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Terms in this set (54)

Severe sepsis is sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion (Dellinger et al., 2013). It represents the progression of sepsis with an amplified SIRS (see Fig. 37-4). All tissues are involved and are hypoxic to some degree. Some organs are experiencing cell death and dysfunction at this time. Microthrombi formation is widespread with clots forming where they are not needed. This process uses up or consumes much of the available platelets and clotting factors, a condition known as disseminated intravascular coagulation (DIC). The amplified SIRS and cytokine release increase capillary leakiness, injure cells, and increase cell metabolism. Damage to endothelial cells reduces anticlotting actions and triggers the formation of even more small clots, increasing DIC. Anaerobic metabolism continues, and cell uptake of oxygen is poor. The continued stress response triggers the continued release of glucose from the liver and causes hyperglycemia. The more severe the response, the higher the blood glucose level (Kleinpell et al., 2013; Schell-Chaple & Lee, 2014).
Despite the severity of this stage and the fact that it may be present for 24 hours or more, it is often missed. One of the reasons it may be missed is that the cardiac function is hyperdynamic in this phase. The pooling of blood and the widespread capillary leak stimulate the heart, and cardiac output is increased 751with a more rapid heart rate and an elevated systolic blood pressure. In addition, the patient's extremities may feel warm and there is little or no cyanosis. Even though the patient may "look" better, the pathologic changes occurring at the tissue level are serious and have caused significant damage. The WBC count at this time may no longer be elevated.