Septic shock

An overview of septic shock (Septic shock) also called septic shock or toxic shock. By pathogenic microorganisms and their toxins in the human microcirculation of a state of induced tissue hypoxia and metabolic disorders, cell damage and even multiple organ failure. Elderly, infant and chronic diseases, chronic malnutrition, immune deficiency and cancer patients after surgery or larger patients particularly vulnerable. Etiology of septic shock caused by bacterial pathogens, viruses, rickettsia body, the spirochetes, fungi and parasites. With Gram-negative bacteria was mostly about 1 / 3 as meningococcus, Escherichia coli, Pseudomonas aeruginosa and Klebsiella spp. , and other types of bacteria. Can be found in Gram-positive bacteria, such as pneumococcal, gold aureus, Streptococcus and clostridium difficile, and so on. Epidemic hemorrhagic fever virus is easily aroused. Rickettsia body, the spirochetes, fungi, parasites, it is less see. Existing diabetes, cirrhosis, cancer, burns, organ transplants, long-term use of immunosuppressive drugs. radiation therapy or long-term indwelling catheter easily secondary septic shock. Pathogenesis and pathology of septic shock in the pathogenesis of complex, the in-depth study of cells, Micro-structure and molecular level. When the lower body resistance, the invading organism or normal body to a place of the large population of pathogen, the release of toxic products, With his motive for the activation of the human body fluids and cell-mediated response system, the generation of various inflammatory mediators and bioactive substances, Cong body caused a series of pathophysiological changes in hemodynamic changes dramatically, resulting in circulatory failure. Generally considered G-bacteria cell wall lipopolysaccharide (Lipopoly isoenzyme LPS), G + P wall rhizomorph wall acid (teichoicacid) sugar and peptide anhydride (pepticlog lycan); Mold zymosan (Zymosan); The grape toxin (poisoning toxic shock syndrome -1, TSST-1) can damage cells, or to form antigen-antibody complex tissue damage, triggering septic shock. As for viruses, rickettsiae and parasitic body of toxic substances have not yet been clarified. Grandfather of septic shock Pathogenesis of mainly concentrated in the G-rhizomorph wall lipopolysaccharide (LPS) with the way the humoral interaction, which is the focus of the study was to stimulate the macrophage cells and release cytokines area. (1) bioactive substances, cytokines in the pathogenesis of septic shock mechanism role. 1. Bioactive substances in the role of LPS, P wall acid, peptide sugar anhydride, TSST-1, Zymosan such as by alternative means (alternative pathway) and the classical way (es ssical pathway) activation of complement, classic way to be antigen complexes activated alternative means by the direct activation of these products. Complement activation of C2b, C4a with bradykinin-like role, increased vascular permeability, have Inc, C5a, said allergic toxins, can mast cells, the blood Aeromonas alkaline cells release histamine, causes vasodilation, increased permeability, Local edema formation, but also turned the smooth muscle spasticity; neutrophil activation, neutrophil aggregation and adhesion to endothelial cells and further platelet aggregation, thrombus formation. Eventually lead to changes in blood flow mechanics. Many factors, vascular endothelial cell injury, Damage to the membrane phospholipid membrane phospholipase role in the release of arachidonic acid (Arachidonic Łaci d), the latter by the cyclooxygenase or lipoxygenase respectively role of prostaglandin-like (prostaglandin. PGs), PGI2 (prostacyclin, PGI2) Thromboxane (PAF, TXA2) and leukotriene (Leucotriene. LT), these bioactive substances with a strong vascular damage, affecting vascular tone, stimulation of microvascular permeability and increase platelet aggregation, hypoxia - ischemia, oxygen free radicals, lysosomes, 5-HT by platelet-activating factor, plasminogen activator release, resulting in circulatory disturbance. LPS, wall phosphorus acid, peptide sugar anhydride also directly activate coagulation system and endothelial cells, Macrophages have damaged tissue factor activated coagulation system, leading to clotting mechanism obstacles and DIC occurred. As the process of the former kininase into kininase, bradykinin enzyme Kininogenase release bradykinin; plus vascular endothelial cells produce the flaccid decomposition factor, Macrophages of nitrous oxide (nitric oxide), Myocardial inhibitory factor (MDF) and endogenous opioids (Opiod) release into the blood could be seen in blood pressure dropped. 2. The role of cytokines (1) interleukin-between - I (Interleukin-1. IL-1) When the body of phagocyte various pathogens, endotoxins, peptide sugar anhydride, Zymogan or immune complexes, phagocytic cells synthesis and secretion of IL-1, IL-1 play a variety of biological activity, known : ?٠IL-1 stimulation of the hypothalamus part of vascular endothelial cells release of prostaglandin (PG) - induced fever; ?ڠwill vascular endothelial cells forefront (PGI2), the former clotting substances, anti-plasminogen inhibitor, Platelet activating factor, thereby promoting DIC; ?۠make alkaline cell to release histamine tablets. neutrophils release of lysosomal enzymes, further injury and vascular tissue; ?ܠexcited ACTH / endorphin central endorphin release, the EP antagonistic catecholamine, smooth muscle relaxation, enhanced vascular permeability, blood pressure dropped; ?ݠpromote tumor necrosis factor (TNF) production of vascular endothelial injury; ?ޠC3 for the synthesis of vascular endothelial injury; ?ߠstimulation of bone marrow granulocyte multinucleated cells mature into blood circulation; ?࠭ake TH cells between leukocyte-2 (IL-2), B cells produce antibodies. (2), tumor necrosis factor (TNF) in LPS local inflammation or blood macrophage phagocytosis. promote its synthesis and secretion of TNF, It was found that LPS binding protein and lipopolysaccharide (LPS-binding protein) complexes formed After stimulate macrophage TNF have the capacity stronger. Rats injected TNF can cause low blood pressure, accelerated respiration, if sustained for a few hours, we have a serious metabolic acidosis and death. But if anti-TNF injection early, a protective role. After the mice were injected with TNF also have a fever reaction was directly proportional to dose. (2) microcirculation of the occurrence and development of microorganisms and toxins to the body's response to the release of bioactive substances, Cytokines interaction and mutual influence, causing tissue damage, dysfunction, particularly cycling and microcirculation dysfunction shock is the central link. 1. Early shock in recent years, many authors discovered through animal experiments septic shock is not the only part of the predicate microcirculation, but the entire circulatory system and microvascular spasm at the beginning rather than expansion. To the conclusion that early animal experiment is due to the unreasonable, that is a big dose of bacterial endotoxin injection or to make animal models in vivo, massive catecholamine, to vasospasm, actual clinical patients is not a massive toxins or bacteria entered, but a small number of persistent or intermittent access, thus in 1987 the European septic shock discussions in the past to rectify the erroneous view. Early endotoxin shock due to myocardial the role of myocardial contractility beginning of a slight weakening, but peripheral expansion, reduced cardiac output and vascular resistance is also low, it showed the high-power high-low resistance-heated row shock. 2. With shock-cells, vascular endothelial cells in the foregoing factors, substances role, significantly increased vascular permeability, oozing, plasma concentration, capillary leakage, Vascular the platelet release of 5-HT and other vasoactive substances under contraction, increased peripheral resistance. Where muscle while inhibiting cytokine release, a further weakening of cardiac contractility and cardiac output decrease, resulting low power - that is, low-emission high resistance cold shock. Shock transition from warm to cold shock causes according to the length of time that species, individual and age. 3. Shock late hemoconcentration, paste, easy condensate, plus pathogens, toxins and cytokines vascular endothelial the direct effect Platelet aggregation and damage, activation of the coagulation system and outside coagulation system, First, to disseminated intravascular coagulation (DIC), with a secondary that is the development of fibrinolysis. As cardiac output and blood pressure to further reduce, when damaged cells to calcium intake and discharge blocked, further decline in vascular tone, and the various vasoactive drugs can not afford to respond. To ensure that the heart and brain blood supply, a large number of organizations so that the release of histamine skin, muscle, kidney, lung, liver, gastrointestinal tract, such as lack of blood perfusion. Stasis of blood in the capillary network so that the increased pressure, plasma extravasation, effective recycling to reduce the volume again, This pathophysiological process finally serious blood dynamic change, from the functions of tissues and organs to shape change, formation of multiple organ failure. (3) the principal organs of the pathological changes of pulmonary : septic shock when the pulmonary microcirculation inadequate, Pulmonary surfactant diminishing, and the size of alveolar not maintain a certain tension, which occurred atelectasis. When the lungs occurred DIC, the micro - thrombosis induced lung congestion, hemorrhage, interstitial edema, alveolar membrane formation of a transparent, thus lung consolidation. CENTRAL : shock myocardial fibrosis, necrosis, or fracture, interstitial edema, decreased myocardial contractility, coronary perfusion, Myocardial ischemia and hypoxia. Subcellular structure changed, the sarcoplasmic reticulum Ca + + perturbation weakened ability, Na-K-ATPase pump inactivation, metabolic disorders, acid poisoning can induce heart failure. Kidney : To ensure the shock when the heart and brain blood supply, blood volume redistribution where renal artery, renal perfusion was reduced. Early in shock there oliguria even intermittent anuria. In a serious and sustained shock can cause renal tubular necrosis, interstitial edema, acute renal failure. DIC, glomerular vascular plexus extensive thrombosis, renal cortical necrosis. Brain : brain tissue oxygen demand, and the high sugar content of the low yuan, mainly rely on continuous supply of blood. Shock cerebral hypoperfusion, astrocytoma occurred swelling and oppression vascular endothelial cells also swelling, caused microcirculation and blood flow abnormalities and increased brain hypoxia, brain edema. Liver and gastrointestinal : shock to cause hypoxia, hypoxia-lasting liver metabolism of amino acids and protein decomposition products of functional impairment, glycogen depletion. The same was true District liver cell degeneration and necrosis. Shock gastrointestinal mucosa in the same period of the existence of the micro-cycle changes, ischemic injury to the mucosa can form ulcers, performance of the patient or vomiting blood.