Detection and Treatment of Patients with Severe Sepsis

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Pathophysiology
Pathophysiology of infection, inflammation response, and sepsis leading to septic shock (the cascade) is a major area of interest in the literature. Under normal circumstances, when a pathogen enters a human host and tissue damage occurs, the host initiates an inflammatory response to repair the tissue. The main types of pathogens include viruses, bacteria, and parasites (Porth & Matfin, 2009; Raghavan & Marik, 2006). Cellulitis is an example of an acute infection, which affects the skin and or subcutaneous tissue often in lower limbs. Cellulitis is caused by streptococcus pyogenes and staphylococcus aureus (multi-resistant bacteria) and is transmitted by direct contact, entering the body via broken skin such as ulcers and or following trauma. The presentation of cellulitis often includes pain (localised), erythema, fever and swelling. Infections such as cellulitis have a propensity to become systemic through distribution in the blood and lymph (Hadzovic-Cengic et al., 2012). The inflammation response to an infection involves the release of both pro and anti-inflammatory mediators. When excessive pro-inflammatory mediators such as cytokines are released they cause inflammation in a systemic manner that can cause sepsis or systemic inflammatory response syndrome (being the non-specific response to non-infectious cause) (Sagy, Al-Qaqaa, & Kim, 2013). Pro-inflammatory mediators also activate the complement system, which results in increased inflammation and upregulation of specific receptors that lead to cellular injury and apoptosis seen in severe sepsis and organ dysfunction (Ward, 2008). Organ dysfunction can occur in one or more organs such as the lungs, liver, kidneys and or heart and often results from a lack of...

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.... (2012). Severe sepsis in pre-hospital emergency care: analysis of incidence, care, and outcome. American Journal of Respiratory and Critical Care Medicine, 186(12), 1264-1271. doi:10.1164/rccm.201204-0713OC
Trautmann, M., Scheibe, C., Wellinghausen, N., Holst, O., & Lepper, P. M. (2010). Low endotoxin release from escherichia coli and bacteroides fragilis during exposure to moxifloxacin. Chemotherapy, 56(5), 364-370. doi:10.1159/000321622
Vincent, J. L., & De Backer, D. (2013). Circulatory Shock. New England Journal of Medicine, 369(18), 1726-1734. doi: 10.1056/NEJMc1314999
Ward, P. A. (2008). Sepsis, apoptosis and complement. Biochemical Pharmacology, 76(11), 1383-1388. doi:10.1016/j.bcp.2008.09.017
Zawistowski, C. A. (2013). The management of sepsis. Current Problems in Pediatric and Adolescent Health Care, 43(10), 285. doi:10.1016/j.cppeds.2013.10.005

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