Toxic particles appear
Introduction
Introduction When laboratory tests are performed on patients with sepsis, the white blood cell count is significantly increased, usually up to (20 ~ 30) x 109 / L or more, or decreased, left shift, immature type, and toxic particles appear. For example, sepsis is a common complication of severe trauma, burns, shock, and major surgery, and is one of the important causes of death in critically ill patients. At present, it is generally believed that the activation of neutrophils, lymphocytes and mononuclear macrophage systems and the release of endogenous mediators play a key role in the pathophysiological mechanisms of post-traumatic sepsis.
Cause
Cause
Under normal circumstances, when microorganisms invade the human body, the body's immune defense system will respond quickly and appropriately; however, when the immune defense ability is defective, the reaction is too high or too low, it can cause sepsis through endogenous inflammation. Occurrence and development. The key factor in the early stage is cytokines. Under endotoxin stimulation, monocytes produce inflammatory factors such as tumor necrosis factor (TNF) and interleukin-1 (IL-1), which promote neutrophils and endothelial cells. Adhesion, activation of the coagulation system, release a large number of inflammatory mediators, including other cytokines, leukotrienes and proteases, as well as anti-inflammatory mediators such as IL-6, IL-10. Both IL-1 and TNF have synergistic effects with many of the same biological effects.
Studies in animal models of sepsis have shown that inhibition of IL-1 and TNF can improve organ function and improve survival. IL-8 is able to chemotaxis of neutrophils, leading to prolonged inflammation. IL-6 and IL-10 may play a negative regulatory role, inhibit the production of TNF, enhance the role of acute phase reaction substances and immunoglobulins, and inhibit the function of T lymphocytes and macrophages. However, in numerous clinical studies, only one study suggests that changes in the concentration of TNF have physiological effects that can affect cytokine levels downstream of the immune cascade.
Arachidonic acid metabolites are involved in the development and progression of sepsis. Animal and clinical trials have observed that cyclooxygenase inhibitors (ibuprofen) can lower body temperature and slow heart rate by inhibiting the production of these substances. Reduces ventilation per minute and corrects lactic acidosis, but does not reduce mortality. It was further confirmed that thromboxane A2 (contracted blood vessels), prostacyclin (dilated blood vessels), and prostaglandin E2 involved the occurrence of fever, tachycardia, shortness of breath, ventilatory dysfunction, lactic acidosis, and the like.
Sepsis is a common complication of severe trauma, burns, shock, and major surgery, and is one of the important causes of death in critically ill patients. At present, it is generally believed that the activation of neutrophils, lymphocytes and mononuclear macrophage systems and the release of endogenous mediators play a key role in the pathophysiological mechanisms of post-traumatic sepsis.
Examine
an examination
The main manifestations of sepsis are:
1 sudden chills, followed by high fever up to 40-41 ° C, or low temperature, acute onset, serious illness, rapid development;
2 headache, dizziness, nausea, vomiting, bloating, pale or flushing, cold sweat. Indifference or irritability, embarrassment and coma;
3 speed up, rapid pulse, shortness of breath or difficulty;
4 liver spleen can be swollen, severe cases of jaundice or subcutaneous bleeding ecchymosis.
Laboratory inspection:
1 white blood cell count is significantly increased, generally up to (20 ~ 30) x 109 / L or more, or reduced, left shift, naive type increased, toxic particles appear;
2 may have different degrees of acidosis, azotemia, hemolysis, protein in urine, blood cells, ketone bodies, etc., metabolic imbalance and signs of liver and kidney damage;
3 When the cold is hot, blood is drawn for bacterial culture. It is easier to find bacteria. If the disease progresses, the infection is not controlled, and septic shock and rapid development may occur as multiple organ dysfunction or even failure.
The clinical manifestations of sepsis are still different due to the different pathogens of infection.
Diagnosis
Differential diagnosis
Sepsis is a general term for surgical infections such as body temperature, respiration, and circulatory changes. It is the damage caused by endotoxin, exotoxin produced by pathogens and the absorption of various inflammatory mediators they mediate. When the performance of sepsis combined with hypoperfusion, such as lactic acidosis, oliguria, acute changes in consciousness, etc., is called pyemia syndrome. If the bacteria invade the blood circulation and the blood culture is positive, it is called bacteremia. Sepsis and bacteremia are often secondary to infections after severe trauma and various purulent infections. The pathogenic bacteria are complex, numerous, and toxic. Generally, the onset is rapid, the condition is heavy, the change is fast, and the organ is often insufficiently perfused. However, attention should be paid to differential diagnosis.
