Irreversible sepsis, in spite of advancements in topical therapy and antimicrobial agents, remains the leading cause of death in major thermal injury. A defect in intracellular bactericidal capacity in leukocytes from severely burned patients appears to correspond with increases in bacterial wound colonization and ultimate sepsis. This leukocyte defect has been demonstrated by abnormally low nitroblue tetrazolium reduction (NBT) and oxygen consumption of white cells in patients with major thermal injury. The subcellular mechanisms responsible for decreased bactericidal capacity were therefore investigated. Nicotinamide-adenine dinucleotide (NADH) and nicotinamide-adenine phosphodinucleotide (NADPH) oxidase activity was measured in patients with major bums, controls (normals), and in patients with nonburn stress or infection. NADH and NADPH oxidase levels in leukocytes from bum patients were not significantly different from those of normal nonchallenged controls but were significantly lower than the leukocyte values found in the patients with nonbum infections or stress. This NADH and NADPH defect in the subcellular leukocyte fraction suggests that it may be a significant factor in the reduced bactericidal function of the intact leukocyte in thermally injured patients.
|Original language||English (US)|
|Number of pages||3|
|Journal||Journal of Trauma - Injury, Infection and Critical Care|
|State||Published - Jan 1979|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine