Delire M
Department of Clinical Research, Behringwerke AG, Marburg.
Ann Biol Clin (Paris). 1988;46(4):272-5.
Septic complications are still the major cause of death in patients with severe injuries, whether due to polytrauma, large burns, or difficult surgical operations. The very high incidence of such infectious episodes in spite of the continuous development of new broad spectrum antibiotics and appropriate intensive care managements, may suggest that any kind of severe injury leads to a state of acquired immunologic deficiencies. Thus an intensive relation has been demonstrated between the extend of body burned surfaces and the neutrophil chemotaxis whose dramatic decline could originate either from an intraleukocytic defect, or from inhibitory factors released by the damaged tissues. Furthermore, any important tissular destruction has been shown to stimulate the clonal proliferation of T suppressor lymphocytes which could be considered as a physiological protective mechanism against the development of an autoimmunization towards self-structures released by the wound in the blood stream. Factors able to activate T suppressor lymphocytes after injury are multiple and among them most important are: HLA-bearing cell wall components, histamine released by tissue mast cells, soluble factors produced at the level of the wound, bacterial endotoxins, arachidonic acid metabolites, etc. Finally, it has been mentioned that this state of immune deficiency after injury may still be exacerbated by iatrogenic measured like catheters, antibiotherapy, corticotherapy, and mainly by malnutrition.
脓毒症并发症仍然是重伤患者死亡的主要原因，无论这些重伤是由多发伤、大面积烧伤还是复杂外科手术引起的。尽管新型广谱抗生素不断发展以及采取了适当的重症监护管理措施，但此类感染性事件的发生率仍然很高，这可能表明任何一种严重损伤都会导致获得性免疫缺陷状态。因此，已证实身体烧伤面积的大小与中性粒细胞趋化性之间存在密切关系，中性粒细胞趋化性的显著下降可能源于白细胞内缺陷，也可能源于受损组织释放的抑制因子。此外，任何严重的组织破坏都已显示会刺激抑制性T淋巴细胞的克隆增殖，这可被视为一种生理保护机制，以防止针对伤口在血流中释放的自身结构发生自身免疫。损伤后能够激活抑制性T淋巴细胞的因素多种多样，其中最重要的有：携带HLA的细胞壁成分、组织肥大细胞释放的组胺、伤口部位产生的可溶性因子、细菌内毒素、花生四烯酸代谢产物等。最后，有人提到，损伤后的这种免疫缺陷状态仍可能因诸如导管、抗生素治疗、皮质激素治疗等医源性措施而加重，主要是因营养不良而加重。
