Abstract
The delicate biochemistry of coagulation and anticoagulation is greatly affected by
deviations from the optimal temperature required for the interactions between various
coagulation enzymes, cellular receptors, and intracellular mechanisms. Hyperthermia
will lead to a prothrombotic state and, if sufficiently severe such as in heatstroke,
a consumption coagulopathy, which will clinically manifest with the simultaneous appearance
of intravascular thrombotic obstruction and an increased bleeding tendency. Hypothermia
slows down the coagulation process, but as this seems to be adequately balanced by
impairment of anticoagulant and fibrinolytic processes, its clinical effects are modest;
however, hypothermia may be modestly linked to a somewhat higher risk of localized
thrombosis. Restoration of a normal body temperature in patients affected by hyper-
or hypothermia is the cornerstone for the management of associated coagulation derangements.
Keywords
hyperthermia - hypothermia - coagulation - inflammation - thrombosis - disseminated
intravascular coagulation
