A case of Kounis syndrome after a hornet sting and literature review

Abstract

BackgroundAcute coronary syndrome after hymenoptera stings or exposure to environment toxins is referred to as the Kounis syndrome or allergic myocardial ischaemia with or without infarction. We report a case of hornet (Vespa affinis) sting causing Kounis syndrome in Sri Lanka and present a review of literature.Case presentationA 60-year -old female with diabetes mellitus and known allergy to bee venom was stung by a hornet on the right hand. Within 30 minutes she developed hypotension and wide spread T wave inversion in the 12 leads ECG that remained unchanged about 5 hours and reversed back to normal.ConclusionHymenoptera stings can induce acute coronary syndrome either by direct effect of venom constituents on the coronary endothelium or through inflammatory mediators induced allergic reaction on coronary vasculature. Early recognition of Kounis syndrome is needed in hornet stings to implement necessary treatments.

Wasp sting induced STEMI with complete coronary artery occlusion: a case of Kounis syndrome

“…MI following Hymenoptera stings can be prolonged or severe in atopic individuals and in some cases anaphylaxis may ensue, with urticaria, circulatory collapse and bronchospasm11; however, it remains a rare cause of MI.…”

Kounis syndrome secondary to amoxicillin/clavulanic acid administration: a case report and review of literature

“…Type I variant includes patients with normal or nearly normal coronary arteries without predisposing factors for coronary artery disease in whom acute allergic attacks can induce either coronary artery spasm alone without raised cardiac enzymes and troponins [ 2 , 10 , 11 ]. Type II variant includes patients with culprit but quiescent pre-existing atheromatous disease in whom the acute allergic attacks can induce either coronary artery spasm, or plaque rupture manifesting as acute myocardial infarction [ 2 , 10 ]. Recently described type III variant includes patients with stent thrombosis in whom thrombus harvesting and staining with hematoxycillin-eosin and Giemsa shows the presence of eosinophils and mast cells respectively, in the pathology specimens.…”

“…Recently described type III variant includes patients with stent thrombosis in whom thrombus harvesting and staining with hematoxycillin-eosin and Giemsa shows the presence of eosinophils and mast cells respectively, in the pathology specimens. Furthermore, type III variant is diagnosed in patients with stent implantation who died suddenly and histological examination of coronary intima, media or adventitia adjacent to stent was found to be infiltrated by eosinophils and/or mast cells [ 1 , 2 , 10 ]. However, in all these types, the prognosis depended on the magnitude of the initial allergic response, the patient’s sensitivity, co-morbidities, the site of antibody antigen reaction, the allergen concentration and the route of allergen entrance [ 1 , 2 ].…”

“…Furthermore, type III variant is diagnosed in patients with stent implantation who died suddenly and histological examination of coronary intima, media or adventitia adjacent to stent was found to be infiltrated by eosinophils and/or mast cells [ 1 , 2 , 10 ]. However, in all these types, the prognosis depended on the magnitude of the initial allergic response, the patient’s sensitivity, co-morbidities, the site of antibody antigen reaction, the allergen concentration and the route of allergen entrance [ 1 , 2 ]. Our patient was 74 years old and had type 2 diabetes mellitus and dyslipidaemia as a predisposing factor for coronary artery disease.…”

“…Kounis syndrome (allergic angina and allergic myocardial infarction) has been described as coincidental occurrence of acute coronary syndromes with conditions associated with mast cell activation, such as allergies or hypersensitivity and anaphylactoid insults [ 1 , 2 ]. It is caused by inflammatory mediators such as histamine, neutral proteases, arachidonic acid products such as leukotrienes, platelet activating factor and a variety of cytokines and chemokines released during the activation process [ 1 ].…”