• D Rixen, J H Siegel, N Espina, and M Bertolini.
• Department of Anatomy, Cell Biology and Injury Sciences, New Jersey 07103, USA.
• Shock. 1997 Jan 1;7(1):17-28.

AbstractThe time course of nitric oxide (NO) production in posttrauma critical illness was monitored, and its relationship to posttrauma "sepsis/SIRS" and physiologic patterns was described. Eighty multiple trauma patients were studied (514 samples) during their course in the intensive care unit (Injury Severity Score 27.6; 36% deaths). Plasma NO was estimated from NO3 + NO2 by the Griess test and compared with that of 10 healthy controls (HC). At each sample period, the patient was categorized as having bacteremic sepsis (BAC), sepsis syndrome (SS), or systemic inflammatory response syndrome (SIRS), and classified by Physiologic State Severity Classification (PSSC) into normal stress response (A-State), metabolic insufficiency (B-State), or respiratory insufficiency (C2-State), each quantified by their physiologic "distance" from reference state of recovering trauma patients (R-State). A severity index (L2PDEATH), based on a logistic model of state distances from R-State, quantified probability of death. Deaths showed increased NO (p < .05) over survivors or HC by day 3 posttrauma. A fall in vascular tone in deaths was related to the increased NO (p < .0001). The level of NO was higher as sepsis worsened: BAC > SS > SIRS > HC (all simultaneous, p < .05). PSSC and L2PDEATH correlated with incidence > HC and level of NO. In conclusion, the severity of posttrauma critical illness was classified by PSSC and quantified by the L2PDEATH index. These reflect progressively increased NO levels and suggest worsening sepsis status. The reduced total peripheral resistance (TPR)-to-flow relationship (vascular tone) in deaths characteristic of the more severe septic PSSC states appeared related to the increased plasma NO.

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