Critical Care Medicine 978-1-4963-0291-5 chapter 27

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SECTION II • Medical and Surgical Crises

TRIGGER

IL-8

TNF

RADICALS

O 2

IL-1

TNF IL-1

PAF

IL-6

MONONUCLEAR CELLS

ENZYMES

PROSTAGLANDINS

ADHESION

FIGURE 27-3. Simplified representation of the early biochemical events in sepsis syndrome. In most cases, an inflammatory stimulus ( upper left ) activates tissue-based and circulating mononuclear cells. The resulting production of tumor necrosis factor (TNF) and interleukin-1 (IL-1) can activate diverse nucleated cells. In response to TNF, other cells, especially neutrophils ( upper right ), release additional interleukins, more TNF, oxidant radicals, prostaglandins, leukotrienes, and proteases. TNF and IL-1 also activate adhesion molecules on neutrophils and vascular endothelium, resulting in cellular binding and vessel injury ( bottom ). Simultaneously, activation of tissue factor on white blood cells and endothelial cells results in accelerated clotting and inhibition of fibrinolysis.

Although routine clotting assays (e.g., prothrombin and activated partial thromboplastin times) may be near normal, abnormalities of clotting and anticlot- ting systems can be detected using more sensitive laboratory tests. The complex interrelationship among the three major pathways that mediate sep- sis (inflammation, coagulation, and fibrinolysis) is still being elucidated by ongoing research. It is also clear, however, that counterregulating immunosup- pressive activity begins from the very first stages of the proinflammatory response. One highly simpli- fied schema depicting these interactions is illus- trated in Figure 27-4. CLINICAL DIAGNOSIS Sepsis has many classic presentations: Group B Streptococcal sepsis in newborns, meningococ- cemia in young children, and staphylococcal toxic shock syndrome of adults. Unfortunately, such “classic presentations,” which include recovery of a

specific organism, are exceptional. Sepsis is a clini- cal diagnosis, not one made by noting a single spe- cific laboratory value or positive culture. Because a central tenet of improving the response to sepsis is early identification and intervention, detection of organ dysfunction at the earliest possible stage is a high priority. To this end, the quick qSOFA score, an abbreviated and user-friendly version of the well validated but more difficult to use sequential organ failure assessment (SOFA) score, has been devel- oped, tested and advocated. Three clinically observ- able elements comprise qSOFA: (1) alteration of mental status (e.g., obtundation or confusion); (2) respiratory rate >22/min; and (3) systolic blood pressure less than 100 mm Hg. If two of these three elements are present, sepsis is likely or imminent. Although the qSOFA may not be infallible, more traditional clinical signs and measures are less spe- cific or less reliable for organ dysfunction. For example, although fever is present in more than 90% of diagnosed cases, it may reflect

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