Splanchnic blood flow and blood volume are highly variable in critically ill patients, depending on the underlying disease, compensatory mechanisms, and therapeutic interventions. During low blood flow states or hypoxemia, adaptive mechanisms include profound reductions in splanchnic blood flow and volume. The splanchnic organs are both source and target of systemic inflammation and significant derangements in splanchnic blood flow and metabolism may occur under these conditions. Therapeutic interventions such as vasoactive drugs or nursing procedures may have additional effects on splanchnic tissue perfusion and metabolic demands.
Although transient reduction of splanchnic perfusion may be life-saving under certain circumstances, splanchnic hypoperfusion may contribute to the pathogenesis of systemic inflammation, sepsis, and multiple organ failure via several mechanisms, including ischemia and reperfusion injury, increased mucosal permeability, translocation of endotoxin and bacteria, and local activation of cytokines and their inflammatory mediators. The clinical syndromes of systemic inflammation, sepsis, and multiple organ failure are associated with a high morbidity and mortality, and are major contributors to the high cost of modern intensive care.