Sepsis is defined as an exaggerated, overwhelming, and uncontrolled systemic inflammatory response to an initially localized infection or tissue injury, which can lead to severe sepsis and septic shock if left untreated (Daniels , 2009; Robson and Daniels, 2013; septic shock can be classified as acute circulatory failure as a result of massive vasodilation, an increase of capillary permeability and a decrease in vascular resistance in the body, which causes refractory hypotension despite adequate fluid resuscitation. This leads to irreversible tissue ischemia, end-organ failure, and ultimately death (McClelland & Moxon, 2014; Sagy, Al-Qaqaa & Kim, 2013, Dellinger et al, 2013). According to the Clinical Excellence Commission (2014), approx 6,000 deaths per year are caused by sepsis in Australia alone. These mortality figures are higher than those for breast cancer (2,864) and prostate cancer (3,235) combined (Cancer Australia, 2014). Despite advances in modern medicine and a greater understanding of the need for timely recognition and intervention (Dellinger et al, 2013), sepsis remains the leading cause of death from infection worldwide (McClelland, 2014). Studies undertaken by The Sepsis Alliance (2014) and Schmidt et al, (2014) state that 40% of patients diagnosed with severe sepsis do not survive. For the purposes of this assignment, a case study was selected to relate the signs and symptoms of sepsis to the underlying pathophysiology of the sepsis continuum. In order to maintain patient confidentiality, names, dates and times have been changed or omitted, in line with the Australian Nurses and Midwives Code of Professional Conduct (ANMCC, 2008). Mr M...... center of sheet ..... .-1 (PAI-1) from endothelial cells and monocytes, activating the extrinsic coagulation pathway. This also leads to the activation of factor X and the production of fibrin. Extrinsic pathway In septic patients, increased levels of PAI-1 inhibit plasminogen activator (t-PA), which converts plasminogen to plasmin. Fibrin release inhibits fibrinolysis by activating thrombin-activatable fibrinolysis inhibitor (TAFI). Furthermore, the release of PAF causes platelet aggregation. This combination of inhibition of fibrinolysis, fibrin filament production, and platelet aggregation contributes to a state of coagulopathy. This can lead to microcirculatory dysfunction with isolated or multiple organ dysfunction and cell death. Mr. Hertz's coagulation profile showed a fibrinogen level of 5.6 g/L, indicating that coagulopathy was occurring in his system. Role of activated protein C