Necrotizing soft tissue infections (NSTI) have a 90-day mortality rate of 18–22%. Tools are needed for estimating the prognosis and severity of NSTI upon admission. We evaluated soluble urokinase-type plasminogen activator receptor (suPAR) levels at admission as a prognostic marker of NSTI severity and mortality. In a prospective, observational cohort study, suPAR was measured in 200 NSTI patients. We compared admission suPAR levels in survivors and non-survivors, patients with septic shock and non-shock, amputation and non-amputation, correlations with Simplified Acute Physiology Score II (SAPS II) and the Sequential Organ Failure Assessment (SOFA) score. Admission suPAR levels were higher in septic shock vs. non-septic shock patients (9.2 vs. 5.8 ng/mL, p-value < 0.001) and non-survivors vs. survivors (11 vs. 6.1 ng/mL, p-value < 0.001) and correlated with SAPS II (r = 0.52, p < 0.001) and SOFA score (r = 0.64, p < 0.001). Elevated suPAR upon admission was associated with 90-day mortality (log-rank test p < 0.001), however not after adjustment for age, sex, and SOFA score. The AUC for suPAR and 90-day mortality was 0.77. We found that suPAR is a promising candidate for prognosis and severity in patients with NSTI.

Purpose: To determine the effects of a blockade of nitric oxide (NO) synthesis on hyperbaric oxygen (HBO2) therapy during cyanide (CN) intoxication. Methods: 39 anesthetized female Sprague-Dawley rats were exposed to CN intoxication (5.4 mg/kg intra-arterially) with or without previous nitric oxide synthase (NOS) inhibition by L-NG-nitroarginine methyl ester (L-NAME) injection (40 mg/kg intraperitoneally). Subsequently, either HBO2 therapy (284 kPa/90 minutes), normobaric oxygen therapy (100% oxygen/90 minutes) or nothing was administered. Intracerebral microdialysis was used to measure the interstitial brain concentration of lactate, glucose, glycerol and lactate/pyruvate ratios. Results: L-NAME potentiated CN intoxication by higher maximum and prolonged lactate (in mM: 0. 5+/- 0.3 vs. 0.7 +/- 0.4, P < 0.005) concentrations compared with solely CN-intoxicated rats. The same trend was found for mean glucose, glycerol and lactate/pyruvate ratio levels.During HBO2 treatment a sustained reduction occurred in mean lactate levels (in mM: 0.5 +/- 0.5 vs. 0.7 +/- 0.4, P < 0.01) regardless of NOS blockade by L-NAME. The same trend was found for mean glucose and glycerol levels. Conclusion: The results suggest that blocking NOS using L-NAME can worsen acute CN intoxication. HBO2 treatment can partially overcome this block and continue to ameliorate CN intoxication.