Cardiac Tamponade and Heart Failure Due to Myopericarditis as a Presentation of Infection with the Pandemic H1N1 2009 Influenza A Virus

Abstract

We describe a fatal case of myopericarditis presenting with cardiac tamponade in a previously healthy 11-year-old child. Pandemic H1N1 2009 influenza A virus sequences were identified in throat and myocardial tissues and pericardial fluid, suggesting damage of myocardial cells directly caused by the virus. CASE REPORTHere, we report a fatal case of myopericarditis presenting with cardiac tamponade associated with infection with the pandemic A/H1N1 2009 influenza virus in a previously healthy 11-year-old girl with no known risk factors, including obesity, for severe, complicated pandemic influenza.The patient developed a high fever (39.2°C) with coughing and vomiting on the evening of 28 October. The next morning, she was visited by a general practitioner, who prescribed antipyretic, antibiotic, and cortisone treatments. About 36 h after the onset of symptoms, the girl presented to the emergency unit of the district hospital with asthenia and dizziness. She was pale and afebrile at 35°C, with tachycardia of 140 beats/min and tachypnea of 32 breaths/min. Routine blood samples were analyzed. The white blood cell count was elevated at 23.8 ϫ 10 9 cells/liter, and C-reactive protein was elevated at 21.6 mg/liter. Her creatine kinase (CK) level was elevated at 5,814 IU/liter (normal range, 26 to 140 IU/liter), the troponin level was 4.24 ng/ml (normal range, 0 to 0.060 ng/ml), the myoglobin level was 1,849.4 ng/ml (normal range, 12 to 76 ng/ml), and the lactate dehydrogenase level was 1,408 IU/liter (normal range, 266 to 500 IU/liter). Her chest X-ray was reported to be clear. An electrocardiogram (ECG) showed sinus tachycardia with diffuse ST segment elevation. An urgent echocardiogram was performed, which demonstrated normal ventricle size, severely compromised pump function (ejection fraction, 20 to 30%), diffuse ipokinesia, and a small pericardial effusion, consistent with myopericarditis with a predominant myocarditic component. Metabolic lactic acidosis was also detected and treated with intravenous administration of Na ϩ -HCO 3 . Because of the need for specialized care and treatment, the patient was transferred to a regional pediatric hospital, but during ambulance transport she had loss of consciousness and needed respiratory assistance. Clinical conditions worsened during transfer to the pediatric intensive care unit (ICU): a peripheral pulse was absent, the central pulse was weak, and the capillary refill time was Ͼ5 s. Cardiac frequency (CF) detected by the monitor was 110 beats/min with a wide QRS interval. CF rapidly decreased. Atropine was administered, and cardiopulmonary resuscitation (CPR) maneuvers were performed. The central pulse became absent, and the echocardiogram showed no contractile activity.The pathological exam showed macroscopic changes such as increased ventricular size (left ventricle thickness, 2.2 cm; right ventricle thickness, 0.35 cm); the left/right ventricle size ratio was 6.28, versus a normal value of 3.1. Pericardial effusion (150 ml) was detected. Pulmonary congestion leading ...

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