Correct!
4. Shock liver
This patient most likely has acute liver failure secondary to shock liver. Heatstroke leads to an inflammatory response similar to the systemic inflammatory response syndrome (SIRS). SIRS is mediated by circulating messenger RNA releasing cytokines and high-mobility group box 1 protein (HMGB1) with activation of leukocytes and endothelial cells. This process can result in disseminated intravascular coagulation (DIC), multiorgan failure, and death. Although it has been two days since the patient was exposed to high temperatures, multiorgan system dysfunction and failure may peak within 24 to 48 hours (1).
Viral hepatitis can also cause liver transaminases to be elevated greater than 1,000 U/L; however, this patient has suspected heatstroke and his initial presentation with severe hypotension makes shock liver more likely. Alcoholic hepatitis presents with moderately elevated liver transaminases (<500 U/L) with AST:ALT ratio >2. Ethanol levels were negative in this patient. Acute cholecystitis is unlikely as an elevation of alkaline phosphatase would be expected. Autoimmune hepatitis is a rare disorder that requires exclusion of other diseases that have a similar presentation. In this patient, shock liver is more likely.
In severe heatstroke injury, it is recommended to check liver function tests, PT/INR, ammonia, CK, LDH, myoglobin and urinalysis, CRP daily and having a low threshold for blood cultures as heatstroke can cause reduced intestinal blood flow with gastrointestinal ischemia. N-acetycysteine is recommended for acute liver failure as well as monitoring for and treating cerebral edema with 3% hypertonic saline or mannitol.
Is there an increased risk of exercise-related death in people with sickle cell trait? (Click on the correct answer to be directed to the fifth of six pages)