Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Introduction: The present study aimed to explore the clinical features and long-term outcomes associated with neurologic impairment in patients with cardiac arrest (CA) who received extracorporeal cardiopulmonary resuscitation (ECPR). Methods: A total of 37 adult CA patients who underwent venoarterial extracorporeal membrane oxygenation and were admitted to our department between January 2015 and February 2022 were divided according to neurologic impairment. Baseline and CPR- and ECMO-related characteristics were compared between the two groups. ⋯ Conclusions: The incidence of neurologic impairment was higher in patients who received ECPR and was closely related to 28-day mortality and discharge survival. NP >12 hours combined with IABP support and serum Cr levels were independent risk factors for neurologic impairments in ECPR-supported patients. Neurologic impairment significantly adversely affected the long-term outcomes of ECPR-supported patients after discharge.
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Ischemic postconditioning (I/Post) reduces I/R injury by activating endogenous cardioprotection mechanisms, such as the JAK/signal transducer and activator of transcription 3 (STAT3) and PI3K/Akt pathways, which offer a traditional approach to myocardial protection. According to a previous study, cardioprotection by I/Post may be lost in aged mice, and in our previous research, hypoxic postconditioning (H/Post) lacked a protective effect in senescent cardiomyocytes, which was associated with low expression of long noncoding RNA H19. The N6-methyladenosine (m 6 A) modification is a dynamic and reversible process that has been confirmed to play a role in cardiovascular diseases. ⋯ Furthermore, ALKBH5 knockdown exacerbated injury following H/Post in senescent cardiomyocytes. In addition, ALKBH5 regulated STAT3 expression by mediating its m 6 A modification and long noncoding RNA H19/miR-124-3p. ALKBH5 also alleviated the H/Post injury induced by the low expression of STAT3 in senescent cardiomyocytes.
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The original guidelines of cardiopulmonary resuscitation focused on the establishment of an airway and rescue breathing before restoration of circulation through cardiopulmonary resuscitation. As a result, the airway-breathing-circulation approach became the central guiding principle of resuscitation. Despite new guidelines by the American Heart Association for a circulation-first approach, Advanced Trauma Life Support guidelines continue to advocate for the airway-breathing-circulation sequence. ⋯ In severely injured patients, a paradigm shift should be considered, which prioritizes restoration of circulation before ETI and positive pressure ventilation while maintaining a focus on basic airway assessment and noninvasive airway interventions. For this patient population, the most reasonable current strategy may be to target a simultaneous resuscitation approach, with immediate efforts to control hemorrhage and provide basic airway interventions while prioritizing volume resuscitation with blood products and deferring ETI until adequate systemic perfusion has been attained. We believe that a circulation-first sequence will improve both survival and neurologic outcomes for a traumatically injured patient and will continue to advocate this approach, as additional clinical evidence is generated to inform how to best tailor circulation-first resuscitation for varied injury patterns and patient populations.
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Significant numbers of patients who survive sepsis exhibit psychiatric and cognitive impairments, termed post-sepsis syndrome. Understanding the underlying pathophysiology is essential to develop effective therapies. Translocator protein 18 kDa (TSPO) is a multifaceted mitochondrial protein implicated in inflammation, oxidative stress, and steroidogenesis in the central nervous system. ⋯ RNA-seq analysis of the hippocampus revealed the upregulation of genes (C1qb, C1qc, and Tyrobp) in C1q complement pathways correlated significantly with anxiety-like behavior that appeared long after CLP surgery. The expressions of these genes predicted other behavioral traits, including depressive-like behavior in the tail suspension test and grip power impairment, supporting the role of the C1q pathway in post-sepsis syndrome. Because the C1q pathway has recently attracted interest as a tag for pathological synaptic elimination, the current study suggests the C1q pathway is involved in the psychiatric and cognitive impairments observed in post-sepsis syndrome.
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Background: Furosemide is a commonly used loop diuretic in critical care. However, its effect on the progression of oliguric acute kidney injury across different central venous pressure (CVP) remains unknown. This study therefore aims to investigate the association between furosemide 6-12h (defined as the use of furosemide within 6 h after the diagnosis of AKI according to the urine output [UO] criteria set by the Kidney Disease: Improving Global Outcomes [KDIGO] guidelines) and the progression of AKI across different CVP 6-12h (defined as CVP within 6 h after the diagnosis of AKI by the KDIGO UO criteria) levels. ⋯ In addition, for patients with CVP 6-12h ≥12 mm Hg, furosemide 6-12h is also significantly associated with lower risk of 28-d mortality (adjusted OR was 0.47 at 95% CI of 0.25-0.92, P = 0.026) in the multivariate logistic regression analysis, and there was a similar trend in the IPTW analysis (adjusted OR was 0.55 at 95% CI of 0.28-1.10, P = 0.092). Conclusions: Among the identified early-stage AKI patients in critical care, the use of furosemide was associated only with lower risk of oliguric AKI progression and 28-d mortality within the high CVP group. These findings suggest the potential of CVP as a guidance or reference point in the usage of furosemide among early-stage oliguric AKI patients in the ICU.