Background Sepsis and septic shock are life-threatening global health challenges associated with high mortality rates. Early identification of high-risk patients is critical for improving outcomes. In the present study, the association between the neutrophil-to-lymphocyte-to-albumin ratio (NLAR) and mortality in septic patients was evaluated.
Methods A retrospective study was performed at a tertiary hospital in Vietnam. Patients ≥18 years of age diagnosed with sepsis or septic shock based on the Sepsis-3 criteria were included. Exclusion criteria included recent corticosteroid use within 7 days, autoimmune diseases, hematological disorders, and active cancer within 5 years. NLAR was calculated from complete blood counts and albumin levels within the first 24 hours of intensive care unit admission. Receiver operating characteristic (ROC) curves were used to determine the predictive ability of NLAR for in-hospital mortality.
Results The present study included 141 patients with a mean age of 72 years. Non-survivors were significantly older with higher rates of mechanical ventilation. NLAR was significantly elevated in non-survivors compared with survivors (0.88 [0.57–1.24] vs. 0.44 [0.28–0.77], P<0.001). In ROC analysis, the area under the curve for NLAR was 0.70 (P<0.001). Using a cutoff value of 0.56, NLAR showed a sensitivity of 77.8% and a specificity of 61.5% for predicting in-hospital mortality.
Conclusions Elevated NLAR on admission was associated with a higher mortality rate in sepsis patients. NLAR could be used as an early prognostic marker for sepsis mortality.
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Background The use of biomarkers to predict patient outcomes may be crucial for patients admitted to the intensive care unit (ICU) following surgery because biomarkers guide clinicians in tailoring treatment plans accordingly. Therefore, we aimed to identify potential biomarkers to predict the prognosis of patients with Fournier’s gangrene (FG) admitted to the ICU after surgery.
Methods We enrolled patients with FG admitted to our Hospital between January 2013 and December 2022. We retrospectively analyzed patient characteristics, factors related to management, scores known to be associated with the prognosis of FG, and laboratory data.
Results The study population included 28 survivors and 13 nonsurvivors. The initial serum lactate level taken in the emergency department; white blood cell, neutrophil, and platelet counts; delta neutrophil index and international normalized ratio; albumin, glucose, HCO3, and postoperative lactate levels; and the laboratory risk indicator for necrotizing fasciitis differed between survivors and nonsurvivors. Postoperative lactate and initial albumin levels were independent predictors of mortality in patients with FG. In the receiver operating characteristic curve analysis, the postoperative lactate level was the best indicator of mortality (area under the curve, 0.877; 95% confidence interval, 0.711–1.000). The optimal cutoff postoperative lactate level for predicting mortality was 3.0 mmol/L (sensitivity, 80.0%; specificity, 95.0%).
Conclusions Postoperative lactate and initial albumin levels could be potential predictors of mortality in patients with FG admitted to the ICU after surgery, and the optimal cutoff postoperative lactate and initial albumin levels to predict mortality were 3.0 mmol/L and 3.05 g/dl, respectively. Large-scale multicenter prospective studies are required to confirm our results.
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Acute Crit Care. 2020;35(2):67-76. Published online May 15, 2020
Background Sepsis-induced cardiomyopathy (SIC) occurs frequently in critically ill patients, but the clinical features and prognostic impact of SIC on sepsis outcome remain controversial. Here, we investigated the predictors and outcomes of SIC.
Methods Patients admitted to a single medical intensive care unit from June 2016 to September 2017 were retrospectively reviewed. SIC was diagnosed by ejection fraction (EF) <50% and ≥10% decrease in baseline EF that recovered within 2 weeks.
Results In total, 342 patients with sepsis met the inclusion criteria, and 49 patients (14.3%) were diagnosed with SIC; the latter were compared with 259 patients whose EF was not deteriorated by sepsis (non-SIC). Low systolic blood pressure and increased left ventricular end-diastolic diameter (LVEDD) were identified as predictors of SIC. SIC and non-SIC patients did not differ significantly in terms of 28-day all-cause mortality (24.5% vs. 26.3%, P=0.936). Acute Physiology and Chronic Health Evaluation II (APACHE II; hazard ratio [HR], 1.10; 95% confidential interval [CI], 1.02 to 1.18; P=0.009) and delta neutrophil index (DNI; HR, 1.02; 95% CI, 1.00 to 1.08; P=0.026) were independent risk factors for 28-day mortality with SIC. DNI, APACHE II, and lactate were identified as risk factors for 28-day mortality in sepsis patients as a whole.
Conclusions SIC was not associated with increased mortality compared to non-SIC. Low systolic blood pressure and increased LVEDD were predictors of SIC. High APACHE II score and elevated DNI, which reflect sepsis severity, predict 28-day all-cause mortality.
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Background Flecainide acetate is a drug used primarily for cardiac arrhythmia. Some studies also imply that flecainide acetate has the potential to regulate inflammatory-immune responses; however, its mechanism of action is contended. We determined the effects of flecainide acetate on lipopolysaccharide (LPS)-stimulated human neutrophils in vitro and on mortality in a septic rat model.
Methods Neutrophils from human blood were cultured with varying concentrations of flecainide acetate (1 μM, 10 μM, or 100 μM) with or without LPS (100 ng/ml). To assess neutrophil activation, the protein levels of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6 and IL-8 were measured after a 4-hour culture period. To assess the intracellular signaling pathways, the levels of phosphorylation of p38 mitogen-activated protein kinase (p38), extracellular signal-regulated kinase (ERK) 1/2, and c-Jun N-terminal kinase (JNK) were measured after a 30-minute culture period, and the nuclear translocation of nuclear factor (NF)-κB was measured after a 1-hour culture period. Additionally, the survival rate was investigated in a rat sepsis model.
Results Flecainide acetate down-regulated the activation of proinflammatory cytokines, including TNF-α and IL-6 and IL-8, and intracellular signaling pathways including ERK 1/2 and NF-κB. Flecainide acetate also improved the survival rate in the rat sepsis model.
Conclusions Collectively, these findings indicate that flecainide acetate can improve survival in a rat sepsis model by attenuating LPS-induced neutrophil responses. We therefore suggest that flecainide acetate plays an important role in modulating inflammatoryimmune responses.
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BACKGROUND Hypothermia is known to suppress inflammation in various experimental and clinical settings. We wanted to investigate how the suppressed inflammation by hypothermia is affected during rewarming. METHODS Mice were being assigned to normothermia (37degrees C) or hypothermia (32degrees C). After 30 minutes at the assigned temperature, lipopolysaccharide was administered intratracheally. The mice were then randomly grouped and subjected to 4 hours of normothermia (N), 24 hours of normothermia (NN), 4 hours of hypothermia (H), or 4 hours of hypothermia followed by normothermia for the next 20 hours (HN). In another experiment, other HN mice were treated with varying doses of anti-TNF-alpha or anti-IL-1beta antibodies (0, 6.25, 12.5, 25, and 50 microg/250 microl) immediately prior to rewarming. RESULTS The neutrophil counts of BAL fluid (x104/ml) were 23.0 +/- 13.1 in the N, 6.4 +/- 3.1 in the H (p = 0.002 vs N), 20.4 +/- 10.2 in the NN, and 49.7 +/- 21.0 in the HN (p = 0.005 vs H; p < 0.001 vs NN). Myeloperoxidase activity of the lung (unit/microg) was 6.7 +/- 2.9, 7.9 +/- 1.9, 17.8 +/- 4.0 (p < 0.001 vs N), and 12.9 +/- 5.9 (p = 0.034 vs H, p = 0.028 vs NN), respectively. Compared with control HN, total WBC and neutrophil counts of mice treated with anti-TNF-alpha antibody or anti-IL-1beta antibody prior to rewarming were lower at all tested doses. The combination of both anti-TNF-alpha or anti-IL-1beta antibodies was not increasingly reducing the neutrophilic sequestration. CONCLUSIONS Rewarming from induced hypothermia resulted in augmentation of neutrophilic sequestration of endotoxin-injured lung. Treatment with antibodies against TNF-alpha or IL-1beta prevented this rebound of neutrophilic infiltration.
BACKGROUND Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the leading causes of death after lungresection. Neutrophil elastase is thought to be an important mediator in the pathogenesis of ALI. Sivelestat is a new neutrophil elastase inhibitor which may improve the outcome in patients with ALI/ARDS after lung resection. The objective of this study was to determine whether or not sivelestat can reduce mortality in patients with ALI after pulmonary resection for lung cancer. METHODS This study was a retrospective case-control study of twenty three patients who developed ALI/ARDS within seven days of lung resection for lung cancer. The control group (n = 12) received standard care, while the sivelestat group (n = 11) received a continuous infusion of sivelestat (0.2 mg/kg/hr) for seven days in addition to standard care. RESULTS There was no significant difference in the baseline characteristics between the control and sivelestat groups, except for heart rate. Six of twelve patients (50%) in the control group survived, while seven of twelve patients (64%) survived in the sivelestat group (p = 0.34). There was also no significant difference between the two groups in the progression to ARDS. In the sivelelestat group, survivors had lower APACHE II and SOFA scores than the patients in the control group. CONCLUSIONS There was no additional effect of a neutrophil elastase inhibitor in the treatment of ALI after pulmonary resection for lung cancer.
BACKGROUND This study was to clarify the influence of collapse and re-ventilation of lung on the development of pulmonary edema in rabbit. METHODS: Animals were randomly assigned to one of three groups: Sham group receiving two lung ventilation (n=14), Collapse group receiving collapse of right lung (n=14), Reventilation group receiving collapse of right lung for 3 hours followed by reventilation of collapsed right lung for 3 hours (n=14). The lung of rabbits were ventilated with 50% oxygen through the tracheostomy.
Right main bronchus was secured by thoracotomy in all animal. Collapse and reventilation were performed using by bulldog forcep. Mean arterial pressure, heart rate, arterial oxygen tension (PaO2), peripheral blood leukocyte and platelet counts were recorded at 0, 1, 2, 3, 4, 5 and 6 hour after the start of experiment. The wet to dry (W/D) weight ratio of lung, lung injury score and leukocyte counts, percentage of polymorphonuclear leukocyte (PMNL), concentration of albumin, and interleukin-8 (IL-8) in bronchoalveolar lavage fluid (BALF) were measured 6 hour after the start of experiment in both lung. RESULTS: W/D weight ratio of lung, lung injury score and leukocyte counts, percentage of PMNL, concentration of albumin and IL-8 in BALF were significantly increased in both lung of reventilation group. And the degree of increases is more significant in right than left lung. CONCLUSIONS: These findings suggest that reventilation of collapsed lung causes the bilateral pulmonary edema in rabbit mainly by activating neutrophil and IL-8 responses, which may play a central role in non cardiogenic pulmonary edema.