Sepsis is a systemic inflammatory disease. The cause of sepsis is bacterial infection and immune dysfunction. The most common symptoms are high fever, chills, and rapid onset, accelerated heart rate, coma, and hepatosplenomegaly. Timely treatment is required to avoid shock. 1. Common symptoms 1. Chills, high fever, or low fever, with rapid onset and progression. 2. Mental apathy or irritability, coma. 3. Fast heart rate, weak pulse, rapid or difficult breathing. 4. Enlarged liver and spleen. 5. Shock. Shock in Gram-positive bacterial sepsis occurs late and the limbs are warmer. G-bacteria septic shock occurs early, lasts for a long time, and causes cold limbs. 2. Causes 1. Bacterial endotoxins (20%): Bacterial endotoxins can induce sepsis. The uncontrolled inflammatory response, immune dysfunction, hypermetabolic state and multi-organ dysfunction that occur in the pathophysiological process of sepsis can all be triggered directly or indirectly by endotoxins. 2. Inflammatory mediators (10%): Infectious factors in sepsis activate the body's mononuclear macrophage system and other inflammatory response cells, causing them to produce and release a large amount of inflammatory mediators. In sepsis, endogenous inflammatory mediators, including vasoactive substances, cytokines, chemokines, oxygen free radicals, acute phase reactants, bioactive lipids, plasma enzyme system products and fibrinolytic pathways, interact with each other to form a network effect and cause extensive damage to various systems and organs throughout the body. At the same time, some cytokines, such as tumor necrosis factor (TNF)-α, may play an important role in the occurrence and development of sepsis. 3. Immune dysfunction (10%): The main characteristics of immune disorders in sepsis are loss of delayed hypersensitivity reactions, inability to eliminate pathogens, and susceptibility to nosocomial infections. The mechanism of immune dysfunction in sepsis is, on the one hand, dysfunction of T cells, important regulatory cells of the immune system, the drift of inflammatory mediators toward anti-inflammatory response, the decrease of pro-inflammatory factors and the increase of anti-inflammatory factors; on the other hand, it manifests as immune paralysis, that is, cell apoptosis and immune unresponsiveness, and T cells do not proliferate or secrete cytokines in response to specific antigen stimulation. 4. Intestinal bacteria/endotoxin translocation (8%): Since the 1980s, people have noticed that stress causes dysfunction in the intestine, the body's largest reservoir of bacteria and endotoxins. The resulting infection caused by intestinal bacteria/endotoxin translocation is closely related to subsequent sepsis and multiple organ dysfunction. Studies have shown that the stress response after severe injury can cause damage to the intestinal mucosal barrier, dysbiosis of the intestinal flora and a decline in the body's immune function, leading to intestinal bacteria/endotoxin translocation, triggering the body's excessive inflammatory response and organ damage. |
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