Combined, converted, and prophylactic use of resuscitative endovascular balloon occlusion of the aorta for severe torso trauma: a retrospective study.

Introduction: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is used as an intra-aortic balloon occlusion in Japan; however, protocols for its effective use in different conditions have not been established. This study aimed to summarize the strategies of REBOA use in severe torso trauma. Methods: Twenty-nine cases of REBOA for torso trauma treated at our hospital over 5 years were divided into hemodynamically unstable (HU) (n = 12), cardiac arrest (CA) (n = 13), and hemodynamically stable (HS) (n = 4) groups. We retrospectively examined patient characteristics, trauma mechanism, injury site, severity score, intervention type, and survival rates at 24 h in each group. Results: In the HU group, 9 and 3 patients survived and died within 24 h, respectively; time to intervention (56.6 versus 130.7 min, P = 0.346) tended to be shorter and total occlusion time (40.2 versus 337.7 min, P = 0.009) was significantly shorter in survivors than in nonsurvivors. In the CA group, 10 patients were converted from resuscitative thoracotomy with aortic cross-clamp (RTACC); one patient survived. All four patients in the HS group survived, having received prophylactic REBOA. Conclusion: The efficacy of REBOA for severe torso trauma depends on the patient's condition. If the patients are hemodynamically unstable, time to intervention and total occlusion time could correlate with survival. The combined use of REBOA with definitive hemostasis could improve outcomes. Conversion from RTACC in the cardiac arrest patients and prophylactic use in the hemodynamically stable patients can be one of the potentially effective options, although further studies are needed.

A longitudinal change of syndecan-1 predicts risk of acute respiratory distress syndrome and cumulative fluid balance in patients with septic shock: a preliminary study.

BACKGROUND: The purpose of this study is to investigate the time course of syndecan-1 (Syn-1) plasma levels, the correlation between Syn-1 and organ damage development, and the associations of Syn-1 level with cumulative fluid balance and ventilator-free days (VFD) in patients with septic shock. METHODS: We collected blood samples from 38 patients with septic shock upon their admission to ICU and for the first 7 days of their stay. Syn-1 plasma level, acute respiratory distress syndrome (ARDS), other organ damage, VFD, and cumulative fluid balance were assessed daily. RESULTS: Over the course of 7 days, Syn-1 plasma levels increased significantly more in patients with ARDS than in those without ARDS. Patients with high levels of Syn-1 in the 72 h after ICU admission had significantly higher cumulative fluid balance, lower PaO2/FiO2, and fewer VFD than patients with low levels of Syn-1. Syn-1 levels did not correlate with sequential organ failure assessment score or with APACHE II score. CONCLUSIONS: In our cohort of patients with septic shock, higher circulating level of Syn-1 of cardinal glycocalyx component is associated with more ARDS, cumulative positive fluid balance, and fewer VFD. Measurement of Syn-1 levels in patients with septic shock might be useful for predicting patients at high risk of ARDS.

Increased PD-1 Expression and Altered T Cell Repertoire Diversity Predict Mortality in Patients with Septic Shock: A Preliminary Study.

Sepsis causes impairment of innate and adaptive immunity by multiple mechanisms, including depletion of immune effector cells and T cell exhaustion. Although lymphocyte dysfunction is associated with increased mortality and potential reactivation of latent viral infection in patients with septic shock, the relation between viral reactivation and lymphocyte dysfunction is obscure. The objectives of this study were 1) to determine the relation of lymphocyte dysfunction to viral reactivation and mortality, and 2) to evaluate recovery of lymphocyte function during septic shock, including T cell receptor (TCR) diversity and the expression of programmed death 1 (PD-1). In 18 patients with septic shock and latent cytomegalovirus (CMV) infection, serial blood samples were obtained on days 1, 3, and 7 after the onset of shock, and immune cell subsets and receptor expression were characterized by flow cytometry. TCR diversity of peripheral blood mononuclear cells was analyzed by Multi-N-plex PCR, and CMV DNA was quantified using a real-time PCR kit. A decrease of TCR diversity and monocyte HLA-DR expression were observed in the early stage of septic shock, while CD4+ T cells displayed an increase of PD-1 expression. Significant lymphopenia persisted for at least 7 days following the onset of septic shock. Normalization of TCR diversity and PD-1 expression was observed by day 7, except in patients who died. CMV reactivation was detected in 3 of the 18 patients during the first week of their ICU stay and all 3 patients died. These changes are consistent with the early stage of immune cell exhaustion and indicate the importance of normal lymphocyte function for recovery from septic shock. Ongoing lymphocyte dysfunction is associated with CMV reactivation and dissemination, as well as with unfavorable outcomes.

Flavopiridol inhibits interferon-γ-induced nitric oxide production in mouse vascular endothelial cells.

Flavopiridol (FP), a synthetic flavone, is a cyclin-dependent kinase inhibitor and possesses an anti-cancer activity. The effect of FP on interferon (IFN)-γ-induced nitric oxide (NO) production in mouse vascular endothelial cell line END-D was examined. FP significantly inhibited IFN-γ-induced NO production in END-D cells via reduced expression of an inducible NO synthase. FP inhibited the activation of STAT1, and subsequently IRF1 as a downstream molecule of STAT1, which is essential for IFN-γ-induced NO production. FP did not affect the cell surface expression of IFN-γ receptor. Taken together, FP was suggested to inhibit IFN-γ-induced NO production in vascular endothelial cells via preventing intracellular IFN-γ signaling. FP might be useful as an immunomodulatory drug as well as an anti-cancer drug.

Beneficial effects of the heme oxygenase-1/carbon monoxide system in patients with severe sepsis/septic shock.

PURPOSE: We evaluated the relations among the arterial carbon monoxide (CO) concentration, heme oxygenase (HO)-1 expression by monocytes, oxidative stress, plasma levels of cytokines and bilirubin, and the outcome of patients with severe sepsis or septic shock. METHODS: Thirty-six patients who fulfilled the criteria for severe sepsis or septic shock and 21 other patients without sepsis during their stay in the intensive care unit were studied. HO-1 protein expression by monocytes, arterial CO, oxidative stress, bilirubin, and cytokines were measured. RESULTS: Arterial blood CO, cytokine, and bilirubin levels, and monocyte HO-1 protein expression were higher in patients with severe sepsis/septic shock than in non-septic patients. Increased HO-1 expression was related to the arterial CO concentration and oxidative stress. There was a positive correlation between survival and increased HO-1 protein expression or a higher CO level. CONCLUSIONS: Arterial CO and monocyte HO-1 protein expression were increased in critically ill patients, particularly those with severe sepsis or septic shock, suggesting that oxidative stress is closely related to HO-1 expression. The HO-1/CO system may play an important role in sepsis.