Pathophysiology The pathophysiology of infection, inflammatory 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, affecting the skin and/or subcutaneous tissue, often in the lower extremities. Cellulitis is caused by Streptococcus pyogenes and Staphylococcus aureus (multi-resistant bacteria) and is transmitted by direct contact, entering the body through skin lesions such as ulcers and/or following trauma. The presentation of cellulitis often includes pain (localized), erythema, fever, and swelling. Infections such as cellulitis have the propensity to become systemic through distribution in the blood and lymph (Hadzovic-Cengic et al., 2012). The inflammatory response to an infection involves the release of both pro- and anti-inflammatory mediators. When excessive proinflammatory mediators such as cytokines are released, they cause inflammation systemically which can cause sepsis or systemic inflammatory response syndrome (the response being nonspecific due to noninfectious cause) (Sagy, Al-Qaqaa, & Kim, 2013). Pro-inflammatory mediators also activate the complement system, which results in increased inflammation and upregulation of specific receptors leading to cell damage 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… middle of paper… (2012). Severe sepsis in the prehospital emergency room: analysis of incidence, treatment and outcome. American Journal of Respiratory and Critical Care Medicine, 186(12), 1264-1271. doi:10.1164/rccm.201204-0713OCTrautmann, M., Scheibe, C., Wellinghausen, N., Holst, O., & Lepper, P. M. (2010). Low release of endotoxins 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/NEJMc1314999Ward, Pennsylvania (2008). Sepsis, apoptosis and complement. Biochemical Pharmacology, 76(11), 1383-1388. doi:10.1016/j.bcp.2008.09.017Zawistowski, California (2013). Management of sepsis. Current Issues in Pediatric and Adolescent Health Care, 43(10), 285. doi:10.1016/j.cppeds.2013.10.005