he SIRS(systemic inflammatory response syndrome) criteria included 2 or more of the following: temperature >38C or <36C, heart rate >90bpm, respiratory rate >20/min, PaCO2<32mmHg, WBC count >12000/mm3 or <4000/mm3 or >10% immature bands. The SIRS criteria does not necessarily dictate a dysregulated , life threatening response. It is also present in many hospitalized patients. Instead, organ dysfunction can be identified as an acute change in total SOFA score > 2 points consequent to infection. The baseline SOFA score is assumed to be 0 in patients that has no pre-existing organ dysfunction. A SOFA score > 2 reflects an overall mortality risk with suspected infection. qSOFA(quick SODA) incorporates altered mentation, systolic BP of 100mHg or less, and respiratory rate >22/min, provides a simple bedside criteria to identify adult patients with suspected infection whose condition are likely to worsen. Additional screening includes a multivariable logistic regression identified that any 2 of 3 clinical variables – GCS 13 or less, systolic BP 100mmHg or less, and respiratory rate 22/min or greater.
Second on the sepsis continuum, the patient needs to present 2 of the SIRS criteria and a positive culture of sputum, blood, or urine that reflects growth of bacteria.
Severe sepsis is classified when there is sepsis and hypo-perfusion with organ dysfunction that is unresponsive to fluid resuscitation. It has more recently been viewed as endothelial dysfunction resulting from overwhelming inflammatory mediation, in conjunction with profound, unopposed coagulation. The capillary vasculature sustains a significant injury due to the cascade of events that ends in capillary occlusion. The greater the occlusion, the greater risk for organ failure because cellular level circulation requires a functional capillary network for delivery of oxygen and nutrients and removal of cellular metabolic waste products.
When infection or injury prompts an initially widespread inflammatory response (SIRS), the normally smooth surface of the microvascular endothelium is roughened and damaged by the response. In addition, the release of inflammatory mediations promotes vasodilation with an increase in capillary permeability. This causes little holes in the endothelium that the systemic mediators try to facilitate the healing of. The four main factors associated with severe sepsis is hyperinflammation, hypercoagulation, microvascular obstruction, and endothelial responses that leads to accelerated formation of microclots on the non-smooth surface of the endothelium. This consumes plates and inhibits clot lysis. This progresses to uncontrolled alterations in the vascular tone with vasodilation. In severe sepsis, the balance between vasodilators(nitric oxide) and vasoconstrictors(endoth