Salbutamol
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Myocardial infarction and myocarditis: case report A 12-year-old girl developed myocardial infarction and myocarditis during treatment with salbutamol for asthma. The girl presented to emergency department (ED) with complaints of severe chest pain after inhaling salbutamol. Prior to admission, she had been prescribed inhalation of salbutamol for asthma by a practitioner in the family medicine. She had used salbutamol for 2 days prior to the ED admission. On the first day, she used her inhaler as prescribed, two puffs thrice a day. On the second day, she used three puffs over 20 minutes in the morning prior to presenting to the ED. Physical examination in the ED showed that she was feeling nauseated and agitated; tachycardic (150 /min), mildly hypotensive (90/48mm Hg) and poorly perfused (capillary refill of 3seconds). A 2/6 systolic murmur was also heard at the second intercostal space along the left sternal border. However, the ED team did not detect any clinical manifestations of asthma. Therefore, the girl’s salbutamol treatment was terminated immediately. Chest X-ray showed heart enlargement and pulmonary congestion. Electrocardiogram (ECG) revealed deep-Q waves, ST-segment depression, and inverted-T waves in the left precordial leads. Initial blood chemistry results revealed leukocyte count of 9 300/mm3, haemoglobin level of 11 g/dL, platelet count of 2 20 000/mm3, C-reactive protein level of 12 mg/L and an erythrocyte sedimentation rate of 15mm/h. The first set of cardiac enzymes was troponin-I 1050 IU/mL, creatine kinase 250 IU/mL and CK-MB isoenzyme 56 IU/mL. Thus, she was immediately transferred to the pediatric intensive care unit (PICU) for further management with the suspicion of myocardial infarction and/or myocarditis (secondary to treatment with salbutamol) due to the alteration in her ECG, the notable increase in her cardiac enzymes and the moderate decrease of her arterial BP. The initial management upon PICU admission included vasoactive support with dopamine, milrinone and unspecified angiotensin-converting enzyme inhibitor. Her hypotension subsequently improved. On the first day of PICU admission, transthoracic echocardiography showed that the left ventricle (LV) was dilated and there was mildmoderate mitral insufficiency. The detection of the second-degree tricuspid regurgitation was made as well (estimated PA pressure was close to 40mm Hg). Her PA pressure was mildly elevated. Furthermore, the parasternal short-axis view disclosed that the RCA was dilated (5mm) and the LCA was branched off from the PA instead of the aorta. Also, there was continuous flow within the interventricular septum (IVS) as a result of collateral vessels between LCA and RCA. Thus, a decision was made to perform cardiac catheterisation and angiography due to the suspicion of Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). Coronary CT angiography revealed that her RCA was dilated. Also, the LCA got its origin from the posterior of the PA. The results confirmed suspicion of underlying
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