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 includes a trigger mechanism for the development of septic shock. Septic process caused by gram-positive flora (enterococcus, staphylococcus, streptococcus). Is complicated by a shock less often. Active exogenous form of infection is exotoxin, produced by living microorganisms. The cause of the shock can be not only aerobic bacterial flora, but also anaerobes, primarily Clostridia perfringens, as well as rickettsia, viruses (v. Herpes zoster, Cytomegalovirus), protozoa and fungi.

For the emergence of shock, in addition to the presence of infection, it is necessary to combine two more factors: reducing 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 the gynecological clinic, the focus of infection in the vast majority of cases is the uterus: septic out-of-hospital abortion, infectious diseases after official abortions performed in the hospital. The development of shock in this situation is facilitated by several factors:

• Pregnant uterus, which is a good entrance gate for infection;
• blood clots and the remains of the fetal egg, serving as an excellent nutrient medium for microorganisms;
• features of the circulation of the pregnant uterus, facilitating the easy entry of bacterial flora into the bloodstream of a woman;
• change hormonal homeostaae (primarily, estrogenic and gestagenic);
• hyperlipidemia of pregnant women, facilitating the development of shock.

Finally, great importance is the allergy of women to pregnancy, as evidenced in the experiment on pregnant animals. The phenomenon of Schwartzman-Sanarelli in pregnant animals (in contrast to non-pregnant animals) develops after a single administration of endotoxin.

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

Pathogenesis of septic shock

In the pathogenesis of septic shock to date, much is unclear. The complexity of studying this problem is that many factors affect the features of the onset and development of septic shock, which include: the nature of the infection (gram-negative or gram-positive); localization of the focus of infection; features and duration of septic infection; characteristic of the "breakthrough" of infection in the bloodstream (massiveness and frequency); the age of the patient and the state of her health preceding the development of the infection; a combination of purulent-septic lesion with trauma and hemorrhage.

Based on the literature data of recent years, the pathogenesis of septic shock can be represented as follows. Toxins of microorganisms 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 rich in proteolytic enzymes that release vasoactive substances are released: kinins, histamine, serotonin, catecholamines, renin.

Primary disorders in septic shock concern peripheral circulation. Vasoactive substances of the kinin type. Gentamina and serotonin cause vasoplegia in the capillary system, which leads to a sharp decrease in peripheral resistance. Normalization and even an increase in the minute volume of the heart (MOS) due to tachycardia, as well as regional arteriovenous shunting (especially pronounced in the lungs and vessels of the celiac zone) can not completely compensate for such a violation of the capillary circulation. There comes a decrease (usually moderate) of blood pressure. A hyperdynamic phase of septic shock develops , in which, despite the fact that peripheral blood flow is quite high, capillary perfusion is reduced. In addition, the absorption of oxygen and energy substances is disrupted due to the direct damaging effect of bacterial toxins at the cellular level. If we consider that in parallel with the emergence of microcirculatory disorders at an early stage of septic shock, the hyperactivation of the platelet and procoagulant links of hemostasis occurs with the development of the DIC of the blood, it becomes evident that already in this phase of shock, metabolic processes in tissues are disrupted with the formation of unoxidized products.

The continuing damaging effect of bacterial toxins leads to a deepening of circulatory disorders. Selective venous spasm in combination with the progression of the ICE syndrome promotes the sequestration of blood in the microcirculation system. Increasing the permeability of the walls of the vessels leads to leakage of the liquid part of the blood, and then of the shaped elements into the interstitial space. These pathophysiological changes lead to hypovolemia. The influx of blood to the heart is significantly reduced, despite a sharp tachycardia, can not compensate for the growing disturbance of peripheral hemodynamics.

Septic shock makes excessive demands on the myocardium, which under unfavorable conditions of existence can not provide adequate supply of the body with oxygen and energy substrates. A number of causes lead to cardiac dysfunction: worsening of coronary blood flow, negative effect of toxins of microorganisms and tissue metabolites, in particular, low molecular weight peptides, united by the term "factor inhibiting the myocardium", reduction of myocardial response to adrenergic stimulation and edema of muscle elements. There is a steady decline in blood pressure. The hypodynamic phase of septic shock develops . In this phase of shock, a progressive impairment of tissue perfusion leads to a further deepening of tissue acidosis against a background of severe hypoxia.

Metabolism occurs through the anaerobic pathway. The final link of anaerobic glycolysis is lactic acid: lactic acidosis develops. All this in combination with the toxic effect of the infection quickly leads to a disruption of the functions of individual parts of tissues and organs, and then to their death. This process is not long. Necrotic changes can occur 6-8 hours after the onset of functional disorders. The lungs, liver, kidneys, brain, gastrointestinal tract, skin are exposed to the greatest damaging effect of toxins in septic shock.

If there is a purulent infection in the body, the lungs work with a high load and high voltage. Septic shock leads to early and significant changes in the function and structure of lung tissue. The pathophysiology of the "shock lung" is first manifested in the disturbance of microcirculation with arteriovenous discharge of blood and the development of interstitial edema, which leads to a violation of the ratio between ventilation and perfusion of the lung tissue. Deepening of tissue acidosis, microthrombosis of pulmonary vessels, insufficient production of surfactant lead to the development of intra-alveolar pulmonary edema, micro-telecautization and the formation of hyaline membranes. Thus, septic shock is complicated by acute respiratory failure, which causes a profound violation of the body's oxygen supply.

With septic shock, perfusion of the renal tissue decreases, a redistribution of renal blood flow occurs with a decrease in the blood supply to the cortical layer. In severe cases, cervical necrosis occurs. The cause of these disorders are a decrease in the total BCC and regional changes resulting from catecholamineemia, the renin-angiotensin effect and the DIC syndrome. There is a decrease in glomerular filtration, the osmolarity of urine is broken - a "shock kidney" is formed, acute renal failure develops. Oligoanuria leads to abnormal shifts in the water-electrolyte balance, elimination of urinary slags is disturbed.

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

Disturbances of microcirculation, accompanied by the formation of platelet-fibrin clots and combined with areas of hemorrhage, are observed in some parts of the brain, in particular in the adenohypophysis and the 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.

For septic shock, extravasation and necrotic skin lesions are associated with a violation of micro-circulation and direct damage to cellular elements by toxin.

Thus, in the pathogenesis of septic shock, the following main points can be singled out. In response to the inflow into the bloodstream of the infection, vasoactive substances are released, membrane permeability increases, and the DVS 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. Progression of pathophysiological changes, in turn, leads to a discrepancy between the energy demands of organs and tissues for the delivery of oxygen and energy substrates. Deep metabolic disturbances that contribute to damage to vital organs develop. Shock lungs, kidneys and liver are formed, heart failure arises, and as the last ethane of homeostatic exhaustion, the body can die.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]