Predictors of poor prognosis in patients with heat stroke

Chun, Jae-Kwon; Choi, Sangchun; Kim, Hyuk-Hoon; Yang, Hee Won; Kim, Chang Seong

doi:10.15441/ceem.18.081

Cited by 5 publications

(5 citation statements)

References 36 publications

(47 reference statements)

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“…Elevated lactate levels are often seen in conditions with low perfusion, such as sepsis, shock, and trauma [25][26][27][28]. Studies have also shown elevated lactate levels in patients with HS [29][30][31], potentially due to factors like hypoxia, ischemia, and hyper-metabolism [29,32]. In this study, the nonsurvival group had signi cantly higher lactate levels compared to the survival group.…”

Section: Discussionmentioning

confidence: 59%

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Predictive Factors and Nomogram for 30-Day Mortality in Heat Stroke Patients: A Retrospective Case-Control Study

Li,

Zhang,

Zhang

et al. 2024

Preprint

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Objective This study aimed to identify early risk factors that impacted the 30-day mortality of heat stroke patients and establish a predictive model to assist clinicians in identifying the risk of death. Methods A retrospective case-control study was conducted, analyzing the clinical data of 72 patients with heat stroke admitted to Chongqing Emergency Medical Center between May 2016 and October 2023. The patients were divided into two groups to implement a control study: one comprising individuals who had died within 30 days of symptom onset, and the other consisting of those who had survived. The study analyzed the risk factors affecting 30-day mortality, plotted receiver operating characteristic (ROC) curves to evaluate patient’s mortality, and developed a model to predict the risk of death in heat stroke patients. The calibration curve and decision curve were used to evaluate the accuracy and clinical prediction efficiency of the nomogram. Results Within a 30-day period, 21 patients (29.167%) died. The APACHE II score, the ratio of lactate to albumin (Lac/Alb ratio), the core temperature at 30 minutes after admission were the independent risk factors for 30-day death in heat stroke patients. The area under the ROC curve for predicting mortality based on the APACHE II score was 0.820 (95% CI 0.716–0.924, P < 0.001). The best cut-off value was 29, with a sensitivity of 57.1% and a specificity of 92.2%. Moreover, the area under the ROC curve for predicting mortality based on the Lac/Alb ratio was 0.902 (95% CI 0.830–0.975, P < 0.001). The optimal cut-off value was 0.160, with a sensitivity of 90.5% and a specificity of 88.2%. The area under the ROC curve based on the core temperature at 30 minutes after admission was 0.700 (95% CI 0.544–0.855, P = 0.008). The optimal cut-off value was determined to be 39.5℃, with a sensitivity of 61.9% and a specificity of 80.4%. Finally, the area under the ROC curve for predicting death due to heat stroke using the combination of these three factors was 0.917 (95% CI 0.851–0.983, P < 0.001), with a sensitivity of 76.2% and a specificity of 92.2%. Conclusion The nomogram developed using these three indicators can be used in combination to predict 30-day mortality in heat stroke patients.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Predictive Factors and Nomogram for 30-Day Mortality in Heat Stroke Patients: A Retrospective Case-Control Study

Li,

Zhang,

Zhang

et al. 2024

Preprint

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“…The causes of death in heatstroke closely resemble the end-stage clinical features of sepsis, which are respiratory failure, acute respiratory distress syndrome, nosocomial pneumonia, renal failure, GI bleeding, stress gastritis, anemia, deep venous thrombosis, electrolyte abnormalities, hyperglycemia, hepatic dysfunction, and disseminated intravascular coagulation. [ 21 ] Consequently, bacterial translocation and endotoxemia from the GI system caused by systemic insults associated with heat stress lead to a systemic inflammatory response that mimics sepsis, and that can deteriorate rapidly to multiple organ failure and death. [ 15 ]…”

Section: Discussionmentioning

confidence: 99%

Targeted temperature management in patients with severe heatstroke

Jung¹,

Kim²,

Yang³

et al. 2020

Medicine

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Rationale: Unprecedented heatwaves over the past several years are getting worse with longer duration in the course of global warming. Heatstroke is a medical emergency with multiple organ involvement and life-threatening illness with a high mortality rate of up to 71%. Uncontrolled damage to the central nervous system can result in severe cerebral edema, permanent neurological sequelae, and death. However, regarding the therapeutic aspects of heat stroke, there was no therapeutic strategy after the rapid cooling of the core body temperature to <39°C to prevent further injury. Patient concerns: Each of 3 patients developed a change of mental statuses after the exposure to summer heatwaves or relatively high environmental temperatures with high humidity in the sauna. Diagnoses: The patients were diagnosed with severe heatstroke since they showed cerebral edema and multiple organ dysfunction based on the results from laboratory tests and the findings in brain computed tomography scan. Interventions: The patients underwent induced therapeutic hypothermia (<36°C) between 24 and 36 hours in the management of severe heatstroke. Outcomes: The patients survived from cerebral edema and multiple organ dysfunction. Lessons: We believe that targeted temperature management (<36°C) will help treat severe heatstroke. Thus it should be considered for reducing the chance of development of complications in multiple organs, especially in the central nervous system, when managing patients with severe heatstroke.

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“…In this context, biomarkers that would aid in the early detection of injury and predict delayed brain damage would be crucial. Notably, S100 calcium‐binding protein β (S100β) (Chun et al., 2019; Li et al., 2020) and neuron‐specific enolase (NSE) (Li et al., 2020) have been recently proposed as potential biomarkers of heatstroke encephalopathy.…”

Section: Brainmentioning

confidence: 99%

“…However, additional work refutes these findings during exercise in the heat (Cheuvront et al., 2008) and passive heat stress (Shepley et al., 2021) models in humans. Nonetheless, two recent studies in heatstroke patients demonstrated elevated S100β protein in the serum and cerebrospinal fluid of heatstroke patients (Chun et al., 2019; Li et al., 2020), with one study finding that the heatstroke patients with poor prognosis (defined as not being able to live without assistance at hospital discharge) having serum S100β concentrations ∼5 times higher than in heatstroke patients with a good prognosis (Chun et al., 2019). NSE is a dimeric isoform of the glycolytic enzyme enolase expressed mainly in neurons (Kaiser et al., 1989).…”

Section: Brainmentioning

confidence: 99%

Biomarkers of heatstroke‐induced organ injury and repair

Schlader

Davis

Bouchama

2022

Experimental Physiology

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New Findings What is the topic of this review?The status and potential role of novel biological markers (biomarkers) that can help identify the patients at risk of organ injury or long‐term complications following heatstroke. What advances does it highlight?Numerous biomarkers were identified related to many aspects of generalized heatstroke‐induced cellular injury and tissue damage, and heatstroke‐provoked cardiovascular, renal, cerebral, intestinal and skeletal muscle injury. No novel biomarkers were identified for liver or lung injury. Abstract Classic and exertional heatstroke cause acute injury and damage across numerous organ systems. Moreover, heatstroke survivors may sustain long‐term neurological, cardiovascular and renal complications with a persistent risk of death. In this context, biomarkers, defined as biological samples obtained from heatstroke patients, are needed to detect early organ injury, and predict outcomes to develop novel organ preservation therapeutic strategies. This narrative review provides preliminary insights that will guide the development and future utilization of these biomarkers. To this end, we have identified numerous biomarkers of widespread heatstroke‐associated cellular injury, tissue damage and repair (extracellular heat shock proteins 72 and 60, high mobility group box protein 1, histone H3, and interleukin‐1α), and other organ‐specific biomarkers including those related to the cardiovascular system (cardiac troponin I, endothelium‐derived factors, circulation endothelial cells, adhesion molecules, thrombomodulin and von Willebrand factor antigen), the kidneys (plasma and urinary neutrophil gelatinase‐associated lipocalin), the intestines (intestinal fatty acid‐binding protein 2), the brain (serum S100β and neuron‐specific enolase) and skeletal muscle (creatine kinase, myoglobin). No specific biomarkers have been identified so far for liver or lung injury in heatstroke. Before translating the identified biomarkers into clinical practice, additional preclinical and clinical prospective studies are required to further understand their clinical utility, particularly for the biomarkers related to long‐term post‐heatstroke health outcomes.

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Predictors of poor prognosis in patients with heat stroke

Cited by 5 publications

References 36 publications

Predictive Factors and Nomogram for 30-Day Mortality in Heat Stroke Patients: A Retrospective Case-Control Study

Predictive Factors and Nomogram for 30-Day Mortality in Heat Stroke Patients: A Retrospective Case-Control Study

Targeted temperature management in patients with severe heatstroke

Biomarkers of heatstroke‐induced organ injury and repair

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