Heat stroke induces coagulofibrinolytic activation, which leads to life-threatening
disseminated intravascular coagulation (
DIC). However, treatment strategies for
DIC in
heat stroke have not yet been established, and also, the time course changes in coagulofibrinolytic markers have not been thoroughly evaluated. We report a severe
heat stroke case with
DIC who was eventually saved by anti-
DIC treatments in accordance with changes in coagulofibrinolytic markers.
CASE PRESENTATION: A 45-year-old man was found unconscious outside, and his body temperature was elevated to 41.9 °C. For
heat stroke, we performed an immediate tracheal intubation under the
general anesthesia along with cooling by iced
gastric lavage, cold fluid administration, and an intravascular cooling using Thermogard™. About 4 h after admission, his core temperature fell to 37 °C. We assessed coagulofibrinolytic
biomarkers and treated in accordance with changes in these parameters. This case exhibited a biphasic change varying from an enhanced to a suppressed fibrinolytic type of
DIC depending on the relative balance between fibrinolytic activation and the level of
plasminogen activator inhibitor-1 (PAI-1). In the early phase with
consumption coagulopathy and enhanced fibrinolysis, we transfused a large amount of fresh frozen plasma (FFP) and platelets with
tranexamic acid, an
antifibrinolytic agent, possibly providing relief for the
bleeding tendency.
Anticoagulant therapy using recombinant human
thrombomodulin-α (rh-TM-α) and
antithrombin III (ATIII) concentrate was especially effective for
DIC with a suppressed fibrinolytic phenotype in the later phase, after which organ failure that included severe
hepatic failure was remarkably improved.
CONCLUSION: