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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Objective: The aim of the study is to explore the impact of early serum phosphate levels on the prognosis of critically ill patients with sepsis. Methods: In this retrospective large cohort study, data of patients with sepsis were obtained from the Medical Information Mart for Intensive Care IV database. Patients were retrospectively divided into a control group and three study groups according to their daily serum phosphate levels within 2 days of intensive care unit (ICU) admission. ⋯ After stratification in the hypophosphatemia group, subgroup analysis showed that only the association between the mild hypophosphatemia group and 28-day mortality reached statistical significance (hazard ratio = 0.76, 95% CI = 0.65-0.89, P = 0.001). Conclusions: Mild hypophosphatemia might improve the short-term prognosis of patients with sepsis, and hyperphosphatemia is an independent risk factor for the outcomes of septic patients. After ICU admission, the serum phosphate levels on the second day had a better independent correlation with 28-day mortality, which prompted us to reconsider the optimal timing of phosphate evaluation.
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Background: The Society for Cardiovascular Angiography and Intervention (SCAI) Shock Classification can define shock severity. We evaluated the vasoactive-inotropic score (VIS) combined with the SCAI Shock Classification for mortality risk stratification. Methods: This was a single-center retrospective cohort analysis including Mayo Clinic cardiac intensive care unit patients from 2007 to 2015. ⋯ A gradient of in-hospital mortality was observed according to the VIS at 1 h and the increase in VIS from 1 to 24 h. Conclusions: Higher vasoactive drug requirements portend a higher risk of mortality, particularly a high VIS early after admission. The VIS provides incremental prognostic information beyond the SCAI Shock Classification, emphasizing the continuum of risk that exists across the spectrum of shock severity.
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Acute respiratory distress syndrome (ARDS) is characterized by uncontrolled inflammation, which manifests as leukocyte infiltration and lung injury. However, the molecules that initiate this infiltration remain incompletely understood. We evaluated the effect of the nuclear alarmin IL-33 on lung damage and the immune response in LPS-induced lung injury. ⋯ We found that IL-33 promoted inflammation through NKT cells in ARDS. In summary, our results demonstrated that the IL-33/ST2 axis promotes the early uncontrolled inflammatory response in ARDS by activating and recruiting iNKT cells. Therefore, IL-33 and NKT cells may be therapeutic target molecules and immune cells, respectively, in early ARDS cytokine storms.
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Background : Critically ill patients with sepsis often require packed cell transfusions (PCTs). Packed cell transfusion causes changes in body's core temperature. Objective : To trace the course and amplitude of body core temperature after PCT in adults with sepsis. ⋯ In a linear regression model, body core temperature increased by a mean 0.06°C in the first 24 h after PCT and decreased by a mean 0.65°C for every 1.0°C increase before PCT. Conclusions : Among critically ill patients with sepsis, PCT itself causes only mild and clinically insignificant temperature changes. Thus, significant changes in core temperature during the 24 h after PCT may indicate an unusual clinical event that requires clinicians' immediate attention.
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Contrast-induced acute kidney injury (CI-AKI) is a serious and common complication in patients receiving intravenous iodinated contrast medium (CM). Clinically, congestive heart failure is the most critical risk factor for CI-AKI and always leads to renal congestion for increased central venous pressure and fluid overload. Here, we aimed to investigate a novel CI-AKI rat model based on renal congestion. ⋯ Simultaneously, Mdivi-1 alleviated oxidative stress, apoptosis, and inflammatory responses induced by CM toxicity. We concluded that renal congestion exacerbated CM toxicity and presented a novel CI-AKI rat model. Excessive mitochondrial fission plays a crucial role in CM reno-toxicity and is a promising target for preventing and treating CI-AKI.