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Síndrome compartimental abdominal y síndrome de distres intestinal agudo


, : Síndrome compartimental abdominal y síndrome de distres intestinal agudo.

La Hipertensi n Intraabdominal (HIA) y el S ndrome Compartimental Abdominal (SCA) son entidades frecuentes en los pacientes graves y cursan con una alta mortalidad. En esta revisi n se actualizan los aspectos m s debatidos sobre la HIA y el SCA: factores desencadenantes, epidemiolog a, pron stico, m todos de medici n de la presi n intraabdominal (PIA), consecuencias fisiopatol gicas y medidas terap uticas, tanto m dicas como quir rgicas. Se plantea que, simult neamente a los mecanismos de lesi n estrictamente f sicos, como la compresi n directa de vasos y rganos intraabdominales, la transmisi n de la PIA a otros compartimentos y el descenso del gasto card aco, pueden intervenir tambi n una serie de mediadores inmunoinflamatorios generados en el propio intestino. La hipoperfusi n, la isquemia mantenida y el fen meno isquemia-reperfusi n actuar an sobre la microbiota, el epitelio y sistema inmune intestinal desencadenando el S ndrome de Distr s Intestinal Agudo, una respuesta inflamatoria sist mica y una eventual disfunci n multiorg nica que pueden aparecer en fases tard as del SCA. Seriously ill patients frequently present intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) as complications, and the associated mortality is very high. This review offers an update on the most controversial aspects of these entities: factors favoring their appearance, the most common causes, prognosis, and methods of measuring intra-abdominal pressure (IAP), physiopathological consequences in relation to the different organs and systems, and the currently accepted treatment measures (medical and/or surgical). Simultaneously to the strictly physical mechanisms of injury, such as direct compression of intra-abdominal organs and vessels, the transmission of IAP to other compartments, and the drop in cardiac output, a series of immune-inflammatory mediators generated in the intestine itself may also intervene. Hypoperfusion, sustained ischemia and the ischemia-reperfusion phenomenon, would act upon the microbiota, intestinal epithelium and intestinal immune system, triggering a systemic inflammatory response and multiorgan dysfunction that appears in the final stages of ACS.

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