Sepsis: A Case Study

Sepsis During sepsis, platelets, neutrophils, macrophages, endothelial cells along with pro-inflammatory and anti-inflammatory cytokines are overreacting as a response to a widespread infection. The overreaction of these cells and activated protein C deficiency not only results in vasodilation, damage to endothelium, increased capillary permeability, hypercoagulability but also enhances platelet aggregation and the development of micro-thrombin (Pearson Education, 2015, p. 600). Consequently, blood clots form throughout the microcirculation leading to the obstruction of blood flow and decreased tissue perfusion (Pearson Education, 2015, p.600). Moreover, sepsis can also cause dysfunction of multiple organs in severe cases. Sepsis is known

1281). Damage to the pulmonary endothelium triggers the release of neutrophils in a great amount, and the neutrophils stimulate the release of other inflammatory mediators such as tumor necrosis factor, prostaglandin, leukotrienes, histamine and platelet-activating factor (McKane, 2010, 1281). Consequently, capillary membrane becomes more permeable which further allows more fluids, proteins and red blood cells casts to flow into alveoli (McKane, 2010, p.1281). It later causes the lungs to collapse resulting in atelectasis and reduce the lungs compliance (McKane, 2010, p.1281). In addition, pulmonary vasoconstriction can result from platelet aggregation, atelectasis and inactivated surfactant (McKane, 2010, p. 1281). Subsequently, the lungs have to work harder for gas exchange and it later impairs oxygen delivery to body organs, especially the heart and brain. Stroke can also result from ARDS due to intravascular thrombus formation, blockage in the microcirculation, decreased oxygen concentration and increased carbon dioxide

174). Sepsis commonly associates with DIC as a response to systemic inflammation; pro-inflammatory cytokines excessively produce during DIC resulting in damage to the vascular endothelium (Dressler, 2009, p.174). Damaged endothelial cells trigger the release of abundant tissue factors leading to the activation of coagulation extensively (Dressler, 2009, p.174). A great amount of thrombin develops in the circulation that exhausts the natural ability of the body to produce anticoagulants such as anti-thrombin, protein C and protein S (McKane, 2010, p.1051). As a result, fibrin clots interrupt blood flow through tissues and organs leading to hypoperfusion, ischemia, infarction and necrosis (McKane, 2010, p. 1052). Due to a high consumption of pro-coagulation factors and platelets during DIC, the liver and bone marrow are unable to catch up with production of clotting factors (Dressler, 2009, p.174). Thus, DIC can result in thrombocytopenia which causes an extensive bleeding at multiple injury sites in the body (McKane, 2010, p.1051). DIC also contributes to the development of cerebral vascular accident due to the interruption of blood flow and excessive bleeding at various sites. In conclusion, DIC not only associates with sepsis, but also can predispose to ARDS and CVA