Septic shock - Causes and pathogenesis

Septic shock most often complicates the course of purulent-infectious processes caused by gram-negative flora: E. coli, Proteus, Klebsiella, Pseudomonas aeruginosa. When these bacteria are destroyed, endotoxin is released, which triggers the development of septic shock. The septic process caused by gram-positive flora (enterococcus, staphylococcus, streptococcus) is complicated by shock less often. The active principle of this type of infection is an exotoxin produced by living microorganisms. Shock can be caused not only by aerobic bacterial flora, but also by anaerobes, primarily Clostridia perfringens, as well as rickettsia, viruses (v. Herpes zoster, Cytomegalovirus), protozoa and fungi.

For shock to occur, in addition to the presence of infection, a combination of two more factors is required: a decrease in the overall resistance of the patient's body and the possibility of massive penetration of the pathogen or its toxins into the bloodstream. Such conditions often occur in pregnant women.

In a gynecological clinic, the source of infection in the vast majority of cases is the uterus: septic extra-hospital abortion, infectious diseases after artificial abortions performed in a hospital. Several factors contribute to the development of shock in such a situation:

• the pregnant uterus, which is a good entry point for infection;
• blood clots and remnants of the fertilized egg, which serve as an excellent nutrient medium for microorganisms;
• features of the blood circulation of the pregnant uterus, which facilitate the easy entry of bacterial flora into the woman’s bloodstream;
• changes in hormonal homeostasis (primarily estrogenic and gestagenic);
• hyperlipidemia of pregnancy, which facilitates the development of shock.

Finally, the allergization of women by pregnancy is of great importance, which is confirmed in an experiment on pregnant animals. The Schwartzman-Sanarelli phenomenon in pregnant animals (unlike non-pregnant animals) develops after a single injection of endotoxin.

Septic shock can complicate limited or diffuse peritonitis that occurs as a complication of inflammatory diseases of the uterine appendages.

Pathogenesis of septic shock

There is still much that is unclear in the pathogenesis of septic shock. The complexity of studying this problem is that many factors affect the characteristics of the onset and development of septic shock, including: the nature of the infection (gram-negative or gram-positive); localization of the infection; characteristics and duration of the septic infection; characteristics of the "breakthrough" of infection into the bloodstream (massiveness and frequency); the age of the patient and her state of health preceding the development of the infection; a combination of purulent-septic lesions with trauma and hemorrhage.

Based on the literature data of recent years, the pathogenesis of septic shock can be presented as follows. Microorganism toxins entering the bloodstream destroy the membrane of the cells of the reticuloendothelial system of the liver and lungs, platelets and leukocytes. In this case, lysosomes are released, rich in proteolytic enzymes, which set in motion vasoactive substances: kinins, histamine, serotonin, catecholamines, renin.

Primary disorders in septic shock concern the peripheral circulation. Vasoactive substances such as kinins, gnetamine and serotonin cause vasoplegia in the capillary system, which leads to a sharp decrease in peripheral resistance. Normalization and even an increase in the cardiac output (CO) due to tachycardia, as well as regional arteriovenous shunting (especially pronounced in the lungs and vessels of the celiac zone) cannot fully compensate for such a violation of capillary circulation. A decrease (usually moderate) in arterial pressure occurs. A hyperdynamic phase of septic shock develops, in which, despite the fact that the peripheral blood flow is quite high, capillary perfusion is reduced. In addition, the absorption of oxygen and energy substances is impaired due to the direct damaging effect of bacterial toxins at the cellular level. If we take into account that, in parallel with the occurrence of microcirculatory disorders at the early stage of septic shock, hyperactivation of the platelet and procoagulant links of hemostasis occurs with the development of DIC syndrome, it becomes obvious that already in this phase of shock, metabolic processes in tissues are disrupted with the formation of under-oxidized products.

The continuing damaging effect of bacterial toxins leads to the deepening of circulatory disorders. Selective spasm of venules in combination with the progression of DIC syndrome contributes to the sequestration of blood in the microcirculation system. Increased permeability of the vessel walls leads to leakage of the liquid part of the blood, and then of formed elements into the interstitial space. These pathophysiological changes lead to hypovolemia. Blood flow to the heart is significantly reduced, despite sharp tachycardia, and cannot compensate for the increasing disturbance of peripheral hemodynamics.

Septic shock places excessive demands on the myocardium, which, under unfavorable conditions of existence, cannot provide the body with an adequate supply of oxygen and energy substrates. A complex of reasons leads to cardiac dysfunction: deterioration of coronary blood flow, negative effect of microbial toxins and tissue metabolites, in particular low-molecular peptides, united by the concept of "factor that depresses the myocardium", decreased myocardial response to adrenergic stimulation and edema of muscle elements. A persistent decrease in arterial pressure occurs. The hypodynamic phase of septic shock develops. In this phase of shock, progressive disruption of tissue perfusion leads to further deepening of tissue acidosis against the background of severe hypoxia.

Metabolism occurs via the anaerobic pathway. The final link of anaerobic glycolysis is lactic acid: lactic acidosis develops. All this, combined with the toxic effect of the infection, quickly leads to dysfunction of individual tissue areas and organs, and then to their death. This process is short-lived. Necrotic changes can occur 6-8 hours after the onset of functional disorders. The lungs, liver, kidneys, brain, gastrointestinal tract, and skin are most susceptible to the damaging effects of toxins in septic shock.

In the presence of a purulent infection in the body, the lungs work under high load and great strain. Septic shock leads to early and significant changes in the function and structure of the lung tissue. The pathophysiology of "shock lung" is initially manifested in a violation of microcirculation with arteriovenous shunting of blood and the development of interstitial edema, which leads to a violation of the relationship between ventilation and perfusion of the lung tissue. Deepening tissue acidosis, microthrombosis of the pulmonary vessels, insufficient production of surfactant lead to the development of intraalveolar pulmonary edema, microatelectasis and the formation of hyaline membranes. Thus, septic shock is complicated by acute respiratory failure, in which a profound violation of the oxygen supply to the body occurs.

In septic shock, renal tissue perfusion decreases, renal blood flow is redistributed with a decrease in the blood supply to the cortex. In severe cases, cortical necrosis occurs. The cause of these disorders is a decrease in the total circulating blood volume and regional changes resulting from catecholaminemia, the renin-angiotensin effect and DIC syndrome. Glomerular filtration decreases, urine osmolarity is impaired - a "shock kidney" is formed, and acute renal failure develops. Oliguanuria leads to pathological shifts in water-electrolyte balance, and the elimination of urinary waste is impaired.

Liver damage in septic shock is indicated by an increase in organ-specific enzymes and bilirubinemia in the blood. The glycogen-forming function of the liver and lipid metabolism are disrupted, and lactic acid production increases. The liver plays a certain role in maintaining DIC syndrome.

Microcirculation disorders, accompanied by the formation of platelet-fibrin thrombi and combined with areas of hemorrhage, are observed in some parts of the brain, in particular in the adenohypophysis and diencephalic region.

Spasm and microthrombosis in the vessels of the intestine and stomach lead to the formation of erosions and ulcers of the mucous membrane, and in severe cases - to the development of pseudomembranous enterocolitis.

Septic shock is characterized by extravasations and necrotic skin lesions associated with impaired microcirculation and direct damage to cellular elements by the toxin.

Thus, the following main points can be distinguished in the pathogenesis of septic shock. In response to the entry of an infectious agent into the bloodstream, vasoactive substances are released, membrane permeability increases, and DIC syndrome develops. All this leads to a violation of peripheral hemodynamics, a disorder of pulmonary gas exchange, and an increase in the load on the myocardium. The progression of pathophysiological changes, in turn, leads to a discrepancy between the energy demands of organs and tissues and the ability to deliver oxygen and energy substrates. Deep metabolic disorders develop, contributing to damage to vital organs. "Shock" lungs, kidneys, and liver are formed, heart failure occurs, and as the last stage of homeostatic exhaustion, the death of the organism may occur.

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