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.