The present study aimed to analyze and compare the prognostic performances of the Revised Trauma Score (RTS), Injury Severity Score (ISS), Shock Index (SI), and Modified Early Warning Score (MEWS) for in-hospital mortality in patients with traumatic brain injury (TBI). This retrospective observational study included severe trauma patients with TBI who visited the emergency department between January 2018 and December 2020. TBI was considered when the Abbreviated Injury Scale was 3 or higher. The primary outcome was in-hospital mortality. In total, 1108 patients were included, and the in-hospital mortality was 183 patients (16.3% of the cohort). Receiver operating characteristic curve analyses were performed for the ISS, RTS, SI, and MEWS with respect to the prediction of in-hospital mortality. The area under the curves (AUCs) of the ISS, RTS, SI, and MEWS were 0.638 (95% confidence interval (CI), 0.603–0.672), 0.742 (95% CI, 0.709–0.772), 0.524 (95% CI, 0.489–0.560), and 0.799 (95% CI, 0.769–0.827), respectively. The AUC of MEWS was significantly different from the AUCs of ISS, RTS, and SI. In multivariate analysis, age (odds ratio (OR), 1.012; 95% CI, 1.000–1.023), the ISS (OR, 1.040; 95% CI, 1.013–1.069), the Glasgow Coma Scale (GCS) score (OR, 0.793; 95% CI, 0.761–0.826), and body temperature (BT) (OR, 0.465; 95% CI, 0.329–0.655) were independently associated with in-hospital mortality after adjustment for confounders. In the present study, the MEWS showed fair performance for predicting in-hospital mortality in patients with TBI. The GCS score and BT seemed to have a significant role in the discrimination ability of the MEWS. The MEWS may be a useful tool for predicting in-hospital mortality in patients with TBI.

Regional cerebral oxygen saturation (rSO ₂ ) is recommended for monitoring cerebral perfusion status. We aimed to investigate the association between rSO ₂ and neurological outcomes and correlating parameters with rSO ₂ in cardiac arrest survivors. This observational study included adult comatose cardiac arrest survivors who underwent targeted temperature management and were monitored with rSO ₂ between June 2021 and February 2023. We collected rSO ₂ values monitored after admission to the intensive care unit at initial, last, 24 hours, 48 hours, and 72 hours after return of spontaneous circulation. We calculated the minimum, maximum, and average rSO ₂ values. The primary outcome was the 6-month neurological outcome assessed using the Cerebral Performance Category (CPC) scale, dichotomized into good (CPC 1 or 2) or poor (CPC 3–5). Among the 78 included patients, 33.3% (26 patients) had poor neurological outcomes. The poor neurological outcome group exhibited lower maximum rSO ₂ (78.5 [70.0–86.8] vs 89.0 [78.3–95.00], P = .006) and lower last rSO ₂ (58.0 [45.3–71.8] vs 70.0 [56.2–85.3], P = .010). Initial, minimum, and average rSO ₂ did not differ between neurological outcome groups. The rSO ₂ significantly changed over 24 hours, 48 hours, and 72 hours after return of spontaneous circulation ( P = .001). Maximum rSO ₂ (odds ratio [OR] 0.931; 95% confidence intervals [CIs] 0.885–0.980), last rSO ₂ during 72 hours (OR 0.950; 95% CIs 0.918–0.983) and rSO ₂ at 48 hours (OR 0.959; 95% CIs 0.920–0.998) were independently associated with poor neurological outcomes. Among hemoglobin, PCO ₂ , PO ₂ , and mean arterial pressure (MAP), hemoglobin correlated with rSO ₂ in both neurological outcomes, while MAP only showed an association with rSO ₂ in the poor neurological outcomes group ( R = 0.292). Lower maximum, 48 hours, and last rSO ₂ values were associated with poor neurological outcomes. The rSO ₂ was dependent on MAP in patients with poor neurological outcomes.

Objective Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence.Methods We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence.Results During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia.Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Background and Objectives: Shift work is associated with an increased risk of acute coronary syndrome (ACS) and higher rates of smoking and alcohol consumption. This study examines how smoking and alcohol intake may influence the effect of shift work on ACS risk, indicating a complex interaction among these factors in individuals engaged in shift work. Materials and Methods: This investigation utilized data from the Korean Genome and Epidemiology Study (KoGES). Shift work was the primary exposure, and the main outcome was ACS, defined as either myocardial infarction or angina pectoris diagnosed from 2003 to 2020. Cox proportional regression analysis was employed to assess the impact of shift work, smoking, and alcohol intake on ACS incidence. Additionally, we performed an interaction analysis to examine the effects of shift work in conjunction with smoking and alcohol intake on ACS incidence. Results: Out of 10,038 participants enrolled during the study period, 3696 (36.8%) met the inclusion criteria. The incidence rate of ACS was 11.88 per 1000 person-years in the shift work group compared to 5.96 per 1000 person-years in the non-shift work group. Using Cox proportional logistic regression, shift work was found to be associated with a hazard ratio (HR) of 1.74 (95% CI, 1.20, 2.53) compared to the non-shift work group. Smoking and alcohol consumption did not exhibit a significant HR for ACS incidence, with HRs of 1.31 (95% CI, 0.98, 1.75) and 0.83 (95% CI, 0.65, 1.07), respectively. In the interaction model, after adjusting for other covariates, shift work was not significantly associated with ACS incidence in current smokers (HR 1.05, 95% CI 0.49, 2.23). However, among non-current smokers, shift work emerged as a significant risk factor for ACS incidence (HR 2.26, 95% CI 1.44, 3.55) (p for interaction < 0.01). No interaction was found between alcohol consumption and shift work in relation to ACS incidence. Conclusions: Shift work is an independent risk factor for acute coronary syndrome (ACS), particularly among non-current smokers. This finding highlights the need to address both lifestyle and occupational factors when developing strategies to mitigate ACS risk among shift workers. Employers and policymakers should consider implementing targeted workplace interventions to reduce this risk. These may include optimizing shift schedules to minimize circadian disruption, providing regular health screenings focused on cardiovascular health, and promoting healthy lifestyle habits such as balanced nutrition, regular physical activity, and stress management programs. Additionally, workplace wellness initiatives could focus on reducing other modifiable risk factors, such as providing resources for smoking cessation and limiting exposure to occupational stressors. Integrating these strategies into occupational health policies can contribute to the early detection and prevention of ACS, ultimately improving the cardiovascular health of shift workers.

Current treatment recommendations for hyperkalemic cardiac arrest focus exclusively on the addition of antihyperkalemic therapies and are otherwise identical to those for cardiac arrest caused by non-hyperkalemic etiologies. We were unable to find any studies that specifically examine the hemodynamic effects of cardiopulmonary resuscitation in hyperkalemic cardiac arrest compared to cardiac arrest from non-hyperkalemic etiologies. We hypothesized that myocardial ischemic contracture would be less severe in hyperkalemic cardiac arrest compared with ventricular fibrillation cardiac arrest, resulting in higher cerebral perfusion pressure, brain tissue oxygen tension, and coronary perfusion pressure during cardiopulmonary resuscitation. Twenty-two pigs randomly underwent either electrically induced ventricular fibrillation arrest or hyperkalemic arrest induced by potassium infusion. Hemodynamic, echocardiographic, and brain tissue oxygen tension measurements were obtained during advanced cardiovascular life support and compared using linear mixed-effects models. Two animals developed massive hemothorax associated with cardiopulmonary resuscitation and were excluded from further analysis. The remaining 20 animals had no internal organ injury due to cardiopulmonary resuscitation and were included in the study. Left ventricular wall thickness was significantly lower in the hyperkalemic arrest group than in the ventricular fibrillation arrest group (group effect, P = 0.019). The decrease in end-diastolic volume over time was significantly less pronounced in the hyperkalemic arrest group (group-time interaction, P = 0.010). Coronary perfusion pressure (group effect, P = 0.041) and cerebral perfusion pressure (group effect, P = 0.020) were significantly lower in the hyperkalemic arrest group. Although not significant, brain tissue oxygen tension was also lower in the hyperkalemic arrest group. In conclusion, the left ventricular wall thickness was smaller, and the decrease in end-diastolic volume over time was less pronounced in the hyperkalemic arrest group. However, perfusion pressure was poorer, and cerebral oxygenation was not better in the hyperkalemic arrest group.

Background: Despite the established concordance between core temperature and brain temperature (BT) in out-of-hospital cardiac arrest (OHCA) patients, the relationship between BT and neurological outcomes in those who received targeted temperature management (TTM) has yet to be elucidated. Thus, this study aimed to explore the relationship between BT and neurological outcome in OHCA patients who received TTM. Methods: This observational study involved adult patients (≥18 years) with OHCA who received TTM at 33 °C between April 2021 and December 2023. We recorded BTs at the initiation of TTM (BTINI) and during the maintenance phase of TTM (BTMAIN). A neurological outcome at 6 months was the primary outcome. Poor outcome was considered as Cerebral Performance Categories 3, 4, and 5. Results: Of the 149 included patients with OHCA, 109 (73.2%) patients exhibited poor outcomes. Compared with the good outcome group, the BTINI (35.8 °C [interquartile range (IQR), 33.4–36.3 °C] vs. 33.4°C [IQR, 32.6–35.4 °C]) and BTMAIN (33.1 °C [IQR, 32.8–33.2 °C] vs. 32.6 °C [IQR, 32.2–32.9 °C]) were lower in the poor outcome group. Multivariate analysis after adjusting for confounders revealed that BTINI (odds ratio (OR), 0.223; 95% confidence interval (CI), 0.054–0.917; p = 0.038) and BTMAIN (OR, 0.078; 95% CI, 0.019–0.322; p < 0.001) were associated with poor outcomes. Conclusions: BTs at the initiation of TTM and during the maintenance phase of TTM at 33 °C are associated with poor outcomes.