Sepsis and septic shock - causes, symptoms, treatment. Septic shock: when there is still a chance to “fan” the spark of life How to recover from aseptic shock

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, a microbiological blood test 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 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.
Increased life expectancy of patients with diabetes mellitus and malignant tumors, who have a high level of predisposition to sepsis.

Sepsis remains the most common cause of death in intensive care units and one of the most fatal conditions. For example, in the United States, about 100,000 people die from sepsis every year.

Sepsis, systemic inflammatory response and septic shock are consequences of an excessive response to stimulation by bacterial antigens of cells that carry out innate immune responses. 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:

A systemic inflammatory response can be a consequence of antigenic stimulation by exo- and endogenous antigens, and can also be the result of inflammation in masses of necrobiotically altered tissues. 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 degrees Celsius, or below 36 degrees.
Respiratory rate is above 20 min-1. Respiratory alkalosis with carbon dioxide tension in arterial blood below 32 mmHg. Art.
Tachycardia with a heart rate greater than 90 min-1.
Neutrophilia when the content of polymorphonuclear leukocytes in the blood increases to a level above 12-10 9 / l, or neutropenia when the content of neutrophils in the blood is below 4-10 9 / l.
A shift in the leukocyte formula, in which band neutrophils make up more than 10% of the total number of polymorphonuclear leukocytes circulating in the blood.

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.

Induction (course) of septic shock

In septic shock, hypercytokinemia increases the activity of inducible 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. This reduces the level of excitation of receptors in the transport-damper section of the systemic circulation. The activity of vagal cardiac neurons decreases, and as a result of tachycardia, the minute volume of blood circulation increases.

Despite the increase in minute volume of blood circulation, some of the body's cells in septic shock 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. In the activated state, these cells perform adhesion and exocytosis, which destroys the walls of microvessels. Ischemia in sepsis partly occurs due to spasm of resistive vessels and precapillary sphincters, which is associated with a deficiency in the activity of constitutional nitric oxide synthetase of endothelial cells and other cells.

The reaction of the systemic circulation to the occurrence of an inflammatory focus of a certain prevalence is aimed at the destruction and elimination of sources of foreign antigens, including one’s own necrobiotically altered tissues. At the same time, the increase in minute volume of blood circulation (MVR) is partly a consequence of the release into the blood and suprasegmental action of primary proinflammatory cytokines (tumor necrosis factor-alpha, etc.), which increases MOC. The growth of IOC increases the delivery of leukocytes to the site of inflammation. In addition to the increase in IOC, the systemic inflammatory response and sepsis are characterized by a decrease in total peripheral vascular resistance through dilatation of resistance vessels in the periphery.

This increases the delivery of leukocytes into the capillaries. If under physiological conditions neutrophils easily pass through arterioles, capillaries and venules, then with hypercytokinemia they are retained by the endothelial cells of the venules. The fact is that hypercytokinemia, increasing the expression of adhesive molecules on the surface of both endothelial cells and neutrophils, causes adhesion of polymorphonuclear cells to the second type of endothelial cells lining the wall of venules. Adhesion is the initial stage of pathogenic inflammation, which has no protective significance.

Before stable adhesion, through the simultaneous expression and connection with each other of adhesion molecules of endothelial cells and polymorphonuclear leukocytes, rolling (rolling) of neutrophils occurs on the surface of the endothelium. Rolling and adhesion are necessary stages in the transformation of neutrophils into cells that carry out inflammation and are capable of exophagocytosis. These are the stages of inflammation, after the implementation of which the sequence of causes and consequences that make up this protective-pathogenic reaction almost completely unfolds.

Inflammation of this origin is purely pathological in nature and occurs in all organs and tissues, damaging the elements of the executive apparatus. 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. Adhesion leads to obstruction of the venules, which increases the hydrostatic pressure in the capillaries and the mass of ultrafiltrate entering the interstitium.

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

In the induction 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). The receptor consists of the TL receptor and the leukocyte surface marker CD 14.

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.

Most experienced clinicians easily recognize the condition of septic shock (SS). If the same medical researchers are asked to define this pathological condition, then many different definitions will be given, largely contradicting each other. The fact is that the pathogenesis of septic shock remains largely unclear. Despite numerous studies of the pathogenesis of septic shock, antibiotics remain the drugs whose action constitutes the main etiopathogenetic element of therapy for septic shock.

At the same time, the mortality rate among patients in septic shock is 40-60%. Research aimed at reducing the effects of some of the mediators of septic shock has not led to the development of effective therapy. At present, it remains unclear whether the treatment system should be focused on blocking the action of any one of the leading links in the pathogenesis of septic shock, or whether treatment should be strictly individualized for each patient.

Septic shock is a set of disorders of functional systems in which arterial hypotension and insufficient volumetric blood flow velocity in the periphery are not reversed under the influence of intravenous infusions of certain plasma-substituting agents. This is the result of the action of some of the mechanisms of innate immune reactions not limited by systemic regulation. Innate immune responses have their own bactericidal effects and also prepare and induce acquired cellular and humoral immune responses.

Innate immune responses are largely caused by the interaction of pathogen ligands with the body's humoral and cellular receptors. One of these receptors is TL-receptors (English toll-like, with the properties of a barrier, “alarm”, “forward guard”). Currently, more than ten types of mammalian TL receptors are known. The connection of a ligand of bacterial origin with the TL receptor triggers a complex of cellular reactions. As a result of these reactions, a bactericidal effect is exerted, inflammation is induced and preparation for a specific immune reaction occurs. When the complex reaction of the innate immune system is excessive, septic shock occurs.

There are several levels at which it may be possible to block the pathological response of the innate immune systems that causes septic shock. The first of them is the level of interaction of exogenous bacterial ligands with humoral and cellular receptors of innate immune systems. 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.

Gram-positive pathogens release components of their wall that are similar in structure to endotoxin. These components can cause septic shock by interacting with cellular receptors (receptors on the outer surface of mononuclear phagocytes). It should be noted that when examining a patient it is very difficult to determine the mechanism of induction of septic shock.

The occurrence of septic shock is a necessary condition for hypercytokinemia, that is, an increase in the concentration of primary proinflammatory cytokines in the circulating blood. In this regard, various methods have been proposed to block the action of primary proinflammatory cytokines (monoclonal antibodies to tumor necrosis factor-alpha, etc.), which did not reduce mortality in septic shock. The fact is that only one element of the immunopathological reaction was affected. Choosing one anti-inflammatory cytokine as the target of therapy means influencing only one of many simultaneous and equally important links in the pathogenesis of septic shock.

So, we can assume that a number of evolutionarily ancient ligands belonging to gram-negative and gram-positive bacteria, as well as mycobacteria and fungal pathogens are currently known. These exogenous ligands are able to interact with a small number of humoral and cellular receptors, causing sepsis and septic shock. In this regard, it cannot be excluded that in the future the pathological reaction of the innate immune systems can be optimally blocked by acting on the humoral and cellular ligand receptors of bacteria responsible for the occurrence of septic shock.

To recognize their ligands, TL receptors require auxiliary molecules. Obviously, the humoral receptor (plasma protein) that binds to elements of the outer membrane of gram-positive bacteria has yet to be identified.

Before the molecular complex of the bacterial wall component and the humoral receptor binds to the TL receptor, it binds to CD 14. As a result, the TL receptor is activated, that is, it begins to transmit a signal to the cell genes to begin the expression of primary proinflammatory cytokines and bactericidal agents. It is fundamentally possible to prevent the induction of septic shock by targeting CD14. In addition, it seems theoretically possible to block the pathogenesis of septic shock in the embryo by blocking TL receptors, as well as the transmission of the signal generated by them at the post-receptor intracellular level.

Etiology and pathogenesis:

Septic shock is the most common cause of death in surgical hospitals and intensive care units. The terms “sepsis”, “severe sepsis”, “septic shock” correspond to different degrees of severity of the pathological reaction of the body and immune system to infection. Sepsis as a syndrome is mainly characterized by signs of infection and inflammation. In severe sepsis, the volumetric flow rate of blood decreases in various organs, which causes combined disorders of functional systems (multiple systemic failure). The onset of septic shock is marked by persistent arterial hypotension. The mortality rate for sepsis is 16%, and for septic shock - 40-60%.

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. Previously, severe sepsis and septic shock were associated exclusively with gram-negative aerobic bacilli. Currently, the frequency of gram-positive infection as a cause of sepsis is equal to the frequency of sepsis caused by invasion of gram-negative microorganisms into the internal environment. This happened due to the widespread use of intravascular catheters and other devices that are somehow located in the internal environment, as well as due to the increasing incidence of pneumonia. Fungal, viral and protozoal infections can also cause septic shock.

The systemic inflammatory response is induced by the release from the site of inflammation of the pathogenic bacteria themselves, their toxins, as well as cytokines with the properties of inflammatory mediators. The endotoxin of gram-negative aerobic bacilli has been studied to the greatest extent as an inducer of a systemic inflammatory response. In addition, other bacterial products (toxins) are known that can cause a massive release of inflammatory mediators by the cells of the innate immune system. Such bacterial products include formyl peptides, exotoxins, enterotoxins, hemolysins-proteoglycans, as well as lipoteichoic acid, which is produced by gram-positive microorganisms.

Bacterial toxins stimulate the release of cytokines by mononuclear phagocytes with the properties of inflammatory mediators, which first cause and then enhance the systemic inflammatory response. Toxins bind to their cellular receptors, activating regulatory proteins. In particular, the transcription factor NF-kB is activated in this way. In the activated state, NF-kB enhances the expression of cytokine genes with the properties of inflammatory mediators.

Activation of NF-kB primarily increases the production of tumor necrosis factor-alpha and interleukin-1 by mononuclear phagocytes. These cytokines are called primary proinflammatory cytokines. Tumor necrosis factor-alpha and interleukin-1 stimulate the release of mononuclear phagocytes, as well as immunocompetent cells of interleukins 6 and 8 and other mediators of the inflammatory reaction: thromboxanes, leukotrienes, platelet activating factor, prostaglandins and activated fractions of the complement system.

It is believed that nitric oxide serves as the main mediator of systemic vasodilation, a decrease in total peripheral vascular resistance and arterial hypotension in patients in a state of septic shock. The inducible form of nitric oxide synthetase is expressed and released by endothelial and other cells only under certain conditions. One of these conditions is the effect of primary proinflammatory cytokines on endothelial cells. By inducing the expression of an inducible form of the synthetase in endothelial, vascular smooth muscle cells and mononuclear phagocytes, primary proinflammatory cytokines increase the release of nitric oxide at the systemic level.

Enhancing the effect of nitric oxide at the systemic level reduces total peripheral vascular resistance and causes arterial hypotension. In this case, nitric oxide serves as a substrate for the formation of peroxynitrite, that is, the product of the reaction of NO with free oxygen radicals, which has a direct cytotoxic effect. This does not exhaust the role of nitric oxide in the pathogenesis of septic shock. It has a negative inotropic effect on the heart and increases the permeability of the microvascular wall. Inhibition of cardiac contractility in septic shock also occurs due to the negative inotropic effect of tumor necrosis factor-alpha.

Tumor necrosis factor-alpha causes mitochondrial swelling and damages mitochondrial respiratory enzyme chains. As a result, a deficiency of free energy occurs in the cell, and cell death occurs due to hypoergosis. It is known that mitochondria are the main source of free oxygen radicals released into the cytosol of the cell. The action of manganese superoxide dismutase inactivates O2-, which is released by a chain of respiratory enzymes.

At the same time, the antioxidant prevents apoptosis, which is caused by tumor necrosis factor-alpha. This suggests that the mechanism of apoptosis under the influence of tumor necrosis factor-alpha is associated with the release of free oxygen radicals by mitochondria. The production of free oxygen radicals by mitochondria increases under the influence of tumor necrosis factor-alpha. At the same time, free oxygen radicals released by mitochondria damage the chains of their respiratory enzymes.

A certain activity of mitochondrial respiratory enzyme chains is a necessary condition for the apoptotic effect of tumor necrosis factor-alpha. The experiment showed that inhibition of tissue respiration in mitochondria causes cell resistance to the apoptotic effect of tumor necrosis factor-alpha.

It can be assumed that cells with a particularly high content of mitochondria and increased activity of respiratory enzyme chains have a particularly pronounced sensitivity to the action of tumor necrosis factor-alpha, which damages the mitochondrial respiratory enzyme chains and causes cell hypoergosis. Such cells are cardiomyocytes. Therefore, the effect of the factor is especially pronounced at the level of the myocardium, the contractility of which decreases during shock. In this case, the systemic damaging effect of tumor necrosis factor-alpha on mitochondria may underlie tissue hypoxia in septic shock.

In response to the action of phlogogens released during septic shock, the expression of adhesion molecules on the surface of endothelial cells and neutrophils increases. In particular, an integrin complex (CD11/CD18) appears on the surface of neutrophils, which occurs simultaneously with the appearance on the surface of the endothelial cell of intercellular adhesion molecules complementary to the integrin complex. Expression of the integrin complex on the surface of neutrophils is one of the consequences of the activation of these cells.

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.

In septic shock, an increase in the expression and release of proinflammatory cytokines causes a pathological reaction of the release of endogenous immunosuppressants into the interstitium and blood. This causes the immunosuppressive phase of septic shock.

Inducers of immunosuppression in septic shock are: 1) cortisol and endogenous catecholamines; 2) interleukins 10 and 4; 3) prostaglandin E2; 4) soluble tumor necrosis factor receptors; 5) endogenous antagonist of the interleukin-1 receptor, etc. Soluble factor receptors bind it in the blood and intercellular spaces. With immunosuppression, the content of type 2 histocompatibility antigens on the surface of mononuclear phagocytes decreases. Without such antigens on their surface, mononuclear cells cannot act as antigen-presenting cells. At the same time, the normal reaction of mononuclear cells to the action of inflammatory mediators is inhibited. All this can cause nosocomial infections and death.

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.

In septic shock, the following signs of juxtacapillary shunting of the blood are revealed:
1) lactic acidosis;
2) a decrease in the arteriovenous oxygen difference, that is, the difference in oxygen content between arterial and venous blood.

In septic shock, the capacitance vessels are dilated, which leads to general venous hyperemia. Dilatation of arterioles and veins is expressed in septic shock differently in different areas. This determines the pathological variability of pre- and postcapillary vascular resistance. Pathological variability causes an abnormal redistribution of minute volume and circulating blood volume. Vascular dilation in septic shock is most pronounced at the site of inflammation. Vasodilation during septic shock is associated with an increase in the content of endogenous vasodilators in the blood and a decrease in the sensitivity of alpha-adrenergic receptors of the vascular wall to endogenous catecholamines.

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.

The experiment showed that the total cross-sectional area of ​​the capillaries in experimental animals in a state of septic shock decreases. This is a consequence of pathogenic cell-cell interactions involving endothelial cells. A decrease in the total lumen of capillaries in patients in a state of septic shock is manifested by inhibition of reactive hyperemia. Reactive hyperemia is inhibited by disorders of local regulation of blood flow through microvessels and a decrease in the ability of blood cells to pass through capillaries. In particular, this ability is reduced by the appearance of adhesive molecules on the surface of neutrophils and monocytes. In addition, this ability decreases due to a decrease in the deformability of neutrophils and erythrocytes.

It is known that during septic shock the activity of constitutional (constantly inherent in the cellular phenotype) nitric oxide synthetase decreases. The action of constitutional synthetase increases blood flow in the periphery. A decrease in the activity of this enzyme reduces blood flow in the periphery, which inhibits reactive hyperemia. In patients in a state of septic shock, swelling of endothelial cells, deposits of fibrin in microvessels and intercellular spaces, an increase in the adhesive ability of neutrophils and endothelial cells, as well as the formation of aggregates of neutrophils, platelets and erythrocytes in venules, arterioles and capillaries are detected. In some cases, the opening of arteriolo-venular anastomoses occurs as a cause of juxtacapillary shunting.

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. A drop in cardiac preload and total peripheral vascular resistance are not all the causes of arterial hypotension in septic shock.

It is also caused by the negative effect of septic shock mediators on the heart. Both the left and right ventricles of the heart in septic shock successively go through the stages of rigidity (insufficient diastolic function) and dilatation (insufficient systolic function). Rigidity and dilatation are not associated with a drop in blood flow through the coronary arteries and an increase in the need for oxygen by cardiomyocytes. The pumping function of the heart in septic shock is inhibited by tumor necrosis factor-alpha, as well as interleukin-1. Inhibition of the pumping function of the heart in septic shock is partly due to pulmonary arterial hypertension and a decrease in the sensitivity of beta-adrenergic receptors of the heart.

It can be assumed that in the majority of 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 cardiogenic shock, lactic metabolic acidosis is caused by severe circulatory hypoxia. In this case, the oxygen tension in mixed venous blood is below 30 mmHg. Art. 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. In the case of septic shock, the reasons for the decrease in the cell's capture of free energy during aerobic biological oxidation are the cytotoxic effects (direct or indirect) of endotoxin, nitric oxide, and tumor necrosis factor-alpha. The pathogenesis of septic shock largely consists of disorders of biological oxidation and is determined by cell hypoergosis as a consequence of tissue hypoxia, which developed under the influence of endotoxemia.

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.

In 2016, new definitions of sepsis and septic shock. Because existing data on epidemiology, prognosis, and treatment relate to conditions diagnosed according to previously used definitions, and because the equivalent of the previously used term “severe sepsis” under the new nomenclature is “sepsis,” in this edition of the guideline these concepts are used in parallel ( , ). The new definitions do not include the term "infection" - below are presented in the traditional sense of the word.

Table 18.8-1. Definition and diagnostic criteria for sepsis and septic shock

Definitions and criteria	Previous (1991, 2001)	Proposed New (2016)
	SIRS resulting from infection	life-threatening organ dysfunction caused by dysregulation of the body's response to infection; this response results in organ and tissue damage (corresponding to the previous concept of "severe sepsis")
severe sepsis	sepsis causing failure or dysfunction of organs (or organ systems →see below); equivalent to the concept of “sepsis” in the new nomenclature	the equivalent is "sepsis" see above
diagnostic criteria for organ dysfunction	used to diagnose severe sepsis ()	used to diagnose sepsis - a sudden increase in SOFA score by ≥2 points ()a, in the presence or suspicion of infection
septic shock	a form of severe sepsis with acute circulatory failure characterized by persistent hypotension (systolic blood pressure<90 мм рт. ст., средние <65 мм рт. ст. или снижение систолического давления на >40 mmHg Art.) despite appropriate infusion therapy (with the need to use vasopressors in the future)	sepsis, in which circulatory, cellular and metabolic abnormalities are so severe that they significantly increase mortality diagnosed if, despite proper fluid therapy, the following persists: 1) hypotension requiring the use of vasopressors to maintain mean arterial pressure ≥65 mm Hg. Art., and 2) plasma lactate concentration >2 mmol/l (18 mg/dl)
scale proposed for early detection of patients at increased risk of death	not defined, both criteria for CVS and organ dysfunction were used, as well as expanded criteria for diagnosing sepsis that included them ()	Quick SOFA (qSOFA) score - ≥2 with the following symptoms: 1) impaired consciousness b 2) systolic blood pressure ≤100 mm Hg. Art. 3) respiratory rate ≥22/min
determining the severity of the inflammatory response	used in the definition of sepsis - SIRS, i.e. ≥2 of the following symptoms: 1) body temperature>38 °C or<36 °C 2) heart rate >90/minv 3) respiratory rate >20/min or PaCO2<32 мм рт. ст. 4) leukocyte count >12,000/µl or<4000/мкл, или >	not shown (it has been established that the inflammatory response is only one and not the most important component of the body's response to infection; emphasis is placed on organ dysfunction, suggesting that it significantly increases the risk of death)
a In patients without acute organ dysfunction, the SOFA score is usually 0. b result of assessment on the Glasgow Coma Scale (→)<15 баллов c May be absent in patients taking β-blockers. PaCO2 - partial pressure of carbon dioxide in arterial blood, SIRS - systemic inflammatory response syndrome based on: Intensive Care Med. 2003; 29:530–538, also JAMA. 2016; 315:801–810. doi:10.1001/jama.2016.0287

Table 18.8-2. Traditional diagnostic criteria for sepsis-associated organ dysfunctiona

1) tissue hypoperfusion associated with sepsis or 2) dysfunction of organs or organ systems caused by infection, i.e. ≥1 s of the following dysfunctions: a) hypotension caused by sepsis b) lactate concentration >ULN c) diuresis<0,5 мл/кг/ч в течение >2 hours despite appropriate fluid therapy d) PaO2/FiO2<250 мм рт. ст., если легкие не являются очагом инфицирования, либо <200 мм рт. ст., если легкие являются очагом инфицирования e) creatininemia >176.8 µmol/l (2 mg/dl) f) bilirubinemia >34.2 µmol/l (2 mg/dl) e) platelet count<100 000/мкл g) coagulopathy (INR >1.5)

a Previously proposed criteria for the diagnosis of severe sepsis. FiO2 is the concentration of oxygen in the inspired air, expressed as a decimal fraction, ULN is the upper limit of normal, PaO2 is the partial pressure of oxygen in arterial blood

Table 18.8-3. Sepsis-associated organ dysfunction score (SOFA)a

Organ or system	Result
respiratory system
PaO2/FiO2, mmHg Art. (kPa)				<200 (26,7)б	<100 (13,3)б
blood clotting
platelet count, × 103/µl
liver
bilirubinemia, µmol/l (mg/dl)		20–32 (1,2–1,9)	33–101 (2,0–5,9)	102–204 (6,0–11,9)
circulatory system	SBP ≥70 mmHg.	GARDEN<70 мм рт.ст.	dobutamine (any dose) or dopamine<5в	norepinephrine ≤0.1 or adrenaline ≤0.1, or dopamine 5.1–15v	norepinephrine >0.1 or adrenaline >0.1, or dopamine >15v
nervous system
Glasgow Coma Scale
kidneys
creatininemia, µmol/l (mg/dl) or diuresis, ml/day		110–170 (1,2–1,9)	171–299 (2,0–3,4)	300–440 (3,5–4,9)
and the calculator is in Polish - http://www.mp.pl/oit/wpraktyce/show.html?id=57427 b during artificial ventilation of the lungs in doses of catecholamines given in mcg/kg/min and used for ≥1 hour FiO2 - concentration of oxygen in inspired air, expressed as a decimal fraction, MAP - mean arterial pressure, PaO2 - partial pressure of oxygen in arterial blood based on: Intensive Care Med. 1996; 22:707–710

Infection is an inflammatory response to microorganisms in tissues, fluids, or body cavities that are normally sterile.

Microbiologically confirmed infection- isolation of pathogenic microorganisms (or determination of their antigens or genetic material) from body fluids or tissues that are normally sterile.

Clinical suspicion of infection- presence of clinical symptoms strongly indicating infection, e.g. leukocytes in the systemic fluid of the body, which is normally sterile (except for blood), perforation of internal organs, radiography shows a picture of pneumonia in combination with purulent discharge from the respiratory tract, an infected wound.

Multiple organ dysfunction syndrome (MODS)- severe organ dysfunction during an acute illness, indicating the impossibility of maintaining homeostasis without therapeutic intervention.

Bacteremia - live bacteria in the blood. Viremia - viruses are capable of replication in the blood. Fungemia - live fungi in the blood (candidemia - live Candida fungi in the blood).

The type of microorganisms does not determine the course of sepsis, since microbes should not be present in the blood. In most cases there are no pre-existing immune disorders, although these are risk factors for sepsis.

Infections and inflammations that cause sepsis initially affect various organs, including the abdominal cavity (eg, peritonitis, cholangitis, acute pancreatitis), urinary system (pyelonephritis), respiratory tract (pneumonia), central nervous system (neuroinfections), pericardium, bones and joints, skin and subcutaneous tissue (wounds resulting from trauma, bedsores and post-operative wounds), reproductive system (including blastocyst infections). The source of infection is often hidden (eg, teeth and periodontal tissues, paranasal sinuses, tonsils, gallbladder, reproductive system, abscesses of internal organs).

Iatrogenic risk factors: vascular cannulas and catheters, bladder catheter, drainages, implanted prostheses and devices, mechanical ventilation, parenteral nutrition, transfusion of contaminated fluids and blood products, wounds and bedsores, immune disorders as a result of pharmacological treatment and radiation therapy, etc.

Pathogenesis

Sepsis is an abnormal response of the body to an infection involving components of the microorganism and endotoxins, as well as mediators of the inflammatory response produced by the host body (cytokines, chemokines, eicosanoids, etc., responsible for SIRS) and substances that damage cells (for example, oxygen free radicals ).

Septic shock (hypotension and tissue hypoperfusion) is a consequence of an inflammatory reaction caused by inflammatory mediators: insufficient vascular filling - relative (dilation of blood vessels and decreased peripheral vascular resistance) and absolute (increased vascular permeability) hypovolemia, less often - decreased myocardial contractility (usually in septic shock, cardiac output is increased, provided that the vessels are adequately filled with fluid). Hypotension and hypoperfusion lead to decreased oxygen delivery to tissues and their hypoxia. Finally, a decrease in oxygen delivery and consumption increases anaerobic metabolism in cells and leads to lactic acidosis. Other elements of septic shock: acute respiratory distress syndrome (ARDS), acute renal failure, disturbances of consciousness caused by ischemia of the central nervous system and the effects of inflammatory mediators, disorders of the digestive tract - paralytic intestinal obstruction due to ischemia and damage to the mucous membrane, which leads to the movement of bacteria from the lumen gastrointestinal tract into the blood (bacterial translocation) and bleeding (hemorrhagic gastropathy and stress ulcers →, ischemic colitis →), acute liver failure →, decreased adrenal reserve (relative adrenal insufficiency).

CLINICAL PICTURE AND NATURAL COURSE

Symptoms of sepsis →Definition and. Other symptoms depend on the organs initially affected. If the progression of the infection is not stopped in the early stages of sepsis, then symptoms of dysfunction of other organs begin to appear: the respiratory system (acute respiratory failure - ARDS; →) the cardiovascular system (hypotension, shock) and the kidneys (acute kidney injury, initially prerenal →), as well as hemostasis disorders (DIC →; initially, as a rule, thrombocytopenia) and metabolic disorders (lactic acidosis). If effective treatment is not started, shock worsens, multiple organ failure develops, and death occurs.

Table 18.8-4. Expanded diagnostic criteria and consequences of sepsis

presence of infection (confirmed or suspected) and some of the following criteria

general indicators – body temperature >38 °C or<36 °C – tachycardia >90/min – tachypnea >30/min (or artificial ventilation) – mental status disorders – significant edema or positive fluid balance (>20 ml/kg/day) – hyperglycemia (>7.7 mmol/l), in the absence of diabetes mellitus

inflammatory indicators – leukocytosis >12,000/μl or leukopenia (number of white blood cells<4000/мкл) – presence of >10% immature forms of neutrophils – C-reactive protein >2 standard deviations from the mean – procalcitonin >2 deviations from the mean value

hemodynamic parameters and tissue perfusion parameters – decreased blood pressure (systolic<90 мм рт. ст., среднее <70 мм рт. ст., падение систолического на >40 mmHg Art. in people with arterial hypertension) – serum lactate concentration > upper limit of normal – slowing down capillary refill

emerging and increasing symptoms of organ dysfunction – hypoxemia (PaO2 /FiO2<300 мм рт. ст., а если имеются первичные заболевания дыхательной системы <200) – acute oliguria (diuresis<0,5 мл/кг/ч в течение >2 hours, despite adequate fluid resuscitation) – increase in creatininemia by >44.2 µmol/l (0.5 mg/dl) within 48 hours – hemostasis disorders (platelet count<100 000/мкл, МНО >1.5, aPTT >60 s) – concentration of total bilirubin in blood plasma >70 µmol/l (4 mg/dl) – paralytic intestinal obstruction (peristalsis cannot be heard)

DIAGNOSTICS

Additional research methods

1. Laboratory research: to assess the degree of organ dysfunction (arterial and venous blood gasometry, plasma lactate concentration [determine within several hours after the onset of severe sepsis], hemostasis study, kidney and liver function tests), as well as the intensity of the inflammatory process (complete blood count, CRP or procalcitonin [PCT], now much less common than ESR; a decrease in PCT may suggest a reduction in the duration of antibiotic therapy in patients with diagnosed infection, and a negative PCT result may justify the decision to discontinue empirical antibiotic therapy in patients in whom infection is suspected. sepsis, but later infection was not confirmed).

2. Microbiological studies

1) blood - ≥2 samples, including ≥1 from a separately punctured vein and one from each vascular catheter inserted >48 hours; All samples must be cultured to identify aerobic and anaerobic pathogens;

2) others depending on the suspected etiology - material from the respiratory tract, urine, other body fluids (eg, cerebrospinal fluid, pleural fluid), smears or discharge from wounds.

3. Imaging studies: radiography (especially of the lungs), ultrasound and CT (especially of the abdominal cavity).

Diagnostic criteria

It is indicated to carry out etiotropic and symptomatic therapy in parallel. The prognosis primarily depends on prompt initiation of antibiotics and fluids. Initial algorithm of actions (so-called task sets) → .

Table 18.8-5. T. n. "challenge packs" according to the Surviving Sepsis Campaign

Within 3 hours: 1) determine the concentration of lactate in the blood 2) take a blood sample for culture (before using antibiotics) 3) use broad-spectrum antibiotics 4) infuse 30 mL/kg crystalloid solutions if hypotension occurs or if blood lactate concentration is ≥4 mmol/L (36 mg/dL).

Within 6 hours: 5) use vasoconstrictors (for hypotension unresponsive to initial fluid resuscitation) to maintain mean arterial pressure (MAP) ≥65 mmHg. Art. 6) with persistent arterial hypotension, despite fluid resuscitation (MAP<65 мм рт. ст.), или если начальная концентрация лактата составляет ≥4 ммоль/л (36 мг/дл), занесите в документацию обновлённую оценку волемии и тканевой перфузии, выполненную по одной из следующих методик: a) assessment of vital functions and objective examination of the circulatory and respiratory systems, with assessment of capillary refill, pulse and skin condition b) performing 2 of the following studies: CVP, Scv O2, bedside echocardiography of the circulatory system, dynamic assessment of the response to fluid loading using lower limb elevation in the supine position, or using trial infusion therapy 7) re-determine the lactate concentration if it was initially elevated.

CVP - central venous pressure, Scv O2 - oxygen saturation of hemoglobin in blood from the superior vena cava

Etiotropic therapy

1. Antimicrobial therapy: initial (empirical), as soon as possible, that is within 1 hour (each hour of delay increases mortality), but before this (unless this is possible and does not slow down the treatment by more than 45 minutes), it is necessary to collect the appropriate material for microbiological testing (→ Diagnosis). Use ≥1 broad-spectrum IV antibiotic; take into account activity against the most likely etiological factors (bacteria, fungi, viruses), penetration into the source of infection, as well as the local sensitivity of microorganisms. In case of septic shock, at the initial stage it is recommended to use ≥2 antibiotics from different groups that are active against the most likely bacterial pathogens. The routine use of ≥2 antibiotics from different groups targeting the same suspected or confirmed pathogen is not recommended for sepsis or bacteremia associated with neutropenia, or for severe infections with bacteremia or sepsis without shock. Although in these situations the use of combined antibiotic therapy is not excluded in order to expand the spectrum of antibacterial action (that is, the use of ≥2 antibiotics from different groups active against ≥2 confirmed or suspected bacteria). Combination antibiotic therapy (in the sense given above, that is, aimed at a single pathogen) is usually used when infection with Pseudomonas or Acinetobacter is suspected or confirmed (this tactic is recommended especially for antibiotic-resistant strains), as well as in shock with S. pneumoniae bacteremia (in another situation a β-lactam antibiotic with a macrolide is used). The patient's condition should be assessed daily for the possibility of switching to antibiotic therapy with a narrower spectrum or monotherapy. For septic shock, this modification is recommended over several days as clinical improvement is achieved and signs of infection resolution; this refers to combination (directed at the same pathogen) therapy, both empirical and specific, depending on the sensitivity of the pathogens. Specific therapy (in most cases monotherapy) based on antibiotic sensitivity should be used as early as possible. When dosing, the pharmacokinetic and pharmacodynamic characteristics of the drugs should be taken into account, for example:

1) the use of large saturating doses - for example. vancomycin;

2) dosing of certain drugs based on body weight or serum concentrations - aminoglycosides and vancomycin;

3) consideration of the issue of continuous or long-term IV administration of drugs whose action is dependent on time, at which their concentration is above the MIC - mainly β-lactam antibiotics;

4) administration of 1-r/d drugs, the effect of which depends on their maximum concentration, and having a clear post-antibiotic effect - aminoglycosides;

5) properties of drugs in patients with sepsis or in a state of septic shock - for example. An increase in the volume of distribution of hydrophilic antibiotics and glomerular filtration (renal clearance), which occurs especially in patients undergoing resuscitation with solutions, suggests the use of higher doses. Duration of treatment: usually 7–10 days (longer if response to treatment is slow, the source of infection cannot be completely removed, neutropenia → or other immune disorders, some microorganisms, S. aureus bacteremia; a shorter course of treatment may be warranted in some patients , especially with rapid clinical improvement after sanitation of the source of infection located in the abdominal cavity or associated with urosepsis, as well as with uncomplicated [that is, without anatomical disorders] pyelonephritis). The role of determining procalcitonin levels in reducing the duration of antibiotic therapy →see. higher.

2. Elimination of the source of infection- infected tissues or organs (eg gallbladder, necrotic segment of the intestine), catheters (intravenous catheter, which can be a source of infection, should be removed immediately after new vascular access has been secured), implanted prostheses and devices; drainage of abscesses, empyema and other foci of infection. The least invasive but effective intervention is preferred (eg, if possible, performing percutaneous rather than surgical drainage of abscesses). In the case of infected pancreatic necrosis, surgical intervention is expected to be delayed.

Symptomatic treatment

Mandatory for sepsis (according to previous terminology - severe sepsis) and septic shock.

1. Initial anti-shock measures: rapid initiation, especially IV administration of solutions → see below, as well as evaluation of effectiveness are at least as important as tactics according to individual algorithms and achievement of target parameters. The most important thing, in addition to improving the general clinical condition (and such simple parameters as heart rate, blood pressure, oxygen saturation of arterial hemoglobin, respiratory rate, body temperature, diuresis), is considered to be a decrease (normalization) of elevated lactate concentrations in patients with hypoperfusion, and also achieving mean arterial pressure ≥65 mm. rt. Art. for septic shock (if vasoconstrictors are used →see below). Previously, it was recommended to achieve “normal” central venous pressure (CVP; 8–12 mm Hg, mean arterial pressure ≥65 mm Hg, spontaneous diuresis ≥0.5 ml/kg/h) within the first 6 hours from the start of treatment and central venous hemoglobin oxygen saturation (superior vena cava, SvO2) ≥70% or mixed venous blood ≥65% The current SSC guidelines do not directly list all of these goals, although measurements of these parameters can serve to assess the clinical situation. however, further hemodynamic assessment (such as cardiac assessment, e.g. echocardiography) if there is doubt about the type of shock (e.g. cardiogenic shock may co-occur with septic shock), and preference is given to the use of dynamic (rather than static) hemodynamic parameters to predict response to transfuse solutions → If, after achieving the target mean arterial pressure (after transfusion of solutions and the use of vasopressors), a decrease in the lactate concentration (or the target level of oxygen saturation of venous hemoglobin) is not achieved within the first few hours, the appropriateness should be considered, depending on the circumstances (frequency heart rate, left ventricular function, response to fluids, hemoglobin level), ≥1 of the following: further fluid transfusion, red blood cell transfusion to achieve hematocrit ≥30%, use of dobutamine (max. dose 20 mcg/kg/min).

2. Treatment of cardiovascular system disorders

1) proper filling of the vascular bed with solutions - in patients with tissue hypoperfusion and suspected hypovolemia Infusion should be started with ≥30 mL of crystalloid/kg in during the first 3 hours, with simultaneous monitoring for signs of hypervolemia. Some patients may require immediate (or later) large fluid transfusions. Large volumes of fluid (eg >30 ml/kg) should be given in portions (eg 200–500 ml), and response to treatment should be assessed each time they are transfused (see also). The SSC (2016) guidelines do not indicate the superiority of balanced crystalloids over 0.9% NaCl (but generally prefer balanced solutions, especially when large volumes of IV administration are required →), but give preference to crystalloids over solutions gelatin. The latter, however, do not have the same contraindications as hydroxyethyl starch (HES) solutions. Transfusion of albumin solutions (usually 4% or 5% concentration) is recommended in addition to crystalloid transfusions initially and during subsequent solution therapy in patients requiring large volumes of crystalloid transfusions.

2) vasopressors - norepinephrine (preferred), if ineffective, vasopressin or adrenaline should be added; Vasopressin can also be used to reduce the dose of norepinephrine. Indications: persistent hypotension that persists despite transfusion of an appropriate volume of fluid. It should be administered (as quickly as possible) through a catheter inserted into the vena cava and blood pressure monitored invasively (insert the catheter into the artery). It is suggested that the use of dopamine be limited to a small group of patients, especially those with bradycardia and reduced cardiac output, as well as those with a low risk of cardiac arrhythmia.

3) treatment that increases myocardial contractility - dobutamine: Consideration should be given to administration in patients with hypoperfusion that persists despite appropriate hydration and use of vasopressors. When dosing (→131), it should be taken into account that the goal is to eliminate hypoperfusion. Administration should be discontinued if hypotension increases and/or arrhythmia occurs.

3. Treatment of respiratory failure→ . Mechanical ventilation is usually necessary. Treatment of pneumonia →.

4. Treatment of kidney failure: the main importance is stabilization of the cardiovascular system (normalization of blood pressure); if necessary, renal replacement therapy (it has not been established whether early initiation is more effective, but is likely not recommended if oliguria and hypercreatininemia are the only indicators for renal replacement therapy).

5. Treatment acidosis: aimed at eliminating the cause. Leaving the pathophysiological aspects aside, NaHCO3 can be prescribed intravenously at blood pH<7,15; но клинические эффекты не определены.

6. Corticotherapy: If hypotension persists despite adequate hydration and the use of vasopressors, IV hydrocortisone 200 mg/day can be considered (at least until shock resolves). If hydrocortisone is not available and another glucocorticoid without significant mineralocorticoid effect is used, fludrocortisone 50 mcg 1 x daily (which can also be used in combination with hydrocortisone) should be given in addition.

7. Glycemic control: in case of hyperglycemia caused by severe sepsis (>10 mmol/l in 2 consecutive measurements), insulin should be prescribed (usually intravenous infusion); the target is glycemia<10 ммоль/л (180 мг/дл), чем <6,1 ммоль/л (110 мг/дл). В начальной фазе лечения инсулином требуется контроль гликемию каждые 1–2 ч, a после стабилизации - каждые 4–6 ч. Следует избегать гипогликемии. Лабораторные исследования капиллярной крови на гликемию могут быть у таких пациентов ошибочны. У пациентов с артериальным катетером для прикроватного определения гликемии рекомендуется набирать кровь из катетера (не капиллярную).

8. Additional treatment

1) transfusion of blood products

a) red blood cell mass, if hemoglobin<7 г/дл, для достижения концентрации 7,0–9,0 г/дл; исключения: переливание эритроцитарной массы при гемоглобине >7 g/dL if there is tissue hypoperfusion, active bleeding, or significant coronary artery disease;

b) platelet concentrate - regardless of other factors, if the platelet count is ≤10,000/μl; transfusion may be useful if the platelet count is 10,000–20,000/µL and there is a condition at increased risk of bleeding (including sepsis or septic shock); invasive procedures may require platelet counts ≥50,000/µL;

c) fresh frozen plasma and cryoprecipitate - mainly when there is active bleeding or invasive procedures are planned;

2) nutrition - whenever possible, by the enteral route, in an amount tolerated by the patient (it is not necessary to satisfy the full calorie requirement);

3) prevention of stress ulcers- proton pump inhibitor or H2 blocker in patients with risk factors for bleeding (in severely ill patients, the most significant is coagulopathy and mechanical ventilation lasting >48 hours);

4) prevention of venous thromboembolic disease(VTE) → . Pharmacological prophylaxis should be used unless there are contraindications due to bleeding or a high risk of bleeding; It is recommended to use LMWH rather than fractionated heparin, and, if possible, initiate mechanical prophylaxis (only if there are contraindications to pharmacological prophylaxis).

5) algorithm of actions during mechanical ventilation l light- including the use of sedatives in the smallest possible doses, ensuring the established (best tolerated) level of sedation, avoid muscle relaxants with the exception of ARDS (for ARDS with PaO2 / FiO2<150 мм рт. ст. рекомендуется рассмотреть целесообразность их введения до 48 ч), показано приподнятое положение изголовья кровати на 30–45° с целью предотвращения ИВЛ-ассоциированной пневмонии.

6) treatment of DIC → - etiotropic treatment of sepsis is of primary importance.

Symptoms often begin with chills and include fever and hypotension, oliguria and confusion. Acute failure of several organs, such as the lungs, kidneys and liver, may occur. Treatment is intensive fluid resuscitation, antibiotics, surgical removal of infected or necrotic tissue and pus, supportive care, and sometimes blood glucose monitoring and corticosteroids.

Sepsis is an infection. Acute pancreatitis and serious trauma, including burns, may present with symptoms of sepsis. The inflammatory reaction is usually manifested by two or more signs:

• Temperature >38 °C or<36 °С.
• Heart rate >90 beats/min.
• Respiratory rate >20 per minute or PaCO 2<32 мм рт.ст.
• Leukocyte count >12x109/l or<4х109/л или >10% immature forms.

However, at present, the presence of these criteria is only a presumptive factor and is not sufficient to make a diagnosis.

Severe sepsis is sepsis accompanied by signs of failure of at least one organ. Cardiovascular failure is usually manifested by hypotension, respiratory failure - by hypoxemia.

Septic shock is severe sepsis with hypoperfusion and hypotension that does not resolve with adequate intensive fluid therapy.

Causes of septic shock

Septic shock occurs more often in newborns, patients over 35 years of age, and pregnant women. Predisposing factors include diabetes mellitus; cirrhosis; leukopenia.

Pathophysiology of septic shock

The pathogenesis of septic shock is not fully understood. Inflammatory agents (eg, bacterial toxin) lead to the production of mediators including tumor necrosis factor and IL-1. These cytokines induce neutrophil-endothepial cell adhesion, activate blood coagulation mechanisms and lead to the formation of microthrombi. They also promote the release of other neurotransmitters, including leukotrienes, lipoxygenase, histamine, bradykinin, serotonin and IL-2. They are counteracted by anti-inflammatory mediators such as IL-4 and IL-10 as a result of a negative feedback mechanism.

First, the arteries and arterioles dilate, and cardiac output increases. Later, cardiac output may decrease, blood pressure drops, and typical signs of shock appear.

Even at the stage of increased cardiac output, vasoactive mediators cause blood flow to bypass the capillaries (distribution defect). Capillaries fall out of this shunt along with capillary obstruction by microthrombi, which reduce the delivery of O2 and reduce the excretion of CO2 and other waste products. Hypoperfusion leads to dysfunction.

Coagulopathy may develop due to intravascular coagulation involving major coagulation factors, increased fibrinolysis, and more often a combination of both.

Symptoms and signs of septic shock

Patients with sepsis typically present with: fever, tachycardia and tachypnea; Blood pressure remains normal. Other signs of infection are also usually present. The first sign of both severe sepsis and septic shock may be confusion. Blood pressure usually drops, but paradoxically, the skin remains warm. Oliguria may occur (<0,5 мл/кг/ч). Органная недостаточность приводит к появлению определенных дополнительных симптомов.

Diagnosis of septic shock

Sepsis is suspected when a patient with a known infection develops systemic symptoms of inflammation or organ dysfunction. If there are signs of systemic inflammation, the patient should be examined for the presence of infection. This requires a thorough history, physical examination and laboratory tests, including a general urinalysis and urine culture (especially in patients with indwelling catheters), and blood cultures of suspicious body fluids. In severe sepsis, blood levels of procalcitonin and C-reactive protein are elevated and may aid diagnosis, but these values ​​are not specific. Ultimately the diagnosis is based on the clinic.

Other causes of shock (eg, hypovolemia, myocardial infarction) should be identified by history, physical examination, cardiogram, and serum cardiac markers. Even without myocardial infarction, hypoperfusion can lead to cardiac signs of ischemia, including nonspecific ST-T abnormalities, T wave inversions, and supraventricular and ventricular premature beats.

Hyperventilation with respiratory alkalosis (low PaCO 2 and elevated blood pH) appears early as compensation for metabolic acidosis. Serum HCO; usually low and serum lactate levels elevated. Shock progresses, metabolic acidosis worsens, and blood pH decreases. Early respiratory failure leads to hypoxemia with Pa02<70 мм рт.ст. Уровень мочевины и креатинина обычно прогрессивно возрастают.

Almost 50% of patients with severe sepsis develop relative adrenal insufficiency (i.e., normal or slightly elevated basal cortisol levels. Adrenal function can be tested by measuring serum cortisol at 8 a.m.

Hemodynamic measurements may be used when the type of shock is unclear or when large volumes of fluid are needed. Echocardiography (including transesophageal echocardiography) is the main method for assessing the functional state of the heart and the presence of vegetations.

Treatment of septic shock

• Infusion therapy with 0.9% saline solution.
• 02-therapy.
• Broad-spectrum antibiotics.
• Drainage of abscesses and removal of necrotic tissue.
• Normalization of blood glucose levels.
• Corticosteroid replacement therapy.

Patients with septic shock should be treated in the intensive care unit. Constant monitoring of the following parameters is indicated: system pressure; CVP, PAOP or both; pulse oximetry; ABGs; blood glucose, lactate and electrolyte levels; renal function, and possibly sublingual PCO 2 . Diuresis control.

If hypotension persists, dopamine can be given to increase mean blood pressure to at least 60 mmHg. If the dopamine dose exceeds 20 mg/kg/min, another vasoconstrictor, usually norepinephrine, may be added. However, vasoconstriction caused by an increased dose of dopamine and norepinephrine poses a threat to both organ hypoperfusion and acidosis.

02 is given using a mask. Tracheal intubation and mechanical ventilation may subsequently be necessary if breathing becomes compromised.

Parenteral administration of antibiotics should be prescribed after taking blood, various media (fluids, body tissues) for antibiotic sensitivity and culture. Early empirical therapy, initiated immediately after sepsis is suspected, is important and can be decisive. The choice of antibiotic should be reasonable, based on the intended source, on clinical conditions.

Treatment regimen for septic shock of unknown etiology: gentamicin or tobramycin, in combination with cephalosporins. In addition, ceftazidime may be used in combination with a fluoroquinolone (eg, ciprofloxacin).

Vancomycin should be added if resistant staphylococci or enterococci are suspected. If the source is localized in the abdominal cavity, a drug effective against anaerobes (for example, metronidazole) should be included in the therapy.

Corticosteroid therapy uses replacement doses rather than pharmacological doses. The regimen consists of hydrocortisone in combination with fludrocortisone for hemodynamic instability and for 3 subsequent days.

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 in whom sepsis is diagnosed or suspected 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 mm Hg. 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.

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Septic shock is a severe complication of infection that is life-threatening. It reduces tissue perfusion, resulting in poor oxygen supply. If measures are not taken in a timely manner, everything can end in damage to internal organs and death of the patient. The probability of death of the patient is about 50%. Septic shock is often typical for the elderly, children, and immunocompromised patients.

Reasons

Please note that septic shock is most often triggered by pathogenic microflora:

• Anaerobic and aerobic streptococcus.
• Escherichia coli.
• Bacteroides.
• Clostridia.
• Beta-hemolytic streptococcus.
• Klebsiella.
• Other pathogenic microorganisms.

It is worth noting that Staphylococcus aureus and beta-hemolytic streptococcus produce an exotoxin, leading to. Sepsis is an inflammatory response. When toxic substances are in the blood, the production of inflammatory cytokines is stimulated. This reaction causes the adhesion of leukocytes and neutrophils.

Types of septic shock

It all depends on where the pathology is localized and how it proceeds. Highlight:

• Pulmonary-pleural appearance.
• Peritoneal.
• Intestinal.
• Biliary.
• Cutaneous.
• Urodynamic.
• Obstetric.
• Cutaneous.
• Vascular.
• Phlegmonous.

Depending on how the pathology proceeds, there are:

• Fulminant.
• Progressive.
• Erased.
• Early.
• Terminal.
• Recurrent.

Symptoms

Signs depend on the pathogen, as well as on the state of the immune system. Please note that the following symptoms often appear:

• Worried about severe chills.
• A high temperature appears.
• On the body you can notice a hemorrhagic, papular rash.
• Intoxication of the body gradually increases.
• Appears.

Nonspecific symptoms include:

• Enlarged spleen, liver.
• Chills.
• Sharp weakness.
• Physical inactivity.
• The stool is disturbed (constipation is a concern).

If antibacterial therapy is not carried out in a timely manner, everything ends in disruption of the internal organs and death of the patient. In the case of septic shock, thrombosis is sometimes observed, which is accompanied by hemorrhagic syndrome.

Important! Antibacterial therapy makes it possible to reduce intoxication. In the case of septic shock with massive infection, an acute inflammatory process begins to develop. It is dangerous when polyarthritis occurs due to septic shock. In some patients it all ends with polyserositis, myocarditis, and glomerulonephritis.

Other symptoms that occur with septic shock include:

• , an x-ray may show pneumonia.
• Septic abortion is especially dangerous for a woman because there is no inflammatory reaction in the uterus. In this case, the vessels begin to become clogged with blood clots, microbes, and purulent masses. After some time, toxic anemia develops and skin color changes. It is dangerous when everything ends in extensive superficial necrosis.
• Tachypnea develops due to the disruption of the heart and blood vessels. In this case, the breathing rate increases.
• Septic pneumonia is a fairly common complication of sepsis.
• Liver damage. With sepsis, the liver begins to noticeably enlarge, severe pain appears in the side, and the level of transaminase and bilirubin in the blood increases. After some time, the amount of total protein decreases. It all ends in liver failure.
• Kidney damage. When blood pressure drops sharply, blood volume decreases and diuresis occurs. Urine is low in density, indicating inflammation. In the kidneys you can notice an organic, functional lesion of an organic nature.
• Intestinal problems. Please note that sepsis is accompanied by intestinal paresis, a severe disorder of the digestive process. A putrefactive process develops in the intestines and is accompanied by septic diarrhea and dysbacteriosis.
• Trophic disorders. When blood microcirculation is disrupted, bedsores appear.
• The spleen enlarges.

Treatment methods

It is important to understand that septic shock is a fairly threatening condition. In this case, the patient is hospitalized and undergoes intensive therapy. The disease develops rapidly and can lead to serious complications and death.

Therapy must be comprehensive, and the pathogenic flora leading to pathology must be taken into account. The main method of treatment is taking antibiotics and anti-inflammatory drugs. Additionally, hormonal therapy is required.

For septic shock, at least two antibiotics with a wide spectrum of action are used. If a specific pathogen is isolated, antibiotics are prescribed against the specific infection. All drugs are administered parenterally - into a muscle or into a vein.

During treatment, blood cultures are constantly taken to identify pathogenic microbes. Antibacterial therapy will last several months until the bacterial culture is negative.

To improve the body's resistance, the patient is injected with interferon and anti-staphylococcal plasma. In severe cases, corticosteroids are used. It is especially important to strengthen the immune system, so additionally consult an immunologist.

Sometimes surgery is necessary to remove dead tissue. Depending on where the inflammatory focus is localized, surgery is performed.

To maintain organs in normal condition they use Norepinephrine, Dopamine Hydrochloride, Dobutamine, other medicines to normalize blood pressure.

Thus, it is important to do everything to prevent. Septic shock is a condition that requires immediate hospitalization to help prevent organ failure.