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[Translocation and multiple organ failure]
T H Jensen1, L Heslet, A Fomsgaard
1Rigshospitalet, anaestesi- og intensiv afdeling, København.
Abstract:
A review of bacterial translocation and multiple organ failure (MOF) is presented. Splanchnic ischaemia plays a central role in the development of MOF, but the exact mechanism of translocation is unclear. The concentration of endotoxins and bacteria in the gut is high. The critically ill patient is often treated with antibiotics with a broad antibacterial spectrum and overgrowth of Gram negative bacteria will take place in the gut favouring the translocation phenomenon. The regime of selective gut decontamination is discussed. Regional and systemic oxygen kinetics together with metabolic markers are important in detecting splanchnic ischaemia. Hepatic vein catheterisation and gastric mucosa pHi are discussed. The regional inflammation in the gut is often initiated by endotoxins, which stimulate the cytokines IL-1, IL-6 and TNF. Another important factor that can accentuate inflammation of the gut is reperfusion injury. A proposal for treatment of splanchnic ischaemia and translocation is discussed i.e.: optimizing central haemodynamic parameters, optimizing the regional microcirculation, treatment with antibodies to endotoxins, gut decontamination and early enteral nutrition. When splanchnic hypoperfusion is detected it cannot be ignored. It may be possible to correct the hypoperfusion with early gastrointestinal resuscitation and to thereby reduce the duration and mortality of MOF. The above mentioned suggestions are all very demanding of resources, but have to be considered in gut directed therapy.
Insights
Bacterial translocation contributes to multiple organ failure (MOF) via splanchnic ischemia. Early gastrointestinal resuscitation and gut-directed therapies may reduce MOF duration and mortality.
Area of Science:
- Gastroenterology
- Critical Care Medicine
- Pathophysiology
Context:
- Splanchnic ischemia is a key factor in multiple organ failure (MOF).
- Bacterial translocation from the gut is implicated in MOF pathogenesis.
- Critically ill patients often receive broad-spectrum antibiotics, potentially promoting bacterial overgrowth.
Purpose:
- To review the mechanisms of bacterial translocation and its link to MOF.
- To discuss diagnostic methods for splanchnic ischemia.
- To propose treatment strategies for splanchnic ischemia and bacterial translocation.
Summary:
- High gut endotoxin and bacterial concentrations, exacerbated by antibiotics, can drive translocation.
- Splanchnic ischemia, detected by oxygen kinetics and gastric pHi, initiates gut inflammation via endotoxins and cytokines.
- Reperfusion injury can worsen gut inflammation.
Impact:
- Early detection and treatment of splanchnic hypoperfusion are crucial.
- Strategies include optimizing hemodynamics, microcirculation, using anti-endotoxin antibodies, gut decontamination, and early enteral nutrition.
- Gut-directed therapy, though resource-intensive, may reduce MOF duration and mortality.