At an early stage of septic shock is observed. Septic shock: when there are still chances to "fan" the spark of life. Diagnostic criteria for septic shock

Sepsis is a pathological process, which is based on the reaction of the body in the form of a generalized (systemic)
inflammation for an infection of various nature (bacterial, viral, fungal).

Synonyms: septicemia, septicopyemia.

Software code ICD10
The usefulness of the etiological principle underlying the classification of sepsis in ICD10, from the standpoint of modern knowledge and actual clinical practice, seems to be limited. Orientation to bacteremia as the main diagnostic sign with low excretion of the pathogen from the blood, as well as the significant duration and laboriousness of traditional microbiological studies, make it impossible to widely practical use of the etiological classification (Table 31-1).

Table 31-1. Classification of sepsis according to ICD-10

EPIDEMIOLOGY

There are no domestic data. It is estimated that over 700,000 cases of severe sepsis are diagnosed annually. about 2000 cases daily. Septic shock develops in 58% of cases of severe sepsis.

At the same time, sepsis served as the main cause of death in non-coronary intensive care units and occupied 11th place 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).

In the course of a multicenter epidemiological cohort prospective study, which included 14 364 patients, 28 intensive care units and intensive care units in Europe, Israel and Canada, it was found that patients with sepsis accounted for 17.4% of cases (sepsis, severe sepsis, septic shock) from all patients who underwent through an intensive stage of treatment; while in 63.2% of cases it became a complication of hospital infections.

PREVENTION

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

SCREENING

A screening method of diagnosis in a patient with a local focus of infection can be considered the criteria for systemic inflammatory response syndrome (see Classification).

CLASSIFICATION

The current classification of sepsis is based on the diagnostic criteria and classifications proposed by the American College of Pulmonary and Society of Critical Medicine (ACCP / SCCM) consensus conferences. The issues of terminology and classification of sepsis were reviewed 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 effects of various strong irritants (infection, injury, surgery and etc.)	It is characterized by two or more of the following: temperature ≥38 ° C or ≤36 ° C Heart rate ≥90 per minute RR\u003e 20 per minute or hyperventilation (PaCO2 ≤32 mm Hg) blood leukocytes\u003e 12 or<4x109/мл, или количество незрелых forms\u003e 10%
Sepsis is a syndrome of a 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, which is not eliminated by fluid therapy and requires the appointment 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 of the same chain in the body's response to inflammation due to microbial infection. Severe sepsis and septic (synonym - infectious-toxic) shock constitute an essential part of the systemic inflammatory response of the body to infection and are the result of the progression of systemic inflammation with the development of dysfunctions of systems and organs.

BACTERIA AND SEPSIS

Bacteremia (the presence of infection in the systemic circulation) is one of the possible, but not required 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 the technique of blood sampling and the use of modern technologies for the determination of microorganisms in the most severe patients, the frequency of positive results, as a rule, does not exceed 45%. The detection of microorganisms in the bloodstream without clinical and laboratory evidence of systemic inflammation syndrome should be regarded as transient bacteremia. The clinical significance of bacteremia may be as follows:

confirmation of the diagnosis and determination of the etiology of the infectious process;
evidence of a mechanism for the development of sepsis (eg, catheter-associated infection);
justification of the choice of antibiotic therapy regimen;
evaluating the effectiveness of therapy.

The role of the polymerase chain reaction in the diagnosis of bacteremia and the interpretation of the results obtained 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 there is a high likelihood of an infectious process.

ETIOLOGY

Today, most large medical centers the frequency of gram-positive and gram-negative sepsis was approximately equal. Sepsis caused by fungal flora such as Candida has ceased to be an exception. The risk of its occurrence is significantly increased in patients with a high index of severity of the general condition, with prolonged stay in the intensive care unit (more than 21 days), who are on full parenteral nutrition, who received 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-systemic damage in sepsis is primarily associated with the uncontrolled spread of pro-inflammatory mediators of endogenous origin from the primary focus of infectious inflammation with subsequent activation under their influence of macrophages, neutrophils, lymphocytes and a number of other cells in other organs and tissues, with the secondary release of similar endogenous substances, damage to the endothelium and decreased organ perfusion and oxygen delivery. Dissemination of microorganisms may be absent altogether or be short-term, subtle. However, even in such a situation, the release of pro-inflammatory cytokines at a distance from the focus is possible. Exo and endotoxins of bacteria can also activate the overproduction of cytokines from macrophages, lymphocytes, endothelium.

The cumulative effects of mediators form the systemic inflammatory response syndrome. Three main stages began to be distinguished in its development.

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

A special place among the mediators of inflammation is occupied by the cytokine network, which controls the processes of realization of immune and inflammatory reactivity. The main producers of cytokines are T cells and activated macrophages, as well as, to one degree or another, other types of leukocytes, endothelial cells of postcapillary venules, platelets, and various types of stromal cells. Cytokines act with priority in the focus of inflammation and on the territory of the reacting lymphoid organs, eventually performing a number of protective functions, participating in the processes of wound healing and protection of body cells from pathogenic microorganisms.

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

Small amounts of mediators are able to activate macrophages, platelets, 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 to TNFα and others, called anti-inflammatory mediators. By maintaining a balance and controlled relationship between pro and anti-inflammatory mediators under normal conditions, prerequisites are created for wound healing, destruction of pathogenic microorganisms, and maintenance of homeostasis. To 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 the bone marrow, hyperproduction of acute phase proteins in the liver, and the development of generalized forms of the immune response.

3rd stage. Generalization of the inflammatory response.

With 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, accumulate there in quantities sufficient to realize their long-distance effects. In the case of the inability of the regulatory systems to maintain homeostasis, the destructive effects of cytokines and other mediators begin to dominate, which leads to impaired capillary endothelial permeability and function, triggering disseminated vascular coagulation syndrome, the formation of distant foci of systemic inflammation, and the development of mono and multiple organ dysfunction. Apparently, any disorders of homeostasis that can be perceived by the immune system as damaging or potentially damaging can also act as factors of systemic damage.

At this stage of the systemic inflammatory reaction syndrome, from the standpoint of the interaction of pro and anti-inflammatory mediators, it is possible to conditionally distinguish two periods. The first, the initial one, is the period of hyperinflammation, characterized by the release of ultra-high concentrations of pro-inflammatory cytokines, nitric oxide, which is accompanied by the development of shock and the early formation of multiple organ failure syndrome (MOF). However, already at the moment, there is a compensatory release of anti-inflammatory cytokines, the rate of their secretion, concentration in 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 reactivity under the influence of environmental factors, 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. The factors triggering 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, exotoxins. In this regard, the complex of reactions in response to invasion by gram-positive microorganisms is more complex. TNFα is the key pro-inflammatory mediator. The pivotal role of TNFα in the development of sepsis is associated with the biological effects of this mediator: an increase in the procoagulant properties of the endothelium, activation of neutrophil adhesion, induction of other cytokines, stimulation of catabolism, fever, and the synthesis of “acute phase” proteins. Generalization of the damaging effects is mediated by the widespread prevalence of TNFα receptors 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 sharply increases under hypoxic conditions due to the expression of cytokine receptors on the cell surface.

In the genesis of acute vascular insufficiency, underlying septic shock syndrome, the leading role is played by nitric oxide, the concentration of which increases tens of times as a result of stimulation of macrophages TNFα, IL1, IFN, and further the secretion of nitric oxide is carried out by cells of vascular smooth muscle, and already monocytes themselves are activated under its action. Under normal conditions, nitric oxide plays the role of a neurotransmitter, is involved in vasoregulation, phagocytosis. It is characteristic that microcirculation disturbances in sepsis are of a heterogeneous nature: dilatation zones are combined with areas of vasoconstriction. Risk factors for the development of septic shock are oncological diseases, the severity of the patient's condition on the SOFA scale of more than 5 points, chronic obstructive pulmonary diseases, old age.

As a result of dysfunction of the liver, kidneys, intestines, new, distal in relation to cytokines, factors of damaging effects appear. These are intermediate and final products of normal metabolism in high concentrations (lactate, urea, creatinine, bilirubin), components and effectors of regulatory systems accumulated in pathological concentrations (kallikreinkinin, clotting, 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 the clinical picture of the systemic inflammatory reaction syndrome (tachycardia, fever or hypothermia, dyspnea, leukocytosis or leukopenia with a shift in the leukocyte count) and a variety of syndromes characteristic of organ dysfunction (septic encephalopathy, septic shock, acute respiratory depression, liver failure).

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

The emergence 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 for which are hypoxemia, bilateral infiltrates on the radiograph, a decrease in the ratio of the partial pressure of oxygen in arterial blood to the inspiratory fraction of oxygen (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 dilatation of the capillary vascular bed. The skin becomes marbled, acrocyanosis develops; they are usually hot to the touch, high humidity, profuse sweat is characteristic, the limbs are warm, and the vascular spot slows down when pressed on the nail bed. In the later stages of septic shock (the "cold" shock phase) the 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.

Evaluation 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 the 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 presence of bilateral infiltrates on chest x-ray, or need for mechanical ventilation
Liver	An increase in the bilirubin content above 20 μmol / L within 2 days or an increase in the level of transaminases 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 / l plasma lactate 1.5 times higher than normal
CNS	Glasgow score less than 15

DIAGNOSTICS

ANAMNESIS

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

PHYSICAL STUDY

The main goal of the study is to establish the source of the 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 criteria for a systemic inflammatory response and the presence of a focus of infection. The criteria for the focus of infection are 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 syndrome of infection (in particular cholangitis).

LABORATORY RESEARCH

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

A 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 %). Increased ESR,

Due to its low specificity, the reactive protein cannot be recognized as diagnostic markers of sepsis.

Negative blood culture results do not exclude sepsis. Blood for microbiological examination 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 taken for microbiological examination from the alleged focus of infection (cerebrospinal fluid, urine, lower respiratory tract secretions, etc.).

INSTRUMENTAL STUDIES

Instrumental diagnostic methods cover all the methods necessary to identify the focus of infection. The 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, 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;
lung atelectasis;
pneumothorax, hydrothorax;
exacerbation of chronic obstructive pulmonary disease;
acute renal failure;
toxic liver damage;
toxic encephalopathy;
embolism by amniotic fluid.

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

INDICATIONS FOR CONSULTATION OF OTHER SPECIALISTS

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

EXAMPLE FORMULATING A DIAGNOSIS

Endometritis. Sepsis. Acute respiratory failure.

TREATMENT

Effective intensive therapy for sepsis is possible only with the full surgical debridement of the site 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 of extirpation of the uterus, especially with its purulent melting, or the removal of a tubo-ovarian formation containing pus.

The main goal of this therapy is to optimize oxygen transport in conditions of increased oxygen consumption, which is 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, immunosubstitution therapy, correction of blood coagulation disorders, prevention of deep vein thrombosis and thromboembolic complications, prevention of stress and gastrointestinal bleeding in patients with sepsis.

ANTIBACTERIAL THERAPY

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

the range of suspected pathogens, depending on the localization of the primary focus;
the level of resistance of nosocomial pathogens according to microbiological monitoring data of a particular 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.

Evaluation of the effectiveness of antibiotic therapy is carried out no earlier than 48-72 hours.

HEMODYNAMIC SUPPORT

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

Localization of the primary focus	The nature of the infection	1st row means	Alternative remedies
Abdominal cavity	Community-acquired	Amoxicillin + clavulanic acid +/– amino glycoside Cefotaxime + metronidazole Ceftriaxone + metronidazole	Ampicillin / sulbactam +/– aminoglycoside Levofloxacin + metronidazole MoxifloxacinOfloxacin + metronidazole Pefloxacin + metronidazole Ticarcillin + clavulanic acid Cefuroxime + metronidazole Ertapenem
	Nosocomial AP ACHE<15, без ПОН	Cefepime +/– metronidazole Cefoperazone / sulb ktam	Imipenem Levofloxacin + metronidazole Meropenem Ceftazidime + metronidazole Ciprofloxacin + metronidazole
	Nosocomial AP ACHE\u003e 15 and / or PON	ImipenemMeropenem	Cefepime + metronidazole Cefoperazone / sulbactam +/– amikacin Ciprofloxacin + metronidazole +/– amikacin
Lungs	Nosocomial pneumonia outside the ICU	Levofloxacin Cefotaxime Ceftre Iaxone	ImipenemMeropenemOfloxacinPefloxacinCephepimErtapenem
	Nosocomial pneumonia in ICU, APACHE<15, без ПОН	Cefepime Ceftazidime + Amikacin	Imipenem Meropenem Cefoperazone / sulbactam +/– amikacin Ciprofloxacin +/– amikacin
	Nosocomial pneumonia in ICU, APACHE\u003e 15 and / or PON	ImipenemMeropenem	Cefepime +/– amikacin
Kidney	Community-acquired	Ofloxacin CefotaximeCeftriac sleep	Levofloxacin Moxifloxacin Ciprofloxacin
Kidney	Nosocomial	LevofloxacinOfloxacinCipro floxacin	ImipenemMeropenemCefepime
Associated catheter		Vancomycin Linezolid	Oxacillin + gentamicin Cefazolin + gentamicin Rifampicin + ciprofloxacin (co-trimoxazole) Fusidic acid + ciprofloxacin (co-trimoxazole)

In sepsis with PON and septic shock, it is necessary to strive to quickly achieve (the first 6 hours after admission) the target values \u200b\u200bof the following parameters: central venous pressure 8-12 mm Hg, mean blood pressure more than 65 mm Hg, urine output 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 improves 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.

Crystalloid and colloidal infusion solutions are used for infusion therapy in the framework of targeted intensive care of sepsis and septic shock with practically the same result. All infusion media have their own advantages and disadvantages. Taking into account the 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 characteristics of the patient: the degree of hypovolemia, the phase of the syndrome of disseminated intravascular coagulation, the presence of peripheral edema and the level of blood albumin, 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 evasion and no clinically significant effect on hemostasis. Albumin transfusion will be useful only if the albumin level drops below 20 g / L and there are no signs of its "leak" into the interstitium. The use of fresh frozen plasma is indicated for consumption coagulopathy and a decrease in the coagulation potential of blood. According to most experts, the minimum concentration of hemoglobin for patients with severe sepsis should be in the range of 90-100 g / l. The wider use of donor erythrocyte mass 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 drugs of first choice for correcting hypotension in patients with septic shock.

Dobutamine should be considered the drug of choice for increasing cardiac output and oxygen delivery at normal or elevated preload levels. Due to the 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 in sepsis.

Acute respiratory failure is one of the leading components of multiple organ dysfunction. Its clinical and laboratory manifestations in sepsis correspond to the syndrome of acute lung injury, and with the progression of the pathological process - to acute respiratory distress syndrome. Indications for artificial ventilation in severe sepsis are determined by the development of parenchymal respiratory failure: with a decrease in the respiratory index below 200, tracheal intubation and the beginning of respiratory support are indicated. With a respiratory index above 200, readings are determined on an individual basis. The presence of adequate consciousness, the absence of high costs for the work of breathing, pronounced tachycardia (heart rate up to 120 per minute), normalization of venous blood return and SaO2\u003e 90% against the background of oxygen support for spontaneous breathing completely allow refraining from transferring to artificial ventilation of the lungs, but not from strict monitoring the dynamics of the patient's condition. Optimum blood oxygen saturation (approximately 90%) can be maintained with various oxygen therapy methods (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-aggressive under the following conditions: peak airway pressure below 35 cm H2O, inspiratory oxygen fraction below 60%, tidal volume below 10 ml / kg, non-inverted inhalation ratio to exhale. The selection of the parameters of the respiratory cycle is carried out until the criteria for the adequacy of artificial ventilation are achieved: PaO2 is more than 60 mm Hg, SaO2 is more than 93%, PvO2 is 35–45 mm Hg, SvO2 is more than 55%.

NUTRITIVE SUPPORT

The development of SNP syndrome in sepsis is usually accompanied by manifestations of hypermetabolism. In this situation, the coverage of energy needs occurs due to the destruction of one's own cellular structures, which aggravates the existing organ dysfunction and enhances endotoxicosis. Nutritional support is considered as a method that prevents the development of severe depletion (protein-energy deficiency) against the background of pronounced hypercatabolism and hypermetabolism, which are the most characteristic metabolic characteristics of a generalized inflammatory response of an 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 carrying out 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 / (kg x day);
glucose: 30–70% of non-protein calories while maintaining glycemic levels below 6.1 mmol / L;
lipids: 15–20% of 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 the protocols of early and late initiation of enteral tube feeding.

For effective synthesis of endogenous protein, it is important to observe the metabolic ratio of non-protein calories / total nitrogen in the range of 1 g nitrogen to 110-130 kilocalories. Carbohydrates do not need to be administered in a dose of more than 6 g / (kgx day) due to the risk of hyperglycemia and activation of catabolic processes in skeletal muscles. For parenteral administration of fat emulsions, a round-the-clock administration regime is recommended. It is necessary to give preference to 2nd generation fatty emulsions of the MCT / LST type, 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 μg / (kgxmin) and systolic blood pressure less than 90 mm Hg);
intolerance to environments for nutritional support;
severe intractable arterial hypoxemia;
gross uncorrected hypovolemia;
decompensated metabolic acidosis.

GLYCEMIA CONTROL

An important aspect of the complex intensive care of severe sepsis is the constant monitoring of the glycemic level and insulin therapy. High glycemic levels and the need for insulin therapy are factors of poor outcome in patients with diagnosed sepsis. In this regard, it is necessary to strive to maintain the glycemic level in the range of 4.5-6.1 mmol / L. With a glycemic level of more than 6.1 mmol / l, it is necessary to infuse insulin (at a dose of 0.5–1 U / h) to maintain normoglycemia (4.4–6.1 mmol / l). Control of glucose concentration - every 1-4 hours, depending on the clinical situation. When performing this algorithm, a statistically significant increase in survival is recorded.

GLUCOCORTICOIDS

Glucocorticoids for sepsis are used for the following indications:

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

It is necessary to abandon the chaotic empirical administration 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 / essence (for 3-6 injections) should be used in case of refractory septic shock or if 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 a nuclear factor inhibitor and correction of relative adrenal insufficiency. In turn, inhibition of the nuclear factor activity 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 pro-inflammatory 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 inflammation system is realized through several mechanisms:

a decrease in the attachment of selectins to leukocytes, which is accompanied by the protection of the integrity of the vascular endothelium, which plays an important 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 the plasminogen activator inhibitor;
direct anti-inflammatory effect on endothelial cells and neutrophils;
protection of the endothelium from apoptosis.

The introduction of activated protein C (drotrecogin alpha [activated]) at a dose of 24 μg / (kg · h) for 96 hours reduces the risk of death by 19.4%.

INFUSION OF IMMUNOGLOBULINS

The expediency of prescribing an infusion of immunoglobulins (IgG and IgG + IgM) is associated with their ability to limit the excessive effect of pro-inflammatory cytokines, increase the clearance of endotoxin and staphylococcal superantigen, eliminate anergy, and enhance the effect of betalactam antibiotics. The use of immunoglobulins in the framework of immunosubstitution therapy for severe sepsis and septic shock is currently recognized as the only really 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 the introduction of 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 range of the severity index according to ARACHE II 20–25 points.

PREVENTION OF DEEP VEIN THROMBOSIS

The available data now confirm that the prevention of deep vein thrombosis significantly affects the results of treatment of patients with sepsis. For this purpose, both unfractionated heparin and preparations of low molecular weight heparin 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 THE FORMATION OF STRESS IN THE GASTROINAL 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 tract stress ranges from 64 to 87%. The incidence of stress without their prevention in critically ill patients can reach 52.8%. Preventive 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 efficiency 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 formation.

RENAL REPLACEMENT THERAPY

Renal dysfunction causes a rapid decompensation of organ failure due to an increase in endotoxemia due to the development of a systemic inflammatory reaction syndrome, massive cytolysis, pathological proteinolysis, leading to the development of pronounced water-sectoral disorders with generalized endothelial damage, impaired blood coagulation and fibrinolysis, increased permeability of the capillary bed and, as a result, to rapid decompensation (or manifestation) of organ failure (cerebral edema, acute lung injury, distress syndrome, distributive shock and acute cardiac, hepatic and intestinal failure).

The main difference between isolated renal failure (acute or chronic) and acute renal failure in MOF is 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 SNP, substances of medium and high molecular weight (more than 1000 D) are added to the above 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. With respect to these substances, hemodialysis is not effective, and preference is given to convection mass transfer used in hemofiltration and a combination of the above two methods in hemodiafiltration. These methods allow, albeit with some reservations, to remove substances with a molecular weight of up to 100,000 D. They include plasma proteins, including immunoglobulins, circulating immune complexes containing complement and myoglobin, although the clearance of these chemical compounds is much higher when plasma filtration methods are used.

Despite the aforementioned pathophysiological database of treatment modalities, there are currently no extensive and well-controlled studies that conclusively support renal replacement therapy as an integral part of targeted therapy for severe sepsis. Moreover, even with the use of the most pathogenetically substantiated method - venovenous prolonged hemofiltration (rate of 2 l / h for 48 h) - no decrease in blood levels of IL6, IL8, TNFα and a decrease in mortality was observed. In this regard, its use in general practice is not yet justified and is indicated only in the development of acute renal failure.

FORECAST

Mortality in severe sepsis is about 20% in case of mono-organ dysfunction, increasing to 80-100% involving four or more organs.

LIST OF REFERENCES
Abdominal surgical infection: clinical picture, diagnosis, antimicrobial therapy: practical. hands. / Edited by V.S. Savelyeva, B.R. Gelfand. - M .: Literra, 2006 .-- 168 p.
Gelfand B.R., Kirienko P.A., Grinenko T.F. and other Anesthesiology and intensive care: practical. hands. / Under total. ed.B.R. Gelfand. - M .: Literra, 2005 .-- 544 p.
Sepsis at the beginning of the XXI century. Classification, clinical diagnostic concept and treatment. Pathological diagnostics: practical. hands. - M .: Literra, 2006 .-- 176 p.
Surgical infections: practical. hands. / Ed. I.A. Eryukhin and others: ed. 2e, lane. and add. - 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.

Septic shock refers to a serious complication of an infection that is life-threatening. With it, tissue perfusion decreases, because of this, oxygen is poorly supplied. If you do not take action in a timely manner, everything can end in the defeat of the internal organs, the death of the patient. The probability of death of the patient is about 50%. Often, septic shock is characteristic of the elderly, children, and immunodeficient patients.

The reasons

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

Anaerobic and aerobic streptococcus.
E. coli.
Bacteroids.
Clostridia.
Beta-hemolytic streptococcus.
Klebsiella.
Other pathogenic microorganisms.

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

Types of septic shock

It all depends on where the pathology is localized, how it proceeds. Allocate:

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

Depending on how the pathology proceeds, there are:

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

Symptoms

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

Disturbed by severe chills.
A high temperature appears.
A hemorrhagic, papular rash can be seen on the body.
Intoxication of the organism gradually increases.
Appears.

Non-specific symptoms include:

Enlarged spleen, liver.
Chills.
Severe weakness.
Physical inactivity.
Stool is disturbed (constipation worries).

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

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

Other symptoms that occur with septic shock include:

, X-ray may show pneumonia.
A septic abortion is especially dangerous for a woman because there is no inflammatory reaction in the uterus. In this case, the vessels begin to clog with blood clots, microbes, and purulent masses. After a while, toxic anemia develops, the skin color changes. It is dangerous when everything ends with extensive superficial necrosis.
Tachypnoe develops due to the fact that the work of the heart and blood vessels is disrupted. In this case, the respiratory rate increases.
Septic pneumonia is a fairly common complication of sepsis.
Liver damage. With sepsis, the liver begins to increase markedly, severe pain in the side appears, the level of transaminase and bilirubin rises in the blood. After a while, the amount of total protein decreases. It all ends in liver failure.
Renal damage. When pressure drops sharply, blood volume decreases, diuresis occurs. The urine has a low density, indicating inflammation. In the kidneys, you can see an organic, functional lesion of an organic nature.
Bowel problems. We draw your attention to the fact that sepsis is accompanied by intestinal paresis, severe disturbance of the digestive process. A putrefactive process develops in the intestine, it is accompanied by septic diarrhea, dysbiosis.
Trophic disorders. When microcirculation of blood is disturbed, bedsores appear.
The spleen is enlarged.

Treatment methods

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

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

With septic shock, at least two antibiotics are used, which have a wide spectrum of action. If a specific pathogen is identified, antibiotics are prescribed for a specific infection. All drugs are administered parenterally, either into a muscle or into a vein.

Blood cultures are taken continuously during treatment to identify pathogenic microbes. Antibiotic therapy will last for several months until the culture is negative.

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

Sometimes surgery is needed to remove dead tissue. An operation is performed depending on where the inflammatory focus is located.

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

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

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

Sepsis is an infection. Acute pancreatitis and serious injury, including burns, can present with symptoms of sepsis. The inflammatory response usually manifests itself in two or more symptoms:

Temperature\u003e 38 ° C or<36 °С.
Heart rate\u003e 90 beats / min.
Respiratory rate\u003e 20 per minute or PaCO 2<32 мм рт.ст.
Leukocyte count\u003e 12x109 / l or<4х109/л или >10% immature forms.

However, at present, the presence of these criteria is only a presumed factor is not sufficient for a diagnosis.

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

Septic shock is severe sepsis with hypoperfusion and hypotension, which are not resolved with adequate intensive fluid therapy.

Causes of septic shock

Septic shock is more common in newborns, patients over 35, and pregnant women. Contributing factors include diabetes mellitus; cirrhosis of the liver; leukopenia.

Pathophysiology of septic shock

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

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

Even at the stage of increased cardiac output, vasoactive neurotransmitters cause blood flow to bypass capillaries (distribution defect). Capillaries fall out of this shunting along with capillary obstruction by microthrombi, which reduce the delivery of 02 and reduce the excretion of CO2 and other waste products. Hypoperfusion leads to dysfunction.

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

Symptoms and signs of septic shock

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

Diagnosis of septic shock

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

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

Hyperventilation with respiratory alkalosis (low PaCO 2 and high blood pH) appears early as a compensation for metabolic acidosis. Serum NSO; usually low and serum lactate levels are elevated. Shock progresses, metabolic acidosis worsens, and blood pH drops. Early respiratory failure leads to hypoxemia with PaO2<70 мм рт.ст. Уровень мочевины и креатинина обычно прогрессивно возрастают.

Nearly 50% of patients with severe sepsis develop relative adrenal insufficiency (ie, normal or slightly elevated basal cortisol levels. Adrenal function can be monitored by measuring serum cortisol at 8 am.

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

Treatment for septic shock

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

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

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

02 is given with a mask. Tracheal intubation and mechanical ventilation may be necessary subsequently if breathing is impaired.

Parenteral administration of antibiotics should be prescribed after collection of blood, various media (fluids, body tissues) for antibiotic sensitivity and culture. Early empiric therapy, started immediately after suspected sepsis, is important and can be critical. The choice of antibiotic must be justified, based on the intended source, and on a clinical basis.

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

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

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

Septic shock is a serious complication of infectious diseases that can be life threatening. Septic shock is characterized by a decrease in tissue perfusion, which markedly disrupts the delivery of oxygen and nutrients to the tissues. This condition leads to failure of many internal organs, which pose a mortal threat to the patient. The probability of death in septic shock is 30 - 50%!

Often, septic shock is recorded in children, the elderly and in patients with severe immunodeficiency conditions.

Septic shock - causes and factors of development

Septic shock can be caused by a variety of pathogenic microorganisms. The bacteria that cause septic shock generally belong to the class of endotoxin-producing bacteria. Often, the following pathogenic microbes are the cause of septic shock:

colibacillus;
aerobic and anaerobic streptococci;
clostridia;
bacteroids;
beta-hemolytic streptococcus;
staphylococcus aureus;
klebsiella;
other pathogenic microorganisms.

It is noteworthy that beta-hemolytic streptococcus and Staphylococcus aureus produce a specific virulent exotoxin that can cause toxic shock syndrome in a patient.

Septic shock (and sepsis) is an inflammatory response to a trigger factor. As a rule, it is a microbial endotoxin, less often an exotoxin. Endotoxins are specific substances (lipopolysaccharides) that are released during the lysis (destruction) of gram-negative bacteria. These toxins activate specific immune mechanisms in the human body, which leads to the development of the inflammatory process. Exotoxins are substances that a gram-negative bacteria release to the outside.

Toxins enter the bloodstream and stimulate the production of inflammatory cytokines, including: tumor necrosis factor, interleukin-1, interleukin-8 in the vascular endothelium. This reaction leads to adhesion (adhesion) of neutrophils, leukocytes, endothelial cells with the formation of specific toxic substances.

Types of disease: classification of septic shock

The classification of septic shock is based on the localization of the pathology, the features of its course and the stage of compensation.

Depending on the localization of the pathological process, septic shock is:

pulmonary pleural;
intestinal;
peritoneal;
biliary;
urodynamic or urinemic;
obstetric or hysterogenic;
cutaneous;
phlegmonous or mesenchymal;
vascular.

Downstream septic shock is:

lightning fast (or instant);
early or progressive;
erased;
recurrent (or septic shock with an intermediate stage);
terminal (or late).

According to the stage of compensation, septic shock is divided into the following types:

compensated;
subcompensated;
decompensated;
refractory.

Symptoms of septic shock: how the disease manifests itself

Symptoms for septic shock largely depend on the pathogenic pathogen, the patient's immunity and the source of infection.

The onset of septic shock can be quite violent and accompanied by symptoms such as:

strong;
hemorrhagic or papular rash;
gradual, slowly increasing intoxication;
myalgia.

Common but non-specific symptoms of sepsis include the following:

enlargement of the spleen;
enlarged liver;
intense sweating (after chills);
hypodynamia;
severe weakness;
stool disorder (usually constipation).

Lack of antibiotic therapy leads to multiple disorders of internal organs and death of the patient. With septic shock, thrombosis is possible, combined with hemorrhagic syndrome.

If, with septic shock, the patient is given adequate antibiotic therapy, then the manifestations of intoxication decrease after 2-4 weeks from the onset of the disease. Against the background of septic shock, due to massive infection and the inflammatory process, arthralgias develop. In severe cases, the patient may develop polyarthritis. In addition, against the background of this condition, the patient may develop symptoms of glomerulonephritis, polyserositis and myocarditis.

Other symptoms that occur with septic shock against a background of various disorders are:

Symptoms of septic shock in severe disseminated intravascular coagulation and respiratory distress. In this case, the development of interstitial edema is possible, which entails the appearance of polymorphic shadows and discoid atelectasis in the lungs. Similar changes in the lungs are observed in other severe forms of septic shock. It is noteworthy that the radiographic images of the lungs are almost the same as in pneumonia.
Septic abortion. As a rule, during a septic abortion, bleeding does not occur, since in this case the inflammatory reaction is noted in the uterus. As a rule, the vessels are clogged with microbes, blood clots and bloody discharge mixed with purulent masses. Possible development of toxic anemia and a change in skin color. The patient sometimes develops petechial hemorrhages, which can form on the mucous membrane, on the skin and in internal organs. In some cases, it comes to the formation of extensive superficial necrosis.
Tachypnoe for septic shock. Due to a violation of the activity of the cardiovascular system, a patient with septic shock develops tachypnea. The breathing rate can be up to 40 breaths / exhalations per minute.
Septic pneumonia. This is a fairly common complication of the septic process in the body.
Liver damage with septic shock. Pathology is accompanied by a noticeable increase in liver size. The liver is painful, and an increase in the level of transaminases, bilirubin, is found in the blood. The prothrombin index, total protein and protein fractions decrease. This situation leads to the development of acute liver failure with irreversible changes.
Kidney damage with septic shock. With a sharp decrease in the volume of circulating blood and a decrease in blood pressure, diuresis also decreases. Urine acquires a low density and markers of the inflammatory process are found in it. In the kidneys, functional and organic lesions are possible, which are irreversible.
Intestinal motility disorders. With septic shock, intestinal paresis and severe disorders of parietal digestion may develop. A putrefactive process starts in the intestine, septic diarrhea and dysbiosis appear. It is quite difficult to compensate for such violations.
Trophic disorders. Pressure ulcers occur early enough in septic shock. This occurs due to microcirculation disorders.
Enlarged spleen.

Patient actions for septic shock

Septic shock is a life-threatening condition. The patient should be hospitalized immediately and intensive care should be started. The disease develops quite rapidly, leading to severe complications up to death. Therefore, it is important to get the patient to the hospital as soon as possible.

The diagnosis of "septic shock" is made on the basis of characteristic symptoms that develop during a massive infectious process. The diagnosis is confirmed by a series of laboratory and instrumental studies.

First of all, the treatment of septic shock should be comprehensive and take into account the type of pathogenic flora that caused the pathology. The main therapeutic measure for septic shock is massive antibiotic therapy, anti-inflammatory therapy, and immunomodulatory therapy. It is also possible to carry out hormone therapy.

Antibacterial therapy. Massive antibiotic therapy for septic shock should be accompanied by the use of at least two broad-spectrum antibacterial drugs. If the pathogenic pathogen is isolated and its sensitivity is determined, then targeted antibiotic therapy is performed against a specific infection. Antibiotics for septic shock are administered parenterally (into a vein, into a muscle, into a regional artery, or by the endolymphatic route).

When conducting antibiotic therapy, blood cultures are regularly performed to identify pathogenic microbes. Antibiotic treatment can take several months until the culture results are negative and doctors achieve a lasting clinical recovery.

To improve the body's resistance, a leukocyte suspension, interferon, hyperimmune antistaphylococcal plasma can be administered to the patient. In severe cases, hormonal corticosteroids are used. Correction of immune disorders in septic shock is carried out with the obligatory consultation of an immunologist.

Surgery. The most important component in the treatment of septic shock is the removal of dead tissue. Depending on the localization of the focus, various surgical interventions are performed.
Supportive care. To maintain vital functions of the most important organs and systems, drugs such as dopamine hydrochloride and other drugs that maintain normal blood pressure levels are used. Oxygen mask inhalations are carried out to ensure proper oxygenation.

Complications of septic shock

With septic shock, the activity of most internal organs and systems is disrupted. This condition is fatal.

Prevention of septic shock

Prevention of septic shock is measures that prevent blood poisoning from developing. With septic shock, it is important to prevent the development of internal organ failure and to maintain the normal functioning of the patient's body.

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, factors of the triggering mechanism of shock (the entrance gate of the infection and the duration of action of this gate). It is important that bacteremia can occur with or without sepsis. That is, bacteremia ceases to be an obligate symptom 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 about 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 during autopsy. Thus, bacterial shock is a manifestation of the general resorptive action of toxins.

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

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

Depleting diseases associated with surgical pathology (blood diseases, oncopathology, systemic diseases), as well as the state of hormonal levels, are of significant importance in reducing the activity of defense mechanisms. When assessing the condition of a patient with suspected septic shock, it should be borne in mind that it can be initially changed by immunosuppressants, radiation therapy, vitamin deficiencies, chronic intoxication (drug addiction, alcoholism).

Primary purulent focus (or gateway for an infection) and the duration of these gates is a mandatory factor related to the triggering mechanism of septic shock.

Primary purulent foci in sepsis are most often acute purulent surgical diseases (carbuncles, mastitis, abscesses, phlegmon, etc.) or purulent wounds, both post-traumatic and postoperative. Sepsis resulting from local purulent processes and purulent wounds has long been known. Sepsis as a complication of various extensive operations, resuscitation measures and invasive diagnostic procedures, that is, nosocomial (or iatrogenic) sepsis, grows with the expansion of the volume and complexity of surgical interventions and modern medical manipulations and has recently received the name "disease of medical progress".

The existing opinion about the possibility of the so-called primary, or cryptogenic, sepsis is, apparently, erroneous and is a consequence of imperfect knowledge and diagnosis. The diagnosis of cryptogenic sepsis leads the doctor away from the search for the primary focus and, consequently, complicates the correct diagnosis and full treatment.

The gateway for an infectious disease is usually 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 a surgical clinic there is a peritoneal form of septic shock, and the biliary tract (biliary form) occupies the next most frequent entry gate for an infection in postoperative septic shock. The development of antibiotic-associated pseudomembranous colitis with the appearance at the first stage of diarrheal syndrome of varying severity can be considered as an intestinal variant of postoperative sepsis. Adipose tissue can become the entrance gate, especially in cases where purulent inflammation occurs with the phenomena of progressive cellulite of the perirenal, retroperitoneal, intermuscular tissue. The increasing importance in the practice of intensive care is acquired by unusual ways of penetration of the infection: with prolonged intubation of the trachea and tracheostomy, with catheterization of the central vessels. Therefore, a vascular, or angiogenic, form of septic shock can occur not only as a consequence of purulent thrombophlebitis, complicating the course of the wounded process, but as an independent complication.

One-stage lysis of microorganisms contained in the focus and circulating in the blood under the influence of an effective bactericidal drug in a high dose (Gelzheimer-Jarisch reaction) can become a shockogenic factor.

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 (superoxides O, etc.), kinins (bradykinin), granulocyte proteases, collagenases, etc.

In septic shock, as in sepsis, hydralases are released into the blood, not only from the 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 total proteolytic activity of the blood increases according to the severity of the systemic inflammatory response.

As septic shock develops, mechanisms are activated that compensate for the effect of systemic vasodalation. This can be attributed to the action of catecholamines, angiotensin, adrenal cortex 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 that 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.

The clinical picture of septic shock

In the development of septic shock (SS), the initial (often very short-term) "hot" period (or hyperdynamic phase) and the subsequent, more prolonged, "cold" period (hypodynamic phase) are distinguished.

With SS, signs of damage to the vital organs are always revealed. The defeat of 2 organs or more is classified as a syndrome of multiple organ failure.

The degree of CNS dysfunction can range from mild stunning to deep coma. About 1 out of 4 patients with septic syndrome develop 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 noises, the appearance of diffuse moist rales, an increase in arterial hypoxemia. The earliest and clearest sign of organ dysfunction typical for septic shock is renal dysfunction, which is established by an 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 rise in the activity in the blood of hepatic transaminases and other markers of cell-liver failure. 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 deteriorate, there is a decrease in cardiac output, which marks the beginning of the decompensated phase of septic shock.

Diagnosis of septic shock.

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

Dynamic determination of blood pressure, heart rate, SV and IOC, CVP level; determination of hourly urine output;

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

Dynamics of T body (with the definition of the gradient between the internal and peripheral T body of the patient);

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

Blood cultures for sterility.

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

Pathogenetic criteria for the differential diagnosis of septic shock include the definition of surrogate markers of the septic process: C-reactive protein, phospholipase A2, procalcitonin (PCT). Determination of the PCT level in plasma is important precisely in patients with sepsis with an outcome in septic shock, since its level increases tenfold in case of SS compared with a definitely significant increase in septic processes. Correction of SS therapy also requires reliable laboratory criteria for the state of the lipid peroxidation system and antioxidant defense of the body.

Treatment for septic shock.

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

Stabilization of hemodynamics is achieved primarily by an adequate volemic load: a quick infusion of 1-2 liters of crystalloid solutions with the consolidation of the effect by colloidal solutions (in a ratio of 2: 1) under the control of hemodynamic monitoring (Hell, CVd, SV) and the rate of diuresis. Inotropic support is of decisive importance in hemodynamic stabilization, which ensures relief of hemodynamic disturbances and maintenance of an adequate level of tissue perfusion. The first choice for inotropic support against the background of SS is dopamine, which is used either in small doses - 1-4 μg / kg min (increases blood flow in the kidneys, mesecterial, cerebral and coronary vessels), or in medium doses - 5-10 μg / kg min (mycocardial).

To reduce the damaging effect of tissue hypoxia, antihypoxants are used: blood substitutes based on fumarate (mafusol) and succinate (reamberen), 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 of a patient with surgical sepsis, the scope of surgical intervention should include the most complete necrectomy, adequate drainage with double-lumen tubes. Sanitation of the septic focus should be urgent and the basis of surgical participation should not be the position - "the patient is too heavy to intervene", but on the contrary - "the patient is too sick to postpone the intervention ...". Any intensive therapy of SS may become ineffective precisely because of the presence of undiagnosed or poorly operated foci of wound infection.

Carbapenems - meronem or thienam - are considered the first choice drugs for bacterial SS. Considering the widest possible spectrum of antibacterial activity of these drugs and significant resistance to -lactamases. The initial dose of carbopenem should be maximal (1–2 g) and administered intravenously by microbolus (for meronem) or drip over 60 minutes (for thienam). Subsequent injections are determined by the preservation of renal functions and are 5000-1000 mg every 8 hours.

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

Improvement of consciousness and general appearance of the patient;

Disappearance of peripheral cyanosis and pinking of the skin, its warming on the hands and feet with a decrease in the temperature gradient to 4-5 С;

Reducing shortness of breath and increasing PaO2 at a stable level;

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

An increase in the rate of diuresis.

The determinant of exit from SS is the response of the patient's vital functions to the treatment.