Ampicillin/sulbactam-induced Kounis syndrome with cardiogenic shock

Anaphylactic cardiogenic shock is a complex and extremely dangerous complication of anaphylaxis; it involves complex patho-physiological mechanisms, and its treatment remains unclear to date. During anaphylactic shock, the main contributors to coronary hypoperfusion, leading to myocardial damage, are systemic vasodilatation, reduced venous return, leakage of plasma and volume loss due to increased vascular permeability, and diminished cardiac output (1). However, experimental and clinical evidence has shown that the heart, particularly the coronary arteries, is the main target of anaphylaxis. The experimental evidence of a rapid increase in left ventricular end-diastolic pressure during the initial phase of anaphylactic shock is attributed to coronary vasoconstriction than to leakage of plasma and volume loss (2). This is supported by clinical evidence that anaphylactic cardiogenic shock does not always respond to fluid replacement but needs anti-allergic and myocardial infarction protocol treatment (3).