septic shock are described below.

Diagnostics

Septic shock, as a phase of generalized sepsis, is diagnosed by the severity of all the symptoms of the pathology in the “warm” and “cold” stages and clear signs of the last stage - secondary or irreversible shock.
The diagnosis should be made immediately based on the following clinical manifestations:

the existence of a purulent focus in the body;
fever with chills, followed by a sharp drop in temperature below normal;
acute and threatening drop in blood pressure;
high heart rate even at low temperatures;
depression of consciousness;
pain in different areas of the body;
acute decrease in urine output;
hemorrhages under the skin in the form of a rash, in the whites of the eyes, nosebleeds, necrosis of areas of the skin;
convulsions.

In addition to external manifestations, during laboratory tests the following is observed:

deterioration of all indicators of laboratory blood tests in comparison with the first phases of sepsis (severe leukocytosis or leukopenia, ESR, acidosis, thrombocytopenia);
acidosis, in turn, leads to critical conditions: dehydration, blood thickening and blood clots, organ infarctions, impaired brain function and coma;
the change in the concentration of procalcitonin in the blood serum exceeds 5.5 - 6.5 ng/ml (an important diagnostic indicator for the development of septic shock).

Diagram of septic shock

Treatment

Treatment combines medication, therapeutic and surgical methods used simultaneously.

As in the phase of severe sepsis, emergency surgical treatment is carried out for all primary and secondary purulent metastases (in internal organs, subcutaneous and intermuscular tissue, in joints and bones) as soon as possible, otherwise any therapy will be useless.

In parallel with the rehabilitation of purulent foci, the following urgent measures are performed:

Perform artificial ventilation to eliminate manifestations of acute respiratory and heart failure
To stimulate heart function, increase blood pressure, and activate renal blood flow, Dopamine and Dobutamine are infused.
In patients with severe hypotension (less than 60 mmHg), Metaraminol is administered to ensure blood supply to vital organs.
Massive intravenous infusions of medicinal solutions are carried out, including dextrans, crystalloids, colloid solutions, glucose under constant monitoring of central venous pressure and diuresis (urine excretion) in order to:
- elimination of blood supply disturbances and normalization of blood flow indicators;
- removal of bacterial poisons and allergens;
- stabilization of electrolyte and acid-base balance;
- prevention of pulmonary distress syndrome (acute respiratory failure due to the development of edema) - infusion of Albumin and Protein;
- relief of hemorrhagic syndrome (DIC) in order to stop tissue bleeding and internal bleeding;
- replenish fluid loss.
When cardiac output is low and vasoconstrictors are ineffective, the following are often used:
- Glucose-insulin-potassium mixture (GIK) for intravenous infusion;
- Naloxone for bolus - rapid jet injection into a vein (if a therapeutic effect is obtained, after 3 - 5 minutes they switch to infusion).
Without waiting for tests to identify the pathogen, antimicrobial therapy is started. Depending on the development of internal pathologies of systems and organs, penicillins, cephalosporins (up to 12 grams per day), aminoglycosides, and carbapenems are prescribed in large doses. The combination of Impinem and Ceftazidime is considered the most rational, which gives a positive result even in the case of Pseudomonas aeruginosa, increasing the survival rate of patients with severe concomitant pathology.

Important! The use of bactericidal antibiotics can worsen the situation, as a result of which a switch to bacteriostatic drugs (Clarithromycin, Dirithromycin, Clindamycin) is possible.

To prevent superinfection (re-infection or complications during antibacterial therapy), Nystatin 500,000 units up to 4 times a day, Amphotericin B, bifidum are prescribed.

Suppress allergic manifestations by using glucocorticosteroids (Hydrocortisone). The use of Hydrocortisone in a daily dose of up to 300 mg (up to 7 days) for shock can accelerate the stabilization of vascular blood flow and reduce deaths.
Administration of the activated APS protein drotrecogin-alpha (Zigris) for 4 days at a dose of 24 mcg/kg/hour reduces the likelihood of patient death during the critical phase of acute renal failure (contraindication - no risk of bleeding).

In addition, if it is determined that the causative agent of sepsis is staphylococcal flora, intramuscular injections of anti-staphylococcal immunoglobulin are added, infusions of anti-staphylococcal plasma, human immunoglobulin are restored, and intestinal motility is restored.

Prevention of septic shock

To prevent the development of septic shock, you must:

Timely surgical opening and sanitation of all purulent metastases.
Prevention of the deepening development of multiple organ dysfunction with the involvement of more than one organ in the septic process.
Stabilization of improvements achieved during the severe shock stage.
Maintaining blood pressure at minimally normal levels.
Prevention of the progression of encephalopathy, acute renal and hepatic failure, disseminated intravascular coagulation syndrome, development of the state of “shock” lung, elimination of the state of acute anuria (urinary retention) and dehydration.

Complications of septic shock are described below.

Complications

At worst– death (if this result can be considered as a complication).
At its best– serious damage to internal organs, brain tissue, central nervous system with long-term treatment. The shorter the period of recovery from shock, the less severe tissue damage is predicted.

Forecast

Septic shock is fatal to the patient, so both early diagnosis and prompt intensive treatment are essential.

The time factor is crucial in predicting this condition, since irreversible pathological changes in tissues occur within 4–8 hours; in many cases, the time for providing assistance is reduced to 1–2 hours.
The probability of death with septic shock reaches more than 85%.

This video talks about septic shock due to TBI:

Which leads to hypoxia of many organs. Shock can occur as a result of insufficient filling of the vascular system with blood and dilation of blood vessels. The disease belongs to a group of disorders in which blood flow to all tissues of the body is limited. This leads to hypoxia and dysfunction of vital organs such as the brain, heart, lungs, kidneys, and liver.

Causes of septic shock:

neurogenic shock occurs as a result of damage to the nervous system;
anaphylactic shock develops as a result of a violent antibody reaction;
cardiogenic shock occurs as a result of acute heart failure;
neurogenic shock occurs due to dysfunction of the nervous system.

The type of microorganism causing the infection is also important; for example, pneumococcal sepsis can occur due to pneumonia. In hospitalized patients, surgical incisions or pressure ulcers are common sites of infection. Sepsis can accompany bone infections, called bone marrow inflammation.

Infection can occur anywhere where bacteria and other infectious viruses can enter the body. The most common cause of sepsis is bacterial infections (75-85% of cases), which, if not treated promptly, can lead to septic shock. Septic shock is characterized by a decrease in blood pressure.

Patients at increased risk include:

with a weakened immune system (particularly with diseases such as cancer or AIDS);
in children under 3 years of age;
old age;
using drugs that block the normal functioning of the immune system;
after a long illness;
after surgical operations;
with elevated sugar levels.

The basis for the occurrence and treatment of sepsis is the immune system, which responds to infection by causing inflammation. If inflammation spreads throughout the body, the immune system will respond to infection by attacking not only the attacking microbes, but also healthy cells. In this way, even parts of the body begin to suffer. In this case, septic shock may occur, accompanied by bleeding and damage to internal organs. For this reason, patients diagnosed or suspected of having sepsis should be treated in intensive care units.

Treatment of sepsis requires a two-pronged approach. Therefore, you should not underestimate any signs and report symptoms to your doctor immediately. To make a correct diagnosis, a specialist will immediately prescribe tests that will determine the type of pathogen and develop effective treatment.

Today, sepsis is combated using causal treatment. It consists in the use of broad-spectrum antibiotics.

It should be remembered that sepsis is a very dangerous set of symptoms that can lead to septic shock and even death of the patient. Symptomatic therapy should restore impaired vital functions. Usually during treatment:

carry out dialysis when the slightest signs of renal failure appear;
a drip is placed to eliminate blood supply disturbances;
use glucocorticoids to capture the inflammatory response;
gives platelet transfusions;
carry out measures to strengthen respiratory functions;
in case of carbohydrate imbalance, insulin administration is recommended.

Septic shock - symptoms

It is worth remembering that sepsis is not a disease, but a certain set of symptoms caused by the body’s violent reaction to an infection, which can lead to progressive failure of many organs, septic shock and death.

The main symptoms of sepsis that may indicate septic shock are:

a sharp increase in temperature above 38C;
a sudden decrease in this temperature to 36 degrees;
increased heart rate;
the amount and frequency of breathing increases;
white blood cell count > 12,000/ml (leukocytosis) or< 4.000/мл (лейкопения);
sudden jumps in blood pressure.

If at least three of the above factors are confirmed during a medical examination, sepsis will most likely lead to the development of septic shock.

Before starting treatment, the doctor will certainly prescribe the necessary diagnostic tests, without which it is difficult to accurately determine the nature of the lesion. First of all, this is a microbiological study, a blood test. Of course, before starting treatment, depending on the clinical picture, you may need to analyze urine, cerebrospinal fluid, and mucus from the respiratory tract.

But due to the threat to the patient’s life, the diagnostic period must be shortened as much as possible; test results must be known as soon as possible. Treatment of a patient with suspected septic shock should begin immediately after diagnosis.

In severe cases, the patient may be subjected to mechanical ventilation and maintenance of peripheral venous pressure in the range of 12-15 mmHg. Art., to compensate for increased pressure in the chest. Such manipulations may be justified in case of increased pressure in the abdominal cavity.

If, during the first 6 hours of treatment, in patients with severe sepsis or septic shock, hemoglobin oxygen saturation does not occur, a blood transfusion may be necessary. In any case, it is important to carry out all activities quickly and professionally.

Description:

Septic shock is a complex pathophysiological process that occurs as a result of the action of an extreme factor associated with the breakthrough of pathogens and their toxins into the bloodstream, which, along with damage to tissues and organs, causes excessive, inadequate tension of nonspecific adaptation mechanisms and is accompanied by hypoxia, tissue hypoperfusion, and profound metabolic disorders processes.

Symptoms:

Symptoms of septic shock depend on the stage of shock, the microorganism that caused it, and the age of the patient.

Initial stage: decreased urination, sudden increase in temperature above 38.3°, diarrhea and loss of strength.

Late stage: restlessness, feeling, irritability, thirst due to decreased blood flow to brain tissue, increased heart rate and rapid breathing. In infants and older adults, the only signs of shock may be low blood pressure, confusion, and rapid breathing.

Low body temperature and decreased urination are common late signs of shock. Complications of septic shock include disseminated intravascular coagulation, renal and peptic ulcers, and liver dysfunction.

Causes:

Septic shock (infectious-toxic, bacteriotoxic or endotoxic) develops only in generalized infections that occur with massive bacteremia, intense destruction of bacterial cells and the release of endotoxins that disrupt the regulation of the volume of the vascular bed. Septic shock can develop not only with bacterial, but also with viral infections, protozoan infestations, fungal sepsis, severe injuries, and so on.

Treatment:

For treatment the following is prescribed:

The first step is to stop the progression of shock. Typically, intravenous fluids are given and pulmonary artery pressure is monitored. Infusion of whole blood or plasma can raise pulmonary artery pressure to a satisfactory level. To overcome hypoxia may be required. Inserting a catheter into the urinary tract allows you to accurately estimate the amount of urine released per hour.

Antibiotics (intravenously) are immediately prescribed to fight the infection. Depending on which microorganism is the causative agent of the infection, complex treatment with antibiotics is carried out (usually an aminoglycoside is used in combination with penicillin). If a staphylococcal infection is suspected, a cephalosporin is used. If the infection is caused by non-spore-forming anaerobic microorganisms, chloromycetin or cleocin is prescribed. However, these drugs can cause unpredictable reactions. All products should be used only as directed by your doctor. If abscesses are present, they are excised and drained to cleanse the purulent focus.

If fluids do not relieve shock, dopastat is used to increase blood pressure to maintain blood perfusion in the brain, liver, gastrointestinal tract, kidneys, and skin. Bicarbonate (intravenously) is used as a remedy for acidosis. Intravenous corticosteroid infusions can improve blood perfusion and cardiac output.

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3.5. The Operator has the right to transfer Personal Data and Data to third parties not specified in clause 3.4. of this Privacy Policy in the following cases:

3.5.1. The user has expressed his consent to such actions;

3.5.2. The transfer is necessary as part of the User’s use of the Site or the provision of Services to the User;

3.5.3. The transfer occurs as part of the sale or other transfer of a business (in whole or in part), and all obligations to comply with the terms of this Policy are transferred to the acquirer.

3.6. The Operator carries out automated and non-automated processing of Personal Data and Data.

4. CHANGE OF PERSONAL DATA.

4.1. The User guarantees that all Personal Data is current and does not relate to third parties.

4.2. The User may change (update, supplement) Personal Data at any time by sending a written application to the Operator.

4.3. The user has the right to delete his Personal Data at any time; to do this, he just needs to send an email with a corresponding application to Email: Data will be deleted from all electronic and physical media within 3 (three) business days.

5. PROTECTION OF PERSONAL DATA.

5.1. The Operator ensures proper protection of Personal and other data in accordance with the Law and takes necessary and sufficient organizational and technical measures to protect Personal data.

5.2. The applied protection measures, among other things, make it possible to protect Personal Data from unauthorized or accidental access, destruction, modification, blocking, copying, distribution, as well as from other unlawful actions of third parties.

6. PERSONAL DATA OF THIRD PARTIES USED BY USERS.

6.1. Using the Site, the User has the right to enter data of third parties for their subsequent use.

6.2. The User undertakes to obtain the consent of the subject of personal data for use through the Site.

6.3. The Operator does not use personal data of third parties entered by the User.

6.4. The Operator undertakes to take the necessary measures to ensure the safety of personal data of third parties entered by the User.

7. OTHER PROVISIONS.

7.1. This Privacy Policy and the relationship between the User and the Operator arising in connection with the application of the Privacy Policy are subject to the law of the Russian Federation.

7.2. All possible disputes arising from this Agreement shall be resolved in accordance with the current legislation at the place of registration of the Operator. Before going to court, the User must comply with the mandatory pre-trial procedure and send the relevant claim to the Operator in writing. The period for responding to a claim is 7 (seven) working days.

7.3. If for one reason or another one or more provisions of the Privacy Policy are found to be invalid or unenforceable, this does not affect the validity or enforceability of the remaining provisions of the Privacy Policy.

7.4. The Operator has the right to change the Privacy Policy, in whole or in part, unilaterally at any time, without prior agreement with the User. All changes come into force the next day after they are posted on the Site.

7.5. The user undertakes to independently monitor changes in the Privacy Policy by familiarizing himself with the current version.

8. OPERATOR CONTACT INFORMATION.

8.1. Contact Email.