The trigger of the coagulopathy that complicates heat stroke is obscure, but direct platelet activation by heat is a possibility we set out to study. Platelet rich plasma (PRP), prepared from blood donors, was incubated at increasing temperatures (38-45 degrees C) and then platelet aggregation was undertaken in response to decreasing low doses of ADP (less than 2.0 mumol/l). Hyperaggregability was manifested when the incubation temperature reached 43 degrees C and was maximum at 44 degrees C before complete inhibition of responses at 45 degrees C. The platelet hyperactivity induced by heating at 44 degrees C persisted after reincubating PRP samples at 37 degrees C. These platelet responses could not be triggered in PRP samples prepared from subjects after the overnight ingestion of aspirin or after the addition of aspirin to PRP before starting the heating procedure. However, aspirin was less effective when added to PRP after the appearance of the heat-induced hyperaggregability. In conclusion, these results indicate that platelets can be activated directly by heat. This mechanism which may be operational in heat stroke, is unaffected by cooling (body cooling being basic in the management of heat stroke) but can be prevented by the early administration of aspirin.

Summary The trigger of the coagulopathy that complicates heat stroke is obscure, but direct platelet activation by heat is a possibility we set out to study. Platelet rich plasma (PRP), prepared from blood donors, was incubated at increasing temperatures (38–45°C) and then platelet aggregation was undertaken in response to decreasing low doses of ADP (<2.0 μmol/l). Hyperaggregability was manifested when the incubation temperature reached 43°C and was maximum at 44°C before complete inhibition of responses at 45°C. The platelet hyperactivity induced by heating at 44°C persisted after reincubating PRP samples at 37°C. These platelet responses could not be triggered in PRP samples prepared from subjects after the overnight ingestion of aspirin or after the addition of aspirin to PRP before starting the heating procedure. However, aspirin was less effective when added to PRP after the appearance of the heat‐induced hyperaggregability. In conclusion, these results indicate that platelets can be activated directly by heat. This mechanism which may be operational in heat stroke, is unaffected by cooling (body cooling being basic in the management of heat stroke) but can be prevented by the early administration of aspirin.

We report a 61-year-old male patient who presented with one month history of exertional dyspnea, persistent dry cough, abdominal pain with distension, poor appetite, and weight loss. This case illustrates a rare presentation of hepatocellular carcinoma with mobile right atrial thrombus and pulmonary embolism along with disseminated tumor thrombosis at multiple sites. Furthermore, this case reiterates that an early detection and diagnosis may have increasing importance in the advent of new therapies for treating advanced hepatocellular carcinoma