Inflammatory mediators and neonatal sepsis. Rarely has so little been known by so many about so much.
Many questions remain unanswered (and probably many more remain unasked) about neonatal sepsis. In addition, many mediators of inflammation have been implicated in neonatal sepsis at one time or another. The goal of this article is to put together what the authors view as some of the more important outstanding questions with what is known about some of the more important mediators. We address four questions specifically: (1) Why is neonatal sepsis different from all other (adult) sepsis? (2) 41Is control of pulmonary hypertension the white whale or red herring in neonatal septic shock? (3) Is sepsis more like dominoes or like 52 pick-up? and (4) Is disruption of QO2/VO2 coupling a legitimate clinical concern or a laboratory anomaly?
Meadow
W
W
Department of Pediatrics, University of Chicago, Illinois, USA.
Rudinsky
B
B
D000328:Adult; D000818:Animals; D001424:Bacterial Infections / Q000503:physiopathology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology / Q000517:prevention & control; D007231:Infant, Newborn; D018836:Inflammation Mediators / Q000494:pharmacology*; D008171:Lung Diseases / Q000209:etiology / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D012772:Shock, Septic / Q000503:physiopathology; D014692:Ventilation-Perfusion Ratio
D018836:Inflammation Mediators; D009569:Nitric Oxide; D010100:Oxygen