Daily Ards Research Analysis

BackgroundFluid resuscitation represents conventional therapy for shock; however, the optimal fluid choice remains controversial. Sodium bicarbonate administration during resuscitation has shown potential benefits in modulating acidosis and hemodynamic parameters. This study aims to evaluate the clinical effects of sodium bicarbonate compared to conventional resuscitation fluids in patients with shock. We conducted a comprehensive literature search across the PubMed, Embase, Web of Science, and China National Knowledge Infrastructure (CNKI) databases, encompassing studies published in both Chinese and English. Publication bias was assessed using funnel plots and Egger's test. Sensitivity analyses were performed to evaluate the robustness of the findings. For studies exhibiting substantial heterogeneity, meta-regression was applied to explore potential sources of variability. Subgroup analyses examined the influence of shock type, control interventions, and temporal factors. A total of 4137 articles were reviewed. Ultimately, 18 studies meeting the predefined inclusion criteria were selected for analysis, comprising data from 1411 participants. Analysis of the included studies indicated that Sodium bicarbonate administration was associated with a reduction in the duration of intensive care unit (ICU) stay (MD = -1.42 days, 95% CI: -1.87 to -0.97) and total hospitalization length (MD = -2.78 days, 95% CI: -4.33 to -1.23). Sodium bicarbonate treatment lowered lactic acid levels (MD = -0.97 mmol/L, 95% CI: -1.28 to -0.67) and decreased the incidence of complications, including multiple organ dysfunction syndrome (MODS), acute respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC). Furthermore, improvements were observed in coagulation parameters, Including thrombin time (TT), activated partial thromboplastin time (APTT), and prothrombin time (PT). The inflammatory response was also attenuated, as evidenced by reduced circulating levels of interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-alpha (TNF-α).ConclusionThis study suggests that Sodium bicarbonate may confer potential therapeutic effects in patients with shock compared to alternative interventions. Further research is required to investigate its efficacy across diverse shock etiologies and therapeutic approaches.

BACKGROUND: Fluid balance management is critical in moderate and severe traumatic brain injury (TBI) due to impaired cerebrovascular autoregulation. This study systematically reviews the association of fluid volume management with outcomes in moderate to severe TBI. METHODS: We conducted a systematic literature search on MEDLINE, EMBASE, CINAHL, The Cochrane Database, and bibliographies of included articles. Studies assessing fluid volume management and outcomes in moderate/severe TBI patients were included. Risk of bias, publication bias, and heterogeneity were comprehensively assessed. Primary outcomes were short/long-term mortality and neurological outcomes. Secondary outcomes included the effect on intracranial pressure, development of acute kidney injury (AKI), refractory intracranial hypertension (RIH), pulmonary edema/acute respiratory distress syndrome, length of stay, and length of mechanical ventilation. Fluid balance groups were categorized into restrictive, euvolemic, and liberal. RESULTS: Out of 2668 studies identified, 12 studies (seven observational and five randomized controlled trials [RCTs]) involving 9184 TBI patients were included. Euvolemic fluid balance was associated with lower odds of mortality compared to restrictive (odds ratio [OR] = 0.39, 95% confidence interval [CI]: 0.27 to 0.57, CONCLUSIONS: Euvolemic fluid balance may improve key outcomes in TBI patients, including reduced mortality and better neurological outcomes. These findings underscore the need for RCTs to further assess euvolemic fluid management protocols in neurocritical care and their potential to inform clinical guidelines.

The interaction between the brain and the lungs is bidirectional: ICU patients with acute brain injury develop pulmonary complications, while ARDS patients frequently manifest neurological sequelae. Research is indeed focusing on both aspects of this cross-talk. On one side, ARDS survivors experience poor neurological outcomes both in the short and long term, with high incidence of delirium and post- discharge neurocognitive impairment. The underlying mechanisms have been investigated either in the pre-clinical and in the clinical field. Ventilator associated brain injury is the new recent term used to indicate the brain damage consequent to mechanical ventilation and leading to neuroinflammation and increased brain cells apoptosis. Moreover, prolonged hypoxia, deep sedation, loss of cerebral autoregulation and complications from vv-ECMO during ARDS are potentially sources of brain damage. On the other side, pulmonary complications in patients with acute brain injury follow a double-hit model, recently implemented in a triple-hit hypothesis. According to this theory, the primary brain injury leads to sympathetic hyperactivity, with inflammation and oxidative stress. Thus, the lungs become more vulnerable to develop complications such as neurogenic pulmonary edema and pneumonia. Finally, immune dysregulation and microbiome alterations due to brain-lung cross-talk lead to the worsening of lung injury. In this context, mechanical ventilation strategies aiming to guarantee adequate gas exchange and brain oxygen delivery are essential to prevent this phenomenon cascade. This review purpose is to examine the mechanisms behind brain-lung cross talk, starting from pathophysiological mechanisms, in order to suggest potential new research and therapeutic approaches.