Zdziarski P, Simon K
Wojskowa Stacja Sanitamo-Epidemiologiczna we Wrocławiu.
Pol Merkur Lekarski. 2001 Oct;11(64):362-9.
Sepsis is defined as systemic inflammatory response syndrome (SIRS) caused by infection. Massive activation of humoral and cellular mechanisms of host defense is present and can lead to a multiple organ dysfunction syndrome. Sepsis is good example, that inflammation binds with considerable energetic and metabolic effort of organism i.e. demand for oxygen, protein and microelements. The effort during SIRS exceeds compensatory abilities of organism, cause shock and death. The high mortality (40-70% in the case of septic shock) is a good illustration of the therapeutic problem. In the paper pathogenesis, diagnosis and therapy of sepsis was described. Pathogenetic importance of intoxication was explained--massive intoxication (for example by Staphylococcal enterotoxin) without infection cans lead to SIRS too. Precious advice in selection of antibiotic were given. Advantage penicillins and karbapenems over cephalosporins result from binding to PBP 2 or 1, considerably smaller release of free endotoxin and smaller induction Jarish-Heixhaimer's reaction. The side effect stimulates inflammation and deepens SIRS by release toxins and increase of TNF-alpha.
脓毒症被定义为由感染引起的全身炎症反应综合征（SIRS）。宿主防御的体液和细胞机制被大量激活，可导致多器官功能障碍综合征。脓毒症是一个很好的例子，即炎症伴随着机体相当大的能量和代谢消耗，也就是对氧气、蛋白质和微量元素的需求。SIRS期间的这种消耗超过了机体的代偿能力，导致休克和死亡。高死亡率（脓毒性休克时为40%-70%）很好地说明了治疗问题。本文描述了脓毒症的发病机制、诊断和治疗。解释了中毒的发病学重要性——无感染的大量中毒（例如由葡萄球菌肠毒素引起）也可导致SIRS。给出了选择抗生素的宝贵建议。青霉素和碳青霉烯类相对于头孢菌素类的优势源于它们与PBP 2或1的结合、游离内毒素释放量显著减少以及贾-赫反应诱导程度较小。副作用通过释放毒素和增加TNF-α来刺激炎症并加深SIRS。
