Complex Management of a Rare Case of Fulminant Myocarditis Due to Influenza A
Presenter
Sara Hazaveh, M.D., Hackensack University Medical Center, Hackensack, NJ
Sara Hazaveh, M.D., Vishad Sheth, M.D. and Bernard Kim, M.D., Hackensack University Medical Center, Hackensack, NJ
Learning Objectives:
- The importance of early recognition of fulminant myocarditis due to its severe complications.
- Highlight complications of ECMO for managing myocarditis and understand the role of left ventricular unloading with impeller.
- Appreciate the complex and multidisciplinary management of fulminant myocarditis.
Keywords: Cardiogenic Shock and Heart Failure
Introduction Acute myocarditis is usually caused by viral infections and can range from silent to fulminant disease with a high mortality. Fulminant myocarditis (FM) is rarely caused by influenza A and can have severe complications with shock and cardiac arrest. We present a case of FM leading to cardiogenic shock requiring veno-arterial extracorporeal membrane oxygenation (VA-ECMO). This case highlights the importance of early recognition of influenza FM to initiate mechanical support devices promptly. It also explores left ventricular (LV) overload as a complication of VA-ECMO requiring LV assist device and the importance of addressing concomitant right ventricular (RV) failure. Clinical Case A 64-year-old female with hypertension presented to a local hospital with a two day history of dyspnea. On arrival blood pressure was 82/30, heart rate 48, she was afebrile and hypoxic to 80% requiring non-invasive ventilation. Electrocardiogram was without ischemic changes. Laboratory findings notable for lactate of 6.6, troponin 21.7 (normal <0.05), and BNP 2256 (normal < 100). Norepinephrine and vasopressin were started for hemodynamic support. Chest X-ray had bilateral interstitial and alveolar infiltrates, and she was started on broad spectrum antibiotics for superimposed pneumonia. Respiratory pathogen panel was positive for influenza A. She was found to have an ejection fraction (EF) of 10% with global hypokinesis. On day 2, she was intubated requiring 100% FiO2 on mechanical ventilation. Upon transfer to our tertiary care hospital, she underwent left heart catheterization which was negative for coronary artery disease. Due to refractory shock, VA-ECMO was initiated. On day 3, axillary impella 5.5 was placed for LV venting. On day 4, repeat echocardiogram revealed an improvement of EF to 30-35% but with remaining RV dysfunction. She was decannulated from ECMO on day 5 as vasopressor requirements were minimal but soon after had worsening shock and hypoxia. Milrinone, epinephrine, and inhaled nitric oxide (iNO) were added and she was placed back on VA-ECMO. As patient's shock continued to improve, ECMO and impella were decannulated on day 13. Follow up echocardiogram on day 15 showed an improvement in EF to 60-65%. She was weaned off mechanical ventilation on day 20, and on discharge was off all inotropic support and oxygen. Discussion FM due to influenza A is rare and mechanical circulatory support devices like VA-ECMO used promptly can prevent multi-organ system failure and mortality. VA-ECMO generates a retrograde flow towards the aortic valve resulting in a higher afterload and increases the LV end diastolic pressure.These unwanted consequences of VA-ECMO may hinder recovery in FM. LV distention also predisposes the lungs to congestion and intracardiac thrombosis. Therefore, use of impella in addition to VA-ECMO can help in reducing such complications. RV dysfunction can also be present due to FM, LV failure, or pulmonary hypertension caused by viral acute respiratory distress syndrome. Therefore, interventions that target RV function can help recovery. iNO can improve RV bloodflow and milrinone can provide inotropic support. This case of influenza induced FM had marked recovery by employing these physiological principles.