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Septic shock with cardiac complications. Septic shock in intensive care

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

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

In the literature, septic shock is usually referred to as infectious-toxic, bacteriotoxic or endotoxic shock. This emphasizes 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, but also with viral infections, protozoan infestations, fungal sepsis, etc. In general clinical practice, the problem septic shock has now acquired particular relevance due to the widespread increase in septic diseases. The number of patients with sepsis has increased 4-6 times in recent years. This was facilitated by the widespread, often irrational use of antibiotics that suppress competitive flora and create conditions for the selection of pathogens insensitive to them, as well as the use of glucocorticosteroids and immunosuppressants that inhibit defense mechanisms. An important role is played by the increase in the average age of patients, as well as the predominance of “hospital” flora resistant to antibiotics in the etiology of sepsis.

The development of nosocomial sepsis and septic shock can be caused by various factors. The likelihood of infection and the risk of developing septic shock are associated with some diagnostic and therapeutic procedures and contamination of intravenous media. A large percentage of septic conditions are associated with postoperative complications. Certain emergency conditions, such as pancreatitis, fat embolism, hemorrhagic shock, ischemia, and various forms of trauma that cause tissue damage, may increase the likelihood of developing sepsis. Chronic diseases complicated by changes in immune system, may increase the risk of generalized infection. The etiology of septic shock is most often dominated by 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 provided insight into many of the pathogenetic mechanisms of septic shock. It has now been proven that 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 increased action of various endogenous molecular substances, which trigger the pathogenesis of sepsis. If in a normal state such molecular reactions can be regarded as adaptation reactions, 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, leading to endothelial damage and causing organ dysfunction.

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

tumor necrotizing factor (TNF);

interleukins (IL-1, IL-4, IL-6, IL-8);

platelet activating factor (PAF);

leukotrienes (B4, C4, D4, E4);

thromboxane A2;

prostaglandins (E2, E12);

prostacyclin;

interferon gamma.

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

Potential mediators of the septic inflammatory response:

endotoxin;

exotoxin, part of the cell wall of a gram-negative bacterium;

complement, products of arachidonic acid metabolism;

polymorphonuclear leukocytes, monocytes, macrophages, platelets;

histamine, cell adhesion molecules;

coagulation cascade, fibrinolytic system;

toxic oxygen metabolites and other free radicals;

kallikrein-kinin system, catecholamines, stress hormones.

The development of the septic process is complicated by the fact that sepsis mediators can interact with each other, activating each other. Consequently, in the development of septic shock, unlike other types of shock, the interaction of endotoxin with the body’s mediator systems plays an important role. It is generally accepted that septic shock, like anaphylactic shock, is an immunopathological condition when, in response to a “breakthrough infection,” phagocytosis is disrupted or reduced, blocking substances appear in the blood and a secondary immune deficiency develops. Endotoxin also plays the role of an inducer of macrophages and cascade systems, persisting even after disturbances of homeostasis. 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.

Disorders of hemodynamics and oxygen transport during 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 disruption of the distribution of blood flow and organ perfusion, even against the background of normal blood pressure and high CO. Microcirculatory disorders 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. For early stage septic shock, accompanied by circulatory hyperdynamia, is usually characterized by a decrease in total vascular resistance with a reflexively caused (from baroreceptors) increase in CO and cardiac function. This may be due to the direct effect 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 its delivery index increase significantly, while oxygen extraction is within normal limits. 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 circulatory regime and impaired oxygen transport. At this stage of shock, increased cardiac performance remains: the work of the left ventricle is significantly increased, but CI is only slightly higher than normal. As a result of the predominance of the activity of norepinephrine, the alpha-adrenomimetic effect 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 are reduced, and oxygen extraction is significantly increased. A blockade of oxygen utilization develops at the subcellular level with the accumulation of lactate.

In the later stages of development of septic shock, despite prolonged vasoconstriction and redistribution of blood in the periphery, a decrease in preload is observed, explained by the devastation of the capillary functioning bed and, most importantly, fluid extravasation. This determines the development of secondary hypovolemic syndrome. Together with myocardial depression, hypovolemia forms a hypodynamic syndrome. The stage of the hypodynamic circulatory regime is characterized by low levels of CO, oxygen delivery and consumption against the background of increased extraction of the latter. Oxygen extraction drops sharply in terminal stage shock. A significant increase in oxygen extraction against the background of reduced oxygen delivery and consumption is caused not only by perfusion insufficiency and hypoxemia, but also by a significant disruption 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 failure.

It has been established that the determining factor in the specificity 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 a major role. Hyper- and hypodynamic syndromes with 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, leading to their microembolization and capillary dilatation. Changes in cell membrane permeability can lead to transmembrane flux 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 liver failure, then by kidney failure, which forms multiple organ failure syndrome(SPON). As MODS develops, each organ is unable to function adequately, which leads to the emergence of new factors that have a damaging effect on other organs and systems of the body.

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

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

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 blood circulation, and subsequently in the form of organ damage.

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

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

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

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

Chills and hyperthermia are replaced by a decrease in body temperature, often with its critical drop to subnormal numbers. The skin temperature of the distal extremities, even to the touch, is significantly lower than normal. A decrease in body temperature is combined with a distinct vegetative reaction in the form of heavy sweats. Cold, pale cyanotic, wet hands and feet are one of the pathognomonic symptoms of the unfavorable course of a generalized infection. At the same time, relative signs of a decrease in venous return are revealed in the form of desolation of the peripheral venous subcutaneous network. Frequent, 130-160 per minute, weak filling, sometimes arrhythmic, 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 progressive renal dysfunction with severe symptoms such as azotemia and increasing oligoanuria (diuresis less than 10 ml/h).

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

It is generally accepted that the supply of oxygen to the body is quite adequate at a hemoglobin concentration of >100 g/l, SaO2 >90% and CI>2.2 l/min/m2. However, in patients with pronounced redistribution of peripheral blood flow and peripheral shunting, oxygen supply, even with these indicators, may be inadequate, resulting in hypoxia with a high oxygen debt, which is characteristic of the hypodynamic stage of septic shock. High oxygen consumption by tissues in combination with low transport of the latter indicates the possibility of an unfavorable outcome, while increased oxygen consumption in combination with an increase in its transport is a sign favorable for almost all types of shock.

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

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

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

In the late stage of septic shock, hematological studies usually reveal moderate anemia (Hb 90-100 g/l), hyperleukocytosis up to 40x109/l and higher with a maximum increase in LII to 20 or more. Sometimes the number of eosinophils increases, which reduces LII, despite a clear shift in the leukocyte formula towards immature forms of neutrophils. Leukopenia with the absence of neutrophilic shift may be observed. When assessing the leukocyte reaction, it is necessary to pay attention to the decrease in the absolute concentration of lymphocytes, which can be 10 times or more below the normal value.

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

When examining blood CBS in the early stages of septic shock, compensated or subcompensated metabolic acidosis is often determined against the background of hypocapnia and high level lactate, the concentration of which reaches 1.5-2 mmol/l or more. In the early stage of septicemia, temporary respiratory alkalosis is most characteristic. Some patients experience metabolic alkalosis. In the later stages of development of septic shock, metabolic acidosis becomes uncompensated and, due to base deficiency, often exceeds 10 mmol/l. The level of lactate acidemia reaches 3-4 mmol/l or more and is a criterion for the reversibility of septic shock. As a rule, a significant decrease in PaO2, SaO2 and, consequently, a decrease in the oxygen capacity of the blood is determined. It should be emphasized that the severity of acidosis largely correlates with the prognosis.

In the diagnosis and treatment of septic shock, it is becoming more and more necessary to dynamically determine indicators of central hemodynamics (MOS, SV, CI, OPSS, etc.) and oxygen transport (a-V - difference in oxygen, CaO2, PaO2, SaO2), which make it possible to evaluate and determine the stage of shock and the body’s compensatory reserves. SI in combination with other factors characterizing the characteristics of oxygen transport in the body and tissue metabolism serve as criteria not only for the effectiveness of oxygen supply, but also for guidance in the prognosis of septic shock and the choice of the main direction of intensive therapy for circulatory disorders with outwardly identical manifestations of this pathological process - hypotension and low rate of diuresis.

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

Diagnostic criteria for septic shock:

the presence of hyperthermia (body temperature >38-39 °C) and chills. In elderly patients, paradoxical hypothermia (body temperature<36 °С);

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

hyper- or hypodynamic circulatory disorder syndrome. Clinical manifestations: tachycardia (heart rate = 100-120 per minute), Adsist< 90 мм рт.ст. или его снижение на 40 мм рт.ст. и более от среднего в отсутствие других причин гипотензии;

microcirculation disorders (cold, pale, sometimes slightly or intensely jaundiced skin);

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

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

vomiting, diarrhea;

leukocyte count >12.0 109/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 the prodrome of septic shock: disturbance of consciousness (change in behavior and disorientation); hyperventilation, determined by eye, and presence of a focus of infection in organism.

In recent years, a scoring 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, mmHg
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 adrenaline<0,1 (мгкгмин) или норадреналин < 0,1 (мгкгмин)	Dopamine >15 (mgkgmin) or adrenaline >0.1 (mgkgmin) norepinephrine >0.1 (mgkgmin)
	Glasgow Coma Scale score, 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, dynamically, daily, against the background of intensive therapy.

Treatment.

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

Intensive treatment should be carried out in three fundamental directions.

First in terms of time and significance - reliable elimination of the main etiological factor or disease that started and maintains the pathological process. If the source of infection is not eliminated, any modern therapy will be ineffective.

Second - treatment of septic shock is impossible without correction of disorders common to most critical conditions: hemodynamics, gas exchange, hemorheological disorders, hemocoagulation, water-electrolyte shifts, metabolic insufficiency, etc.

Third - direct impact on the function of the affected organ, up to temporary prosthetics, should begin early, before the development of irreversible changes.

Antibacterial therapy, immunocorrection and adequate surgical treatment of septic shock are important in the fight against infection. Early treatment with antibiotics should be initiated before culture is isolated and identified. This is of particular importance in patients with compromised immunity, where a delay in treatment of more than 24 hours may result in an unfavorable outcome. For septic shock, immediate use of broad-spectrum parenteral antibiotics is recommended. The choice of antibiotics is usually determined by the following factors: the likely pathogen and its sensitivity to antibiotics; underlying disease; patient's immune status and pharmacokinetics of antibiotics. As a rule, a combination of antibiotics is used, which ensures their high activity against a wide range of microorganisms before the results of microbiological testing become known. Combinations of 3-4th generation cephalosporins (stizone, cefepime, etc.) with aminoglycosides (amikacin) are often used. The dose of amikacin is 10-15 mg/kg body weight. Antibiotics that have a short half-life must be prescribed 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 may be changed. In cases where it was possible to identify the microflora, the choice of antimicrobial drug becomes straightforward. It is possible to use monotherapy with antibiotics that have a narrow spectrum of action.

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

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

In the interests of optimal correction of homeostasis, the clinician must simultaneously provide correction of various pathological changes. It is believed that for an adequate level of oxygen consumption it is necessary to maintain an SI of at least 4.5 l/min/m2, while the DO2 level must be more than 550 ml/min/m2. Tissue perfusion pressure can be considered restored provided that the average blood pressure is at least 80 mm Hg and the peripheral vascular resistance is about 1200 dynes s/(cm5 m2). At the same time, it is necessary to avoid excessive vasoconstriction, which inevitably leads to decreased tissue perfusion.

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

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

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

Vasoconstrictors can have harmful effects and should be used to restore peripheral vascular resistance to normal limits of 1100-1200 dynes s/cm5m2 only after optimizing the volume of blood volume. Digoxin, glucagon, calcium, calcium channel antagonists should be used strictly individually.

Respiratory therapy is indicated for patients with septic shock. Breathing support eases the load on the DO2 system and reduces the oxygen cost of breathing. Gas exchange improves with good blood oxygenation, so oxygen therapy, ensuring airway patency and improving the drainage function of the tracheobronchial tree are always required. It is necessary to maintain PaOz at a level of at least 60 mm Hg, and hemoglobin saturation at least 90%. The choice of treatment method for ARF in septic shock depends on the degree of gas exchange disturbance 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 purpose, rheological infusion media are used (reopolyglucin, plasmasteril, HAES-steril, reogluman), as well as chimes, complamin, trental, etc.

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

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

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

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

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

Rational correction of hemodynamics. The following fundamental therapeutic tasks must be completed within 24-48 hours.

Necessarily:

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

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

average blood pressure is at least 80 mm Hg;

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

If possible:

oxygen consumption level of at least 150 ml/(min*m2);

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

This requires:

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

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

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

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

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

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

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

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

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

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

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

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

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

Causes of septic shock:

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

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

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

Patients at increased risk include:

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

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

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

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

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

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

Septic shock - symptoms

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

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

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

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

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

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

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

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

Septic shock - causes and development factors

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

Escherichia coli;
aerobic and anaerobic streptococci;
clostridia;
bacteroides;
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 the patient.

Septic shock (and sepsis) is an inflammatory response to a trigger. 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 an inflammatory process. Exotoxins are substances that gram-negative bacteria secrete.

Toxins enter the blood and stimulate the production of inflammatory cytokines, including: tumor necrosis factor, interleukin-1, interleukin-8 in the vascular endothelium. This reaction leads to adhesion (sticking) 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 characteristics of its course and the stage of compensation.

Depending on the location of the pathological process, septic shock occurs:

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

Along the way, septic shock occurs:

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 of septic shock largely depend on the pathogenic pathogen, the state of 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 nonspecific symptoms of sepsis include the following:

enlarged spleen;
liver enlargement;
intense sweating (after chills);
physical inactivity;
severe weakness;
bowel dysfunction (usually constipation).

The lack of antibacterial therapy leads to multiple damage to internal organs and death of the patient. With septic shock, thrombosis is possible, combined with hemorrhagic syndrome.

If, during septic shock, the patient is given adequate antibacterial therapy, then the manifestations of intoxication decrease after 2-4 weeks from the onset of the disease. Against the background of septic shock, arthralgia develops due to massive infection and the inflammatory process. 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 the background of various disorders are:

Symptoms of septic shock in severe disseminated intravascular coagulation syndrome and respiratory distress syndrome. In this case, the development of interstitial edema is possible, which entails the appearance of polymorphic shadows and disc-shaped atelectasis in the lungs. Similar changes in the lungs are observed in other severe forms of septic shock. It is noteworthy that the X-ray images of the lungs are almost the same as those of pneumonia.
Septic abortion. As a rule, with a septic abortion, bleeding does not occur, since in this case an inflammatory reaction is observed in the uterus. As a rule, the vessels become clogged with microbes, blood clots and bloody discharge mixed with purulent masses. It is possible to develop toxic anemia and change skin color. The patient sometimes develops petechial hemorrhages, which can form on the mucous membrane, on the skin and in the internal organs. In some cases, it reaches the formation of extensive superficial necrosis.
Tachypneous in septic shock. Due to disruption of the cardiovascular system, a patient with septic shock develops tachypnea. The respiratory rate can reach up to 40 breaths/exhalations per minute.
Septic pneumonia. This is a fairly common complication of the septic process in the body.
Liver damage in septic shock. The pathology is accompanied by a noticeable increase in liver size. The liver is painful, and an increase in the level of transaminases and 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 in septic shock. With a sharp decrease in circulating blood volume and a decrease in blood pressure, diuresis also decreases. Urine becomes low-density and markers of the inflammatory process are found in it. In the kidneys, functional and organic lesions are possible, which are irreversible.
Impaired intestinal motility. With septic shock, intestinal paresis and severe disturbances of parietal digestion are possible. A putrefactive process starts in the intestines, septic diarrhea and dysbacteriosis appear. It is quite difficult to compensate for such violations.
Trophic disorders. Bedsores occur quite early 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 immediately hospitalized and intensive care should be started. The disease develops quite rapidly, leading to severe complications and even death. Therefore, it is important to get the patient to the hospital as quickly as possible.

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

First of all, treatment of septic shock should be comprehensive and take into account the type of pathogenic flora that caused the pathology. The main treatment for septic shock is massive antibacterial therapy, anti-inflammatory therapy and immunomodulatory therapy. Hormonal therapy is also possible.

Antibacterial therapy. Massive antibacterial therapy for septic shock should be accompanied by the use of at least two broad-spectrum antibacterial drugs. If a 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 through the endolymphatic route).

When carrying out antibacterial therapy, blood cultures are regularly performed to identify pathogenic microbes. Treatment with antibiotics may continue for several months until the bacterial culture is negative and doctors achieve lasting clinical recovery.

To improve the body's resistance, the patient can be given a leukocyte suspension, interferon, or hyperimmune antistaphylococcal plasma. In severe cases, hormonal corticosteroid drugs 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 location of the lesion, different surgical interventions are performed.
Maintenance treatment. To maintain the 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. Mask oxygen inhalations are performed to ensure proper oxygenation.

Complications of septic shock

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

Prevention of septic shock

Prevention of septic shock is measures that do not allow blood poisoning to develop. In case of septic shock, it is important to prevent the development of internal organ failure and maintain the normal functioning of the patient’s body.

Septic shock is the last stage of sepsis, dangerous for organ failure and death.

The main reason for the development is ignoring the growing symptoms of general sepsis, the lightning-fast course of some infectious diseases, the reluctance to consult a doctor (or the lack of proper attention from medical personnel to the patient).

When the first symptoms of pathology are detected, you should urgently call an ambulance, since the possibility of survival depends on the speed of initiation of therapy and the degree of organ damage.

Septic shock is a complication of the infectious process, which is manifested by impaired microcirculation and tissue permeability to oxygen.

In essence, this is severe poisoning of the body with bacterial poisons and decay products of tissues damaged during the disease. The pathology is extremely life-threatening and has a high mortality rate, up to 50%.

In ICD 10, the disease is indicated together with the main disease with the additional code R57.2.

Why does it occur?

The precursor of the pathology is considered to be a diffuse infectious process, or sepsis.

The infection is caused by bacteria, protozoa, viruses and other agents entering the body, as well as an immune response to various foreign substances in the bloodstream.

One of the manifestations of the process is inflammation, which is a key link in pathogenesis.

The body's immunity responds to the appearance of foreign bodies in two ways:

Activation of lymphocytes, which recognize and absorb infectious agents.
Release of cytokines and immune hormones.

Normally, this speeds up the fight against the disease. However, with a long-term and widespread infection, cytokines lead to severe vasodilation and a drop in blood pressure.

These factors lead to impaired absorption of oxygen and nutrients into the walls of blood vessels, causing hypoxia of organs and disruption of their function.

Phases of development

Septic shock has three sequential stages:

Hyperdynamic, warm.
Hypodynamic, cold.
Terminal, irreversible.

The first is characterized by a strong rise in temperature, up to 40-41 degrees Celsius, a drop in blood pressure up to collapse, increased breathing and severe muscle pain. The duration varies from 1-2 minutes to 8 hours. It is the body's primary response to the release of cytokines.

Additionally, in the first stage, symptoms of damage to the nervous system may increase - the appearance of hallucinations, depression of consciousness, and incessant vomiting. Preventing collapse is especially important for obstetrics - newborns have a very difficult time with circulatory disorders.

A sign of the second stage is a drop in temperature to 36 degrees and below. Hypotension does not go away, leaving a threat of collapse. Symptoms of cardiac and respiratory failure increase - rhythm disturbances, tachycardia, which abruptly gives way to bradycardia, severe increased breathing. Necrotic areas appear on the skin of the face and mucous membranes - small dark spots.

Hypodynamic septic shock is reversible - oxygen starvation has not yet led to terminal changes in the organs, and most of the resulting side pathologies are still treatable. Typically the duration is from 16 to 48 hours.

The irreversible stage is the last phase of septic shock, which ends in multiple organ failure and death. The process of destruction of the heart muscle progresses, massive necrosis of the lung tissue begins with disruption of the gas exchange process. The patient may develop jaundice and hemorrhages caused by deterioration of blood clotting. Areas of necrosis form in all organs and tissues.

If the patient was able to survive, then the main problem is organ failure and the consequences of hemorrhages due to concomitant DIC. The prognosis at this stage is complicated by the slowing of blood flow, which complicates the already impaired blood circulation.

And also, septic shock has a classification according to the stages of compensation:

Compensated.
Subcompensated.
Decompensated.
Refractory.

Varieties are important for the choice of treatment method. For a person, they differ in the amount of symptoms - the further the disease progresses, the stronger the negative effects are felt. The last stage cannot be treated.

The disease is also classified according to the site of primary infection. This division is important in surgical treatment, when the intervention is aimed at removing purulent formation.

Main features

The following symptoms indicate the development of septic shock:

Temperature above 38 degrees or below 36.
Tachycardia, heart rate over 90 beats per minute, arrhythmia.
Increased respiratory rate, more than 20 chest contractions per minute.
High, more than 12x10^9/l, or low, less than 4x10^9/l, the number of leukocytes in the blood.

The temperature depends on the stage of the disease and an increase in temperature is an indicator that the body is still struggling.

Tachycardia can be replaced by sharp drops in heart rate, which is especially dangerous in the presence of pathology of the heart muscle. The breathing rate reflects the total lack of oxygen to the tissues and the body’s attempt to reflexively restore balance.

Some symptoms of septic shock may also include:

Hallucinations, changes in perception, depression of consciousness, coma.
The appearance of necrotic spots on the skin.
Involuntary bowel movements and urination, blood in stool or urine, little or no urine.

These clinical criteria allow us to identify specific lesions in the body. The first group reflects disorders in the brain, such as stroke.

Necrotic spots reflect a severe lack of blood in the superficial tissues. The last group speaks of damage to the digestive and excretory systems, with damage to the muscular system.

A decrease in the amount of urine indicates the development of kidney failure and the need for artificial blood purification - dialysis.

Diagnostic methods

The study for septic shock begins with a blood test - an immunogram.

Important diagnostic indicators are:

Total leukocyte level.
Cytokine levels.
Leukocyte formula.

The pathology is directly related to the immune system, and its altered state is a direct indicator. White blood cells may be decreased or increased, depending on the stage and strength of the response. More often, patients with this diagnosis experience an excess of one and a half to two times the norm.

Since this process is the result of the entry of a huge amount of cytokines into the blood, their level will be significantly exceeded. In some cases, cytokines may not be detected.

The leukocyte formula helps determine the cause of the pathology. With a microbiological cause, there is an increased number of young forms of leukocytes, which are formed to respond to an emerging infection.

A general laboratory blood test will also help to conduct a differential study to exclude certain pathologies. In septic shock, the ESR will be significantly increased, as a result of changes in the protein composition of the blood - an increase in the concentration of markers of the inflammatory process.

Bacteriological analysis of the discharge to determine the infectious agent is important. The material can be taken from the mucous membranes of the nasopharynx or purulent focus. Blood cultures are required.

Determining the type of pathogen allows you to more accurately select antibiotics.

Another diagnostic method is the study of hemodynamics, in terms of the amount of oxygen transferred and carbon dioxide removed. In shock, there is a sharp decrease in the amount of CO2, which means reduced oxygen consumption.

An ECG is used to diagnose myocardial lesions. In a state of shock, signs of coronary heart disease are noted - a significant jump in the ST segment (“cat’s back”).

How is the treatment carried out?

Therapy for septic shock consists of first aid measures, medication and surgical treatment.

Urgent Care

Most patients with severe infection are sent to the hospital to monitor the development of pathology. However, people often refuse specialized help.

If this condition develops outside the hospital, then you should urgently call an ambulance, accurately determine the patient’s stage and provide emergency assistance.

The hyperthermic stage is determined by the presence of:

Temperatures above 39-40 degrees.
Cramps.
Tachycardia, over 90 beats per minute.
Tachypnea, number of respirations - over 20 per minute.

When the body temperature rises above 41-42 degrees, protein coagulation begins, followed by death, and the work of enzymes stops.

Seizures also indicate the beginning of damage to nerve tissue. Cooling of the body can be done using ice heating pads or a cold water bath.

The hypothermic stage can be determined by:

Temperature below 36 degrees.
Blue discoloration of the skin.
Reduced breathing.
Heart rate drop.

If your heart rate is low, there is a risk of cardiac arrest, so you need to be prepared to start cardiopulmonary resuscitation.

To alleviate the condition, emergency doctors can introduce drugs that increase vascular tone and support heart function. If necessary, artificial ventilation and oxygen supply are performed to improve oxygenation of the brain and other tissues.

In the hospital, the patient is connected to a ventilator and the temperature is lowered or raised.

The location in the intensive care unit allows the team to quickly respond to organ damage, cardiac arrest and take measures to restore the activity of the cardiovascular system.

Drug therapy

For septic shock, the drug treatment algorithm consists of:

eliminating the risk of toxic damage;
reducing hypoglycemia;
preventing blood clotting;
facilitating the penetration of oxygen through the vascular wall and accelerating its absorption in cells;
eliminating the main cause of the disease - sepsis.

The first step is to detoxify the body and restore the electrolyte balance needed to easily transport oxygen and nutrients. For this, infusion therapy with glucose-saline solutions and the introduction of sorbents can be used.

Hypoglycemia is eliminated by administering glucose and glucocorticoids, which accelerate metabolic processes in cells. They also help prevent blood clotting, so they are usually administered along with Heparin.

Steroidal anti-inflammatory drugs increase cell permeability. Vasopressor substances - Adrenaline, Norepinephrine, Dopamine - also contribute to the achievement of this goal. Additionally, inotropic agents such as Dopamine are prescribed.

In the presence of acute renal failure, the administration of solutions is contraindicated - too much fluid in the body will cause swelling and intoxication, therefore for such patients, blood purification is carried out using hemodialysis.

Surgical intervention

Septic shock itself cannot be treated surgically, but side processes such as suppuration, necrosis and abscesses can significantly interfere with recovery. Respiratory and heart failure may be a complication for the operation, and therefore the indications for the operation are determined by a council of doctors.

Radical surgical intervention is performed in the presence of purulent lesions on the extremities - for example, gas gangrene. In this case, the limb is amputated, preventing further development of septicopyemia (or septicemia).

If pus accumulates in certain parts of the body, they are opened and sanitized to remove it, preventing further spread throughout the body. In order to ease the impact on the heart, sanitation is carried out under local anesthesia.

Interventions in pregnant women are particularly difficult. Gynecological sepsis has very complex specifics due to the danger of pregnancy disruption. The spread of bacterial infection often leads to the child dying in the womb.

How is prevention carried out?

It is possible to prevent the development of septic shock by timely treatment of its cause.

To do this, you should contact the clinic in time if symptoms characteristic of bacterial lesions of the body develop.

In case of severe infection, this requires prompt treatment with antibiotics, which have an intensive effect on the existing pathogenic microflora. Surgical correction involves timely removal of purulent foci.

Consequences of septic shock

The main possible complication is multiple organ failure. Gradual organ failure leads to the death of the patient.

Due to the large toxic load, renal and liver failure develops first, with a deterioration in the course of the picture, and then pulmonary and cardiac failure.

Another possible consequence is disseminated intravascular coagulation syndrome. Clinically, two stages are important: hypercoagulation and.

The first is characterized by massive thrombosis, and the second by bleeding.

Massive internal bleeding complicates the situation created by hypotension, and the patient dies within a few days. The syndrome can be prevented either in the first stage, by administering heparin, or in the second, by transfusing plasma with clotting elements that prevent bleeding.

Very often, the clinical picture of the syndrome develops as a consequence of a difficult birth, which in septic shock is dangerous for both the mother and the child, whose immune system is not ready to respond to a bacterial agent. The baby often dies.

In general, even in patients with milder diagnoses, DIC is often fatal, and in conditions of severe sepsis it becomes the primary cause of death. Medical statistics show that the chance of survival is significantly higher when treatment is started in the first phase.

And often, with the development of severe sepsis or septic shock, the patient begins to develop a superinfection - re-infection with another bacterial or viral agent.

Life forecast

As already mentioned, the pathology has a mortality rate of up to 50%. Recovery depends on how quickly treatment was started, how adequate the antibiotics were, and how severe the complications were.

The infectious agent that caused the septic lesion also plays a role. Hospital strains are considered the most dangerous, for example Staphylococcus aureus. It is usually resistant to most antibiotics, which is why the process is most difficult for the patient’s body.

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

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

Potential mediators of the septic inflammatory response:

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

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

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.

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

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

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

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

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

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

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

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

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

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

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

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

Diagnostic criteria for septic shock:

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

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

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

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

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

Treatment.

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

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

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

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

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

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

Vasoconstrictors can have harmful effects and should be used to restore peripheral vascular resistance to normal limits of 1100-1200 dynes s/cm 5 m2 only after optimizing the volume of blood volume. Digoxin, glucagon, calcium, calcium channel antagonists should be used strictly individually.

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

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

The most promising therapeutic measures appear to be those

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

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

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

Rational correction of hemodynamics.

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

Necessarily:

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

If possible:

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

This requires:

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

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

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

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

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

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

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

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

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

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

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

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