Home Coated tongue Septic shock belongs to the group of shocks. What is septic shock, its causes and how dangerous it is

Coated tongue

Septic shock belongs to the group of shocks. What is septic shock, its causes and how dangerous it is

Sepsis is a pathological process, which is based on the body’s reaction in the form of a generalized (systemic)
inflammation to infections of various natures (bacterial, viral, fungal).

Synonyms: septicemia, septicopyemia.

ICD10 CODE
Utility etiological principle, which forms the basis for the classification of sepsis in ICD10, from the standpoint of modern knowledge and real clinical practice seems limited. Focus on bacteremia as the main diagnostic sign with low excretion of the pathogen from the blood, as well as the significant duration and labor intensity of traditional microbiological studies make widespread practical use impossible etiological classification(Table 31-1).

Table 31-1. Classification of sepsis in accordance with ICD-10

EPIDEMIOLOGY

No domestic data available. According to calculations, more than 700,000 cases of severe sepsis are diagnosed annually, i.e. about 2000 cases daily. Septic shock develops in 58% of cases of severe sepsis.

At the same time, sepsis was the main cause of death in the departments intensive care non-coronary profile and ranked 11th among all causes of mortality. Data on the prevalence of sepsis in different countries vary significantly: in the USA - 300 cases per 100,000 population (Angus D., 2001), in France - 95 cases per 100,000 population (Episepsis, 2004), in Australia and New Zealand - 77 per 100,000 population (ANZICS, 2004).

A multicenter epidemiological cohort prospective study involving 14,364 patients in 28 intensive care units in Europe, Israel and Canada found that patients with sepsis accounted for 17.4% of cases (sepsis, severe sepsis, septic shock) of all patients treated through the intensive stage of treatment; Moreover, in 63.2% of cases it became a complication of hospital infections.

PREVENTION

Prevention of sepsis consists of timely diagnosis and treatment of the underlying disease and elimination of the source of infection.

SCREENING

The criteria for systemic syndrome can be considered a screening method for diagnosing a patient with a local focus of infection. inflammatory reaction(see Classification).

CLASSIFICATION

The current classification of sepsis is based on the diagnostic criteria and classification proposed by the American College of Chest Physicians and Society of Critical Care Medicine (ACCP/SCCM) consensus conference. Issues of terminology and classification of sepsis were considered and approved at the Kaluga Consensus Conference (2004) (Table 31-2).

Table 31-2. Classification and diagnostic criteria for sepsis

Pathological process	Clinical and laboratory signs
Systemic inflammatory response syndrome - systemic reaction of the body to the influence of various strong irritants (infection, trauma, surgery and etc.)	Characterized by two or more of the following: temperature ≥38 °C or ≤36 °C Heart rate ≥90 per minute RR >20 per minute or hyperventilation (PaCO2 ≤32 mmHg) blood leukocytes >12 or<4x109/мл, или количество незрелых forms >10%
Sepsis is a syndrome of systemic inflammatory response to invasion of microorganisms	Presence of a focus of infection and two or more signs of systemic inflammatory response syndrome
Severe sepsis	Sepsis combined with organ dysfunction, hypotension, tissue perfusion disorders (increased concentration lactate, oliguria, acute impairment of consciousness)
Septic shock	Severe sepsis with signs of tissue and organ hypoperfusion and arterial hypotension that cannot be eliminated with help infusion therapy and requiring the administration of catecholamines
Additional definitions
Multiple organ dysfunction syndrome	Dysfunction in two or more systems
Refractory septic shock	Persistent arterial hypotension, despite adequate infusion, use of inotropic and vasopressor support

Local inflammation, sepsis, severe sepsis and multiple organ failure are links in one chain in the body's response to inflammation due to microbial infection. Severe sepsis and septic (synonymous with infectious-toxic) shock constitute an essential part of the syndrome of the body's systemic inflammatory response to infection and are a consequence of the progression of systemic inflammation with the development of dysfunction of systems and organs.

BACTEREMIA AND SEPSIS

Bacteremia (presence of infection in the systemic bloodstream) is one of the possible, but not obligatory, manifestations of sepsis. The absence of bacteremia should not affect the diagnosis in the presence of the above criteria for sepsis. Even with the most scrupulous adherence to blood sampling techniques and the use of modern technologies for determining microorganisms in the most severely ill patients, the frequency positive results, as a rule, does not exceed 45%. Detection of microorganisms in the bloodstream without clinical laboratory confirmation of systemic inflammation syndrome should be regarded as transient bacteremia. The clinical significance of bacteremia may include the following:

confirming the diagnosis and determining the etiology infectious process;
evidence of the mechanism of development of sepsis (for example, catheter-related infection);
rationale for choosing an antibiotic treatment regimen;
assessing the effectiveness of therapy.

The role of polymerase chain reaction in the diagnosis of bacteremia and the interpretation of the results remains unclear for practical use. The presence of a suspected or confirmed infectious process is established based on the following signs:

detection of leukocytes in body fluids that are normally sterile;
perforation of a hollow organ;
radiographic signs of pneumonia, the presence of purulent sputum;
clinical syndromes in which the likelihood of an infectious process is high.

ETIOLOGY

Today, most major medical centers the frequency of gram-positive and gram-negative sepsis was approximately equal. Sepsis caused by fungal flora such as Candida is no longer an exception. The risk of its occurrence increases significantly in patients with a high severity index general condition, prolonged stay in the intensive care unit (more than 21 days), on total parenteral nutrition, receiving glucocorticoids; patients with severe renal dysfunction requiring extracorporeal detoxification.

The etiology of gynecological sepsis is determined by the source of infection:

Vaginal source:
―Peptostreptococcus spp.;
―Bacteroides bivus;
―Group B streptococci;
―Gardnerella vaginalis;
- Mycoplasma hominis;
―S. aureus.

Intestinal source:
-E. coli;
-Enterococcus spp.;
―Enterobacter spp.;
-Clostridium spp.;
-Bacteroides fragilis;
- Candida spp.

Sexually transmissible:
―Neisseria gonorrhoeae;
―Chlamydia trachomatis.

Hematogenous:
-Listeria monocytogenes;
―Campylobacter spp.;
- Group A streptococci.

PATHOGENESIS

The development of organ system damage in sepsis is primarily associated with the uncontrolled spread of primary focus infectious inflammation pro-inflammatory mediators of endogenous origin with subsequent activation under their influence of macrophages, neutrophils, lymphocytes and a number of other cells in other organs and tissues, with secondary release of similar endogenous substances, damage to the endothelium and a decrease in organ perfusion and oxygen delivery. Dissemination of microorganisms may be completely absent or short-term and difficult to detect. However, even in such a situation, the release of pro-inflammatory cytokines at a distance from the lesion is possible. Exo and endotoxins of bacteria can also activate the hyperproduction of cytokines from macrophages, lymphocytes, and endothelium.

The total effects exerted by mediators form the systemic inflammatory response syndrome. In its development, three main stages began to be distinguished.

1st stage. Local production of cytokines in response to infection.

A special place among inflammatory mediators is occupied by the cytokine network, which controls the processes of immune and inflammatory reactivity. The main producers of cytokines are T cells and activated macrophages, as well as, to varying degrees, other types of leukocytes, endothelial cells of postcapillary venules, platelets and Various types stromal cells. Cytokines act primarily at the site of inflammation and in the territory of the responding lymphoid organs, ultimately performing a series of protective functions, participating in the processes of wound healing and protecting body cells from pathogenic microorganisms.

2nd stage. Release of small amounts of cytokines into the systemic circulation.

Small amounts of mediators can activate macrophages, platelets, the release of adhesion molecules from the endothelium, and the production of growth hormone. The developing acute phase reaction is controlled by pro-inflammatory mediators (interleukins IL1, IL6, IL8, tumor necrosis factor α, etc.) and their endogenous antagonists, such as IL4, IL10, IL13, soluble receptors for TNFα and others, called anti-inflammatory mediators. By maintaining a balance and controlled relationship between pro- and anti-inflammatory mediators in normal conditions prerequisites are created for wound healing, destruction of pathogenic microorganisms, and maintenance of homeostasis. Systemic adaptive changes during acute inflammation include stress reactivity of the neuroendocrine system, fever, release of neutrophils into the circulation from the vascular and bone marrow depots, increased leukocytopoiesis in bone marrow, hyperproduction of acute phase proteins in the liver, development of generalized forms of the immune response.

3rd stage. Generalization of the inflammatory response.

In case of severe inflammation or its systemic failure, some types of cytokines: TNFα, IL1, IL6, IL10, TGFβ, INFγ (with viral infections) - can penetrate into the systemic circulation and accumulate there in quantities sufficient to realize their long-range effects. If the regulatory systems are unable to maintain homeostasis, the destructive effects of cytokines and other mediators begin to dominate, which leads to disruption of the permeability and function of the capillary endothelium, the initiation of disseminated vascular coagulation syndrome, the formation of distant foci of systemic inflammation, and the development of mono and multiple organ dysfunction. Apparently, any disturbances of homeostasis that can be perceived can act as factors of systemic damage. immune system as damaging or potentially damaging.

At this stage of the systemic inflammatory response syndrome, from the standpoint of the interaction of pro- and anti-inflammatory mediators, it is possible to conditionally distinguish two periods. The first, initial period is a period of hyperinflammation, characterized by the release of ultra-high concentrations of pro-inflammatory cytokines and nitric oxide, which is accompanied by the development of shock and the early formation of multiple organ failure syndrome (MOF). However, already in this moment compensatory release of anti-inflammatory cytokines occurs, the rate of their secretion, concentration in the blood and tissues gradually increases with a parallel decrease in the content of inflammatory mediators.

A compensatory anti-inflammatory response develops, combined with a decrease in the functional activity of immune-competent cells—a period of “immune paralysis.” In some patients, due to genetic determination or altered by factors external environment reactivity, the formation of a stable anti-inflammatory reaction is immediately recorded.

Gram-positive microorganisms do not contain endotoxin in their cell membrane and cause septic reactions through other mechanisms. Factors that trigger a septic response can be cell wall components, such as peptidoglycan and teichoic acid, staphylococcal protein A and streptococcal protein M, located on the cell surface, glycocalyx, and exotoxins. In this regard, the complex of reactions in response to invasion by gram-positive microorganisms is more complex. The key proinflammatory mediator is TNFα. The pivotal role of TNFα in the development of sepsis is associated with the biological effects of this mediator: increasing the procoagulant properties of the endothelium, activation of neutrophil adhesion, induction of other cytokines, stimulation of catabolism, fever and synthesis of “acute-phase” proteins. The generalization of damaging effects is mediated by the wide distribution of receptors for TNFα and the ability of other cytokines to release it. From a practical point of view, it is important that the rate of reactions of the septic cascade increases sharply under hypoxic conditions due to the expression of cytokine receptors on the cell surface.

In the genesis of acute vascular insufficiency, which underlies septic shock syndrome, the leading role is given to nitric oxide, the concentration of which increases tens of times as a result of stimulation of macrophages by TNFα, IL1, IFN, and subsequently the secretion of nitric oxide is carried out by the cells of vascular smooth muscles, and the monocytes themselves are activated under it action. Under normal conditions, nitric oxide acts as a neurotransmitter and is involved in vasoregulation and phagocytosis. It is characteristic that microcirculation disorders in sepsis are heterogeneous: zones of dilatation are combined with areas of vasoconstriction. Risk factors for developing septic shock - oncological diseases, the severity of the patient’s condition on the SOFA scale is more than 5 points, chronic obstructive pulmonary diseases, old age.

As a result of dysfunction of the liver, kidneys, and intestines, new damaging factors appear distal to cytokines. These include intermediate and final products of normal metabolism in high concentrations (lactate, urea, creatinine, bilirubin), components and effectors of regulatory systems accumulated in pathological concentrations (kallikreininin, coagulation, fibrinolytic), products of perverted metabolism (aldehydes, ketones, higher alcohols ), substances of intestinal origin such as indole, skatole, putrescine.

CLINICAL PICTURE

The clinical picture of sepsis consists of clinical picture systemic inflammatory response syndrome (tachycardia, fever or hypothermia, dyspnea, leukocytosis or leukopenia with shift leukocyte formula) and a variety of syndromes characteristic of organ dysfunction (septic encephalopathy, septic shock, acute respiratory, cardiac, renal, liver failure).

Septic encephalopathy is most often a consequence of cerebral edema and can be associated with both the development of systemic inflammatory response syndrome and the development of septic shock, hypoxia, concomitant diseases(cerebral atherosclerosis, alcohol or drug addiction, etc.). Manifestations of septic encephalopathy are varied - restlessness, agitation, psychomotor agitation and, conversely, lethargy, apathy, lethargy, stupor, coma.

The appearance of acute respiratory failure in sepsis is most often associated with the development of acute lung injury or acute respiratory distress syndrome, the diagnostic criteria of which are hypoxemia, bilateral infiltrates on a radiograph, a decrease in the ratio of partial pressure of oxygen in arterial blood to the inspiratory oxygen fraction (PaO2/FiO2) below 300, no signs of left ventricular failure.

The development of septic shock is characterized by impaired peripheral circulation due to the development of capillary dilatation vascular bed. Skin acquire a marbled tint, acrocyanosis develops; they are usually hot to the touch, high humidity, profuse sweat is typical, the extremities are warm, and the vascular spot slows down when pressing on the nail bed. IN late stages septic shock (phase of “cold” shock) limbs are cold to the touch. Hemodynamic disorders in septic shock are characterized by a decrease in blood pressure, which cannot be normalized during infusion therapy, tachycardia, a decrease in central venous pressure and pulmonary capillary wedge pressure. Respiratory failure progresses, oliguria, encephalopathy, and other manifestations of multiple organ dysfunction develop.

Assessment of organ dysfunction in sepsis is carried out according to the criteria presented below (Table 31-3).

Table 31-3. Criteria for organ dysfunction in sepsis

System/organ	Clinical and laboratory criteria
The cardiovascular system	Systolic blood pressure ≤90 mm Hg. or mean blood pressure ≤70 mm Hg. for at least 1 hour, despite correction of hypovolemia
urinary system	Diuresis<0,5 мл/(кг · ч) в течение 1 ч при адекватном объёмном восполнении или повышение уровня креатинина в два раза от нормального значения
Respiratory system	PaO2/FiO2 ≤250 or the presence of bilateral infiltrates on the radiograph, or the need for mechanical ventilation
Liver	An increase in bilirubin levels above 20 µmol/l for 2 days or an increase in transaminase levels by two times or more
Coagulation system	Platelet count<100x109/л или их снижение на 50% от наивысшего значения в течение 3 дней, или увеличение протромбинового времени выше нормы
Metabolic dysfunction	pH ≤7.3 base deficiency ≥5.0 mEq/plasma lactate 1.5 times higher than normal
CNS	Glasgow score less than 15

DIAGNOSTICS

ANAMNESIS

Anamnestic data for sepsis are most often associated with the presence of an unsanitized focus of infection of both the pelvic organs (endometritis, peritonitis, wound infection, criminal abortion) and other sources (pneumonia - 50%, abdominal infection - 19% of all causes of severe sepsis, pyelonephritis , endocarditis, ENT infections, etc.).

PHYSICAL INVESTIGATION

The main goal of the study is to determine the source of infection. In this regard, standard methods of gynecological and general clinical examination are used. There are no pathognomonic (specific) symptoms of sepsis. Diagnosis of sepsis is based on the criteria of a systemic inflammatory response and the presence of a focus of infection. Criteria for a focus of infection - one or more signs:

leukocytes in normally sterile biological fluids;
perforation of a hollow organ;
X-ray signs of pneumonia in combination with purulent sputum;
the presence of a high-risk infection syndrome (in particular cholangitis).

LABORATORY RESEARCH

Laboratory diagnosis is based on measuring the number of leukocytes (less than 4 or more than 12x109/l), the appearance of immature forms (more than 10%), assessing the degree of organ dysfunction (creatinine, bilirubin, arterial blood gases).

High specificity for confirming the diagnosis of sepsis of bacterial etiology is the determination of the concentration of procalcitonin in the blood plasma (an increase above 0.5–1 ng/ml is specific for sepsis, above 5.5 ng/ml - for severe sepsis of bacterial etiology - sensitivity 81%, specificity 94 %). Increase in ESR,

Due to low specificity, sreactive protein cannot be considered a diagnostic marker of sepsis.

Negative blood culture results do not rule out sepsis. Blood for microbiological testing must be collected before antibiotics are prescribed. The required minimum sampling is two samples taken from the veins of the upper extremities with an interval of 30 minutes. It is optimal to take three blood samples, which significantly increases the possibility of detecting bacteremia. If necessary, material is collected for microbiological examination from the suspected source of infection ( cerebrospinal fluid, urine, lower secretion respiratory tract etc.).

INSTRUMENTAL RESEARCH

Instrumental diagnostic methods cover all methods necessary to identify the source of infection. Methods of instrumental diagnostics in each case are determined by specialized specialists. To identify the source of infection of the uterine cavity, ultrasound of the uterus and hysteroscopy are performed; to identify the source in the abdominal cavity (uterine appendages) - abdominal ultrasound, computed tomography, magnetic resonance imaging, laparoscopy.

DIFFERENTIAL DIAGNOSTICS

Differential diagnosis of sepsis includes almost all diseases accompanied by tachycardia, shortness of breath, hypotension, leukocytosis, and organ dysfunction. Most often in the practice of an obstetrician-gynecologist, differential diagnosis is carried out with the following conditions:

gestosis;
pulmonary embolism;
acute heart failure;
acute myocardial infarction, cardiogenic shock;
pulmonary edema;
pulmonary atelectasis;
pneumothorax, hydrothorax;
exacerbation of chronic obstructive pulmonary diseases;
acute renal failure;
toxic liver damage;
toxic encephalopathy;
amniotic fluid embolism.

A differential diagnostic criterion confirming sepsis can be a concentration of procalcitonin in the blood plasma above 0.5 ng/ml, for severe sepsis - above 5.5 ng/ml.

INDICATIONS FOR CONSULTATION WITH OTHER SPECIALISTS

If signs of organ dysfunction appear, consultation with an anesthesiologist and resuscitator is indicated. In the absence of a source of infection, consultations with specialized specialists (therapist, neurologist, otorhinolaryngologist, dentist, urologist, infectious disease specialist).

EXAMPLE OF FORMULATION OF DIAGNOSIS

Endometritis. Sepsis. Acute respiratory failure.

TREATMENT

Effective intensive therapy for sepsis is possible only with complete surgical sanitation of the source of infection and adequate antimicrobial therapy. Inadequate initial antimicrobial therapy is an independent risk factor for death in patients with sepsis. At the same time, maintaining the patient’s life, preventing and eliminating organ dysfunction is impossible without targeted intensive therapy. Often the question arises about extirpation of the uterus, especially when it is purulently melted, or about removing a tubo-ovarian formation containing pus.

The main goal of this therapy is to optimize oxygen transport in conditions of increased oxygen consumption, characteristic of severe sepsis and septic shock. This direction of treatment is implemented through hemodynamic and respiratory support. Other aspects of intensive care play an important role: nutritional support, immunoreplacement therapy, correction of hemocoagulation disorders, prevention of deep vein thrombosis and thromboembolic complications, prevention of stress ulcers and gastrointestinal bleeding in patients with sepsis.

ANTIBACTERIAL THERAPY

It is necessary to start antibacterial therapy in the first hours after the diagnosis of sepsis is established, based on the following principles:

spectrum of putative pathogens depending on the location of the primary focus;
level of resistance of nosocomial pathogens according to microbiological monitoring of a specific medical institution;
conditions for the occurrence of sepsis - community-acquired or nosocomial;
the severity of the patient's condition, assessed by the presence of multiple organ failure or APACHE II.

The effectiveness of antibiotic therapy is assessed no earlier than after 48–72 hours.

HEMODYNAMIC SUPPORT

Infusion therapy is one of the initial measures to maintain hemodynamics and, above all, cardiac output. The main objectives of infusion therapy in patients with sepsis are: restoration of adequate tissue perfusion, normalization of cellular metabolism, correction of homeostasis disorders, reduction of the concentration of mediators of the septic cascade and toxic metabolites.

Localization of the primary focus	Nature of infection	1st line remedies	Alternative remedies
Abdomen	Community-acquired	Amoxicillin + clavulanic acid +/– aminoglycoside Cefotaxime + metronidazole Ceftriaxone + metronidazole	Ampicillin/sulbactam +/– aminoglycosideLevofloxacin + metronidazoleMoxifloxacinOfloxacin + metronidazolePefloxacin + metronidazoleTicarcillin + clavulanic acidCefuroxime + metronidazoleErtapenem
	NosocomialAP ACHE<15, без ПОН	Cefepime +/– metronidazole Cefoperazone/sulba ktam	ImipenemLevofloxacin + metronidazoleMeropenemCeftazidime + metronidazoleCiprofloxacin + metronidazole
	NosocomialAP ACHE >15 and/or MODS	ImipenemMeropenem	Cefepime + metronidazoleCefoperazone/sulbactam +/– amikacinCiprofloxacin + metronidazole +/– amikacin
Lungs	Nosocomial pneumonia outside the ICU	Levofloxacin Cefotaxime Ceftr iaxone	ImipenemMeropenemOfloxacinPefloxacinCef epiErtapenem
	Nosocomial pneumonia in the ICU, APACHE<15, без ПОН	Cefepime Ceftazidime + amikacin	ImipenemMeropenemCefoperazone/sulbactam +/– amikacinCiprofloxacin +/– amikacin
	Nosocomial pneumonia in the ICU, APACHE >15 and/or MODS	ImipenemMeropenem	Cefepime +/– amikacin
Kidneys	Community-acquired	Ofloxacin Cefotaxime Ceftriac sleep	LevofloxacinMoxifloxacinCiprofloxacin
Kidneys	Nosocomial	LevofloxacinOfloxacinCipro floxacin	ImipenemMeropenemCefepime
Catheter-associated		Vancomycin Linezolid	Oxacillin + gentamicin Cefazolin + gentamicin Rifampicin + ciprofloxacin (co-trimoxazole) Fusidic acid + ciprofloxacin (co-trimoxazole)

In case of sepsis with MODS and septic shock, it is necessary to strive to quickly achieve (the first 6 hours after admission) the target values of the following parameters: central venous pressure 8–12 mm Hg, mean blood pressure more than 65 mm Hg, diuresis 0.5 ml/(kgxh), hematocrit more than 30%, blood saturation in the superior vena cava or right atrium not less than 70%. The use of this algorithm increases survival in septic shock and severe sepsis. The volume of infusion therapy should be maintained so that the wedge pressure in the pulmonary capillaries does not exceed the colloid-oncotic plasma pressure (to avoid pulmonary edema) and is accompanied by an increase in cardiac output. It is necessary to take into account the parameters characterizing the gas exchange function of the lungs - PaO2 and PaO2/FiO2, the dynamics of the x-ray picture.

For infusion therapy as part of targeted intensive therapy for sepsis and septic shock, crystalloid and colloid infusion solutions are used with almost the same results. All infusion media have both their advantages and disadvantages. Taking into account the available results of experimental and clinical studies to date, there is no reason to give preference to any of the infusion media.

The qualitative composition of the infusion program should be determined by the patient’s characteristics: the degree of hypovolemia, the phase of disseminated intravascular coagulation syndrome, the presence of peripheral edema and blood albumin level, and the severity of acute pulmonary injury.

Plasma substitutes (dextrans, gelatin preparations, hydroxyethyl starches) are indicated for severe deficiency of circulating blood volume. Hydroxyethyl starches with molecular weights of 200/0.5 and 130/0.4 have a potential advantage over dextrans due to a lower risk of membrane escape and lack of clinically significant effects on hemostasis. Albumin transfusion will be useful only if the albumin level decreases to less than 20 g/l and there is no evidence of its “leakage” into the interstitium. The use of fresh frozen plasma is indicated for consumption coagulopathy and a decrease in the coagulation potential of the blood. According to most experts, the minimum hemoglobin concentration for patients with severe sepsis should be in the range of 90–100 g/L. Wider use of donor red blood cells must be limited due to the high risk of developing various complications (acute lung injury, anaphylactic reactions, etc.).

Low perfusion pressure requires the immediate inclusion of drugs that increase vascular tone and/or inotropic function of the heart. Dopamine or norepinephrine are the first-choice drugs for correcting hypotension in patients with septic shock.

Dobutamine should be considered as the drug of choice for increasing cardiac output and oxygen delivery at normal or elevated preload levels. Due to its predominant effect on β1 receptors, dobutamine, to a greater extent than dopamine, contributes to an increase in these indicators.

RESPIRATORY SUPPORT

The lungs very early become one of the first target organs involved in the pathological process during sepsis.

Acute respiratory failure is one of the leading components of multiple organ dysfunction. Its clinical and laboratory manifestations in sepsis correspond to acute lung injury syndrome, and with progression pathological process- acute respiratory distress syndrome. Indications for artificial ventilation of the lungs in severe sepsis are determined by the development of parenchymal respiratory failure: when the respiratory index decreases below 200, tracheal intubation and the beginning of respiratory support are indicated. If the respiratory index is above 200, the readings are determined on an individual basis. The presence of adequate consciousness, the absence of high costs of breathing work, pronounced tachycardia (heart rate up to 120 per minute), normalization of venous blood return and SaO2 >90% against the background of oxygen support for spontaneous breathing allow us to refrain from transferring to artificial ventilation, but not from strict monitoring the dynamics of the patient's condition. Optimal blood oxygen saturation levels (approximately 90%) can be maintained using various oxygen therapy techniques (face masks, nasal catheters) using a non-toxic oxygen concentration (FiO2<0,6). Больным с тяжёлым сепсисом противопоказано применение неинвазивной респираторной поддержки.

It is necessary to adhere to the concept of safe artificial ventilation of the lungs, according to which it is low-invasive if the following conditions are met: peak airway pressure below 35 cm H2O, inspiratory oxygen fraction below 60%, tidal volume less than 10 ml/kg, non-inverted inspiratory ratio to exhale. The selection of respiratory cycle parameters is carried out until the criteria for the adequacy of artificial pulmonary ventilation are achieved: PaO2 more than 60 mm Hg, SaO2 more than 93%, PvO2 35–45 mm Hg, SvO2 more than 55%.

NUTRITIONAL SUPPORT

The development of MOF syndrome in sepsis is usually accompanied by manifestations of hypermetabolism. In this situation, meeting energy needs occurs due to the destruction of one’s own cellular structures, which aggravates existing organ dysfunction and intensifies endotoxicosis. Nutritional support is considered as a method of preventing the development of severe malnutrition (protein-energy deficiency) against the background of pronounced hypercatabolism and hypermetabolism, which serve as the most characteristic metabolic characteristics of a generalized inflammatory reaction of infectious origin. Inclusion of enteral nutrition in the complex

intensive therapy prevents the translocation of microflora from the intestine, the development of dysbiosis, increases the functional activity of the enterocyte and the protective properties of the mucous membrane, reducing the degree of endotoxicosis and the risk of secondary infectious complications.

When providing nutritional support, it is advisable to focus on the following recommendations:

energy value of food: 25–30 kcal/(kgxday);
protein: 1.3–2.0 g/(kgxday);
glucose: 30–70% non-protein calories, maintaining glycemic levels below 6.1 mmol/L;
lipids: 15–20% non-protein calories.

Early initiation of nutritional support within 24–36 hours is more effective than starting from 3–4 days of intensive therapy.

This is especially true for protocols for early and late initiation of enteral tube feeding.

For efficient synthesis of endogenous protein, it is important to maintain a metabolic ratio of non-protein calories/total nitrogen in the range of 1 g of nitrogen to 110–130 kilocalories. Carbohydrates should not be administered in a dose of more than 6 g/(kg x day) due to the fact that there is a risk of developing hyperglycemia and activation of catabolic processes in skeletal muscles. For parenteral administration of fat emulsions, a round-the-clock administration regimen is recommended. It is necessary to give preference to 2nd generation fat emulsions such as MCT/LST, which demonstrate a higher rate of utilization from the bloodstream and oxidation in patients with severe sepsis.

Contraindications to nutritional support:

refractory shock syndrome (dopamine dose more than 15 mcg/(kgxmin) and systolic blood pressure less than 90 mmHg);
intolerance to media for nutritional support;
severe intractable arterial hypoxemia;
severe uncorrected hypovolemia;
decompensated metabolic acidosis.

GLYCEMIC CONTROL

An important aspect of complex intensive care for severe sepsis is constant monitoring of glycemic levels and insulin therapy. High levels of glycemia and the need for insulin therapy are factors of unfavorable outcome in patients with diagnosed sepsis. In this regard, it is necessary to strive to maintain glycemic levels within the range of 4.5–6.1 mmol/l. At a glycemic level of more than 6.1 mmol/l, an insulin infusion (at a dose of 0.5–1 U/hour) should be performed to maintain normoglycemia (4.4–6.1 mmol/l). Monitor glucose concentration every 1–4 hours depending on the clinical situation. When performing this algorithm, a statistically significant increase in survival rate is recorded.

GLUCOCORTICOIDS

Glucocorticoids for sepsis are used for the following indications:

the use of glucocorticoids in high doses in the treatment of septic shock is inappropriate due to the lack of effect on increasing survival and increasing the risk of hospital infections;
the addition of hydrocortisone in doses of 240–300 mg/day for 5–7 days to the complex therapy of septic shock allows to accelerate the moment of hemodynamic stabilization, withdrawal of vascular support and increase survival in the population of patients with concomitant relative adrenal insufficiency.

It is necessary to abandon the chaotic empirical prescription of prednisolone and dexamethasone. In the absence of laboratory evidence of the development of relative adrenal insufficiency, the use of hydrocortisone at a dose of 300 mg / day (for 3-6 injections) should be resorted to in refractory septic shock or when it is necessary to administer high doses of vasopressors to maintain effective hemodynamics. The effectiveness of hydrocortisone in septic shock can mainly be associated with the following mechanisms of action of glucocorticoids in conditions of systemic inflammation: activation of nuclear factor inhibitor and correction of relative adrenal insufficiency. In turn, inhibition of the activity of the nuclear factor leads to a decrease in the synthesis of inducible NO synthetase (nitric oxide is the most powerful endogenous vasodilator), as well as the formation of proinflammatory cytokines, cyclooxygenase and adhesion molecules.

ACTIVATED PROTEIN C

One of the characteristic manifestations of sepsis is a violation of systemic coagulation (activation of the coagulation cascade and inhibition of fibrinolysis), which ultimately leads to hypoperfusion and organ dysfunction. The effect of activated protein C on the inflammatory system is realized through several mechanisms:

reduction in the attachment of selectins to leukocytes, which is accompanied by the preservation of the integrity of the vascular endothelium, which plays a critical role in the development of systemic inflammation;
decreased release of cytokines from monocytes;
blocking the release of TNFα from leukocytes;
inhibition of thrombin production, which potentiates the inflammatory response.

Anticoagulant, profibrinolytic and anti-inflammatory effects are due to:

degradation of factors Va and VIIIa, which leads to suppression of thrombus formation;
activation of fibrinolysis due to suppression of plasminogen activator inhibitor;
direct anti-inflammatory effect on endothelial cells and neutrophils;
protection of the endothelium from apoptosis.

Administration of activated protein C (drotrecogin alfa [activated]) at a dose of 24 mcg/(kg h) for 96 hours reduces the risk of death by 19.4%.

IMMUNOGLOBULIN INFUSION

The advisability of prescribing an infusion of immunoglobulins (IgG and IgG + IgM) is associated with their ability to limit the excessive effect of proinflammatory cytokines, increase the clearance of endotoxin and staphylococcal superantigen, eliminate anergy, and enhance the effect of betalactam antibiotics. The use of immunoglobulins as part of immunoreplacement therapy for severe sepsis and septic shock is currently recognized as the only truly proven method of immunocorrection that increases survival in sepsis. The best effect was recorded when using a combination of IgG and IgM. The standard dosage regimen is to administer 3–5 ml/(kg · day) for three consecutive days. Optimal results with the use of immunoglobulins were obtained in the early phase of shock (“warm shock”) and in patients with severe sepsis and the APACHE II severity index range of 20–25 points.

PREVENTION OF DEEP VEIN THROMBOSIS

Available data now confirm that prevention of deep vein thrombosis has a significant impact on treatment outcomes in patients with sepsis. For this purpose, both unfractionated heparin and low molecular weight heparin preparations can be used. The main advantages of low-molecular-weight heparin preparations are a lower incidence of hemorrhagic complications, a less pronounced effect on platelet function, prolonged action, i.e. the possibility of a single administration per day.

PREVENTION OF STRESS IN THE GASTROINTESTINAL TRACT

This direction plays a significant role in a favorable outcome in the management of patients with severe sepsis and septic shock, since mortality in patients with bleeding from gastrointestinal stress varies from 64 to 87%. The incidence of stress ulcers without their prevention in patients in critical condition can reach 52.8%. Prophylactic use of H2 receptor blockers and proton pump inhibitors reduces the risk of complications by 2 times or more. The main direction of prevention and treatment is maintaining pH above 3.5 (up to 6.0). Moreover, the effectiveness of proton pump inhibitors is higher than the use of H2 blockers. It should be emphasized that, in addition to the above drugs, enteral nutrition plays an important role in the prevention of stress ulcers.

RENAL REPLACEMENT THERAPY

Impaired renal function causes rapid decompensation of organ failure due to an increase in endotoxemia caused by the development of a systemic inflammatory response syndrome, massive cytolysis, pathological proteinolysis, leading to the development of pronounced water-sectoral disorders with generalized endothelial damage, disorders of hemocoagulation and fibrinolysis, increased permeability of the capillary bed and, ultimately, to rapid decompensation (or manifestation) of organ failure (cerebral edema, acute lung injury, distress syndrome, distributive shock and acute cardiac, liver and intestinal failure).

The main difference between isolated renal failure(acute or chronic) from acute renal failure during MODS - in the spectrum of endotoxins formed and accumulated in the body. In isolated renal failure, they are represented by substances of low molecular weight (less than 1000 D) - urea, indoles, phenols, polyamines, neopterins, ammonia, uric acid. These substances can be effectively eliminated by hemodialysis. With MODS, substances of medium and high molecular weight (more than 1000 D) are added to the above-described spectrum of low molecular weight toxins, which include all biologically active substances formed as a result of a systemic inflammatory reaction - TNFα, interleukins, leukotrienes, thromboxane, oligopeptides, complement components. For these substances, hemodialysis is not effective, and preference is given to convective mass transfer, used in hemofiltration, and a combination of the two methods described above for hemodiafiltration. These methods make it possible, albeit with some reservations, to remove substances with a molecular weight of up to 100,000 D. These include plasma proteins, including immunoglobulins, circulating immune complexes containing complement and myoglobin, although the clearance of these chemical compounds is much higher when using plasma filtration methods.

Despite the above-mentioned pathophysiological evidence for treatment modalities, there are currently no large, well-controlled studies supporting renal replacement therapy as an integral part of targeted therapy for severe sepsis. Moreover, even when using the most pathogenetically substantiated method - venovenous prolonged hemofiltration (rate 2 l/h for 48 hours) - there was no decrease in IL6, IL8, TNFα in the blood and no reduction in mortality. In this regard, its use in widespread practice is not yet justified and is indicated only in the development of acute renal failure.

FORECAST

Mortality in severe sepsis is about 20% with single organ dysfunction, increasing to 80–100% with involvement of four or more organs.

BIBLIOGRAPHY
Abdominal surgical infection: clinical picture, diagnosis, antimicrobial therapy: practical work. hands / Edited by V.S. Savelyeva, B.R. Gelfand. - M.: Literra, 2006. - 168 p.
Gelfand B.R., Kirienko P.A., Grinenko T.F. and others. Anesthesiology and intensive care: practical work. hands / Under the general ed.B.R. Gelfand. - M.: Literra, 2005. - 544 p.
Sepsis at the beginning of the 21st century. Classification, clinical diagnostic concept and treatment. Pathoanatomical diagnosis: practical work. hands - M.: Literra, 2006. - 176 p.
Surgical infections: practical work. hands / Ed. I.A. Eryukhina et al.: ed. 2e, lane and additional - M.: Literra, 2006. - 736 p.
Bone R.C., Balk R.A., Cerra F.B. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis: the ACCP/SCCM consensus conference committee // Chest. - 1992. - Vol. 101. - P. 1644–1655.

David C. Dale, Robert G. Petersdorf G. Petersdorf)

Definition. Septic shock is characterized by insufficient tissue perfusion due to bacteremia, most often caused by gram-negative enteric bacteria. Most patients experience hypotension, oliguria, tachycardia, tachypnea and fever. Circulatory failure is caused by diffuse damage to cells and tissues, as well as blood stagnation in the microcirculatory bed.

Etiology and epidemiology. Septic shock can be caused by gram-positive microorganisms, mainly staphylococci, pneumococci and streptococci, but more often it develops with bacteremia as a result of infection with gram-negative pathogens. These include Escherichia coli, Klebsiella, other Enterobacteriaceae, Proteus, Pseudomonas aeruginosa and Serratia. An important cause of septic shock also includes bacteremia due to infection with meningococci or gram-negative anaerobic bacteroids. With bacteremia caused by gram-negative pathogens, shock syndrome is not caused by the penetration of bacteria as such into the bloodstream, it develops under the influence of microbial toxins. The most studied of these toxins is currently endotoxin, which is a substance of the lipopolysaccharide nature of the bacterial wall.

Gram-negative bacteremia and septic shock develop mainly in hospitalized patients, usually against the background of an underlying disease, in which the penetration of infectious agents into the blood is noted. Predisposing factors include diabetes mellitus, liver cirrhosis, leukemia, lymphoma or advanced carcinoma, antineoplastic chemotherapeutic agents and immunosuppressants, as well as a variety of surgical procedures and infections of the urinary, biliary tract and gastrointestinal tract. Special groups include newborns, pregnant women and elderly people with urinary disorders as a result of prostate pathology. The incidence of sepsis due to Gram-negative bacteremia is increasing and is now reported to be 12 per 1000 hospitalized patients in some large urban hospitals. Along with these factors, the widespread use of antibiotics, glucocorticoids, intravenous catheters, humidifiers and other hospital equipment, as well as the increasing life expectancy of patients with chronic diseases, contribute to the increase in the scale of this serious problem (Chapters 84 and 85).

Pathogenesis, pathological human anatomy and physiology. Most of the bacteria that cause gram-negative sepsis are common commensals of the gastrointestinal tract, from which they can spread to adjacent tissues, for example, in peritonitis as a result of perforation of the appendix, or can migrate from the perineal area to the urethra or bladder. Gram-negative bacteremia usually develops against the background of a local primary infection of the genitourinary and biliary tract, gastrointestinal tract or lungs and much less often against the background of infection of the skin, bones and joints. In patients with burns and leukemia, the entry point for infection is often the skin or lungs. In many cases, especially in patients with debilitating diseases, cirrhosis and cancer, it is not possible to identify the primary source of infection. If bacteremia causes metastatic damage to distant areas of the body, then classic abscesses form in them. However, more often, autopsy results in gram-negative sepsis indicate primarily a primary focus of infection and target organ damage, namely: edema, hemorrhages and the formation of hyaline membranes in the lungs, tubular or cortical necrosis of the kidneys, focal necrosis of the myocardium, superficial ulceration of the gastrointestinal mucosa tract, blood clots in the capillaries of many organs.

Basic mechanisms of pathophysiology. Septic shock develops as a result of the impact of bacterial products on cell membranes and components of the blood coagulation and complement systems, which leads to increased coagulation, cell damage and disruption of blood flow, especially microcirculation. Experimental evidence from bacterial and endotoxin administration suggests that many of these reactions begin simultaneously; Most modern ideas about the pathophysiology of septic shock are based on the results of studying the influence of bacterial endotoxin and its toxic component, lipid A.

Endotoxin and other bacterial products activate cell membrane phospholipases, which leads to the release of arachidonic acid and stimulates the synthesis and release of leukotrienes, protaglandins and thromboxanes. Phospholipase A2-containing cells (eg, neutrophils, monocytes, platelets) also produce platelet-activating factor (PAF). These inflammatory mediators have a major effect on vasomotor tone, small vessel permeability, and aggregation of leukocytes and platelets. For example, thromboxane A 2 and prostaglandin F 2 a cause a marked constriction of pulmonary vessels, leukotrienes C4 and D4 increase the permeability of small vessels, and leukotriene B4 and PAF promote aggregation and activation of neutrophils. Although the opposing actions and interactions of these substances are a very complex process, their cumulative effect on the development of shock appears to be quite significant (Chapter 68, “Prostaglandins and Eicosanoids”).

Microorganisms activate the classical complement pathway, and endotoxin activates the alternative pathway; Moreover, both pathways lead to the formation of C3a and C5a, which affect the aggregation of leukocytes and platelets and vascular tone. Complement activation, leukotriene formation, and direct effects of endotoxin on neutrophils cause the accumulation of these inflammatory cells in the lungs, releasing their enzymes and producing toxic acid radicals that damage the pulmonary endothelium and cause acute respiratory distress syndrome. Activation of the coagulation system leads to the formation of thrombin and the formation of blood clots in the microvasculature of many tissues.

Gram-negative bacteria or endotoxin stimulate the release of catecholamines and glucocorticoids from the adrenal glands, histamine from mast cells and serotonin from platelets. Secretion of opioids in the central nervous system, formation of bradykinin from kininogen, and production of the vasoactive arachidonate occur simultaneously in many cells. Tachycardia, hypotension and developing circulatory collapse are the result of the combined effects of substances. Their inhibitors and antagonists are used clinically to modify the course of septic shock. It is now recognized that injection of glucocorticosteroids prior to endotoxin administration to experimental animals provides a protective effect, which is believed to be associated with blocking the release of arachidonic acid from cell membranes. If endotoxin is administered first, the effect after glucocorticoid injection is much less pronounced. The secretion of opioids, i.e. b-endorphins and enkephalins, may play a decisive role in the development of shock. Some experimental results suggest that naloxone, an opiate antagonist, significantly enhances the function of of cardio-vascular system.

Septic shock is accompanied by cell damage and death as a result of direct exposure to endotoxin and other products of bacterial origin, indirect exposure to endogenous mediators, and tissue anoxia. The vascular endothelium is especially susceptible to these effects; experimental data indicate diffuse damage, vacuolization and desquamation of these cells. Anoxia and the release of hormones (eg, catecholamines, glucagon, insulin, glucocorticoids) cause a sharp shift in the conditions of tissue metabolism from aerobic to anaerobic changes and fat metabolism, protein catabolism, hypoglycemia, lactic acidosis. Many of the clinical consequences of septic shock are due to these metabolic changes.

Hemodynamic disorders. At the early stage of shock development, blood accumulates in the capillary bed, and plasma proteins leak into the interstitial fluid. This in turn leads to a sharp decrease in the effective volume of circulating blood, a decrease in cardiac output, as well as systemic arterial hypotension. Subsequently, the activity of the sympathetic nervous system increases, blood vessels constrict and selectively decreases blood flow to the vessels, internal organs and skin. If insufficient perfusion of vital organs continues, metabolic acidosis and severe solid organ damage occur, and shock becomes irreversible. In humans, the kidneys and lungs are especially sensitive to endotoxin; in this case, oliguria and tachypnea, and in some cases pulmonary edema, develop first. In general, in the early stages of shock, the heart and brain are damaged to a lesser extent, so heart failure and coma are late and often terminal manifestations of shock syndrome. There is also experimental evidence that after the introduction of live gram-negative bacteria around the capillary bed of sensitive organs, significant arteriovascular shunting of the blood occurs. This increases tissue anoxia. In some cases, damaged cells appear to be unable to use available oxygen. The overall result of insufficient tissue perfusion is a dramatic decrease in arteriovenous (AV) oxygen difference and lactic acidemia.

In the early stages of septic shock, usually the first thing to do is dilate blood vessels and increase cardiac output, decrease systemic vascular resistance and decrease central venous pressure, and increase stroke volume. In contrast, in the later stages, vasoconstriction with an increase in systemic resistance, a decrease in cardiac output, a decrease in central venous pressure, and a decrease in stroke volume predominate. When examining large groups of patients with septic shock, certain types of clinical and laboratory abnormalities were identified: 1) unchanged cardiac output, blood volume, circulation rate, unchanged or increased central venous pressure, unchanged or increased pH values, decreased peripheral vascular resistance; the skin is warm and dry; despite hypotension, oliguria and lactic acidemia, the prognosis is generally favorable; it is believed that shock in this case is caused by shunting of blood through arteriovenous anastomoses, which leads to impaired perfusion of vital organs; 2) low blood volume and central venous pressure, high hematocrit, increased peripheral vascular resistance, low cardiac output, hypotension, oliguria with a moderate increase in blood lactate levels and unchanged or slightly increased pH; it is possible that before the development of bacteremia, these patients had some hypovolemia, and their prognosis is quite favorable provided that intravascular blood volume is restored, treatment with appropriate antibiotics, elimination or drainage of septic lesions and the administration of vasoactive drugs; 3) unchanged blood volume, high central venous pressure, unchanged or high cardiac output, decreased peripheral vascular resistance against the background of severe metabolic acidosis, oliguria, and very high blood lactate levels, indicating insufficient tissue perfusion or insufficient oxygen uptake; despite the fact that the hands and feet of these patients are warm and dry, the prognosis in these cases is unfavorable; 4) low blood volume, central venous pressure and cardiac output, severe decompensated metabolic acidosis and lactic acidemia; the hands and feet of these patients are cold to the touch and cyanotic. The prognosis in these cases is extremely unfavorable.

These data indicate different stages of septic shock: from hyperventilation, respiratory alkalosis, vasodilation of increased or unchanged cardiac output in the early stage to decreased perfusion with pronounced lactic acidemia and metabolic acidosis, low cardiac output, as well as a slight AV oxygen difference in the irreversible late stage. stage of shock. Moreover, in some patients the correlation between the outcome of shock and hemodynamic disturbances is small.

Complications. Disorders of coagulation processes. Most patients with septic shock have a deficiency of a number of coagulation factors due to their increased consumption. This syndrome is called disseminated intravascular coagulation (DIC). Its pathogenesis consists of the activation of the intrinsic coagulation system by factor XII (Hageman factor) followed by the deposition of fibrin-adhesive platelets on capillary thrombi formed as a result of the generalized Schwarzmann reaction. The formation of platelet masses glued together with fibrin is typical of DIC, characterized by a decrease in the level of factors II, V and VIII, a decrease in the amount of fibrinogen and platelets. The development of moderate fibrinolysis with the appearance of cleavage products is possible. These coagulation abnormalities occur to varying degrees in most patients with septic shock, but clinically there is usually no bleeding, although hemorrhages sometimes occur due to thrombocytopenia or clotting factor deficiency. A more serious consequence of progressive disseminated intravascular coagulation is the formation of capillary thrombi, particularly in the lungs. If there are no signs of bleeding, the coagulopathy does not require special treatment and resolves spontaneously as shock is treated.

Respiratory failure. The most important causes of death in patients with shock include respiratory failure, especially after correction of hemodynamic disorders. Significant factors in the development of acute respiratory failure (ARF) are pulmonary edema, hemorrhage, atelectasis, the formation of hyaline membranes and the formation of capillary thrombi. Severe pulmonary edema may result from a marked increase in capillary permeability. It can develop in the absence of heart failure. Respiratory failure may occur and worsen even after other problems have resolved. Pulmonary surfactant levels decrease with progressive decline in pulmonary respiratory function.

Kidney failure. Oliguria develops early stage shock and is probably due to a decrease in intravascular blood volume and insufficient renal perfusion. If the latter remains insufficient, acute tubular necrosis develops. Sometimes cortical necrosis occurs, similar to that which occurs with the generalized Schwartzmann phenomenon.

Heart failure. Many patients with septic shock develop myocardial failure, even if they did not have heart disease before the onset of shock. Based on experimental data, it is believed that heart failure develops under the influence of a substance formed as a result of the activity of lysosomal enzymes in the zone of tissue ischemia. This substance is called myocardial depression factor (FDM). Functionally, the pathology manifests itself as left ventricular failure, as evidenced by increased pressure in the left ventricle at the end of diastole.

Violations of the functions of other organs. Superficial ulcerations of the mucous membrane of the gastrointestinal tract are often detected, which is manifested by bleeding, as well as liver dysfunction in the form of hypoprothrombinemia, hypoalbuminemia and moderate jaundice.

Clinical manifestations and laboratory data. Bacteremia due to infection with gram-negative pathogens usually begins acutely with chills, fever, nausea, vomiting, diarrhea and prostration. As shock develops, they include tachycardia, tachypnea, hypotension, the patient’s arms and legs become cold to the touch and pale, often cyanotic, the patient is lethargic, and oliguria appears. Shock caused by gram-negative pathogens is easy to diagnose with a pronounced clinical picture, but sometimes clinical signs can be blurred, especially in the elderly, debilitated patients or children. Unexplained hypotension, increasing confusion and disorientation, or hyperventilation may be the only clue to the diagnosis of septic shock. Some patients experience hypothermia, and the absence of fever often makes it difficult to recognize the disease. Jaundice that sometimes appears indicates a biliary tract infection, intravascular hemolysis or toxic hepatitis. As shock progresses, oliguria persists, and signs of cardiac and respiratory failure and coma begin to increase. Death usually results from pulmonary edema, secondary generalized anoxemia due to respiratory failure, cardiac arrhythmia, disseminated intravascular coagulation with hemorrhage, cerebral anoxia, or a combination of these factors. .

Laboratory findings vary greatly and in many cases depend on the cause of the shock syndrome, as well as on the stage of shock. The hematocrit is often elevated and, as circulating blood volume is restored, becomes less than normal. Leukocytosis is usually observed (the number of leukocytes is 15-30 10 9 / l) with a shift in the white blood count to the left. However, the number of leukocytes may be within normal limits, and some patients experience leukopenia. The platelet count usually decreases, and the prothrombin time and partial thromboplastin time may be altered, reflecting the consumption of clotting factors.

There are no specific changes observed in the urine. At first, its specific density is high; if oliguria continues, isosthenuria develops. Blood urea nitrogen (BUN) and creatinine levels are increased and creatinine clearance is decreased.

Simultaneous determination of urine and plasma osmotic pressure can be used to recognize impending renal failure. If the urine osmotic pressure exceeds 400 mOsmol and the urine-to-plasma osmotic pressure ratio exceeds 1.5, renal function is preserved and oliguria is likely due to a decrease in circulating blood volume. On the other hand, an osmotic pressure of less than 400 mOsmol and a urine-to-plasma pressure ratio of less than 1.5 indicate renal failure. Along with this, prerenal azotemia can be judged by such indicators as a urine sodium level of less than 20 mol/L, a urine-to-serum creatinine ratio of more than 40, or a blood urea nitrogen to serum creatinine ratio of more than 20. The types of electrolyte disturbances vary significantly, however, there is a tendency towards hyponatremia and hypochloremia. Serum potassium levels may be high, low, or within the normal range. The bicarbonate concentration is usually low, and the blood lactate level increases. A low pH of the liver and a high level of lactate in it are among the most reliable signs of insufficient tissue perfusion.

At the onset of endotoxin shock, respiratory alkalosis is determined, manifested by low pco2 and high pH of arterial blood, probably as a result of progressive anoxemia and the removal of carbon dioxide against the background of pulmonary hyperventilation, aimed at compensating for lactic acidemia. As shock progresses, metabolic acidosis develops. Anoxemia is often pronounced, with p o2 below 70 mm Hg. Art. The ECG usually shows a decrease in the segment ST, negative wave T and various types of arrhythmias, which may result in a misdiagnosis of myocardial infarction.

Before treatment is started in patients with septic shock, pathogens are detected in blood cultures, but bacteremia may not be consistent. and blood culture results may be negative in some cases. Moreover, the results of bacteriological studies may be distorted, since many patients manage to take antimicrobial drugs by the time of the examination. Negative results do not exclude the diagnosis of septic shock. The results of culture of material from the primary site of infection can help establish the diagnosis, but they may be distorted by the influence of previous chemotherapy. The ability of endotoxin to coagulate the blood of the horseshoe crab Limulus represents the basis of a test for endotoxemia, however it is not available for widespread use and therefore has limited clinical use.

Diagnosis. If the patient has chills, fever, and an obvious focus of infection is identified, septic shock is not difficult to recognize. However, none of these signs may be present. In elderly people and especially in weakened patients, the infection may not be accompanied by a feverish state. In a patient who has no radiological changes in the lungs, but is confused and disoriented due to hyperventilation, the cause of which is not clear, one should think about septic shock. Most often it is confused with diseases such as pulmonary embolism, myocardial infarction, cardiac tamponade, aortic dissection, and “silent” bleeding.

Flow. The basis of rational treatment for sepathic shock is careful monitoring of the patient. Continuous recording of clinical data is very useful. At the patient's bedside, it is especially important to monitor four main indicators:

1. The state of pulmonary blood flow (and preferably left ventricular function) is monitored using a Swan-Ganz catheter. The pressure in the pulmonary vessels is above 15-18 cm of water. Art. indicates stagnation. If a Swan-Ganz catheter is not available, central venous pressure (CVP) should be measured. Insertion of a catheter into large veins or into the right atrium allows one to obtain accurate data on the relationship between the condition of the right ventricle and the volume of circulating blood, which makes it possible to regulate the volume of injected fluid. Central venous pressure is above 12-14 mmH2O. Art. indicates some danger in continuing to administer fluids and the risk of developing sudden pulmonary edema. It is very important to ensure that blood flow through the catheter is free and that the catheter is not in the right ventricle. Every patient with septic shock must have either a Swan-Ganz or CVP catheter inserted.

2. Pulse pressure allows you to estimate the stroke volume of the heart.

3. Constriction of cutaneous vessels indicates peripheral vascular resistance, although it does not completely reflect impaired blood flow in the kidneys, brain or intestines.

4. Hourly measurement of the volume of urine excreted allows you to monitor the level of blood flow in the internal organs and the degree of their perfusion. This usually requires the insertion of an indwelling urinary catheter.

The listed indicators sufficiently fully reflect the condition of patients with septic shock and allow for rational treatment. Indirect measurement results blood pressure do not allow an accurate determination of the hemodynamic state, since in this case the perfusion of vital organs may be adequate in patients with hypotension; conversely, some patients whose blood pressure is within normal limits may develop blood stagnation and insufficient blood flow in the vessels of internal organs. Direct blood pressure measurements may be useful, but are not necessary in practice. If possible, these patients should be treated in intensive care units in hospitals where laboratories are equipped to determine arterial blood pH, blood gases, lactate levels, as well as renal function and blood electrolyte levels.

Treatment. Maintaining respiratory function. In many patients with septic shock, the horn of arterial blood is noticeably reduced. In this regard, it is important for them from the very beginning to ensure free breathing and oxygen supply through a nasal catheter, mask or tracheostomy. Ventilation is provided already in the early stages of shock in order to prevent the development of acidosis and hypoxia.

Restoration of circulating blood volume. Focusing on central venous pressure or pressure in the pulmonary vessels, it is necessary to restore the volume of circulating blood by administering blood (for anemia), plasma or other colloidal solutions. For this purpose, it is preferable to use human serum albumin, as well as appropriate solutions of electrolytes, primarily dextrose in isotonic sodium chloride solution and bicarbonate (the latter has an advantage over lactate in the treatment of a patient with acidosis). In most cases, bicarbonate is administered to bring the blood pH to approximately 7.2-7.3, but not higher. The amount of fluid required for treatment can significantly exceed the normal volume of blood and reaches 8-12 liters in just a few hours. Large amounts of fluid may be required even in cases where the cardiac index is within the normal range. In case of hypotension, oliguria is not a contraindication to continued intensive fluid administration. In order to prevent pulmonary edema in cases where the central venous pressure reaches approximately 10-12 cm of water. Art., and the pressure in the pulmonary artery is 16-18 cm of water. Art., furosemide should be administered to increase diuresis.

Treatment with antibiotics. Before starting treatment, cultures of blood and related fluids and exudates should be performed. The drugs should be administered intravenously, and it is advisable to use bactericidal antibiotics. Once the results of blood cultures and sensitivity tests are obtained, one of the appropriate antibiotics recommended for specific infections, reviewed in Chapter 1, should be prescribed. 88. In the absence of data on the pathogen, the basis for initial therapy should be the principle of choosing a drug with the maximum wide range action and effective against infection by the most likely pathogen. Analysis of clinical data can be of great assistance in the initial selection of antimicrobial agents. For example, if a young woman has dysuria, chills, pain in the sides of the abdomen, and septic shock, then her bacteremia is likely caused by Escherichia coli. In a patient with burns, the cause of gram-negative sepsis is probably Pseudomonas aeruginosa bacteria. During influenza epidemics, drugs should be selected based on their effect on Staphylococcus aureus, since it often causes severe bacterial superinfections and pneumonia.

If the etiology of septic shock is not established, treatment with gentamicin (or tobramycin) and cephalosporin or penicillinase-resistant penicillin preparations should be prescribed simultaneously; Many doctors add carbenicillin to these drugs. Due to the toxic effect on the vestibular part of the VIII pair of cranial nerves, gentamicin, tombramycin and other aminoglycosides should be prescribed with caution to patients with oliguria. If a bacteroides infection is suspected, chloramphenicol (chloramphenicol), 7-chlorlincomycin (clindamycin), or carbenicillin can be added to these drugs. Having received the culture results, the necessary amendments are made to the treatment.

Surgical intervention. Many patients with septic shock have abscesses, infarcts or necrosis of the intestine, inflammation of the gallbladder, infection of the uterus, pyonephrosis or other focal inflammatory processes that require surgical drainage or removal. As a rule, to successfully treat a patient with shock, surgical intervention is necessary, even in cases where his condition is extremely severe. Surgery should not be delayed in order to stabilize his condition, since in these cases it continues to worsen until the septic focus is removed or drained.

Vasoactive drugs. Typically, septic shock is accompanied by maximal stimulation of alpha-adrenergic receptors, so pressor agents that act by stimulating them (norepinephrine, levarterinol, and metaraminol) are generally not indicated. For septic shock, two groups of drugs have proven effective: beta-receptor stimulants (especially isoproterenol and dopamine) and alpha-receptor blockers (phenoxybenzamine and phentolamine).

Dopamine hydrochloride is widely used to treat patients with shock. Unlike other vasoactive agents, it increases renal blood flow and glomerular filtration, sodium excretion, and urine output. The effect is observed when low doses of the drug are administered (1-2 mcg/kg per 1 min). At a dose of 2-10 mcg/(kg min) it stimulates the beta receptors of the heart muscle with a subsequent increase in cardiac output, but without increasing heart rate or blood pressure, at a dose of 10-20 mcg/(kg min) it slightly stimulates alpha receptors , followed by an increase in blood pressure. At a dose of more than 20 mcg/(kg min), stimulation of alpha receptors becomes predominant, while the vasoconstrictor effect can neutralize the dopaminergic effect on the vessels of the kidneys and other internal organs. Treatment should begin with a dose of 2-5 mcg/(kg min) with further increases until urine output increases and blood pressure normalizes. In most patients, a dose of 20 mcg/(kg min) or less is effective. Adverse reactions include ectopic arrhythmias, nausea and vomiting, and sometimes tachycardia. They are usually leveled out when the dose of the drug is reduced.

Isoproterenol counteracts spasm of arterial and venous vessels in the microvasculature through a direct vasodilator effect. Along with this, it has a direct inotropic effect on the heart. Cardiac output is increased by stimulating the myocardium and reducing cardiac workload as a result of decreased peripheral vascular resistance. On average, for an adult, the dose of isoproterenol is 2-8 mcg/min. When administered, ventricular arrhythmias may occur, and in cases where the administration of fluid does not correspond to the degree of reduction of vasospasm, signs of shock may increase.

Phenoxybenzamine, an adrenolytic agent, affects central venous pressure by reducing vascular resistance and increasing the efficiency of blood flow. Thus, it causes a redistribution of blood. Its outflow from the lungs increases, pulmonary edema decreases and gas exchange increases, central venous pressure and residual diastolic pressure in the left ventricle decrease, cardiac output increases, and constriction of peripheral venous vessels decreases. The drug is recommended to be administered intravenously at a dose of 0.2-2 mg/kg. Small doses can be administered in a stream, and large doses over 40-60 minutes. At the same time, fluids should be administered in order to compensate for the increased capacity of the venous vessels, otherwise shock will increase. Phenoxybenzamine (not approved by the Food and Drug Administration for this purpose at the time of publication) is not available for clinical use, and experience with phentolamine is insufficient to recommend it for widespread clinical use.

Treatment with diuretics and cardiac glycosides. It is very important to maintain urinary output in order to prevent necrosis of the renal tubules. Once circulating blood volume has been restored, a diuretic should be prescribed, preferably furosemide, so that the amount of hourly urine excreted exceeds 30-40 ml/h. Patients who remain hypotensive despite elevated central venous pressure or pulmonary vascular pressure may benefit from digoxin, but should be administered with caution due to frequent changes in acid-base balance, hyperkalemia, and renal dysfunction in septic shock.

Glucocorticoids. Numerous experimental data support corticosteroid drugs for manifestations of endotoxemia and septic shock. Steroids appear to protect cell membranes from damage caused by endotoxins, prevent the transformation of arachidonic acid into its vasoactive derivatives, and reduce platelet aggregation and the release of enzymes from leukocytes into the extracellular space. Several studies suggest that steroids may also directly reduce peripheral vascular resistance. Due to the complexity of the clinical picture in patients with endotoxic shock, it is quite difficult to prove the unconditional effectiveness of steroid drugs. Some controlled studies have shown the effectiveness of methylprednisolone (30 mg/kg) or dexamethasone (3 mg/kg) when given at the first sign of shock. In case of an extremely serious condition of the patient, the drug was re-administered at the same dose after 4 hours. The results of these studies and the experience of specialists in many centers indicate early administration of large doses of steroids over a relatively short period (24-48 hours). In the later stages of septic shock, steroids are probably ineffective. Long-term treatment with them is associated with serious problems, such as hyperglycemia, gastrointestinal bleeding, etc., and therefore their use should be avoided.

Other treatments. For bleeding, whole blood, fresh frozen plasma, cryoprecipitate, or platelet mass should be transfused, depending on the cause of the bleeding disorder. Naloxone, inhibitors of prostaglandin synthesis, and prostacyclin are at the stage of experimental study. The use of heparin for disseminated intravascular coagulation remains controversial and controversial. Treatment of patients with bacteremia due to gram-negative pathogens with hyperbaric oxygen therapy has not produced any definitive results.

Prognosis and prevention of the disease. The use of these treatment methods ensures at least temporary survival for most patients. Its effectiveness is evidenced by: .1) correction of brain functions and improvement of general condition; 2) reducing the severity of peripheral cyanosis; 3) warming of the skin of the hands and feet; 4) urine volume 40-50 ml/h; 5) increased pulse pressure; 6) normalization of central venous pressure and pressure in the pulmonary artery; 7) increased blood pressure.

However, the final outcome depends on a number of other factors. Firstly, from the possibility of eliminating the source of infection surgically or using antibiotics. The prognosis for urinary tract infections, septic abortion, abdominal abscesses, gastrointestinal or biliary fistulas, as well as subcutaneous or anorectal abscesses is more favorable than for primary lesions localized in the skin or lungs. However, during extensive operations on the abdominal organs, carried out for life-saving reasons. testimony, he is always very serious. Secondly, the outcome depends on past exposure to the pathogen. In patients with chronic urinary tract infection, bacteremia is rarely complicated by shock caused by gram-negative pathogens, possibly because they develop tolerance to the bacterial endotoxin. Thirdly, the underlying disease matters. If a patient with lymphoma or leukemia develops septic shock during an intractable exacerbation of hematologic disease, they rarely survive; conversely, when hematologic remission is achieved, there is a greater likelihood of successful treatment of shock. In patients with pre-existing heart disease and diabetes mellitus, the prognosis for septic shock is also quite unfavorable. Fourth, metabolic status is important. Severe forms of metabolic acidosis and lactic acidemia, regardless of cardiac status, are associated with a poor prognosis. Fifthly, pulmonary insufficiency, despite the normalization of hemodynamic parameters, is also fraught with an unfavorable prognosis.

The overall mortality rate in septic shock remains at 50%, however, as monitoring of the patient's condition improves and his treatment is more physiologically based, the prognosis will become more favorable.

Unsatisfactory treatment results for septic shock are not due to the lack of effective antibiotics or vasoactive drugs. Obviously, the main obstacle to successful treatment is the delay in starting appropriate treatment. Septic shock is usually recognized too late and too often after irreversible changes have occurred. Since 70% of patients at risk of developing septic shock are hospitalized before they show signs of shock, it is important to closely monitor their condition, treat infections vigorously and early, and perform appropriate surgical procedures before catastrophic complications develop. . It is especially important to prevent infection of venous and urinary catheters, which can become entry points for gram-negative pathogens that cause sepsis, and to remove these catheters in all patients as quickly as possible at the first opportunity. There is preliminary evidence that early treatment for septic shock results in a more favorable prognosis. Finally, the protective effect of the antiserum in experimental animals may be used in human treatment.

Sepsis, being a primary medical problem today, continues to be one of the leading causes of mortality, despite various discoveries in the pathogenesis of this disease and the application of new treatment principles. A severe complication of sepsis is septic shock.

Septic shock is a complex pathophysiological process that arises as a result of the action of an extreme factor associated with the breakthrough of pathogens or 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.

Some known mediators of endothelial damage involved in septic reactions are:

tumor necrotizing factor (TNF);
interleukins (IL-1, IL-4, IL-6, IL-8);
platelet activating factor (PAF);
leukotrienes (B4, C4, D4, E4);
thromboxane A2;
prostaglandins (E2, E12);
prostacyclin;
interferon gamma.

Along with the above-mentioned mediators of endothelial damage, many other endogenous and exogenous mediators are involved in the pathogenesis of sepsis and septic shock, which become components of the inflammatory response.

Potential mediators of the septic inflammatory response:

endotoxin;
exotoxin, part of the cell wall of a gram-negative bacterium;
complement, products of arachidonic acid metabolism;
polymorphonuclear leukocytes, monocytes, macrophages, platelets;
histamine, cell adhesion molecules;
coagulation cascade, fibrinolytic system;
toxic oxygen metabolites and other free radicals;
kallikrein-kinin system, catecholamines, stress hormones.

In the pathogenesis of septic shock, the most important link is microcirculation disorders. They are caused not only by vasoconstriction, but also by a significant deterioration in the aggregate state of the blood with a violation of its rheological properties and the development of disseminated intravascular coagulation (DIC) syndrome or thrombohemorrhagic syndrome. Septic shock leads to disorders of all metabolic systems. Carbohydrate, protein and fat metabolism are disrupted, and the utilization of normal energy sources - glucose and fatty acids - is sharply inhibited. In this case, pronounced catabolism of muscle protein occurs. In general, metabolism shifts to the anaerobic pathway.

Thus, the pathogenesis of septic shock is based on deep and progressive disorders of humoral regulation, metabolism, hemodynamics and oxygen transport. The interrelation of these disorders can lead to the formation of a vicious circle with complete depletion of the body’s adaptive capabilities. Preventing the development of this vicious circle is the main goal of intensive care of patients with septic shock.

Clinical picture septic shock

Changes in the functions of vital organs under the influence of damaging factors of septic shock form a dynamic pathological process, the clinical signs of which are revealed in the form of dysfunctions of the central nervous system, pulmonary gas exchange, peripheral and central circulation, and subsequently in the form of organ damage.

The breakthrough of the infection from the source of inflammation or the entry of endotoxin into the bloodstream triggers the primary mechanism of septic shock, in which the pyrogenic effect of the infection and, above all, endotoxin is manifested. Hyperthermia above 38-39 °C and tremendous chills are key signs in the diagnosis of septic shock. Very often, gradually progressive fever of the hectic or irregular type, reaching extreme values and uncharacteristic for a given age (40-41 ° C in elderly patients), as well as polypnea and moderate circulatory disorders, mainly tachycardia (heart rate more than 90 per minute), are considered a reaction for trauma and surgery. Sometimes such symptoms serve as the basis for a diagnosis of local infection. However, this phase of septic shock is called “warm normotension” and is often undiagnosed. When studying central hemodynamics, a hyperdynamic blood circulation regime is determined (CI more than 5 l/min/m2) without impaired oxygen transport (RTC 800 ml/min/m2 or more), which is typical for the early stage of septic shock.

As the process progresses, this clinical phase of septic shock is replaced by a phase of “warm hypotension,” which is characterized by a maximum increase in body temperature, chills, and changes in the patient’s mental state (excitement, anxiety, inappropriate behavior, and sometimes psychosis). When examining the patient, the skin is warm, dry, hyperemic or pink. Breathing disorders are expressed as hyperventilation, which subsequently leads to respiratory alkalosis and fatigue of the respiratory muscles. There is tachycardia up to 120 beats per minute or more, which is combined with good pulse filling and hypotension (Adsist< 100 мм рт.ст.). Гипотензия скорее умеренная и обычно не привлекает внимание врачей. Уже в этой стадии септического шока выявляются признаки неспособности системы кровообращения обеспечить потребность тканей в кислороде и питательных веществах, а также создать возможность детоксикации и удаления токсичных метаболитов. Для того чтобы поддержать адекватность перфузии тканей и избежать анаэробного окисления, больным необходим более высокий уровень DO 2 (15 мл/мин/кг вместо 8-10 мл/мин/кг в норме). Однако в этой стадии септического шока даже повышенный СВ (СИ 4,3-4,6 л/мин/м 2) не обеспечивает должной потребности в кислороде.

Often, hemodynamic and respiratory changes are combined with distinct disturbances in the functioning of the digestive tract: dyspeptic disorders, pain (especially in the upper abdomen), diarrhea, which can be explained by the peculiarities of serotonin metabolism, initial changes in blood flow in the area of the celiac vessels and activation of the central mechanisms of nausea and vomiting. In this phase of septic shock, there is a decrease in diuresis, sometimes reaching the level of oliguria (urine output less than 25 ml/h).

The clinical picture of the late stage of septic shock is characterized by disturbances of consciousness, severe disorders of pulmonary gas exchange, peripheral and central circulatory failure, organ pathology with signs of liver and kidney failure. The external manifestations of this stage of septic shock are called “cold hypotension.” When examining the patient, attention is drawn to a darkening of consciousness, up to the development of a coma; pale skin; acrocyanosis, sometimes significant; Oligoanuria. Severe tachypnea (more than 40 breaths per minute) is combined with a feeling of lack of air, which does not decrease even with oxygen therapy; Inhalation usually involves accessory muscles.

Chills and hyperthermia are replaced by a decrease in body temperature, often with its critical drop to subnormal numbers. The skin temperature of the distal extremities, even to the touch, is significantly lower than normal. A decrease in body temperature is combined with a distinct vegetative reaction in the form of heavy sweats. Cold, pale cyanotic, wet hands and feet are one of the pathognomonic symptoms of the unfavorable course of a generalized infection. At the same time, relative signs of a decrease in venous return are revealed in the form of desolation of the peripheral venous subcutaneous network. Frequent, 130-160 per minute, weak filling, sometimes arrhythmic, pulse is combined with a critical decrease in systemic blood pressure, often with a small pulse amplitude.

The earliest and clearest sign of organ damage is progressive renal dysfunction with severe symptoms such as azotemia and increasing oligoanuria (diuresis less than 10 ml/h).

Lesions of the gastrointestinal tract manifest themselves in the form of dynamic intestinal obstruction and gastrointestinal bleeding, which can prevail in the clinical picture of septic shock even in cases where it is not of peritoneal origin. Liver damage is characterized by the appearance of jaundice and hyperbilirubinemia.

It is generally accepted that the supply of oxygen to the body is quite adequate when the hemoglobin concentration is >100 g/l, SaO 2 > 90% and SI>2.2 l/min/m2. However, in patients with pronounced redistribution of peripheral blood flow and peripheral shunting, oxygen supply, even with these indicators, may be inadequate, resulting in hypoxia with a high oxygen debt, which is characteristic of the hypodynamic stage of septic shock. High oxygen consumption by tissues in combination with low transport of the latter indicates the possibility of an unfavorable outcome, while increased oxygen consumption in combination with an increase in its transport is a sign favorable for almost all types of shock.

Most clinicians believe that the main objective diagnostic criteria for sepsis are changes in peripheral blood and metabolic disorders.

Most characteristic changes blood: leukocytosis (12 x 10 9 /l) with a neutrophilic shift, a sharp “rejuvenation” of the leukocyte formula and toxic granularity of leukocytes. At the same time, one should remember the nonspecificity of disorders of certain peripheral blood parameters, their dependence on circulatory homeostasis, the constantly changing clinical picture of the disease and the influence of therapeutic factors. It is generally accepted that characteristic objective criteria for septic shock may be leukocytosis with an increase in the leukocyte index of intoxication (LII>10) and thrombocytopenia. Sometimes the dynamics of the leukocyte reaction has a wave-like character: the initial leukocytosis is replaced by leukopenia, coinciding with mental and dyspeptic disorders, the appearance of polypnea, and then a rapid increase in leukocytosis is observed again. But even in these cases, the value of LII progressively increases. This indicator is calculated using the formula [Kalf-Kalif Ya.Ya., 1943]:

where C - segmented neutrophils, P - band neutrophils, Yu - young, Mi - myelocytes, Pl - plasma cells, Mo - monocytes. Li - lymphocytes, E - eosinophils.

The normal value of the index fluctuates around 1. An increase in LII to 4-9 indicates a significant bacterial component of endogenous intoxication, while a moderate increase in the index to 2-3 indicates a limitation of the infectious process or predominant tissue breakdown. Leukopenia with high LII is always an alarming symptom of septic shock.

In the late stage of septic shock with hematological studies As a rule, moderate anemia (Hb 90-100 g/l), hyperleukocytosis up to 40×10 9 /l and higher with a maximum increase in LII to 20 or more are detected. Sometimes the number of eosinophils increases, which reduces LII, despite a clear shift in the leukocyte formula towards immature forms of neutrophils. Leukopenia with the absence of neutrophilic shift may be observed. When assessing the leukocyte reaction, it is necessary to pay attention to the decrease in the absolute concentration of lymphocytes, which can be 10 times or more below the normal value.

Among the data of standard laboratory monitoring, indicators characterizing the state of metabolic homeostasis deserve attention. The most common diagnosis of metabolic disorders is based on monitoring changes in CBS, blood gases and assessing the concentration of lactate in the blood. As a rule, the nature and form of CBS disorders, as well as the level of lactate, depend on the severity and stage of development of shock. There is a fairly pronounced correlation between the concentrations of lactate and endotoxin in the blood, especially in septic shock.

When examining blood CBS in the early stages of septic shock, compensated or subcompensated metabolic acidosis is often determined against the background of hypocapnia and high level lactate, the concentration of which reaches 1.5-2 mmol/l or more. In the early stage of septicemia, temporary respiratory alkalosis is most characteristic. Some patients experience metabolic alkalosis. In the later stages of development of septic shock, metabolic acidosis becomes uncompensated and, due to base deficiency, often exceeds 10 mmol/l. The level of lactate acidemia reaches 3-4 mmol/l or more and is a criterion for the reversibility of septic shock. As a rule, a significant decrease in PaO 2, SaO 2 and, consequently, a decrease in the oxygen capacity of the blood is determined. It should be emphasized that the severity of acidosis largely correlates with the prognosis.

In the diagnosis and treatment of septic shock, it is becoming more and more necessary to dynamically determine indicators of central hemodynamics (MOS, SV, SI, OPSS, etc.) and oxygen transport (a-V - difference in oxygen, CaO 2, PaO 2, SaO 2), which allow you to assess and determine the stage of shock and the body’s compensatory reserves. SI in combination with other factors characterizing the characteristics of oxygen transport in the body and tissue metabolism serve as criteria not only for the effectiveness of oxygen supply, but also for guidance in the prognosis of septic shock and the choice of the main direction of intensive therapy for circulatory disorders with outwardly identical manifestations of this pathological process - hypotension and low rate of diuresis.

Except functional research, diagnosis includes identifying etiological factor- identification of the pathogen and study of its sensitivity to antibacterial drugs. Conduct bacteriological examination blood, urine, wound exudate, etc. Biological tests are used to examine the severity of endotoxemia. Clinics diagnose immune deficiency based on general tests: T- and B-lymphocytes, blast transformation, level of immunoglobulins in the blood serum.

Diagnostic criteria for septic shock:

the presence of hyperthermia (body temperature >38-39 °C) and chills. In elderly patients, paradoxical hypothermia (body temperature<36 °С);
neuropsychiatric disorders (disorientation, euphoria, agitation, stupor);
hyper- or hypodynamic circulatory disorder syndrome. Clinical manifestations: tachycardia (heart rate = 100-120 per minute), Adsist< 90 мм рт.ст. или его снижение на 40 мм рт.ст. и более от среднего в отсутствие других причин гипотензии;
microcirculation disorders (cold, pale, sometimes slightly or intensely jaundiced skin);
tachypnea and hypoxemia (heart rate>20 per minute or PaCO 2<32 мм рт.ст., акроцианоз);
oligoanuria, urine output - less than 30 ml/h (or the need to use diuretics to maintain sufficient diuresis);
vomiting, diarrhea;
leukocyte count >12.0 10 9 /l, 4.0 10 9 /l or immature forms >10%, LII >9-10;
lactate level >2 mmol/l.

Some clinicians identify a triad of symptoms that serve as the prodrome of septic shock: disturbance of consciousness (change in behavior and disorientation); hyperventilation, determined by eye, and presence of a focus of infection in organism.

IN last years finds wide application scoring scale for organ failure associated with sepsis and shock (SOFA scale - Sepsis-related Organ Failure Assessment) (Table 17.1). It is believed that this scale, adopted by the European Society of Intensive Care, is objective, accessible and easy to assess the dysfunction of organs and systems during the progression and development of septic shock.

Table 17.1.

ScaleSOFA

Grade	Index	1	2	3	4
Oxygenation	PaO2/FiO2,	<400	<300	<200	<100
Coagulation	Platelets	<150 10 9 /л	<100 10 9 /л	<50 10 9 /л	<20 10 9 /л
Liver	Bilirubin,	1,2-1,9	2,0-5,9	6,0-11,9 (102-204)	>12
Cardiovascular system	Hypotension or degree of inotropic support	GARDEN<70 мм рт.ст.	Dopamine < 5 or dobuta-min (any dose)	Dopamine >5* or adrenaline<0,1* или норадре-налин < 0,1*	Dopamine >15* or adrenaline >0.1* norepinephrine >0.1*
CNS	Glasgow Coma Scale score, in points	13-14	10-12	6-9	<6
Kidneys	Creatinine, mg/dl, µmol/l. Possible oliguria	1,2-1,9 (110-170)	2,0-3,4 (171-299)	3.5-4.9 (300-440) or<500 мл мочи/сут	> 5,0 (>440) or<200 мл мочи/сут

Dose of cardiotonics in mg per 1 kg of body weight per 1 min for at least

The dysfunction of each organ (system) is assessed separately, dynamically, daily, against the background of intensive therapy.

Treatment.

The complexity of the pathogenesis of septic shock determines a multicomponent approach to its intensive therapy, since treatment of failure of only one organ is unrealistic. Only with an integrated approach to treatment can one hope for relative success.

Intensive treatment should be carried out in three fundamental directions. First in terms of time and significance - reliable elimination of the main etiological factor or disease that started and maintains the pathological process. If the source of infection is not eliminated, any modern therapy will be ineffective. Second - Treatment of septic shock is impossible without correction of disorders common to most critical conditions: hemodynamics, gas exchange, hemorheological disorders, hemocoagulation, water-electrolyte shifts, metabolic insufficiency, etc. Third - direct impact on the function of the affected organ, up to temporary prosthetics, should begin early, before the development of irreversible changes.

Antibacterial therapy, immunocorrection and adequate surgical treatment of septic shock are important in the fight against infection. Early treatment with antibiotics should be initiated before culture is isolated and identified. This is of particular importance in patients with compromised immunity, where a delay in treatment of more than 24 hours may result in an unfavorable outcome. For septic shock, immediate use of broad-spectrum parenteral antibiotics is recommended. The choice of antibiotics is usually determined by the following factors: the likely pathogen and its sensitivity to antibiotics; underlying disease; patient's immune status and pharmacokinetics of antibiotics. As a rule, a combination of antibiotics is used, which ensures their high activity against a wide range of microorganisms before the results of microbiological testing become known. Combinations of 3-4th generation cephalosporins (Longacef, Rocephin, etc.) with aminoglycosides (gentamicin or amikacin) are often used. The dose of gentamicin for parenteral administration is 5 mg/kg/day, amikacin - 10-15 mg/kg body weight. Longacef has a long half-life, so it can be used once a day up to 4 g, Rocephin - up to 2 g once a day. Antibiotics that have a short half-life must be prescribed in large daily doses. Claforan (150-200 mg/kg/day), ceftazidime (up to 6 g/day) and cephalosporin (160 mg/kg/day) are widely used. When treating patients with a septic focus within the abdominal cavity or pelvis, you can resort to a combination of gentamicin and ampicillin (50 mg/kg per day) or lincomycin. If a gram-positive infection is suspected, vancomycin (vancocin) up to 2 g/day is often used. When determining sensitivity to antibiotics, therapy may be changed. In cases where it was possible to identify the microflora, the choice of antimicrobial drug becomes straightforward. It is possible to use monotherapy with antibiotics that have a narrow spectrum of action.

In some cases, along with antibiotics, powerful antiseptics can be included in the antibacterial combination of drugs: dioxidin up to 0.7 g/day, metronidazole (Flagyl) up to 1.5 g/day, solafur (Furagin) up to 0.3-0.5 g/day Such combinations are preferably used in cases where it is difficult to expect sufficient effectiveness from conventional antibiotics, for example, with previous long-term antibiotic therapy.

An important link in the treatment of septic shock is the use of drugs that enhance the body’s immune properties. Patients are administered gamma globulin or polyglobulin, specific antitoxic serums (antistaphylococcal, antipseudomonas).

Powerful intensive therapy will not be successful unless the infection is eliminated surgically. Emergency surgery can be essential at any stage. Drainage and removal of the source of inflammation are required. Surgical intervention should be low-traumatic, simple and reliable enough to ensure the initial and subsequent removal of microorganisms, toxins and tissue decay products from the lesion. It is necessary to constantly monitor the appearance of new metastatic foci and eliminate them.

In the interests of optimal correction of homeostasis, the clinician must simultaneously provide correction of various pathological changes. It is believed that for an adequate level of oxygen consumption it is necessary to maintain an SI of at least 4.5 l/min/m2, while the DO2 level must be more than 550 ml/min/m2. Tissue perfusion pressure can be considered restored provided that the average blood pressure is at least 80 mm Hg, and the peripheral vascular resistance is about 1200 dynes s/(cm 5 m2). At the same time, it is necessary to avoid excessive vasoconstriction, which inevitably leads to decreased tissue perfusion.

Carrying out therapy that corrects hypotension and maintains blood circulation is very important in septic shock, since circulatory disorders are one of the leading symptoms of shock. The first remedy in this situation is to restore adequate vascular volume. At the beginning of therapy, fluid can be administered intravenously at the rate of 7 ml/kg body weight over 20-30 minutes. Improvement in hemodynamics is observed as normal ventricular filling pressure and mean blood pressure are restored. It is necessary to transfuse colloidal solutions, as they more effectively restore both volume and oncotic pressure.

The use of hypertonic solutions is of undoubted interest, since they are able to quickly restore plasma volume by extracting it from the interstitium. Restoring intravascular volume with crystalloids alone requires an increase in infusion by 2-3 times. At the same time, given the porosity of the capillaries, excessive hydration of the interstitial space contributes to the formation of pulmonary edema. Blood is transfused in such a way as to maintain the hemoglobin level within 100-120 g/l or hematocrit 30-35%. The total volume of infusion therapy is 30-45 ml/kg body weight, taking into account clinical (SBP, CVP, diuresis) and laboratory parameters.

Adequate fluid replenishment is critical to improving oxygen delivery to tissues. This indicator can be easily changed by optimizing CO and hemoglobin levels. When carrying out infusion therapy, diuresis should be at least 50 ml/h. If, after replenishing the fluid volume, the pressure continues to remain low, dopamine at a dose of 10-15 mcg/kg/min or dobutamine at a dose of 0.5-5 mcg/(kg-min) is used to increase CO. If hypotension persists, correction can be carried out with adrenaline at a dose of 0.1-1 mcg/kg/min. The adrenergic vasopressor effect of epinephrine may be required in patients with persistent hypotension on dopamine or in those who respond only to high dosages. Due to the risk of deterioration in oxygen transport and consumption, adrenaline can be combined with vasodilators (nitroglycerin 0.5-20 mcg/kg/min, nanipruss 0.5-10 mcg/kg/min). Potent vasoconstrictors, such as norepinephrine 1 to 5 mcg/kg/min or dopamine greater than 20 mcg/kg/min, should be used to treat the severe vasodilation seen in septic shock.

Vasoconstrictors can have harmful effects and should be used to restore peripheral vascular resistance to normal limits of 1100-1200 dynes s/cm 5 m 2 only after optimizing the volume of blood volume. Digoxin, glucagon, calcium, calcium channel antagonists should be used strictly individually.

Respiratory therapy is indicated for patients with septic shock. Breathing support eases the load on the DO 2 system and reduces the oxygen cost of breathing. Gas exchange improves with good blood oxygenation, so oxygen therapy, ensuring airway patency and improving the drainage function of the tracheobronchial tree are always required. It is necessary to maintain PaOz at a level of at least 60 mm Hg, and hemoglobin saturation at least 90%. The choice of treatment method for acute respiratory failure in septic shock depends on the degree of disturbance of gas exchange in the lungs, the mechanisms of its development and signs of excessive load on the respiratory apparatus. When respiratory failure progresses, the method of choice is mechanical ventilation in the PEEP mode.

Particular attention in the treatment of septic shock is given to improving hemocirculation and optimizing microcirculation. For this purpose, rheological infusion media are used (reopolyglucin, plasmasteril, HAES-steril, reogluman), as well as chimes, complamin, trental, etc.

Metabolic acidosis can be corrected if the pH is below 7.2. however, this position remains controversial, since sodium bicarbonate can aggravate acidosis (shift of EDV to the left, ion asymmetry, etc.).

During intensive therapy, coagulation disorders must be eliminated, since septic shock is always accompanied by disseminated intravascular coagulation syndrome.

The most promising therapeutic measures appear to be those

aimed at the starting, initial, cascades of septic shock. It is advisable to use antioxidants (tocopherol, ubiquinone) as protectors of damage to cellular structures, and to inhibit blood proteases - antienzyme drugs (gordox - 300,000-500,000 units, contrical - 80,000-150,000 units, trasylol - 125,000-200,000 units ). It is also necessary to use drugs that weaken the effect of humoral factors of septic shock - antihistamines (suprastin, tavegil) in the maximum dose.

The use of glucocorticoids in septic shock is one of the controversial issues in the treatment of this condition. Many researchers believe that it is necessary to prescribe large doses of corticosteroids, but only once. In each case, an individual approach is required, taking into account the patient’s immunological status, the stage of shock and the severity of the condition. We believe that the use of steroids with high potency and duration of action, which have less pronounced side effects, may be justified. These drugs include the corticosteroids dexamethasone and betamethasone.

In conditions of infusion therapy, along with the task of maintaining water-electrolyte balance, issues of energy and plastic supply must be resolved. Energy nutrition should be at least 200-300 g of glucose (with insulin) per day. The total calorie content of parenteral nutrition is 40-50 kcal/kg body weight per day. Multicomponent parenteral nutrition can be started only after the patient has recovered from septic shock.

K. Martin et al. (1992) developed a scheme for hemodynamic correction in septic shock, which provides effective therapy for circulatory and oxygen transport disorders and can be used in practice.

Rational correction of hemodynamics.

The following fundamental therapeutic tasks must be completed within 24-48 hours.

Necessarily:

SI not less than 4.5 l/(min-m 2);
level DO 2 not less than 500 ml/(min-m2);
average blood pressure is at least 80 mm Hg;
OPSS within 1100-1200 dyne-sDcm^m 2).

If possible:

oxygen consumption level of at least 150 ml/(min-m2);
diuresis not less than 0.7 ml/(kg/h).

This requires:

1) replenish the blood volume to normal values, ensure Pa02 in arterial blood is at least 60 mm Hg, saturation is at least 90%, and the hemoglobin level is 100-120 g/l;

2) if CI is at least 4.5 l/(min-m2), you can limit yourself to monotherapy with norepinephrine at a dose of 0.5-5 mcg/kg/min. If the SI level is below 4.5 l/(min-m2), additional dobutamine is administered;

3) if CI is initially less than 4.5 l/(min-m2), it is necessary to start treatment with dobutamine at a dose of 0.5-5 mcg/(kg-min). Norepinephrine is added when mean blood pressure remains less than 80 mm Hg;

4) in doubtful situations, it is advisable to start with norepinephrine, and, if necessary, supplement therapy with dobutamine;

5) epinephrine, isoproterenol, or inodilators can be combined with dobutamine to control CO levels; to correct BPSS, dopamin or adrenaline can be combined with norepinephrine;

6) in the case of oliguria, use furosemide or small doses of dopamine (1-3 mcg/kg-min);

7) every 4-6 hours it is necessary to monitor the parameters of oxygen transport, as well as adjust treatment in accordance with the final goals of therapy;

8) withdrawal of vascular support can begin after 24-36 hours of stabilization. In some cases, it may take several days for complete withdrawal of vascular agents, especially norepinephrine. In the first days, the patient, in addition to the daily physiological requirement, should receive 1000-1500 ml of fluid as compensation for the vasodilation that occurs after discontinuation of α-agonists.

Thus, septic shock is a rather complex pathophysiological process that requires a mental rather than a formulaic approach in both diagnosis and treatment. The complexity and interconnectedness of pathological processes, the variety of mediators in septic shock create many problems in choosing adequate therapy for this formidable complication of many diseases.

Submitted by J. Gomez et al. (1995), mortality in septic shock. despite rational intensive therapy, it is 40-80 %.

The emergence of promising immunotherapy and diagnostic methods opens up new treatment options that improve the outcome of septic shock. Encouraging results were obtained using monoclonal antibodies to the endotoxin core and to tumor necrosis factor.

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: 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
Organ or system
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: 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, x-ray 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 lungs)

– 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 average

– 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 norms

– 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 total bilirubin in blood plasma >70 µmol/l (4 mg/dl)

– paralytic intestinal obstruction(peristalsis is not 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 a few hours after the onset of severe sepsis], hemostasis studies, renal and liver function tests), as well as the intensity 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 sepsis was suspected, but infection was later 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 expected etiology - material from the respiratory tract, urine, etc. biological fluids(eg, cerebrospinal fluid, pleural fluid), smears or wound discharge.

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 (typically 4% or 5%) in addition to crystalloid transfusions is recommended. initial period and during further therapy with solutions in patients requiring transfusion of large volumes of crystalloids.

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. Coming out pathophysiological aspects NaHCO3 can be prescribed IV 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 action 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/mm3 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.

According to a number of domestic pathophysiologists and clinicians (Kostyuchenko A.L. et al., 2000), the development of septic shock is determined by the virulence of the pathogen, the reactivity of the patient’s body, the factors triggering the shock (entry gates of infection and the duration of action of these gates). It is important that bacteremia can occur with or without sepsis. That is, bacteremia ceases to be an obligate sign of sepsis.

In surgical patients, septic shock most often occurs when bacterial infections. According to the literature, until the 50s, the main causative agent of sepsis was streptococcus, later staphylococcus became the predominant causative agent, and recently the frequency of gram-negative sepsis and the role of opportunistic flora have increased.

The type of microbe, its pathogenicity, toxicity and other biological properties largely determine the clinical course of sepsis. Blood cultures are sterile in approximately 50% of patients with septic syndrome. In a certain percentage of patients who died with a typical clinical picture of septic shock, purulent metastases are not detected at autopsy. Thus, bacterial shock serves as a manifestation of the general resorptive effect of toxins.

Modified body reactivity is considered one of the most significant conditions for the development of septic shock. In the figurative expression of A.P. Zilber (), appropriate conditions are necessary so that E. coli - one of the most common causative agents of septic shock syndrome, living in collaboration with humans, participating in microbial hydrolysis of protein, producing B vitamins, fighting with typhoid, dysentery and putrefactive microbes, suddenly begins to kill its owner.

The age of the patient is essential. With the exception of postoperative complications in obstetrics and neonatology, postoperative septic shock most often develops in patients over 50 years of age.

Debilitating diseases accompanying surgical pathology (blood diseases, cancer pathology, systemic diseases), as well as hormonal conditions, are of significant importance in reducing the activity of protective mechanisms. When assessing the condition of a patient with suspected septic shock, it should be taken into account that it can be initially changed by immunosuppressants, radiation therapy, vitamin deficiencies, chronic intoxications (drug addiction, alcoholism).

Primary purulent focus (or entry point for infection) and the duration of action of these gates are an obligatory factor relevant to the triggering mechanism of septic shock.

The primary purulent foci in sepsis are most often acute purulent surgical diseases (carbuncles, mastitis, abscesses, cellulitis, etc.) or purulent wounds, both post-traumatic and postoperative. Sepsis, which occurs as a result of local purulent processes and purulent wounds, has been known for a long time. Sepsis as a complication of various major operations, resuscitation and invasive diagnostic procedures, that is, nosocomial (or iatrogenic) sepsis, is growing with the expansion of the volume and complexity of surgical interventions and modern medical procedures and has recently been called the “disease of medical progress.”

The existing opinion about the possibility of so-called primary, or cryptogenic, sepsis is apparently erroneous and is a consequence of imperfect knowledge and diagnosis. The diagnosis of cryptogenic sepsis takes the doctor away from searching for the primary focus and, therefore, makes it difficult to make the correct diagnosis and carry out full treatment.

The entrance gate for infection is, as a rule, a determinant of the clinical form of postoperative septic shock. In general, one of the first places is occupied by the urodynamic form of septic shock. Very often in the surgical clinic the peritoneal form of septic shock is encountered, and the next most common place of entry for infection in postoperative septic shock is the biliary tract (biliary form). The development of antibiotic-associated pseudomembranous colitis with the appearance of diarrheal syndrome of varying severity at the first stage can be considered as an intestinal variant of postoperative sepsis. Fatty tissue can become the entrance gate, especially in cases where purulent inflammation occurs with the phenomena of progressive cellulite of the perinephric, retroperitoneal, and intermuscular tissue. Unusual routes of infection are becoming increasingly important in intensive care practice: during prolonged tracheal intubation and tracheostomy, during catheterization of central vessels. Therefore, the vascular, or angiogenic, form of septic shock can occur not only as a consequence of purulent thrombophlebitis, complicating the course of the wound process, but as an independent complication.

A shockogenic factor can be the immediate lysis of microorganisms contained in the lesion and circulating in the blood under the influence of an effective bactericidal drug in a high dose (Helzheimer-Jarisch reaction).

Pathogenesis of septic shock

Sepsis is characterized by massive endothelial damage caused by persistent inflammation due to infectious or non-infectious causes. Severe bacterial infection or septic shock is associated with the appearance in the circulation of both cytokines (TNF-a, IL-1, IL-6, IL-8, IL-10) and their antagonists (IL-1 RA, TNF-RtI and TNF -RtII), as well as complements (C3a, C5a), metabolites (leukotrienes, prostaglandins), oxygen radicals (O superoxides, etc.), - kinins (bradykinin), granulocyte proteases, collagenases, etc.

In septic shock, as in sepsis, there is a release of hydralase into the blood, not only from lysosomes of the tissues of the liver, spleen, and lungs, but also from polymorphonuclear leukocytes (PMNL). At the same time, during the septic process, the activity of natural antiproteases decreases. As a result, the overall proteolytic activity of the blood increases according to the severity of the systemic inflammatory reaction.

As septic shock develops, mechanisms are activated to compensate for the effect of systemic vasodilation. This can be attributed to the action of catecholamines, angiotensin, and adrenal hormones. But the reserves of these compensatory reactions are not programmed for such a pathophysiological situation as septic shock.

As septic shock progresses, the potential of vasodilators exceeds the potential of vasoconstrictors. In different vascular zones, this effect is expressed differently, which determines, to a certain extent, the clinical and morphological manifestations of organ pathology.

Clinical picture of septic shock

In the development of septic shock (SS), an initial (often very short-term) “hot” period (or hyperdynamic phase) and a subsequent, longer, “cold” period (hypodynamic phase) are distinguished.

In case of SS, signs of damage to vital support organs are always revealed. Damage to 2 or more organs is classified as multiple organ failure syndrome.

The degree of central nervous system dysfunction can vary from moderate stupor to deep coma. Approximately 1 in 4 patients with septic syndrome develops adult respiratory distress syndrome (ARDS) as a result of damage to the endothelium of the pulmonary capillaries by activated neutrophils. Clinically, the danger of acute lung injury is manifested by an increase in shortness of breath, a change in respiratory sounds, the appearance of scattered moist rales, and an increase in arterial hypoxemia. The earliest and clearest sign of organ dysfunction typical of septic shock is impaired renal function, which is determined by the increase in oliguria, progression of azotemia and other symptoms of acute renal failure. For the liver, organ damage is characterized by a rapid increase in bilirubinemia, a rapid increase in the activity of liver transaminases and other markers of cellular liver failure in the blood. In the gastrointestinal tract, the damaging effect of the mediator explosion manifests itself in the form of dynamic intestinal obstruction and diapedetic gastric and intestinal bleeding. The systolic and diastolic functions of the ventricles of the heart are depressed and progressively worsen, a decrease in cardiac output occurs, which marks the beginning of the decompensated phase of septic shock.

Diagnosis of septic shock.

The assumption of the possibility of SS requires an immediate transition to intensive monitoring of such a patient in an ICU. Standard monitoring should include:

Dynamic determination of blood pressure, heart rate, stroke volume and blood volume, central venous pressure level; determination of hourly diuresis;

Dynamics of pulse oximeter indicators; dynamic study of gas tension and CBS of arterial and mixed venous blood;

Dynamics of body T (with determination of the gradient between the internal and peripheral T of the patient’s body);

Dynamics of reference biochemical parameters (protein, urea, creatinine, coagulogram, glucose, liver transaminases, etc.);

Blood cultures for sterility.

Diagnosis of SS should include determination of the etiological factor - isolation of pathogens and determination of their sensitivity to antibacterial drugs.

Pathogenetic criteria for the differential diagnosis of septic shock include the determination of surrogate markers of the septic process: C-reactive protein, phospholipase A2, procalcitonin (PCT). Determining the level of PCT in plasma is important specifically in patients with sepsis with an outcome in septic shock, since its level increases tens of times in SS compared to a clearly significant increase in septic processes. To correct SS therapy, reliable laboratory criteria for the state of the lipid peroxidation system and the body's antioxidant defense are also required.

Treatment of septic shock.

Therapeutic measures for septic shock pursue the following main goals: correction of hemodynamic disorders with stabilization of the body's oxygen regime, eradication of infection and relief of organ dysfunctions, including their replacement.

Stabilization of hemodynamics is achieved primarily by an adequate volume load: rapid infusion of 1-2 liters of crystalloid solutions with consolidation of the effect by colloid solutions (in a ratio of 2:1) under the control of hemodynamic monitoring (BP, CVP, CO) and the rate of diuresis. Inotropic support is of decisive importance in stabilizing hemodynamics, ensuring relief of hemodynamic disturbances and maintaining an adequate level of tissue perfusion. The first choice for inotropic support against the background of SS is dopamine, used either in small doses - 1-4 mcg/kg min (increases blood flow in the kidneys, mesecterial, cerebral and coronary vessels), or in medium doses - 5-10 mcg/kg min (mycocardial).

To reduce the damaging effects of tissue hypoxia, antihypoxants are used: blood substitutes based on fumarate (mafusol) and succinate (reamberene), regulatory antihypoxants (cytochrome C, mildronate).

Eradication of infection and sanitation of circulating blood from the pathogen is the main pathogenetic direction of therapy for SS. And the main therapeutic measures in this direction are drainage of the septic focus and adequate antimicrobial therapy. In accordance with the standards of treatment for a patient with surgical sepsis, the scope of surgical intervention should include the most complete necrectomy, adequate drainage with double-lumen tubes. Sanitation of a septic focus should be urgent and the basis of surgical participation should not be the position - “the patient is too sick to intervene,” but, on the contrary, “the patient is too sick to postpone intervention...”. Any intensive therapy for SS may become ineffective precisely because of the presence of undiagnosed or poorly operated foci of wound infection.

The first choice drugs for bacterial SS are carbapenems - meronem or tienam. Given the widest possible spectrum of antibacterial activity of these drugs and significant resistance to β-lactamases. The initial dose of carbopenem should be maximum (1-2 g) and administered intravenously as a microbolus (for meronem) or drip over 60 minutes (for tienam). Subsequent administrations are determined by the preservation of renal function and are 5000-1000 mg every 8 hours.

Clinical criteria for the optimal effectiveness of SS therapy should be considered:

Improving the consciousness and general appearance of the patient;

Disappearance of peripheral cyanosis and pinkness of the skin, warming of the hands and feet with a decrease in the temperature gradient to 4-5 C;

Decrease in shortness of breath and increase in PaO2 at a stable level;

Decrease in heart rate, normalization of systemic blood pressure and central venous pressure with restoration of IOC and SV;

Increased rate of diuresis.

The determinant of exit from SS is considered to be the reaction of the patient’s vital functions to the treatment.

EPIDEMIOLOGY

PREVENTION

SCREENING

CLASSIFICATION

BACTEREMIA AND SEPSIS

ETIOLOGY

PATHOGENESIS

CLINICAL PICTURE

DIAGNOSTICS

ANAMNESIS

PHYSICAL INVESTIGATION

LABORATORY RESEARCH

INSTRUMENTAL RESEARCH

DIFFERENTIAL DIAGNOSTICS

INDICATIONS FOR CONSULTATION WITH OTHER SPECIALISTS

EXAMPLE OF FORMULATION OF DIAGNOSIS

TREATMENT

ANTIBACTERIAL THERAPY

HEMODYNAMIC SUPPORT

NUTRITIONAL SUPPORT

GLYCEMIC CONTROL

GLUCOCORTICOIDS

ACTIVATED PROTEIN C

IMMUNOGLOBULIN INFUSION

PREVENTION OF DEEP VEIN THROMBOSIS

PREVENTION OF STRESS IN THE GASTROINTESTINAL TRACT

RENAL REPLACEMENT THERAPY

FORECAST

Some known mediators of endothelial damage involved in septic reactions are:

Potential mediators of the septic inflammatory response:

Clinical picture septic shock

Diagnostic criteria for septic shock:

ScaleSOFA

Treatment.

Rational correction of hemodynamics.

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