Multiple organ dysfunction syndrome: a narrative review.
ABSTRACT To review multiple organ dysfunction syndrome with respect to: 1) clinical measurement systems; 2) molecular mechanisms; and 3) therapeutic directions based upon molecular mechanisms.
The Medline, Cochrane, and Best Evidence databases (1996 to 2000), conference proceedings, bibliographies of review articles were searched for relevant articles. Key index words were multiple organ failure, multiple system organ dysfunction, sepsis, septic shock, shock, systemic inflammatory response syndrome. Outcomes prospectively defined were death and physiological reversal of end organ failure.
Multiple organ dysfunction/failure (MODS) is the most common cause for death in intensive care units. The recognition of this syndrome in the last 30 yr may be due to advances in early resuscitation unmasking these delayed sequelae in those that would have died previously. Multiple organ dysfunction occurs after shock of varied etiologies and may be the result of unbridled systemic inflammation. As yet, therapy directed to prevent or improve MODS has not dramatically altered outcomes.
Multiple organ dysfunction may serve as useful measure of disease severity for risk adjustment and outcome marker for quality of care and therapy provided. Anesthesiologists treating shock patients will note the subsequent development of MODS in the critical care unit and may be required to provide anesthetic support to these patients.
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ABSTRACT: The liver is one of the major target organs affected in sepsis that are usually accompanied with free radical formation. The use of minus charge for the prevention and cure of various radical related diseases is gaining wide importance in the medicinal field. Here, we investigate whether minus charge stimulation (MCS) inhibits nitric oxide (NO) production induced by lipopolysaccharide (LPS) in the mice liver. The survival rate was compared in LPS-treated group with MCS group. The liver NO radical was measured using electron spin resonance technique. Serum alanine transaminase (ALT) was estimated for liver injury. MCS significantly improved the survival rate of LPS-treated mice and inhibited increase of ALT in serum levels. MCS also reduced NO radical production significantly in the LPS-treated mice liver tissue. In conclusion, our results indicate that MCS prevents LPS-induced liver injury, which may be through the inhibition of liver NO radical production.Journal of Clinical Biochemistry and Nutrition 06/2008; 42(3):222-7. · 1.98 Impact Factor