Abstract
In a case of contrast media-induced anaphylactic shock managed with epinephrine, a 57-year-old male patient developed lactic acidosis without cardiogenic shock or global hypoperfusion, highlighting epinephrine's potential to trigger lactic acidosis. Despite the previous management of similar reactions with antihistamines and corticosteroids, this case required intensive care unit admission and emergency intervention for alarmingly high lactate level. The rapid resolution of acidosis following epinephrine discontinuation underscores the need for careful monitoring and consideration of alternative vasopressor strategies in severe anaphylaxis, illustrating the complex relationship between epinephrine's metabolic effects and anaphylaxis-induced tissue hypoperfusion.