A previously healthy 60-year-old woman, with a recent travel history to South America and the USA, developed flu-like symptoms in late October 2009. The patient was seen by her primary care doctor and a rapid test was positive for influenza A, initially treated with oseltamivir 75 mg orally every 12 h. Then, 3 days later she was admitted to a community hospital with progressive worsening dyspnoea, chest pain, hypotension and tachycardia. A cardiac catheterisation revealed an ejection fraction of 10% with severe left ventricular dysfunction. No evidence of coronary artery occlusive disease was evident. An intra-aortic balloon pump (IABP) was placed at this time to maintain her blood pressure. The patient was intubated and ventilated due to respiratory distress and oseltamivir treatment was continued at the same dose. Due to suspicion of an overimposed bacterial infection empiric broad-spectrum antibiotic treatment was initiated with vancomycin and piperacillin/tazobactam.
Over the subsequent 2 days the patient remained hypotensive despite the use of the IABP and the administration of dobutamine, vasopressin, norepinephrine and milrinone infusions. A percutaneous left ventricular assist device (LVAD) (Impella 2.5; Abiomed-Impella CardioSystems GmbH, Aachen, Germany) was placed for additional support. The patient's status continued to deteriorate despite this aggressive management, prompting the transfer to our tertiary referral centre for further care including possible emergency heart transplantation.
Upon arrival the patient was determined to have multisystem failure with oligoanuric acute renal failure, acute liver failure and respiratory failure. There was evidence of cardiogenic shock: with the Impella LVAD providing 2.4 litres/min of circulatory assistance and with the vasopressor treatment described above, the cardiac index was only 2.1 litres/min/m2. An echocardiogram showed global hypokinesis of the left ventricle, inferior wall akinesis, dilated left atrium, dilated inferior vena cava, moderate mitral regurgitation, mild tricuspid regurgitation, mild aortic regurgitation, a small pericardial effusion and a right ventricular systolic pressure of 35–39 mm Hg.
Upon arrival at our centre the dose of oseltamivir was increased to 150 mg orally every 12 h. Due to lack of clinical improvement the Centers for Disease Control and Prevention (CDC) were contacted for compassionate release of peramivir, a novel intravenous neuraminidase inhibitor. Within 24 h of admission oseltamivir was discontinued and the patient was given peramivir 600 mg intravenously every 24 h for a total of 10 days.
Prior to initiating peramivir treatment, the patient's blood and urine were cultured and found to be negative for bacterial growth. HIV by ELISA and HIV PCR viral loads, were obtained to rule out acute retroviral syndrome. Serology testing for legionella, mycoplasma, chlamydia, coxackie virus A and B, respiratory syncytial virus, and influenza A, subtype H1N1 reverse transcriptase (RT)-PCR were obtained. All results were negative including viral respiratory cultures.
Considering the patient's rapid clinical deterioration, a decision was made to empirically administer intravenous immunoglobulin (Flebogamma 5%) 10g intravenous over 8 h in attempts to boost the innate immunity and control the infection as part of the management of acute viral myocarditis.
The LVAD and vasopressor treatment were continued for haemodynamic support. Within 24 h of the patient's transfer to our institution the LVAD (which had been in place for 5 days) malfunctioned and its flow gradually decreased to 1.4 litres/min despite maximal speed. The LVAD was removed and full venoarterial ECMO (flow=3.1 litres/min) was initiated by cannulating the right common femoral artery and vein. Vasopressors were weaned quickly after ECMO was initiated.