Síndrome séptico: Importancia del diagnóstico temprano

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Abstract

Se realiza un estudio retrospectivo y transversal sobre los pacientes con proceso infeccioso, ingresados en una Unidad de Terapia Intensiva Polivalente (UTIP). Estos representan el 54,2 % de los ingresos totales durante 6 meses y de ellos el 30,1 % muestra síndrome séptico, con una mortalidad los últimos del 24 %. Se estudian 4 grupos de pacientes según el momento de diagnóstico y terapéutica, y se observa que mientras más tarde es el diagnóstico de síndrome séptico, más avanzada la enfermedad hacia etapas más complicadas del fenómeno sepsis/shock séptico y mayor la mortalidad. En aquellos pacientes en los cuales se hizo el diagnóstico al aparecer los elementos clínicos que lo describen, la mortalidad no existe y las complicaciones son menores.

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Most cited references 14

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The pathogenesis of sepsis.

Courtney Bone (1991)

Sepsis and its sequelae (sepsis syndrome and septic shock) are increasingly common and are still potentially lethal diagnoses. Many mediators of the pathogenesis of sepsis have recently been described. These include tumor necrosis factor alpha (TNF alpha), interleukins, platelet activating factor, leukotrienes, thromboxane A2, and activators of the complement cascade. Neutrophil and platelet activation may also play a role. Other agents that may participate in the sepsis cascade include adhesion molecules, kinins, thrombin, myocardial depressant substance, beta-endorphin, and heat shock proteins. Endothelium-derived relaxing factor and endothelin-1 are released from the endothelium and seem to exert a regulatory effect, counterbalancing each other. A central mediator of sepsis does not seem to exist, although TNF alpha has been commonly proposed for this role. Animal studies are difficult to extrapolate to the clinical setting because of cross-species differences and variations in experimental design. Rather than being caused by any single pathogenic mechanism, it is more likely that sepsis is related to the state of activation of the target cell, the nearby presence of other mediators, and the ability of the target cell to release other mediators. Also important is the downregulation or negative feedback of these mediators or the generation of natural inflammation inhibitors, such as interleukin-4 and interleukin-8. Endothelial damage in sepsis probably results from persistent and repetitive inflammatory insults. Eventually, these insults produce sufficient damage that downregulation can no longer occur; this leads to a state of metabolic anarchy in which the body can no longer control its own inflammatory response.