Pathophysiology of Sepsis Inflammatory Response Essay

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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, …show more content…
He describes the pain as intermittent, radiating to left and right sides, lasting 5-10 mins before spontaneously resolving. He denies any nausea, vomiting or altered bowel/bladder habits. He also describes shortness of breath on exertion, on a background of feeling generally unwell by 3/7 days with decreased appetite, lethargy and diaphoresis. He denies any chest pain and has no pain on presentation.

Pathophysiology of Sepsis
Inflammatory Response
Sepsis begins with a systemic inflammatory response to a perceived threat to the immune system (Powers & Burchell, 2010). Tissue injury or invading pathogens stimulate production of phagocytes, such as monocytes and macrophages, which act as the first line of defence against infection. These phagocytes release pro-inflammatory mediators called cytokines, in order to attract neutrophils to the site of infection. The release of cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumour necrosis factor alpha (TNFα), results in release of further chemical agents, such as complement, histamine and prostaglandin. These agents cause localised vasodilation and release of cytotoxic chemicals, in an effort to destroy the invading pathogen. (Daniels, 2009) A rise in inflammatory markers (such as an elevated CRP) demonstrates this inflammatory response (due to release of IL-6).

In a certain sub-group of people with a host predisposition, such as those possessing a genetic variant of a receptor known as a

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