Sepsis and Septic Shock

Definitions of terms related to sepsis are given in Table 45-1. Physiologically similar systemic inflammatory response syndrome can be seen even in the absence of identifiable infection. 

The sites of infections that most frequently led to sepsis were the respiratory tract (21% to 68%), urinary tract (14% to 18%), and intraabdominal space (14% to 22%). Sepsis may be caused by gram-negative (38% of sepsis) or gram-positive bacteria (40%), as well as by fungi (17%) or other microorganisms. 

Candida species (particularly Candida albicans) are a common cause of sepsis in hospitalized patients. 

Sepsis involves a complex interaction of proinflammatory (e.g., tumor necrosis factor-a [TNF-a] interleukin [1L]-1, IL-6) and antiinflammatory mediators (e.g., lL-1 receptor antagonist, lL-4, and lL-10). IL-8, plateletactivating factor, and a variety of prostaglandins, leukotrienes, and thromboxanes are also important. 

TNF-a is considered the primary mediator of sepsis, and concentrations are elevated early in the inflammatory response during sepsis, and there is a correlation with severity of sepsis. TNF-a release leads to activation of other cytokines associated with cellular damage and it stimulates release of arachidonic acid metabolites that contribute to endothelial cell damage. lL-6 is a more consistent predictor of sepsis as it remains elevated for longer periods of time than does TNF-a 

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Appropriate empiric anti-infective therapy decreases 28-day mortality compared to inappropriate empiric therapy (24% versus 39%).22 23,30 Additionally, appropriate therapy administered within 1 hour of sepsis recognition also decreases complications and mortality.22-23,30 Empiric anti-infective therapy should include one, two, or three drugs, depending on the site of infection and causative pathogens (Table 79-3). Anti-infective clinical trials in sepsis and septic shock patients are scarce and have not demonstrated differences among agents therefore, factors that determine selection are ... 

Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004 32 858-873. 

Rivers E, Nguyen B, Havstad S, et al. Early Goal-directed Therapy Collaborative Group. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001 345 1368-1377. 

WJB Dorn Veterans Affairs Medical Center Columbia, South Carolina Chapter 79 Sepsis and Septic Shock... 

Chap. 79 - Sepsis and Septic Shock Universal Program Number 014-999-07-094-H04... 

Hormonal Changes during Sepsis and Septic Shock... 

It has been shown that CGRP is released into the circulation during the development of human sepsis and septic shock (A8). Plasma CGRP levels correlated with the APACHE II score as well as with cardiac index and systemic vascular re-sistence index. There is also a relationship between the initial plasma CGRP levels and the severity of the disease at the time of admission to the ICU. Plasma CGRP levels are related to the hemodynamic changes seen early in septic shock. 

A8. Amalich, F., Sanchez, F. F., Martinez, M Jimenez, M., L6pez, J., Vazques, J. J., and Hernanz, A., Changes in plasma concentrations of vasoactive neuropeptides in patients with sepsis and septic shock. Life Sci. 56, 75-81 (1995). 

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