Heatstroke-induced coagulopathy: Biomarkers, mechanistic insights, and patient management

Heatstroke is increasingly becoming a significant concern due to global warming. Systemic inflammation and coagulopathy are the two major factors that provoke life-threatening organ dysfunction in heatstroke. Dysregulated thermo-control induces cellular injury, damage-associated molecular patterns release, hyperinflammation, and hypercoagulation with suppressed fibrinolysis to produce heatstroke-induced coagulopathy (HSIC). HSIC can progress to disseminated intravascular coagulation and multiorgan failure if severe enough. Platelet count, D-dimer, soluble thrombomodulin, and inflammation biomarkers such as interleukin-6 and histone H3 are promising markers for HSIC. In exertional heatstroke, the measurement of myoglobin is helpful to anticipate renal dysfunction. However, the optimal cutoff for each biomarker has not been determined. Except for initial cooling and hydration, effective therapy continues to be explored, and the use of antiinflammatory and anticoagulant therapies is under investigation. Despite the rapidly increasing risk, our knowledge is limited, and further study is warranted. In this review, we examine current information and what future efforts are needed to better understand and manage HSIC.