Appendicitis Dichotomy

The discussion regarding the pathophysiology of sepsis should include the pathophysiology of disease conduction that led to sepsis. In this case, the disease started from appendicitis. Therefore, the pathophysiology of complicated appendicitis will be discussed first. Then, secondary peritonitis and sepsis will follow.
Complicated Appendicitis and Peritonitis
The pathogeneses of appendicitis believed to be from obstruction of appendiceal lumen by bacteria, stool, lymphoid hyperplasia, intraluminal scarring, tumors, or foreign body (Jacobs, 2014). The obstruction may lead to bacterial overgrowth and luminal distension which may interfere with the flow of lymph and blood (Jacobs, 2014). At this point, the appendix gets inflamed or infected. If not treated, vascular thrombosis and ischemic necrosis occur this eventually leads to perforation (Jacobs, 2014). The abdominal content starts leaking into the peritoneum. The bacteria will infect the peritoneum and peritonitis. The infection remains contain to local are due to
The microbes will be recognized monocytes, macrophages, and neutrophils with pattern recognition receptors such as toll-like receptors (TLR), nucleotide-oligomerization domain (NOD) (Han, Cribbs, & Martin, 2014) (Munford, 2014). At this point, inflammatory response will be activated. These result in tissue phagocytes to production and release cytokines, chemokines, prostanoids, and leukotrienes that increase blood flow to the infected tissue, a permeability of local blood vessels and recruitment of neutrophils (Munford, 2014). Proinflammatory cytokines and other mediators such as tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) will promote increased inflammatory response and produced a response called SIRS (Han et al., 2014)(Munford, 2014). These produced the symptoms like fever, tachycardia, hypercapnia, and