Huasheng Tong

Background: Sepsis-induced lymphopenia is associated with adverse outcomes, yet static assessments at a single time point fail to capture the clinical significance of its dynamic evolution, and the effects of the trajectories of lymphopenia on prognosis are to be elucidated in sepsis. Methods: This retrospective cohort study extracted data from the MIMIC-IV (v3.1) database. Adult septic patients with initial lymphopenia (<1.0 × 10⁹/L) were included. Group-Based Trajectory Modeling (GBTM) identified lymphocyte count trajectories. Kaplan-Meier analysis with log-rank test was used to visualize survival differences. Multivariable Cox and logistic regression assessed associations between trajectories and 7-day, 28-day, ICU, and in-hospital mortality. Subgroup analyses validated result consistency. Results: A total of 1,640 patients were included. GBTM identified 4 distinct lymphocyte count trajectories. Kaplan-Meier analysis revealed that patients in Trajectory 4 (Persistent Low Level, N = 544, 33.2%), characterized by persistent lymphopenia, had the lowest cumulative 7-day and 28-day survival rates. After multivariable adjustment, Trajectory 4 was independently associated with an increased risk of 28-day mortality [adjusted HR = 1.76, 95% CI: 1.266–2.446, P = 0.001], ICU mortality (adjusted OR = 1.831, 95% CI: 1.196–2.832, P = 0.006), and in-hospital mortality (adjusted OR = 1.881, 95% CI: 1.298–2.767, P = 0.001) compared to Trajectory 1 (Sustained Recovery), and these associations remained robust across all predefined subgroups. In contrast, no significant association was observed between Trajectory 4 and 7-day mortality after full adjustment for confounders. Conclusion: Lymphocyte count Trajectory 4 (Persistent Low Level) in initially lymphopenic sepsis patients is independently associated with late (28-day) but not early (7-day) mortality, as well as worse ICU and hospital outcomes. Failure of lymphopenia to recover by days 3–4 may signal a transition to the highest-risk state, suggesting a potential window for immunomodulatory strategies.

Exertional heatstroke (EHS) often leads to multiple organ dysfunction syndrome (MODS) with high mortality. The liver is frequently early damaged in EHS, presenting as acute liver injury (ALI), including acute liver disease (ALD) and acute liver failure (ALF). This study investigates liver enzyme changes in EHS patients, assesses whether ALF independently predicts in-hospital mortality, and tries to create an ALF-based predictive model for EHS. This was a single-center retrospective study. The medical records of EHS patients admitted to the intensive care unit (ICU) of a tertiary hospital from January 1, 2008 to December 31, 2023, were recorded and analyzed. The characteristics of liver damage were analyzed by reviewing the enzymatic indices of EHS patients from day 1 to day 9 after admission. There were 176 male patients ultimately analyzed, comprising 160 survivors and 16 non-survivors. Univariate and multivariate logistic regression analysis showed that prolonged activated partial thromboplastin time (APTT) (OR = 1.029, P = 0.018), increased γ-glutamyltransferase (γ-GGT) (OR = 1.032, P = 0.013), and ALF (OR = 57.238, P = 0.002) were independent risk factors for predicting in-hospital mortality. Approximately half of the patients (48.3%) were diagnosed as ALI. Notably, 81.8% of the ALF cases were diagnosed within 5 days after EHS onset. The predictive model based on increased heart rate (HR) (OR = 1.065, P < 0.001), increased platelet (PLT) count (OR = 0.989, P = 0.034), and increased fibrinogen (Fib) (OR = 0.216, P = 0.002) level had a higher specificity and better predictive performance (SEN = 86.4%, SPE = 90.8%, AUC = 0.936) for occurrence of ALF in EHS. During the early stages of EHS, patients exhibited multiple organ injuries, with a high ALI incidence rate. ALF, prolonged APTT, and elevated γ-GGT levels were the independent risk factors for in-hospital mortality in EHS patients. The predictive model based on HR, PLT, and Fib levels was potentially suitable and practical for early identification and timely management of ALF in EHS patients.

Background: While lactate has emerged as a promising biomarker for assessing the severity in traumatic brain injury (TBI), it fails to reflect the dynamic change of disease. Thus, this study aims to investigate the relationship between arterial lactate trajectories and TBI. Methods: TBI patient data were extracted from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. The group-based trajectory modeling (GBTM) was employed to identify subgroups of lactate trajectories. Subsequently, the impact of lactate trajectories on mortality in TBI patients was analyzed using Cox proportional hazards models and doubly robust estimation methods. Results: Among 509 enrolled TBI patients, three lactate trajectories were established using GBTM. Kaplan-Meier analysis revealed that Trajectory 1 had the highest 7-day mortality. Multivariate Cox regression analysis showed that Trajectory 1 was an independent risk factor for 7-day mortality. The doubly robust analysis also similarly demonstrated that Trajectory 1 had a significantly higher mortality risk compared to other groups. Conclusion: Three lactate trajectories were found in TBI patients, and Trajectory 1 was identified as an independent risk factor for mortality. The study emphasizes the importance of dynamic monitoring to facilitate early identification and timely treatment of individuals in Trajectory 1 with potentially poor prognoses.

Multi-trauma presents significant challenges due to the complexity of injuries and high mortality rates. Early identification and intervention are crucial for improving outcomes in these critically injured patients. This retrospective study analyzed clinical data from multi-trauma patients admitted to the emergency department of Huiyang Sanhe Hospital between January 10, 2020, and September 30, 2022. Univariate and multivariate logistic regression analyses were conducted to identify independent predictors of hospital mortality. A prediction model was developed based on these prognostic markers, visualized using a nomogram, and its discriminative ability and clinical benefit were evaluated. A total of 124 multi-trauma patients were included in the study, with a hospital mortality rate of 26.7%. Univariate and multivariate logistic regression analyses identified trauma-induced coagulopathy (TIC) (OR 4.238, 95% CI 1.46–12.28), blood urea nitrogen (BUN) (OR 1.397, 95% CI 1.09–1.78), and Glasgow Coma Scale (GCS) score (OR 0.720, 95% CI 0.61–0.85) as independent factors of hospital mortality. Therefore, a nomogram incorporating TIC, BUN, and GCS score was constructed and demonstrated excellent predictive performance and clinical impact (AUC 0.898, 95% CI 0.834–0.962). The nomogram developed in this study provided a practical tool for early prediction of hospital mortality in multi-trauma patients. By focusing on TIC, BUN, and GCS score, this model may facilitate rapid bedside assessment and timely intervention. However, further multicenter, prospective studies are required to validate its performance and applicability.

Background: Heat stroke (HS), a potentially fatal heat-related illness, is often accompanied by disseminated intravascular coagulation (DIC) early, resulting in a poorer prognosis. Unfortunately, diagnosis by current DIC scores is often too late to identify DIC. This study aims to investigate the predictors and predictive model of DIC in HS to identify DIC early. Methods: This retrospective study analyzed clinical data of patients with HS in a tertiary hospital from January 1, 2008 to December 31, 2020. Univariate and multivariate logistic regression analyses were employed to identify the risk factors for DIC in HS. The predictive models based on these risk factors were constructed and externally validated, and their predictive efficacy was evaluated using receiver operating characteristic curves. Results: A total of 219 HS patients, including 49 with DIC, were included. The independent risk factors for DIC were identified as follows: neutrophil percentage (Neu%), lymphocyte count, lymphocyte percentage (Lym%), creatine kinase-MB (CKMB), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), neutrophil–lymphocyte ratio (NLR), monocyte–lymphocyte ratio (MLR), and rhabdomyolysis (RM). After logarithmization, the final predictive model based on the logarithm of lactate dehydrogenase (InLDH; odds ratio (OR) = 9.266, 95% confidence interval (95%CI; 4.379–19.607), p < 0.0001) and the logarithm of neutrophil–lymphocyte ratio (InNLR; OR = 3.393, 95%CI (1.834–6.277), p < 0.0001) was constructed with the largest area under the curve (0.928). A nomogram incorporating InLDH and InNLR was developed and showed excellent discrimination and calibration capabilities. Conclusion: Nine independent risk factors were identified for the occurrence of DIC in HS patients. The predictive model based on InLDH and InNLR can effectively predict the incidence of DIC. A nomogram based on InLDH and InNLR was developed to facilitate early identification and timely treatment of DIC in HS patients.

Background: Exertional heatstroke (EHS), a fatal illness, pronounces multiple organ dysfunction syndrome (MODS) and high mortality rate. Currently, no ideal factor prognoses EHS. Decreased monocyte human leukocyte‐DR antigen (mHLA‐DR) has been observed in critically ill individuals, particularly in those with sepsis. While most research focus on the pro‐inflammatory response exploration in EHS, there are few studies related to immunosuppression, and no report targeted on mHLA‐DR in EHS. The present study tried to explore the prognostic value of mHLA‐DR levels in EHS patients.Methods: This was a single‐center retrospective study. Clinical data of EHS patients admitted to the intensive care unit of the General Hospital of Southern Theatre Command between January 1, 2008, and December 31, 2020, were recorded and analyzed.Results: Seventy patients with 54 survivors and 16 nonsurvivors were ultimately enrolled. Levels of mHLA‐DR in the nonsurvivors (41.8% [38.1–68.1]%) were significantly lower than those in the survivors (83.1% [67.6–89.4]%, p < 0.001). Multivariate logistic regression indicated that mHLA‐DR (odds ratio [OR] = 0.939; 95% confidence interval [CI]: 0.892–0.988; p = 0.016) and Glasgow coma scale (GCS) scores (OR = 0.726; 95% CI: 0.591–0.892; p = 0.002) were independent risk factors related with in‐hospital mortality rate in EHS. A nomogram incorporated mHLA‐DR with GCS demonstrated excellent discrimination and calibration abilities. Compared to the traditional scoring systems, the prediction model incorporated mHLA‐DR with GCS had the highest area under the curve (0.947, 95% CI: [0.865–0.986]) and Youden index (0.8333), with sensitivity of 100% and specificity of 83.33%, and a greater clinical net benefit.Conclusion: Patients with EHS were at a risk of early experiencing decreased mHLA‐DR early. A nomogram based on mHLA‐DR with GCS was developed to facilitate early identification and timely treatment of individuals with potentially poor prognosis.

Heatstroke (HS), a severe condition, can develop multiple organ dysfunction syndrome and death. However, at present, no early reliable index exists for risk stratification and prognosis. von Willebrand factor (vWF), a marker of vascular endothelial injury, is a key regulatory target of inflammation and coagulation, which is closely associated with the pathogenesis of HS. vWF was reported as a prognostic marker in several infectious and noninfectious severe illness such as COVID-19, sepsis, and trauma. Although early increased level of vWF is seen in HS, the relationship between vWF and mortality is to be elucidated. Clinical data of patients with HS in a tertiary hospital were recorded and analyzed. It was shown that plasma vWF concentrations at admission were significantly increased in the nonsurvivors (351% ± 105%) compared with survivors (278% ± 104%, p = 0.021). After multivariate logistic regression analysis it was shown that vWF (odds ratio [OR] = 1.010; 95% confidence interval [CI], 1.002–1.18; p = 0.017), hemoglobin (Hb) (OR = 0.954; 95% CI, 0.931–0.979; p < 0.001), and hematocrit (HCT) in blood (OR = 0.859; 95% CI, 0.790–0.934; p < 0.001) were independent factors of in-hospital mortality in HS. The nomogram based on vWF and Hb was constructed in patients with HS. The area under curve under the receiver operating characteristic of this prediction model was 0.860 (95% CI, 0.773–0.923) and cutoff was 0.15, with Youden index 0.5840, which were not significantly different to sequential organ failure assessment ( p = 0.0644), Acute Physiology and Chronic Health Evaluation II (APACHE II) ( p = 0.7976), and systemic inflammatory response syndrome (SIRS) scores ( p = 0.3274). The prediction model that integrated vWF and Hb showed a better predicting efficiency than single variable, and a higher specificity (81.48%) than APACHE II (72.84%) and SIRS (72.84%) scores. In summary, vWF, as an independent risk factor for in-hospital mortality, combined with Hb, could effectively prognosis the mortality in HS patients at early stage.

Heat stroke is a life‐threatening disease with high mortality and complications. Endothelial glycocalyx (EGCX) is essential for maintaining endothelial cell structure and function as well as preventing the adhesion of inflammatory cells. Potential relationship that underlies the imbalance in inflammation and coagulation remains elusive. Moreover, the role of EGCX in heat stroke‐induced organ injury remained unclear. Therefore, the current study aimed to illustrate if EGCX aggravates apoptosis, inflammation, and oxidative damage in human pulmonary microvascular endothelial cells (HPMEC). Heat stress and lipopolysaccharide (LPS) were employed to construct in vitro models to study the changes of glycocalyx structure and function, as well as levels of heparansulfate proteoglycan (HSPG), syndecan‐1 (SDC‐1), heparansulfate (HS), tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐6, Von Willebrand factor (vWF), endothelin‐1 (ET‐1), occludin, E‐selectin, vascular cell adhesion molecule‐1 (VCAM‐1), and reactive oxygen species (ROS). Here, we showed that heat stress and LPS devastated EGCX structure, activated EGCX degradation, and triggered oxidative damage and apoptosis in HPMEC. Stimulation of heat stress and LPS decreased expression of HSPG, increased levels of SDC‐1 and HS in culture supernatant, promoted the production and release of proinflammation cytokines (TNF‐α and IL‐6,) and coagulative factors (vWF and ET‐1) in HPMEC. Furthermore, Expressions of E‐selection, VCAM‐1, and ROS were upregulated, while that of occludin was downregulated. These changes could be deteriorated by heparanase, whereas they meliorated by unfractionated heparin. This study indicated that EGCX may contribute to apoptosis and heat stroke‐induced coagulopathy, and these effects may have been due to the decrease in the shedding of EGCX.