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Table of Contents   
Year : 2021  |  Volume : 14  |  Issue : 3  |  Page : 441-442
Allergic myocardial infarction (Kounis syndrome) in a child with scorpion sting

1 Department of Paediatric Cardiac Sciences, Krishna Institute of Medical Sciences, Secunderabad, Telangana, India
2 Department of Paediatrics, Ankura Hospital, Hyderabad, Telangana, India
3 Department of Paediatrics, Ankura Hospital, Telangana, India

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Date of Submission08-Nov-2020
Date of Decision04-Mar-2021
Date of Acceptance10-May-2021
Date of Web Publication26-Aug-2021

How to cite this article:
Verma S, Mathew R, Khan KM, Gouthami V. Allergic myocardial infarction (Kounis syndrome) in a child with scorpion sting. Ann Pediatr Card 2021;14:441-2

How to cite this URL:
Verma S, Mathew R, Khan KM, Gouthami V. Allergic myocardial infarction (Kounis syndrome) in a child with scorpion sting. Ann Pediatr Card [serial online] 2021 [cited 2022 Dec 6];14:441-2. Available from:


A 4-year-old boy with an alleged history of scorpion bite on the left finger presented with complaints of restlessness, breathing difficulty, and cough. Examination revealed cold peripheries with low volume pulses. There are blood pressure of 80/58/74 mmHg, saturation of 95% on 5 L oxygen, heart rate of 170/min, respiratory rate of 56/min, bilateral basal crepts with normal heart sounds, and no murmur. Temperature of 99°F was noted. Electrocardiogram (ECG) showed ST elevation with tall T-waves in anteroinferior leads suggestive of myocardial ischemia [Figure 1]. Echocardiography revealed severe left ventricular (LV) dysfunction with ejection fraction of 24% [Figure 2]. Chest X-ray showed pulmonary venous congestion [Figure 3]. Prazosin, dobutamine (10 mcg/kg/min), and furosemide infusion were started. Nitroglycerine was given in view of widespread ST changes. By 5 hours, ECG changes normalized [Figure 4]a with improved LV ejection fraction to 80% [Figure 4]b. Such presentation of acute coronary spasm and autonomic crises is related to mast cells destabilization known as Kounis syndrome (KS) or allergic myocardial infarction, first described by Kounis and Zavras in 1991.[1] Many triggers are described ranging from drugs, foreign bodies, insect stings, food, medical conditions, or environmental exposure, most common being antibiotics (27.4%) and insects' bites (23.4%).[2] Mainly described in adults but pediatric cases have been reported worldwide since its first description in 2009.[3],[4] It resulted from hypersensitivity causing release of vasoactive mediators from mast cells such as histamine, leukotrienes, and serotonin and proteases such as tryptase and chymase, either locally or into the systemic circulation.[5] There are two types of KS, namely Type I: without coronary artery disease and predisposing factors with or without increase in cardiac enzymes, Type 2: with coronary artery disease, and rarely, Type 3 also described in patients with coronary artery stent thrombosis. Symptomatic KS is always associated with subclinical, clinical, acute, or chronic allergic reactions accompanied by cardiac symptomatology.[6]
Figure 1: Baseline electrocardiogram on admission showing widespread ST and T changes suggestive of anteroinferior ischemia

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Figure 2: X-ray showed cardiomegaly and pulmonary venous congestion

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Figure 3: Two-dimensional echocardiogram with M mode showing dilated left ventricular with severe left ventricular dysfunction with ejection fraction of 24%

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Figure 4: ECG (a) and ECHO (b) after 5 hours of admission showing normalisation of ischemic pattern and LV function

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Systemic allergic reactions associated with clinical, electrocardiographic, and laboratory findings of acute myocardial ischemia should be suspected as having KS. Although the most frequent ECG finding is ST-segment elevation in the four anterior and inferior leads, the tracing may be normal or show only nonspecific findings.[2],[5] This entity is variant of stress cardiomyopathy but differentiating both is very challenging. Coronary angiography reveals normal coronaries in Type I KS and stress cardiomyopathy.

Treatment of the allergic event alone can abolish symptoms in Type I KS. The use of intravenous corticosteroids such as hydrocortisone (1–2 mg/kg/day) and antihistamines such as diphenhydramine (1–2 mg/kg) and ranitidine (1 mg/kg) is adequate. The administration of vasodilators such as calcium channel blockers and nitrates can abolish hypersensitivity-induced vasospasm. In patients with Type II variant, treatment should be initiated with an acute coronary event protocol together with corticosteroids and antihistamines. Other measures to stabilize the patient such as pain relief, volume expansion, and oxygen should be taken simultaneously to manage this condition.[2],[5],[6]

   Conclusions Top

Allergic myocardial infarction as a cause for LV dysfunction can be suspected with a history of hypersensitivity or allergic reactions resulting in autonomic storm. It can present in severe form like myocardial dysfunction with significant ECG changes. Most of the cases without underlying coronary artery disease can be managed with nitroglycerin or antihistaminic. Even ECG showing widespread ST changes suggestive of ischemia can be reversible with decrease in autonomic storm.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Kounis NG, Zavras GM. Histamine-induced coronary artery spasm: The concept of allergic angina. Br J Clin Pract 1991;45:121-128.  Back to cited text no. 1
Abdelghany M, Subedi R, Shah S, Kozman H. Kounis syndrome: A review article on epidemiology, diagnostic findings, management and complications of allergic acute coronary syndrome. Int J Cardiol 2017;232:1-4.  Back to cited text no. 2
Biteker M, Duran NE, Biteker FS, Ertürk E, Aykan AC, Civan HA, et al. Kounis syndrome secondary to amoxicillin/clavulanic acid use in a child. Int J Cardiol, 2009;136:e3-5.  Back to cited text no. 3
Biteker M, Duran NE, Biteker FS, Civan HA, Kaya H, Gökdeniz T, et al. Allergic myocardial infarction in childhood: Kounis syndrome. Eur J Pediatr 2010;169:27-9.  Back to cited text no. 4
Cepeda PR, Herrejón EP, Aguirregabiria MM. Kounis syndrome. Med Intensiva 2012;36:358-64.  Back to cited text no. 5
Kounis NG. Kounis syndrome: An update on epidemiology, pathogenesis, diagnosis and therapeutic management. Clin Chem Lab Med 2016;54:1545-59.  Back to cited text no. 6

Correspondence Address:
Sudeep Verma
Department of Paediatric Cardiac Sciences, Krishna Institute of Medical Sciences, Secunderabad, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/apc.apc_257_20

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4]