Predicting Prolonged Intensive Care Unit Stay Among Patients With Sepsis-Induced Hypotension

Murphy, David L.; Johnson, Nicholas J.; Hall, Matthew; Kim, Mitchell L.; Shapiro, Nathan I.; Henning, Daniel J.

doi:10.4037/ajcc2019931

Cited by 4 publications

(4 citation statements)

References 24 publications

(20 reference statements)

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“…Increased respiratory rate as a risk factor of respiratory failure identified in this study is simple and convenient to apply for clinicians in their practice. This result is consistent with previous studies [ 7 , 26 ].…”

Section: Discussionsupporting

confidence: 94%

Respiratory failure among patients with COVID-19 in Jiangsu province, China: a multicentre retrospective cohort study

et al. 2021

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This study was a retrospective multicentre cohort study of patients with coronavirus disease 2019 (COVID-19) diagnosed at 24 hospitals in Jiangsu province, China as of 15 March 2020. The primary outcome was the occurrence of acute respiratory failure during hospital stay. Of 625 patients, 56 (9%) had respiratory failure. Some selected demographic, epidemiologic, clinical and laboratory features as well as radiologic features at admission and treatment during hospitalisation were significantly different in patients with and without respiratory failure. The multivariate logistic analysis indicated that age (in years) (odds ratio [OR], 1.07; 95% confidence interval [CI]: 1.03–1.10; P = 0.0002), respiratory rate (breaths/minute) (OR, 1.23; 95% CI: 1.08–1.40; P = 0.0020), lymphocyte count (109/l) (OR, 0.18; 95% CI: 0.05–0.69; P = 0.0157) and pulmonary opacity score (per 5%) (OR, 1.38; 95% CI: 1.19–1.61; P < 0.0001) at admission were associated with the occurrence of respiratory failure. Older age, increased respiratory rate, decreased lymphocyte count and greater pulmonary opacity score at admission were independent risk factors of respiratory failure in patients with COVID-19. Patients having these risk factors need to be intensively managed during hospitalisation.

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Section: Discussionsupporting

confidence: 94%

Respiratory failure among patients with COVID-19 in Jiangsu province, China: a multicentre retrospective cohort study

et al. 2021

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“…Previous researches demonstrated that neutrophils were involved in the development of sepsis 42 . Previous work identified that deleterious accumulation of neutrophils in organs resulted in MODS 43 . Our data showed that LPS injection resulted in severe neutrophil infiltration in lung, liver, kidney, and heart tissues.…”

Section: Discussionmentioning

confidence: 99%

Aerobic exercise improves LPS-induced sepsis via regulating the Warburg effect in mice

Wang

Tang

2021

Sci Rep

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We investigated the impact of aerobic exercise (AE) on multiple organ dysfunction syndrome (MODS), aortic injury, pathoglycemia, and death during sepsis. ICR mice were randomized into four groups: Control (Con), Lipopolysaccharide (LPS), Exercise (Ex), and Exercise + LPS (Ex + LPS) groups. Mice were trained with low-intensity for 4 weeks. LPS and Ex + LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. Histopathological micrographs showed the organ morphology and damage. This study examined the effects of AE on LPS-induced changes in systemic inflammation, pulmonary inflammation, lung permeability, and bronchoalveolar lavage fluid (BALF) cell count, oxidative stress-related indicators in the lung, blood glucose levels, plasma lactate levels, serum insulin levels, plasma high-mobility group box 1 (HMGB1) levels, glucose transporter 1 (Glut1) and HMGB1, silent information regulator 1 (Sirt-1), and nuclear factor erythroid 2-related factor 2 (Nrf-2) mRNA expression levels in lung tissue. AE improved sepsis-associated multiple organ dysfunction syndrome (MODS), aortic injury, hypoglycemia, and death. AE prominently decreased pulmonary inflammation, pulmonary edema, and modulated redox balance during sepsis. AE prominently decreased neutrophil content in organ. AE prominently downregulated CXCL-1, CXCL-8, IL-6, TNF-α, Glu1, and HMGB1 mRNA expression but activated IL-1RN, IL-10, Sirt-1, and Nrf-2 mRNA expression in the lung during sepsis. AE decreased the serum levels of lactate and HMGB1 but increased blood glucose levels and serum insulin levels during sepsis. A 4-week AE improves sepsis-associated MODS, aortic injury, pathoglycemia, and death. AE impairs LPS-induced lactate and HMGB1 release partly because AE increases serum insulin levels and decreases the levels of Glut1. AE is a novel therapeutic strategy for sepsis targeting aerobic glycolysis.

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“…These results demonstrated that AE improved sepsis-induced lung injury in part by decreasing neutrophil content. Besides, deleterious accumulation of neutrophils within remote vital organs led to collateral tissue damage and ultimately multiple organ failure [38]. Hence, deleterious activation of neutrophils was a critical reason leading to host tissue injury and organ damage during sepsis.…”

Section: Discussionmentioning

confidence: 99%

Aerobic Exercise Improves Sepsis via Impairing LPS-induced Lactate and HMGB1 Release in Mice

Wang

Tang

2021

Preprint

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Purpose: In the present study, we attempted to investigate whether aerobic exercise (AE) could prevent sepsis and its complications and explored the related mechanisms. Methods: Forty ICR mice were divided into four groups: Control (Con), Lipopolysaccharide (LPS), Exercise (Ex), and Exercise + LPS (Ex + LPS) groups. Ex and Ex + LPS mice were performed with low-intensity AE for 4 weeks. LPS and Ex + LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. Histopathological micrographs showed the organ injury. This study examined the effects of AE on LPS-induced changes in systemic inflammation, pulmonary inflammation, lung permeability, oxidative stress-related indicators in the lung, blood glucose levels, plasma lactate levels, and plasma high-mobility group box 1 (HMGB1) levels, and bronchoalveolar lavage fluid (BALF) cell count. Sixty mice were used to perform survival rate analysis. Results: AE improved survival rates, MODS, and aortic injury in mice with sepsis. AE decreased LPS-induced oxidative stress injury in lung tissue. AE reduced the infiltration of neutrophils in the lung, liver, kidney, and heart tissues. AE suppressed CXCL-1, CXCL-8, IL-6, and TNF-α mRNA expression but activated IL-1RN, IL-10, Sirt-1, and Nrf-2 mRNA expression in the lung. AE decreased the serum levels of lactate and HMGB1 but increased blood glucose levels during sepsis. Conclusions: AE improves sepsis-associated lung, liver, kidney, heart, and aortic injury and death. AE modulates the inflammatory-anti-inflammatory and oxidative-antioxidative balance in the lung. AE, which can regulate the Warburg effect and impair LPS-induced lactate and HMGB1 release, is a novel therapeutic strategy for sepsis targeting aerobic glycolysis.

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Predicting Prolonged Intensive Care Unit Stay Among Patients With Sepsis-Induced Hypotension

Cited by 4 publications

References 24 publications

Respiratory failure among patients with COVID-19 in Jiangsu province, China: a multicentre retrospective cohort study

Respiratory failure among patients with COVID-19 in Jiangsu province, China: a multicentre retrospective cohort study

Aerobic exercise improves LPS-induced sepsis via regulating the Warburg effect in mice

Aerobic Exercise Improves Sepsis via Impairing LPS-induced Lactate and HMGB1 Release in Mice

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