JMSCR Vol||06||Issue||10||Page 366-371||October 2018
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JMSCR Vol||06||Issue||10||Page 366-371||October 2018 www.jmscr.igmpublication.org Impact Factor (SJIF): 6.379 Index Copernicus Value: 79.54 ISSN (e)-2347-176x ISSN (p) 2455-0450 DOI: https://dx.doi.org/10.18535/jmscr/v6i10.62 Is It Kounis Syndrome? - A Case Report Authors Jyotsnaa M*1, Vijayakumar N2, Umarani R3 *1Post Graduate, Department of Medicine, RMMCH, Chidambaram-608002, Tamilnadu 2Lecturer, Department of Medicine, RMMCH, Chidambaram-608002, Tamilnadu 3Professor, Department of Medicine, RMMCH, Chidambaram-608002, Tamilnadu Abstract “Kounis syndrome”, otherwise known as “allergic angina” or “allergic myocardial infarction”, refers to acute coronary syndrome occurring due to allergic, hypersensitivity or anaphylactoid reaction(1). It results due to activation of mast cells, leading to vasospasm of coronary artery and/or erosion or rupture of atherosclerotic plaque. Here, we present a probable case of Kounis syndrome Type 1 induced by a scorpion sting. Keywords: allergic myocardial infarction, scorpion sting, hypersensitivity. Introduction between endothelial cells lining human Pfister et al published the first case of “allergic atheromatous plaques better than the closed myocardiac infarction” in 1951: a gentleman aged junctions present in the intima of normal 49 years old who developed anterolateral arteries(5,6), and that proteases released on myocardial infarction along with urticaria degranulation of these mast cells lead to plaque following allergy to penicillin(2). erosion/ rupture(4). The term 'allergic myocardial infarction' was first Kounis syndrome has been reported to have used by Zosin et al in 1965(3). multiple etiologies, including In 1991, Kounis and Zavras described the clinical i. Environmental exposures including grass syndrome of "allergic angina": chest pain with cutting, millet allergy, poison ivy, clinical and biochemical findings of classical Hymenoptera, jellyfish and scorpion angina pectoris occurring along with allergic stings, centipede bite, viper venom, latex manifestations(1). Allergic angina progressing to contact, metals; acute myocardial infarction was called "allergic ii. Drugs including analgesics (eg, aspirin), myocardial infarction". anesthetics (eg, propofol, isoflurane, In 1995, Kovanen et al. (4) and Constantinides(5,6) midazolam, etomidate); antibiotics, described the role of cytokine-mediated mast cell anticoagulants, contrast media, NSAIDs, de-granulation in the pathogenesis of the proton pump inhibitors, thrombolytics, condition. They identified that mast cell skin disinfectants and some other drugs precursors could penetrate the open junctions including protamine, iron, iodine, Jyotsnaa M et al JMSCR Volume 06 Issue 10 October 2018 Page 366 JMSCR Vol||06||Issue||10||Page 366-371||October 2018 allopurinol, dextran, clopidogrel, enalapril, leads and normal serum potassium levels, a esmolol, tetanus antitoxin; probable diagnosis of allergic myocardial iii. Foods including fish, shellfish, fruits, infarction or “Type 1 Kounis syndrome” with mushroom Coprinopsis atramentaria, cardiogenic pulmonary edema was made. canned food, vegetables, tomato salad; Coronary angiogram was not done. iv. Conditions like angioedema, anisakiasis, Patient was managed in ICU with prazosin, bronchial asthma, Churg-Strauss intravenous fluids, inotropic and ventilatory syndrome, exercise-induced anaphylaxis, support. During hospitalisation, the patient food allergy, hay fever, mastocytosis, developed ventilator-associated infection with E. scromboid syndrome, serum sickness; coli for which he was managed with antibiotics. v. Coronary and other stents (bare metal or Serial ECGs that were done showed reversion of drug-eluting) the ST segment changes and tall T waves (Figure 2.3). Repeat echocardiograms were done 2 days Case Report and 7 days after admission which revealed mitral A male aged 14 years was brought to the regurgitation and trivial triscuspid regurgitation Emergency Room approximately 2 hours and grade II diastolic dysfunction. It also showed following alleged history of scorpion sting on the increase in Ejection Fraction to 43% and 60% fourth digit of his right foot. respectively. He presented with profuse sweating, drowsiness CK-MB when repeated had normalized. At and breathlessness. His pulse rate was 58 bpm, discharge, patient was stable and advised repeat blood pressure 80/60 mmHg and oxygen Echocardiogram on follow-up. saturation 60%. Priapism was present. JVP was normal. Respiratory system examination revealed Figure 1 basal crepitations in bilateral lung fields. Normal heart sounds were heard; no murmurs were present. Chest X-ray (Figure 1) showed pulmonary oedema and ECG (Figure 2.1 and 2.2) showed ST depression in leads II, III and aVF, tall T waves in V2 to V4 chest leads and q waves in leads I and aVL, simulating anterolateral MI with reciprocal changes and no arrhythmia. Investigations also revealed a CK-MB of 91 IU/L (normal range: 5 to 25 IU/L), positive Troponin T, metabolic acidosis and hypokalemia. Echocardiogram done (Figure 3) showed regional wall motion abnormality, severe mitral regurgitation, dilated left ventricle with poor LV systolic function (Ejection Fraction: 33%), with no significant pulmonary artery hypertension and normal pericardium. Due to the presence of elevated CK-MB, positive Troponin T, ECG changes on anterolateral leads, regional wall motion abnormality on Echocardiogram, absence of ECG changes on all Jyotsnaa M et al JMSCR Volume 06 Issue 10 October 2018 Page 367 JMSCR Vol||06||Issue||10||Page 366-371||October 2018 Figure 2.1 (at presentation) Figure 2.2 (at presentation) Figure 3 Figure 2.3 Discussion endothelial dysfunction or microvascular Three types of Kounis syndrome have been angina(8). The type II variant is found in patients reported(7). The type I variant occurs in patients with preexisting atherosclerotic disease. The with normal coronary arteries without allergic insult causes rupture or erosion of the predisposing risk factors for coronary artery plaque leading to coronary vasospasm or acute disease. It has been described as occurring due to myocardial infarction(7). The type III variant is Jyotsnaa M et al JMSCR Volume 06 Issue 10 October 2018 Page 368 JMSCR Vol||06||Issue||10||Page 366-371||October 2018 thrombosis of coronary arterial stent occurring due spider bite, honeybee sting and snake bite have to allergic reaction, in which histological been reported (18 - 24). examinations would reveal eosinophils and/or Scorpion envenomation induces venom-specific mast cells(7). immunoglobulin E (IgEs), and, thereby, produces The pathogenesis of Kounis syndrome is by mast mast cell-mediated histamine release leading to cells mainly(10), which release the culprit Type 1 hypersensitivity reaction (25). inflammatory mediators and by a subset of platelets bearing FCγRI, FCγTII, FCεRI and Treatment FCεRII receptors (11). The mainstay in Kounis syndrome should be 1. Degranulation of mast cells occurs when management of the allergic reaction. specific antigens induced by the allergy react Simultaneous stabilization of the coronary arteries with IgE antibodies attached to mast cells and with medical or interventional techniques is also produce a significant number of bridged IgE required. antibodies (12). Treatment in scorpion sting-induced Type 1 2. Inflammatory mediators released following Kounis syndrome includes: degranulation cause coronary vasospasm(7,9) - antivenom and dobutamine for cardiovascular leading to ischemia by the following effects, mechanisms. - benzodiazepines for neuromuscular i. Histamine leads to coronary involvement, vasoconstriction, produces tissue factor - adrenaline and fluid resuscitation for expression and activation of platelets. anaphylaxis management, ii. The three neutral proteases chymase, - antihistamines and leukotriene receptor tryptase and cathepsin D can lead to antagonists as second line treatment of degradation of the collagen cap, thereby anaphylaxis, and causing rupture or erosion of the - prazosin, a postsynaptic alpha blocker, to atheromatous plaque(13). Tryptase has reduce sympathetic symptoms and also in properties of both thrombosis and pulmonary edema (cardiogenic) with arterial fibrinolysis (14). Chymase and cathepsin-D hypertension. Oral prazosin is used due to its can additionally convert angiotensin I to rapid onset of action, easily availability and angiotensin II which is a potent high effectiveness. vasoconstricting substance. - Corticosteroids are to be used in interstitial iii. Biosynthesis of leukotrienes – powerful pulmonary edema that is non-cardiogenic. vasoconstrictors – increases during the Type I Kounis syndrome has been reported to acute phase of unstable angina(15,16). have good response when treated with Thromboxane causes aggregation of corticosteroids and histamine (H1 or H2) receptor platelets and vasoconstriction. blockers, along with coronary vasodilators such as iv. In myocardial ischemia, platelet-activating nitrates or calcium channel blockers. factor (PAF) activates both leukocytes and In Type II and Type III Kounis syndrome, the platelets, thereby leading to release of same management is followed and coronary leukotrienes. It also has a direct effect on interventions may be required. vasoconstriction (17). The present case is, therefore, a probable case of Drugs contraindicated in Kounis syndrome Type I Kounis syndrome induced by scorpion i. Morphine – may exacerbate histamine release sting. Cases of Kounis syndrome induced by and related pathologic cascade of events;