03.07.2020

What is septic shock. Sepsis and septic shock - causes, symptoms, treatment Septic shock syndrome

Treatment of septic shock (sepsis) should be immediate and comprehensive. The main direction of therapy is the fight against infection and inflammation.

Treatment of septic shock, which is the most severe complication of infectious diseases, can be intensive conservative or surgical - according to indications. Bacterial-toxic shock requires immediate medical attention, since it threatens the life of the patient - lethal outcome is observed in 30-50% of clinical cases. Shock is often recorded in children and senile patients, as well as in people with immunodeficiency, diabetes, and malignant diseases.

Causal factors

The state of shock is a set of disorders of the body's functions, when the fall in blood pressure and the deficient volumetric velocity of the blood flow (peripheral) cannot be reversed, despite intravenous infusions. Sepsis is one of the most common causes of death of patients in intensive care units; it is one of the most fatal pathological conditions that are difficult to treat with medication.

Bacterial-toxic shock is provoked by pathogenic microbes. Infectious organisms produce aggressive endo- or exotoxins.

Shock is often caused by:

intestinal microflora;
clostridia;
streptococcal infection;
staphylococcus aureus;
introduction of Klebsiella, etc.

Shock is a specific response, an excessive reaction of the human body to the impact of an aggressive factor.

Endotoxins are dangerous substances that are released as a result of the destruction of Gram-negative bacteria. Toxic elements lead to the activity of the human immune apparatus - an inflammatory reaction occurs. Exotoxins are hazardous substances released to the outside by Gram-negative microbes.

The active use of invasive devices (for example, catheters) during intensive care, the widespread use of cytostatics and immunosuppressants, which are prescribed in the complex therapy of oncological diseases and after organ transplantation, contributes to the development of septic shock.

Pathogenetic mechanism

An increase in the expression and release of pro-inflammatory cytokines provokes the release of endogenous immunosuppressants into the interstitium and into the blood fluid. This mechanism is responsible for the immunosuppressive phase of septic shock.

Induce immunosuppression:

internal catecholamine;
hydrocortisol;
interleukins;
prostin E2;
tumor necrotizing factor receptors and others.

Receptors of the aforementioned factor lead to its binding in the blood and in the space between cells. The amount of type 2 tissue compatibility antigens in mononuclear phagocytes drops to critical levels. As a result, the latter lose their antigen-presenting cellular ability, and the normal reaction of mononuclear cells to the action of inflammatory mediators is suppressed.

Arterial hypotension is a consequence of a fall in the total resistance of peripheral vessels. Hypercytokinemia, as well as an upward jump in the content of nitric oxide in the blood, leads to the expansion of arterioles. Due to the increase in heart rate according to the compensatory principle, the volume of blood flow / minute increases. The pulmonary vascular resistance increases. Venous hyperemia develops, which occurs due to the expansion of capacitive vessels. Vascular dilatation is especially pronounced in the source of infectious inflammation.

It is customary to distinguish the following main pathogenetic "steps" of circulatory disorders in the periphery during the development of septic shock:

Increased permeability of the vascular walls.
An increase in the resistance of small vessels, increasing adhesion of cells in their lumen.
Lack of vascular response to vasodilating mechanisms.
Arterio-venular shunting.
Critical decrease in the speed of "running" of blood.

Another factor in reducing blood pressure in septic shock is called hypovolemia, which has such causes as vascular dilatation and loss of the liquid component of the plasma part of the blood in the interstitium due to pathological increased permeability of small vessels (capillaries). Complements the complete pathogenetic picture of the negative impact on the heart muscle of shock mediators. They lead to a state of rigidity and dilatation of the ventricles of the heart. In patients with the development of sepsis, the body's oxygen consumption decreases due to a disorder in tissue respiration. The onset of lactic acidosis is associated with a decrease in the activity of pyruvate dehydrogenase, as well as the accumulation of lactate.

Blood flow disorders in the periphery are of a systemic nature, develop at normal blood pressure, supported by an increase in the minute amount of blood circulation. The pH of the mucous membrane lining the stomach decreases, and the oxygen saturation of hemoglobin in the veins of the liver decreases. There is also a decrease in the protective ability of the intestinal walls, which exacerbates endotoxemia in sepsis.

Types of septic shock

The classification of a life-threatening condition called septic shock is based on the degree of its compensation, the characteristics of the course, and the location of the primary focus of infection.

Depending on the location and nature of the infectious focus, septic shock can be:

pleural-pulmonary;
enteral;
peritoneal;
biliary;
uremic;
gynecological;
skin;
phlegmonous;
vascular.

Depending on the severity of the course, shock can be instantaneous (lightning fast), which develops rapidly, erased (with a blurry picture), early or progressive, terminal (late). There is also such a type of shock as recurrent (with an intermediate period).

Depending on the compensatory stage, shock can be compensated, subcompensated, decompensated, and also refractory.

Manifestations of shock

What will be the clinical picture, as well as the dominant manifestations, depends on the state of the patient's immunity, the gate of infection, the species of the microscopic provocateur.

The shock usually begins strongly, violently. Chills, a drop in blood pressure, a change in body temperature (an increase to 39-40 degrees with its further critical decrease to normal, subnormal numbers), progressive intoxication, muscle pain, and convulsions are considered characteristic early symptoms. Often there is a hemorrhagic rash on the skin. Nonspecific signs of sepsis are hepatomegaly and splenomegaly, increased sweating, physical inactivity, severe weakness and stool disorders, impaired consciousness.

The clinic of septic shock is accompanied by insufficiency of important organs.

Symptoms that indicate this are:

signs of deep DIC and respiratory distress syndrome with the development of pulmonary atelectasis;
tachypnea resulting from dysfunction of the SS system;
septic pneumonia;
liver damage, which is manifested by an increase in its size, the presence of pain, its insufficiency;
kidney damage, characterized by a decrease in daily diuresis, a decrease in urine density;
changes in intestinal motility (intestinal paresis, indigestion, dysbacteriosis);
violation of tissue trophism, evidence of which is the appearance of bedsores on the body.

Bacterial shock can develop at any period of the purulent process, but it is usually observed during an exacerbation of a purulent disease or after surgery. There is an ongoing risk of shock in patients with sepsis.

Diagnosis is based on clinical manifestations, laboratory data (characterized by signs of inflammation in blood and urine tests). Bacterial culture of biological material is carried out, as well as radiography, echography of internal organs, MRI and other instrumental examinations according to indications.

Shock conditions in obstetric (gynecological) practice

Septic shock in gynecology, as a result of purulent-inflammatory pathologies, is caused by several causative factors:

changes in the characteristics of the vaginal microflora;
the development of resistance to most antibiotics in microorganisms;
violation of the cellular-humoral immune mechanism in women against the background of prolonged antibiotic therapy, hormonal drugs and cytostatics;
high allergization of patients;
the use in obstetric practice of invasive diagnostic and therapeutic manipulations involving entry into the uterine cavity.

The main foci of infection causing bacterial shock are the uterus (complicated abortion, remnants of the fetal egg or placenta, inflammation of the endometrium after childbirth, caesarean section), mammary glands (mastitis, postoperative sutures in case of suppuration), appendages (abscesses of the ovaries, tubes). Infection usually occurs in an ascending fashion. Gynecological bacterial shock is caused by inflammation of a polymicrobial nature with a predominance of various bacterial associations of the vaginal flora.

Bleeding from the vagina / uterus, purulent discharge in large quantities, and pain in the lower abdomen join the standard manifestations and signs. In a complicated pregnancy, an inflammatory response of the maternal organism to preeclampsia can be observed.

The principles of treatment of infectious-toxic shock caused by inflammatory gynecological pathology do not differ significantly from shock of another etiology. If conservative methods have not provided the desired therapeutic effect, there may be an extirpation of the uterus and appendages. With purulent mastitis, an abscess is necessarily opened.

Anti-shock therapeutic measures - the main directions

Treatment of such a dangerous condition as bacterial shock requires an integrated approach and does not tolerate delay. Urgent hospitalization indicated.

Massive adequate antimicrobial therapy is considered the most important therapeutic measure. The choice of drugs directly depends on the type of pathogenic microscopic flora that served as a causative factor in the development of shock. Be sure to use anti-inflammatory drugs, as well as drugs whose action is aimed at increasing the body's resistance to the diseased. Hormonal medications may also be used.

Septic shock involves the following treatment:

The use of antimicrobial drugs. Prescribe antibiotics of at least two varieties (groups) of the most extensive range of bactericidal effects. It is necessary to determine the species of the pathogen (by laboratory methods) and purposefully apply antimicrobial agents, choosing those to which the causative microbe is most susceptible. Antibiotics are administered parenterally: intramuscularly, intravenously, intraarterially, by endolymphatic. During antibiotic therapy, crops are periodically done - the patient's blood is examined for the presence of pathogenic microflora in it. Antibiotic treatment should be continued until a special culture shows a negative result.
Supportive care. To improve the body's resistance, the patient may be prescribed a suspension of leukocytes, interferon, antistaphylococcal plasma. In severe, complicated clinical situations, the use of corticosteroids is indicated. To maintain vital parameters (pressure, respiration, etc.), symptomatic therapy is carried out: oxygen inhalations, enteral nutrition, injections of drugs that correct hypotension, metabolic changes and other pathological disorders.
radical treatment. Dead tissue is removed surgically. The volume and nature of the operation directly depends on the focus of infection, its localization. Radical therapy is indicated for the ineffectiveness of conservative methods.

One of the main goals of infusion therapy is the correct maintenance of normal blood flow in the tissues. The volumes of solutions are determined on an individual basis after assessing the actual hemodynamics, response to infusion.

The absence of antimicrobial therapy entails further deterioration and death of the patient.

If the correct antibiotic regimen is prescribed and applied in a timely manner, a decrease in intoxication can be achieved only by the third or fourth week of illness. Due to the fact that the functioning of almost all organs and systems is disrupted during extended septic shock, even a complete set of therapeutic actions does not always provide the desired result. That is why it is necessary to strictly monitor the course of any infectious disease, purulent-inflammatory processes that can provoke the development of bacterial shock, and to carry out their correct treatment.

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

Septic shock is a complex pathophysiological process resulting from the action of an extreme factor associated with a breakthrough into the bloodstream of pathogens or their toxins, 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 injury 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;
gamma interferon.

Along with the above 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, parts of the cell wall of a Gram-negative bacterium;
complement, metabolic products of arachidonic acid;
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, microcirculation disorders are the most important link. 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) or thrombohemorrhagic syndrome. Septic shock leads to disorders of all metabolic systems. Carbohydrate, protein and fat metabolism is disturbed, the utilization of normal energy sources - glucose and fatty acids - is sharply inhibited. In this case, a pronounced catabolism of muscle protein occurs. In general, the 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 relationship of these disorders can lead to the formation of a vicious circle with the complete depletion of the body's adaptive capabilities. Preventing the development of this vicious circle is the main task 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 focus 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, stunning chills are key signs in the diagnosis of septic shock. Very often, gradually progressive fever of a 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), is considered a reaction for trauma and surgery. Sometimes such symptoms serve as the basis for the diagnosis of a local infection. However, this phase of septic shock is called "warm normotension" and is often not diagnosed. In the study of central hemodynamics, a hyperdynamic circulation regime is determined (SI more than 5 l / min / m 2) without impaired oxygen transport (RTC 800 ml / min / m 2 or more), which is typical for the early stage of septic shock.

With the progression of the process, this clinical phase of septic shock is replaced by the phase of "warm hypotension", which is characterized by a maximum increase in body temperature, chills, changes in the patient's mental state (excitation, anxiety, inappropriate behavior, sometimes psychosis). When examining a patient, the skin is warm, dry, hyperemic or pink. Respiratory disorders are expressed by the type of hyperventilation, which further leads to respiratory alkalosis and fatigue of the respiratory muscles. There is tachycardia up to 120 beats or more per minute, 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 disorders 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 (urination less than 25 ml / h).

The clinical picture of the late stage of septic shock is characterized by impaired consciousness, severe disorders of pulmonary gas exchange, peripheral and central circulatory failure, organ pathology with signs of liver and kidney failure. External manifestations of this stage of septic shock are called "cold hypotension". When examining a patient, attention is drawn to the blackout of consciousness, up to the development of a coma; pallor of the 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, as a rule, auxiliary muscles are involved.

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 much lower than normal. The decrease in body temperature is combined with a distinct vegetative reaction in the form of heavy sweats. Cold, pale cyanotic, wet hands and feet is one of the pathognomonic symptoms of an 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, the 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 a progressive impairment of kidney function with severe symptoms such as azotemia and increasing oligoanuria (diuresis less than 10 ml/h).

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

It is generally accepted that the supply of oxygen to the body is quite adequate when the concentration of hemoglobin> 100 g / l, SaO 2 > 90% and SI> 2.2 l / min / m 2. Nevertheless, in patients with a 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 typical for the hypodynamic stage of septic shock. High tissue oxygen consumption 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 that is favorable for almost all shock variants.

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

The most characteristic changes in the 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 keep in mind the non-specificity of disorders of certain indicators of peripheral blood, their dependence on circulatory homeostasis, the constantly changing clinical picture of the disease, and the influence of therapeutic factors. It is generally accepted that leukocytosis with an increase in the leukocyte index of intoxication (LII> 10) and thrombocytopenia can be characteristic objective criteria for septic shock. Sometimes the dynamics of the leukocyte reaction has an undulating character: the initial leukocytosis is replaced by leukopenia, coinciding in time with mental and dyspeptic disorders, the appearance of polypnea, and then a rapid increase in leukocytosis is again observed. But even in these cases, the LII value progressively increases. This indicator is calculated by the formula [Kalf-Kalif Ya.Ya., 1943]:

where C - segmented neutrophils, P - stab, 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 decay. Leukopenia with high LII is always an alarming symptom of septic shock.

In the late stage of septic shock, hematological studies, as a rule, reveal moderate anemia (Hb 90-100 g/l), hyperleukocytosis up to 40×10 9 /l and higher with a limiting increase in LII up to 20 and more. Sometimes the number of eosinophils increases, which reduces LII, despite a distinct shift in the leukocyte formula towards immature forms of neutrophils. There may be leukopenia with no neutrophilic shift. When evaluating 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 control, indicators characterizing the state of metabolic homeostasis deserve attention. The most common diagnosis of metabolic disorders is based on the control of shifts in acid-base balance, blood gases and the assessment of 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 shock development. The correlation between the concentrations of lactate and endotoxin in the blood is quite pronounced, especially in septic shock.

In the study of blood acid-base balance in the early stages of septic shock, compensated or subcompensated metabolic acidosis is often determined against the background of hypocapnia and a high level of 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 have metabolic alkalosis. In the later stages of the development of septic shock, metabolic acidosis becomes uncompensated and often exceeds 10 mmol/l in terms of base deficiency. 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 becomes more and more necessary to dynamically determine the indicators of central hemodynamics (MOS, UO, SI, OPSS, etc.) and oxygen transport (a-V - oxygen difference, CaO 2, PaO 2, SaO 2), which allow assessing and determining the stage of shock and compensatory reserves of the body. SI in combination with other factors that characterize the features of oxygen transport in the body and tissue metabolism serve as criteria not only for the effectiveness of oxygen supply, but also for orientation in the prognosis of septic shock and the choice of the main direction of intensive care for circulatory disorders with outwardly identical manifestations of this pathological process - hypotension and low blood pressure. rate of diuresis.

In addition to a functional study, the diagnosis includes the identification of an etiological factor - the identification of the pathogen and the study of its sensitivity to antibacterial drugs. A bacteriological examination of blood, urine, wound exudate, etc. is carried out. With the help of biological tests, the severity of endotoxemia is examined. In clinics, diagnostics of immune deficiency is carried out on the basis of general tests: T- and B-lymphocytes, blast transformation, the level of immunoglobulins in 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);
neuropsychic disorders (disorientation, euphoria, agitation, stupor);
hyper- or hypodynamic syndrome of circulatory disorders. Clinical manifestations: tachycardia (HR = 100-120 per minute), Adsyst< 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 icteric skin);
tachypnea and hypoxemia (HR>20 per minute or PaCO 2<32 мм рт.ст., акроцианоз);
oligoanuria, urination - 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 a prodrome of septic shock: disturbance of consciousness (change in behavior and disorientation); hyperventilation determined by eye, and the presence of a source of infection in organism.

In recent years, a score scale for assessing organ failure associated with sepsis and shock (SOFA scale - Sepsis-related Organ Failure Assessment) has been widely used (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	PaO 2 /FiO 2 ,	<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 epinephrine >0.1* norepinephrine >0.1*
CNS	Score according to the Glasgow coma scale, 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 cardiotonic drugs in mg per 1 kg of body weight in 1 min for at least

The dysfunction of each organ (system) is assessed separately, in dynamics, 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 the treatment of insufficiency of only one organ is unrealistic. Only with an integrated approach to treatment can we hope for relative success.

Intensive treatment should be carried out in three principal directions. First in terms of time and significance - reliable elimination of the main etiological factor or disease that triggered and maintains the pathological process. With an unresolved focus of infection, 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 and electrolyte shifts, metabolic insufficiency, etc. Third - direct impact on the function of the affected organ, up to temporary prosthetics, should be started early, before the development of irreversible changes.

Antibacterial therapy, immunocorrection and adequate surgical treatment of septic shock in the fight against infection are important. Early antibiotic treatment should be started before culture is isolated and identified. This is of particular importance in immunocompromised patients, where treatment delays of more than 24 hours may result in adverse outcomes. In septic shock, the 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; immune status of the patient 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 examination become known. Combinations of 3rd-4th generation cephalosporins (longacef, rocefin, 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 of body weight. Longacef has a long half-life, so it can be used 1 time per day up to 4 g, rocefin - up to 2 g 1 time per day. Antibiotics that have a short half-life should be given 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. In the treatment of patients with a septic focus within the abdominal cavity or small pelvis, a combination of gentamicin and ampicillin (50 mg / kg per day) or lincomycin can be resorted to. If a gram-positive infection is suspected, vancomycin (Vancocin) up to 2 g/day is often used. When determining sensitivity to antibiotics, therapy can be changed. In cases where it was possible to identify the microflora, the choice of antimicrobial drug becomes direct. It is possible to use monotherapy with antibiotics with a narrow spectrum of action.

In some cases, along with antibiotics, powerful antiseptics can also be included in the antibacterial combination of drugs: dioxidine 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, in previous long-term antibiotic therapy.

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

Powerful intensive care will not be successful if the foci of infection are not removed surgically. Emergency surgery can be essential at any stage. Mandatory drainage and removal of inflammation. Surgical intervention should be low-traumatic, simple and reliable enough to ensure the primary and subsequent removal of microorganisms, toxins and tissue decay products from the focus. It is necessary to constantly monitor the emergence 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 CI of at least 4.5 l/min/m 2 , while the level of DO 2 must be more than 550 ml/min/m 2 . Tissue perfusion pressure can be considered restored, provided that the average blood pressure is not less than 80 mm Hg, and the TPVR is about 1200 dyn s/(cm 5 m 2). At the same time, excessive vasoconstriction, which inevitably leads to a decrease in tissue perfusion, must be avoided.

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

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

Adequate fluid volume replacement 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 blood pressure remains low after volume replacement, dopamine at a dose of 10–15 µg/kg/min or dobutamine at a dose of 0.5–5 µg/(kg min) is used to increase CO. If hypotension persists, adrenaline can be corrected 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 doses. Due to the risk of deterioration of oxygen transport and consumption, adrenaline can be combined with vasodilators (nitroglycerin 0.5-20 µg/kg/min, nanipruss 0.5-10 µg/kg/min). In the treatment of severe vasodilation seen in septic shock, potent vasoconstrictors, such as norepinephrine 1 to 5 μg/kg/min, or dopamine greater than 20 μg/kg/min, should be used.

Vasoconstrictors can have harmful effects and should be used to restore OPSS to normal limits of 1100-1200 dyn s/cm 5 m 2 only after BCC has been optimized. Digoxin, glucagon, calcium, calcium channel antagonists should be used strictly individually.

Respiratory therapy is indicated for patients with septic shock. Breathing support eases the burden on the DO 2 system and reduces the oxygen cost of breathing. Gas exchange improves with good oxygenation of the blood, 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 of at least 90%. The choice of treatment for ARF in septic shock depends on the degree of impaired gas exchange in the lungs, the mechanisms of its development, and signs of excessive load on the respiratory apparatus. With the progression of respiratory failure, 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, rheological infusion media are used (rheopolyglucin, 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 debatable, since sodium bicarbonate can aggravate acidosis (leftward shift of BWW, ionic asymmetry, etc.).

In the process of intensive care, coagulation disorders should be eliminated, since septic shock is always accompanied by DIC.

The most promising are therapeutic measures,

aimed at starting, initial, cascades of septic shock. As protectors of damage to cellular structures, it is advisable to use antioxidants (tocopherol, ubiquinone), and to inhibit blood proteases - antienzymatic drugs (gordox - 300,000-500,000 IU, contrical - 80,000-150,000 IU, trasilol - 125,000-200,000 IU ). It is also necessary to use agents that weaken the effect of humoral factors of septic shock - antihistamines (suprastin, tavegil) at 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 immunological status of the patient, the stage of shock and the severity of the condition. We believe that the use of steroids of high activity and duration of action, which have less pronounced side effects, may be justified. These drugs include the corticosteroids dexamethasone and betamethasone.

Under the conditions of infusion therapy, along with the task of maintaining water-electrolyte balance, the issues of energy and plastic supply are necessarily solved. 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 of 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 correcting hemodynamics in septic shock, which provides effective therapy for circulatory and oxygen transport disorders and can be used in practice.

Rational correction of hemodynamics.

It is necessary to perform the following principal therapeutic tasks within 24-48 hours.

Necessarily:

SI not less than 4.5 l / (min-m 2);
level DO 2 not less than 500 ml/(min-m 2);
mean blood pressure not less than 80 mm Hg;
OPSS within 1100-1200 dyn-sDcm^m 2).

If possible:

the level of oxygen consumption is not less than 150 ml / (min-m 2);
diuresis not less than 0.7 ml/(kg'h).

This requires:

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

2) if SI is not less than 4.5 l / (min-m 2), you can limit yourself to norepinephrine monotherapy at a dose of 0.5-5 μg / kg / min. If the SI level is below 4.5 l / (min-m 2), additional dobutamine is administered;

3) if CI is initially less than 4.5 l/(min-m 2), it is necessary to start treatment with dobutamine at a dose of 0.5-5 µg/(kg-min). Norepinephrine is added when mean BP 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 OPSS, dopamine or epinephrine can be combined with norepinephrine;

6) in case of oliguria, furosemide or small doses of dopamine (1-3 µg/kg-min) are used;

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

8) cancellation of vascular support can be started after 24-36 hours of stabilization period. In some cases, it may take several days for the complete withdrawal of vascular agents, especially norepinephrine. In the first days, the patient, in addition to the daily physiological need, should receive 1000-1500 ml of fluid as compensation for the vasodilation that occurs after the a-agonist withdrawal.

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

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

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

In the literature, septic shock is commonly referred to as infectious-toxic, bacteriotoxic or endotoxic shock. Thus, it is emphasized that this type of shock develops only in generalized infections that occur with massive bacteremia, intense decay of bacterial cells and the release of endotoxins that disrupt the regulation of the volume of the vascular bed. Septic shock can develop not only with bacterial infections, but also with viral infections, protozoan invasions, fungal sepsis, etc. In general clinical practice, the problem of septic shock has now become particularly relevant due to the widespread growth of septic diseases. The number of patients with sepsis in recent years has increased by 4-6 times. This was facilitated by the widespread, often irrational use of antibiotics that suppress the competitive flora and create conditions for the selection of pathogens insensitive to them, as well as the use of glucocorticosteroids and immunosuppressants that suppress defense mechanisms. An important role is played by the increase in the average age of patients, as well as the predominance of the "hospital" flora resistant to antibiotics in the etiology of sepsis.

The development of nosocomial sepsis and septic shock may be due to various factors. The likelihood of infection and the risk of developing septic shock carry with them some diagnostic and therapeutic procedures, contamination of intravenous media. A large percentage of septic conditions are associated with postoperative complications. Several medical emergencies, such as pancreatitis, fat embolism, hemorrhagic shock, ischemia, and various forms of tissue injury, can contribute to an increased chance of developing sepsis. Chronic diseases complicated by changes in the immune system can increase the risk of a generalized infection. The etiology of septic shock is most often gram-negative infection (65-70% of cases), but it can also develop with sepsis caused by gram-positive bacteria.

Advances in molecular biology and immunology have made it possible to understand many of the pathogenetic mechanisms of septic shock. It has now been proven that the infection itself is not the direct cause of numerous pathological changes characteristic of sepsis. Most likely they arise as a result of the body's response to infection and some other factors. This response is due to the increased action of various endogenous molecular substances that trigger the pathogenesis of sepsis. If in the normal state such molecular reactions can be regarded as reactions of adaptation or adaptation, then during sepsis their excessive activation is damaging. It is known that some of these active molecules can be released directly on the endothelial membrane of the target organ, resulting in damage to the endothelium and cause organ dysfunction.

Some known mediators of endothelial injury 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;

gamma interferon.

Potential mediators of the septic inflammatory response:

endotoxin;

exotoxin, parts of the cell wall of a Gram-negative bacterium;

complement, metabolic products of arachidonic acid;

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.

The development of the septic process is complicated by the fact that sepsis mediators can interact with each other, activating each other. Therefore, in the development of septic shock, unlike other types of shock, an important role is played by the interaction of endotoxin with mediator systems of the body. It is generally accepted that septic shock, like anaphylactic shock, is an immunopathological condition when, in response to a "breakthrough of the infection", phagocytosis is impaired or reduced, blocking substances appear in the blood, and a secondary immune deficiency develops. Endotoxin also acts as an inducer of macrophages and cascade systems, which persists even after homeostasis disturbances. In the development of these changes, the leading role belongs to TNF, interleukins (IL-1, IL-6, IL-8), etc. In addition, microbial invasion and toxemia quickly lead to profound metabolic, endocrine and circulatory disorders.

Violations of hemodynamics and oxygen transport in septic shock occupy one of the central places and are very complex. Some researchers argue that the simultaneous and multidirectional action of etiological and pathogenetic factors in septic shock leads to a violation of the distribution of blood flow and organ perfusion even against the background of normal blood pressure and high CO. It is microcirculation disorders that come to the fore in shock, and arterial hypotension is a late symptom of septic shock.

There are two main syndromes of circulatory disorders that characterize the stages of development of septic shock - hyperdynamic and hypodynamic. The early stage of septic shock, accompanied by circulatory hyperdynamia, is usually characterized by a decrease in total vascular resistance with a reflex-induced (from baroreceptors) increase in CO and heart function. This may be due to the direct influence of rapidly accumulating bacterial flora and endotoxins on the cardiovascular system and cellular metabolism. The reasons for the decrease in peripheral vascular resistance are the opening of low-resistance arteriovenous shunts and the direct discharge of blood through them. At the same time, oxygen consumption and the index of its delivery increase significantly, while oxygen extraction is within the normal range. Further manifestation of septic shock is also characterized by significant changes in the sympathetic-adrenal, pituitary-adrenal, kallikrein-kinin and other homeostasis regulation systems. The next stage of septic shock is characterized by a hyperdynamic regime of blood circulation and impaired oxygen transport. In this stage of shock, the increased productivity of the heart persists: the work of the left ventricle is significantly increased, but SI only slightly exceeds the norm. As a result of the predominance of the activity of noradrenaline, the alpha-adrenergic action of which promotes vasoconstriction, the total peripheral vascular resistance increases. The inevitable consequence of this is developing tissue hypoxia. Oxygen consumption and the index of its delivery to tissues decrease, and oxygen extraction increases significantly. A blockade of oxygen utilization at the subcellular level develops with the accumulation of lactate.

In the late stages of the development of septic shock, despite prolonged vasoconstriction and redistribution of blood to the periphery, a decrease in preload is observed, due to the devastation of the functioning capillary bed and, most importantly, fluid extravasation. This determines the development of secondary hypovolemic syndrome. Together with myocardiodepression, hypovolemia forms a hypodynamic syndrome. The stage of the hypodynamic regime of blood circulation is characterized by low rates of CO, delivery and consumption of oxygen against the background of increased extraction of the latter. Oxygen extraction drops sharply in the terminal stage of shock. A significant increase in oxygen extraction against the background of its reduced delivery and consumption is due not only to perfusion insufficiency and hypoxemia, but also to a significant impairment of cellular metabolism and oxygen utilization. Compensatory vasoconstriction with an increase in total vascular resistance can also be observed in the hypodynamic phase of septic shock. A significant increase in pulmonary vascular resistance and pulmonary hypertension become additional factors in the progression of myocardial insufficiency.

It has been established that the determining factor in the specifics of hemodynamic disorders in septic shock is not the characteristics of the microflora, but the systemic reaction of the patient's body, in which damage to the immune system plays an important role. Hyper- and hypodynamic syndromes in both gram-positive and gram-negative bacteremia are observed with almost the same frequency.

It should be emphasized that in septic shock, the main target organ, the lungs, is the first to be damaged. The main cause of lung dysfunction is caused by damage to the endothelium by mediators and inflammatory factors, which increases the permeability of blood vessels, leads to their microembolization and capillary dilatation. Changes in the permeability of the cell membrane can lead to a transmembrane flow of low molecular weight substances and macroions, which is accompanied by impaired cell function. Thus, interstitial pulmonary edema develops.

Once endothelial damage occurs, the target organs and tissues are more likely to develop multiple organ failure. Lung dysfunction may be followed first by hepatic, then by renal failure, which forms multiple organ failure syndrome(SPON). As MODS develops, each of the organs is unable to function adequately, which leads to the emergence of new factors of damaging effects on other organs and body systems.

Clinical picture. 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 focus 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, stunning chills are key signs in the diagnosis of septic shock. Very often, gradually progressive fever of a 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), is considered a reaction for trauma and surgery. Sometimes such symptoms serve as the basis for the diagnosis of a local infection. However, this phase of septic shock is called "warm normotension" and is often not diagnosed. In the study of central hemodynamics, a hyperdynamic circulation regime is determined (SI 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.

With the progression of the process, this clinical phase of septic shock is replaced by the phase of "warm hypotension", which is characterized by a maximum increase in body temperature, chills, changes in the patient's mental state (excitation, anxiety, inappropriate behavior, sometimes psychosis). When examining a patient, the skin is warm, dry, hyperemic or pink. Respiratory disorders are expressed by the type of hyperventilation, which further leads to respiratory alkalosis and fatigue of the respiratory muscles. There is tachycardia up to 120 beats or more per minute, 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 DO2 (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/м2) не обеспечивает должной потребности в кислороде.

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

It is generally accepted that the supply of oxygen to the body is quite adequate when the concentration of hemoglobin is > 100 g/l, SaO2 > 90% and CI > 2.2 l/min/m2. Nevertheless, in patients with a 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 typical for the hypodynamic stage of septic shock. High tissue oxygen consumption 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 that is favorable for almost all shock variants.

Most clinicians believe that the main objective diagnostic criteria for sepsis are changes in peripheral blood and metabolic disorders. The most characteristic changes in the blood: leukocytosis (12 x 109 / l) with a neutrophilic shift, a sharp "rejuvenation" of the leukocyte formula and toxic granularity of leukocytes. At the same time, one should keep in mind the non-specificity of disorders of certain indicators of peripheral blood, their dependence on circulatory homeostasis, the constantly changing clinical picture of the disease, and the influence of therapeutic factors. It is generally accepted that leukocytosis with an increase in the leukocyte index of intoxication (LII> 10) and thrombocytopenia can be characteristic objective criteria for septic shock. Sometimes the dynamics of the leukocyte reaction has an undulating character: the initial leukocytosis is replaced by leukopenia, coinciding in time with mental and dyspeptic disorders, the appearance of polypnea, and then a rapid increase in leukocytosis is again observed. But even in these cases, the LII value progressively increases. This indicator is calculated by the formula:

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

In the late stage of septic shock, hematological studies, as a rule, reveal moderate anemia (Hb 90-100 g/l), hyperleukocytosis up to 40x109/l and higher with a limiting increase in LII up to 20 and more. Sometimes the number of eosinophils increases, which reduces LII, despite a distinct shift in the leukocyte formula towards immature forms of neutrophils. There may be leukopenia with no neutrophilic shift. When evaluating 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.

In the study of blood acid-base balance in the early stages of septic shock, compensated or subcompensated metabolic acidosis is often determined against the background of hypocapnia and a high level of 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 have metabolic alkalosis. In the later stages of the development of septic shock, metabolic acidosis becomes uncompensated and often exceeds 10 mmol/l in terms of base deficiency. 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 PaO2, SaO2 is determined and, consequently, a decrease in the oxygen capacity of the blood. It should be emphasized that the severity of acidosis largely correlates with the prognosis.

In the diagnosis and treatment of septic shock, it becomes more and more necessary to dynamically determine the indicators of central hemodynamics (MOS, UO, SI, OPSS, etc.) and oxygen transport (a-V - oxygen difference, CaO2, PaO2, SaO2), which allow you to evaluate and determine the stage of shock and compensatory reserves of the body. 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 orientation in the prognosis of septic shock and the choice of the main direction of intensive care for circulatory disorders with outwardly identical manifestations of this pathological process - hypotension and low blood pressure. rate of diuresis.

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);

neuropsychic disorders (disorientation, euphoria, agitation, stupor);

hyper- or hypodynamic syndrome of circulatory disorders. Clinical manifestations: tachycardia (HR = 100-120 per minute), Adsyst< 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 icteric skin);

tachypnea and hypoxemia (HR>20 per minute or PaCO2<32 мм рт.ст., акроцианоз);

oligoanuria, urination - less than 30 ml / h (or the need to use diuretics to maintain sufficient diuresis);

vomiting, diarrhea;

leukocyte count >12.0 109/l, 4.0 109/l or immature forms >10%, LII >9-10;

lactate level >2 mmol/L.

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

In recent years, a score scale for assessing organ failure associated with sepsis and shock (SOFA scale - Sepsis-related Organ Failure Assessment) has been widely used (Table 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 1. ScaleSOFA

	Index
oxygenation	PaO2/FiO2, mm Hg
Coagulation	platelets
	Bilirubin, mg/dl, µmol/l		2,0-5,9 (33-101)	6,0-11,9 (102-204)
Cardiovascular system	Hypotension or degree of inotropic support	GARDEN<70 мм рт.ст.	dopamine < 5(mgkgmin)	Dopamine >5 (mgkgmin) or epinephrine<0,1 (мгкгмин) или норадреналин < 0,1 (мгкгмин)	Dopamine >15 (mgkgmin) or epinephrine >0.1 (mgkgmin) norepinephrine >0.1 (mgkgmin)
	Score according to the Glasgow coma scale, in points
	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

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

Treatment.

Intensive treatment should be carried out in three principal directions.

First in terms of time and significance - reliable elimination of the main etiological factor or disease that triggered and maintains the pathological process. With an unresolved focus of infection, 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 be started early, before the development of irreversible changes.

Antibacterial therapy, immunocorrection and adequate surgical treatment of septic shock in the fight against infection are important. Early antibiotic treatment should be started before culture is isolated and identified. This is of particular importance in immunocompromised patients, where treatment delays of more than 24 hours may result in adverse outcomes. In septic shock, the 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; immune status of the patient 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 examination become known. Combinations of 3-4th generation cephalosporins (stizon, cefepime, etc.) with aminoglycosides (amikacin) are often used. The dose of amikacin is 10-15 mg/kg of body weight. Antibiotics that have a short half-life should be given in large daily doses. If a gram-positive infection is suspected, vancomycin (Vancocin) up to 2 g/day is often used. When determining sensitivity to antibiotics, therapy can be changed. In cases where it was possible to identify the microflora, the choice of antimicrobial drug becomes direct. It is possible to use monotherapy with antibiotics with a narrow spectrum of action.

An important link in the treatment of septic shock is the use of drugs that enhance the immune properties of the body. Patients are given gamma globulin, specific antitoxic serums (antistaphylococcal, antipseudomonal).

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 CI of at least 4.5 l/min/m2, while the level of DO2 should be more than 550 ml/min/m2. Tissue perfusion pressure can be considered restored, provided that the mean blood pressure is at least 80 mm Hg, and the TPVR is about 1200 dyn s/(cm5 m2). At the same time, excessive vasoconstriction, which inevitably leads to a decrease in tissue perfusion, must be avoided.

Vasoconstrictors can have deleterious effects and should be used to restore OPSS to normal limits of 1100-1200 dyn s/cm5m2 only after BCC has been optimized. Digoxin, glucagon, calcium, calcium channel antagonists should be used strictly individually.

Respiratory therapy is indicated for patients with septic shock. Breathing support relieves the burden on the DO2 system and reduces the oxygen cost of breathing. Gas exchange improves with good oxygenation of the blood, 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 of at least 90%. The choice of treatment for ARF in septic shock depends on the degree of impaired gas exchange in the lungs, the mechanisms of its development, and signs of excessive load on the respiratory apparatus. With the progression of respiratory failure, the method of choice is mechanical ventilation in the PEEP mode.

Metabolic acidosis can be corrected if the pH is below 7.2. however, this position remains debatable, since sodium bicarbonate can aggravate acidosis (leftward shift of BWW, ionic asymmetry, etc.).

In the process of intensive care, coagulation disorders should be eliminated, since septic shock is always accompanied by DIC.

The most promising are therapeutic measures aimed at starting, initial, cascades of septic shock. As protectors of damage to cellular structures, it is advisable to use antioxidants (tocopherol, ubiquinone), and to inhibit blood proteases - anti-enzymatic drugs (gordox - 300,000-500,000 IU, contrical - 80,000-150,000 IU, trasilol - 125,000-200,000 IU ). It is also necessary to use agents that weaken the effect of humoral factors of septic shock - antihistamines (suprastin, tavegil) at 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 immunological status of the patient, the stage of shock and the severity of the condition. Currently, it is believed that the use of steroids of high potency and duration of action, which have less pronounced side effects, may be justified. These drugs include the corticosteroid dexamethasone.

Rational correction of hemodynamics. It is necessary to perform the following principal therapeutic tasks within 24-48 hours.

Necessarily:

SI not less than 4.5 l/(min-m2);

DO2 level not less than 500 ml/(min-m2);

mean blood pressure not less than 80 mm Hg;

OPSS within 1100-1200 dyn-sDcm^m2).

If possible:

the level of oxygen consumption is not less than 150 ml/(min*m2);

diuresis not less than 0.7 ml / (kg "h).

This requires:

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

if SI is not less than 4.5 l / (min-m2), noradrenaline monotherapy at a dose of 0.5-5 μg / kg / min can be limited. If the CI level is below 4.5 l/(min-m2), additional dobutamine is administered;

if the initial SI is 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 BP remains less than 80 mm Hg;

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

epinephrine, isoproterenol, or inodilators may be combined with dobutamine to manage CO levels; to correct OPSS, dopamine or epinephrine can be combined with norepinephrine;

in the case of oliguria, furosemide or small doses of dopamine (1-3 μg / kg-min) are used;

every 4-6 hours it is necessary to control the parameters of oxygen transport, as well as to correct the treatment in accordance with the ultimate goals of therapy;

the withdrawal of vascular support can be started after 24-36 hours of stabilization period. In some cases, it may take several days for the complete withdrawal of vascular agents, especially norepinephrine. In the first days, the patient, in addition to the daily physiological need, should receive 1000-1500 ml of fluid as compensation for the vasodilation that occurs after the abolition of antagonists.

Thus, septic shock is a rather complex pathophysiological process that requires a meaningful, rather than a stereotyped, approach both in diagnosis and in treatment.

The complexity and interconnectedness of pathological processes, the variety of mediators in septic shock create many problems in choosing an adequate therapy for this terrible complication of many diseases.

Mortality in septic shock, despite rational intensive care, is 40-80 %.

The emergence of promising methods of immunotherapy and diagnostics opens up new treatment options that improve the outcomes of septic shock.

Pathological condition, which has long been known as blood poisoning, is now called septic shock. Shock develops due to a disseminated bacterial infection, in which the infectious agent is carried by the blood from one tissue to another, causing inflammation of various organs and intoxication. There are varieties of septic shock due to the specific action of different types of bacterial infection.

Performance about septic shock is of great clinical importance, tk. it, along with cardiogenic shock, is the most common cause of death in patients who are in the clinic in a state of shock.

The most common causes of septic shock are the following.
1. Peritonitis caused by infectious processes in the uterus and fallopian tubes, including those resulting from instrumental abortion performed under non-sterile conditions.
2. Peritonitis caused by damage to the wall of the gastrointestinal tract, including those caused by intestinal diseases or injuries.

3. Sepsis resulting from an infection of the skin with streptococcal or staphylococcal microflora.
4. A widespread gangrenous process caused by a specific anaerobic pathogen, first in peripheral tissues, and then in internal organs, especially in the liver.
5. Sepsis resulting from infection of the kidneys and urinary tract, most often caused by Escherichia coli.

The skin of a child with sepsis

Features of septic shock. Typical manifestations of septic shock of various origins are as follows.
1. Severe fever.
2. Widespread expansion of blood vessels, especially in infected tissues.

3. An increase in cardiac output in more than half of patients, caused by the expansion of arterioles, which occurs due to general vasodilation, as well as due to an increase in the level of metabolism under the influence of bacterial toxins and high temperature.
4. Change in the rheological properties of the blood (“thickening”) caused by agglutination of erythrocytes in response to tissue degeneration.
5. The formation of microthrombi in the vascular bed is a condition characterized as disseminated intravascular coagulation (DIC). Since coagulation factors are involved in this process, a deficiency of coagulation factors is formed in the remaining circulating blood. In this regard, bleeding is observed in many tissues, especially in the gastrointestinal tract.

Early stages of septic shock against the background of a bacterial infection, symptoms of circulatory collapse do not appear. If the infectious process progresses, the circulatory system is involved due to both the direct action of the infectious principle and the secondary action, namely intoxication, leading to damage to the capillary wall and the release of plasma from the capillaries into the tissues. Then comes the moment from which hemodynamic disturbances develop in the same way as during other types of shock. The final stages of septic shock do not differ significantly from the final stages of hemorrhagic shock, even though the causes of the two conditions are quite different.

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 that trigger the shock mechanism (the entrance gate of infection and the duration of the 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 1950s, the main causative agent of sepsis was streptococcus, later staphylococcus became the predominant pathogen, 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 at 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. Zilbera (), appropriate conditions are necessary so that E. coli, one of the most common pathogens of septic shock syndrome, living in commonwealth with humans, participating in microbial protein hydrolysis, producing B vitamins, fighting typhoid, dysentery and putrefactive microbes, suddenly began to kill his master.

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

Debilitating diseases, concomitant surgical pathologies (blood diseases, oncopathology, systemic diseases), as well as the state of the hormonal background, are essential 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, beriberi, chronic intoxications (drug addiction, alcoholism).

Primary purulent focus (or entrance gate for infection) and the duration of the action of these gates is a necessary factor related to the trigger of septic shock.

The 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 major surgeries, resuscitation 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 procedures, and has recently been called the "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 the imperfection of knowledge and diagnosis. The diagnosis of cryptogenic sepsis takes the doctor away from the search for the primary focus and, therefore, makes it difficult to make a correct diagnosis and conduct a full-fledged 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 there is a peritoneal form of septic shock, and the next place of entry gate for infection in postoperative septic shock is occupied by the biliary tract (biliary form). As an intestinal variant of postoperative sepsis, the development of antibiotic-associated pseudomembranous colitis with the appearance of diarrheal syndrome of varying severity at the first stage can be considered. Fatty tissue can become an entrance gate, especially in cases where purulent inflammation occurs with progressive cellulitis of the perirenal, retroperitoneal, intermuscular tissue. Increasingly important in the practice of intensive care are unusual ways of infection penetration: with prolonged tracheal intubation and tracheostomy, with catheterization of the central vessels. Therefore, the vascular, or angiogenic, form of septic shock can occur not only as a result of purulent thrombophlebitis, which complicates the course of the wounded process, but as an independent complication.

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

The 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, 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, there is a decrease in the activity of natural antiproteases. As a result, the total proteolytic activity of the blood increases according to the severity of the systemic inflammatory reaction.

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

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.

With SS, there are always signs of damage to life-support organs. The defeat of 2 organs or more is classified as a syndrome of multiple organ failure.

The degree of CNS dysfunction may vary from mild stupor to deep coma. Approximately 1 in 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 breath sounds, the appearance of diffuse 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 established by increasing 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 hepatic transaminases and other markers of cellular liver failure in the blood. In the gastrointestinal tract, the damaging effect of a 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, there is a decrease in cardiac output, 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 patients in the ICU. Standard monitoring should include:

Dynamic determination of blood pressure, heart rate, SV and IOC, the level of CVP; 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 the determination of the gradient between the internal and peripheral T of the patient's body);

Dynamics of reference biochemical indicators (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 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 tenfold in 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 the body's antioxidant defense.

Treatment of septic shock.

Therapeutic measures in septic shock have 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 rapid infusion of 1-2 liters of crystalloid solutions with fixing the effect of colloid solutions (at a ratio of 2:1) under the control of hemodynamic monitoring (BP, CVP, CO) and the rate of diuresis. Of decisive importance in the stabilization of hemodynamics is inotropic support, which ensures the relief of hemodynamic disorders and the maintenance of an adequate level of tissue perfusion. The first choice for inotropic support against the background of SS is dopamine, used either in low 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 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 SS therapy. 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 volume 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 involvement should not be the position - "the patient is too heavy to intervene", but vice versa - "the patient is too sick to postpone intervention ...". Any intensive therapy for SS can become ineffective precisely because of the presence of undiagnosed or poorly operated foci of wound infection.

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

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

Improving the 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 C;

Reducing dyspnea and increasing PaO2 at a stable level;

Decrease in heart rate, normalization of systemic blood pressure and CVP with the restoration of the 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 ongoing treatment.

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Causal factors

Pathogenetic mechanism

Types of septic shock

Manifestations of shock

Shock conditions in obstetric (gynecological) practice

Anti-shock therapeutic measures - the main directions

Some known mediators of endothelial injury 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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