Abstract Introduction Hyperthermia is an elevated body temperature with no corresponding change in the hypothalamic set point. Heat stroke (HS) occurs once core body temperature surpasses 40 °C with neurologic dysfunction. In approximately 21% of HS cases, disseminated intravascular coagulation (DIC) occurs from endothelial injury and a Systemic Inflammatory Response Syndrome (SIRS) triggered by direct thermal damage. We present a case of acute-onset DIC following HS unresponsive to rapid cooling and factor replacement. Case Description A 53-year-old male with hypertension and major depressive disorder with psychosis (on duloxetine and apriprazole) presented after being found unresponsive at home without air conditioning on a summer day. His temperature was 43. 4 °C. He was tachycardic 163 (beats/minute), hypertensive (206/166 mmHg), and tachypneic (30 breaths/min), with SpO2 98% saturation with bag valve mask. Physical exam was notable for pinpoint pupils with diminished response, shallow breath sounds, diminished bowel sounds, 1+ reflexes bilaterally, and reduced muscle tone. Initial troponins were 900 ng/mL and repeat was 40, 000 ng/mL. Electrocardiogram was unrevealing. The differential diagnosis included heat stroke, neuroleptic malignant syndrome, and serotonin syndrome. Clinically, we had greater concern for heat stroke given that he did not have clonus or rigidity, bradyreflexia, mydriasis, hyperactive bowels; although he was taking medications with these associated complications. Cooling measures, including direct application of ice packs, 4 liters of cooled crystallized fluids, evaporative cooling, and Arctic Sun were rapidly commenced. He became hypotensive requiring vasopressors. He was intubated for acute hypoxic hypercapnic respiratory failure. Eight hours after arrival, substantial bleeding was observed from his orogastric tube. New onset thrombocytopenia 273 (10⁹/L) to 77 (10⁹/L), PT increase from 39. 9s to 100s, INR increase from 4. 1 to 10 and a fibrinogen less than 60 was transfused. He was transfused 5000 units of 4-factor PCC, 10 units of cryoprecipitate, and 1 unit of FFP for DIC. Unfortunately, his pressor requirements worsened, and he expired 8 hours later. Discussion DIC secondary to hyperthermia represents one complication of heat stroke. The Society of Critical Care Medicine recommends active cooling measures (immersion) at a rate greater than 0. 155 °C/minute. Due to institutional protocol, we used arctic sun and evaporative cooling methods and cooled the patient from 43. 4 to 38. 6 °C in 4. 5 hours. It is uncertain if swifter cooling would have prevented the sudden onset of DIC here. Overall, HS patients require close monitoring for end-organ dysfunction in which DIC can occur requiring prompt intervention of blood products and rapid cooling. This abstract is funded by: None
Ramanathan et al. (Fri,) studied this question.