Pathophysiology of Sepsis Inflammatory Response

explanatory Essay
987 words
987 words

Sepsis is defined as an exaggerated, overwhelming and uncontrolled systemic inflammatory response to an initially localised infection or tissue injury, which may lead to severe sepsis and septic shock if left untreated (Daniels, 2009; Robson & Daniels, 2013; Dellinger et al, 2013; Perman, Goyal & Gaieski, 2012; Vanzant & Schmelzer, 2011). Septic shock can be classified by acute circulatory failure as a result of massive vasodilation, increased capillary permeability and decreased vascular resistance in the body, causing refractory hypotension despite adequate fluid resuscitation. This leads to irreversible tissue ischaemia, 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), approximately 6,000 deaths per annum are caused by sepsis in Australia alone. These mortality figures are higher than breast cancer (2,864) and prostate cancer (3,235) combined (Cancer Australia, 2014). Despite advances in modern medicine and increased understanding of the need for timely recognition and intervention (Dellinger et al, 2013), sepsis remains the primary 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 purpose of this assignment, a case study has been selected in order 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 Australian Nursing and Midwifery Code of Professional Conduct (ANMCC, 2008).

Mr M...

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...-1 (PAI-1) from the endothelial cells and monocytes, activating the extrinsic coagulation pathway. This also leads to activation of factor X and fibrin production.

Extrinsic Pathway
In septic patients, increased levels of PAI-1 inhibit plasminogen activator (t-PA), which converts plasminogen to plasmin. Release of fibrin inhibits fibrinolysis by activation of thrombin-activatable fibrinolysis inhibitor (TAFI). In addition, the release of PAF causes platelet aggregation. This combination of inhibition of fibrinolysis, fibrin strand production and platelet aggregation contribute 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 coagulopathies were underway in his system.

Role of Activated Protein C

In this essay, the author

  • Explains that damage to the endothelial lining activates coagulation factors in the blood, such as tissue factor (tf), which is utilised by the body to repair tissue damage.
  • Explains that the intrinsic pathway is activated when factor xii binds to the damaged endothelial surface and becomes active.
  • Explains that in septic patients, increased levels of pai-1 inhibit plasminogen activator (t-pa) and fibrin release causes platelet aggregation, which contributes to a state of coagulopathy.
  • Explains that sepsis is an exaggerated, overwhelming, and uncontrolled systemic inflammatory response to an initially localised infection or tissue injury.
  • Explains that sepsis begins with a systemic inflammatory response to an perceived threat to the immune system.

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