BackgroundNew biomarkers are needed to assess the severity of necrotizing soft tissue infection (NSTI) at an early stage and to individualize treatment strategies. We assessed pentraxin-3 (PTX3) as a marker of disease severity and risk of death in patients with NSTI.MethodsWe conducted a prospective, observational study in the intensive care unit at Copenhagen University Hospital, where treatment of NSTI is centralized at a national level. We compared PTX3, procalcitonin and C-reactive protein in septic shock versus nonshock patients and in amputated versus nonamputated patients using the Mann-Whitney U test. The prognostic value of the markers for 180-day mortality was assessed using Cox regression analyses.ResultsPatients with NSTI (n = 135) were included over 25 months with up to 2.5-year follow-up; 71 % had septic shock, amputation was undertaken in 20 % and the 180-day mortality was 27 %. Baseline plasma PTX3 level was significantly higher in patients with septic shock (67.3 versus 24.6 ng/mL, p < 0.0001) and in patients who underwent amputation (118.6 versus 43.6 ng/mL, p = 0.019). No significant differences in baseline procalcitonin or C-reactive protein levels were found according to amputation (25.2 versus 7.0 μg/L, p = 0.060 and 202 versus 225 mg/L, p = 0.123), respectively. Baseline PTX3 level above the median was associated with death (p = 0.009, log-rank test) and the univariate Cox regression analysis revealed a significant association between PTX3 level upon admission and 180-day mortality (hazard ratio 2.60 (95 % confidence interval 1.28–5.29), p = 0.008). When adjusted for age, sex, chronic disease and Simplified Acute Physiology Score II, no significant association was found.ConclusionsHigh PTX3 level is associated with septic shock, amputation and risk of death in patients with NSTI, but it is not an independent predictor of 180-day mortality in this patient group.Trial registrationClinicalTrials.gov Identifier: NCT02180906. Date of registration: June 29, 2014.

Purpose Animal studies have demonstrated anti-inflammatory, and anti-nociceptive properties of hyperbaric oxygen therapy (HBOT). However, physiological data are scarce in humans. In a recent experimental study, the authors used the burn injury (BI) model observing a decrease in secondary hyperalgesia areas (SHA) in the HBOT-group compared to a control-group. Surprisingly, a long-lasting neuroplasticity effect mitigating the BI-induced SHA-response was seen in the HBOT-preconditioned group. The objective of the present study, therefore, was to confirm our previous findings using an examiner-blinded, block-randomized, controlled, crossover study design. Patients and methods Nineteen healthy subjects attended two BI-sessions with an inter-session interval of ≥28 days. The BIs were induced on the lower legs by a contact thermode (12.5 cm 2 , 47C°, 420 s). The subjects were block-randomized to receive HBOT (2.4 ATA, 100% O 2 , 90 min) or ambient conditions ([AC]; 1 ATA, 21% O 2 ), dividing cohorts equally into two sequence allocations: HBOT-AC or AC-HBOT. All sensory assessments performed during baseline, BI, and post-intervention phases were at homologous time points irrespective of sequence allocation. The primary outcome was SHA, comparing interventions and sequence allocations. Results Data are mean (95% CI). During HBOT-sessions a mitigating effect on SHA was demonstrated compared to AC-sessions, ie, 18.8 (10.5–27.0) cm 2 vs 32.0 (20.1–43.9) cm 2 ( P =0.021), respectively. In subjects allocated to the sequence AC-HBOT a significantly larger mean difference in SHA in the AC-session vs the HBOT-session was seen 25.0 (5.4–44.7) cm 2 ( P =0.019). In subjects allocated to the reverse sequence, HBOT-AC, no difference in SHA between sessions was observed ( P =0.55), confirming a preconditioning, long-lasting (≥28 days) effect of HBOT. Conclusion Our data demonstrate that a single HBOT-session compared to control is associated with both acute and long-lasting mitigating effects on BI-induced SHA, confirming central anti-inflammatory, neuroplasticity effects of hyperbaric oxygen therapy.

Introduction: This study aimed to assess the capability of a pulse CO-oximeter to continuously monitor carboxyhemoglobin (COHb) during hyperbaric oxygen (HBO2) therapy. We estimated limits of agreement (LOA) between blood gas analysis and pulse CO-oximeter for COHb during HBO2 therapy in patients suffering from acute CO poisoning. Furthermore, we did a medicotechnical evaluation of the pulse CO-oximeter in hyperbaric conditions. Method: We conducted a prospective, non-clinical, observational study in which we included n=10 patients with acute CO poisoning referred for HBO2 therapy. We did five repeated measurements of COHb for each patient during the HBO2 therapy. Bland-Altman analysis for multiple observations per individual was used to assess the agreement. The a priori LOA was ±6% for COHb. For the medicotechnical evaluation continuous measurements were obtained throughout each complete HBO2 therapy. The measurements were visually inspected and evaluated. Results: The Bland-Altman analysis showed that the pulse CO-oximeter overestimated COHb by 2.9 % [±1.0%] and the LOA was ±7.3% [±1.8%]. The continuous measurements by pulse CO-oximetry showed fluctuating levels of COHb and summarized saturations reached levels above 100%. Measurements were not affected by changes in pressure. Conclusion: To our knowledge, this study is the first to asses LOA and demonstrate use of a non-invasive method to measure COHb during HBO2 therapy. The pulse CO-oximeter performed within the manufactures reported LOA (±6%) despite hyperbaric conditions and was unaffected by changes in pressure. However, summarized saturations reached levels above 100%.

Objective: The aim of this study was to evaluate whether monitoring of acute carbon monoxide-poisoned (COP) patients by means of quantitative Romberg’s test (QR-test) during a hyperbaric oxygen (HBO2) therapy regimen could be a useful supplement in the evaluation of neurological status. Method: We conducted a retrospective study (2000-2014) in which we evaluated data containing quantitative sway measurements of acute COP patients (n = 58) treated in an HBO2 regimen. Each patient was tested using QR-test before and after each HBO2 treatment. Data were analyzed using linear mixed models (LMM). In each LMM, sway prior to HBO2 therapy was set as the fixed effect and change in sway after HBO2 therapy was set as the response variable. Patient, treatment number, weight and age were set as random effects for all LMMs. Results: From the LMMs we found that larger values of sway prior to HBO2 produced a negative change in sway. We found no correlation between CO level and sway (P=0.1028; P=0.8764; P=0.4749; P=0.5883). Results showed that loss of visual inputcaused a significant increase in mean sway (P=0.028) and sway velocity (P<0.0001). Conclusion: The Quantitative Romberg’s test is a fast, useful supplement to neurological evaluation and a potential valuable tool for monitoring postural stability during the course of treatment in acute COP patients.