Conclusion.
The pathological basis of sepsis is initially an excessive inflammatory response against invading pathogens, leading to systemic inflammatory response syndrome (SIRS). Evidence reveals that a variety of inflammatory mediators orchestrate the intense inflammation through complicated cellular interactions. More recent data indicate that most septic patients survive this stage and then subjected to an immunoparalysis phase, termed compensatory anti-inflammatory response syndrome (CARS), which is more fatal than the initial phase. Sepsis is a complicated clinical syndrome with multiple physiologic and immunologic abnormalities.
A major shift has occurred in the way investigators view the problem of sepsis. Sepsis may not be attributable solely to an “immune system gone haywire” but may indicate an immune system that is severely compromised and unable to eradicate pathogens. Mechanisms of organ failure and death in patients with sepsis remain unknown, and autopsy studies do not reveal widespread necrosis. Future therapy may be directed at enhancing or inhibiting the patient’s immune response, depending on genetic polymorphisms, the duration of disease, and the characteristics of the particular pathogen.
At present, in order to obtain better prognosis, quick and accurate diagnosis in an early stage of sepsis is above all important. An initial therapy with prompt speed and appropriateness is essential. New therapeutic options based on the scientific evidence may pave the way for the treatment of sepsis and septic shock in the new era. However, recent clinical trials aimed at modulating inflammatory response have failed or shown only modest clinical benefit. Recently, there is a growing consensus that the general strategy of research on
sepsis needs to be reconsidered.
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