Explain the Development of SIRS or MODS?

Multiple hypothesis have been proposed to explain the development of SIRS or MODS. The progression of SIRS to MODS appears to be mediated by excessive production of pro-inflammatory cytokines and other mediators of inflammation. According to the "gut hypothesis" disruption of the gut barrier function results in translocation of enteric bacteria into the mesentery lymph nodes, liver and other organs. Despite a number of advances in the treatment of infections and a better understanding of its path physiology, the mortality and morbidity rates from septicemia are high. Unlike elective surgery and trauma, the response patterns following major infection are unpredictable.

The variability in metabolic and physiological response is relied partly to the patient's age, previous health status, pre-existing disease, previous stress, site of infection and the infective agent. Moreover, the organ system failure may mask the manifestation of systemic infection. Based on cardiac output, two physiological responses have been described. The first is characterized by an increased cardiac output and high systemic perfusion. The second response is characterized by cardiac decomposition, inadequate tissue perfusion and acidosis, and is described as low flow sepsis. Both these responses reflect the body's reaction to systemic infection and are modified by the underlying disease and physiologic reserves of the patient, The invasion of the body by infective agents initiates host responses. There is mobilization of phagocytes and inflammation at the local site. As the infection progresses, fever, tachycardia and other responses occur.