Case Presentation:
A 19 y/o woman presents with dyspnea and chest pain that began one week ago. Dyspnea is worse on exertion. She also complains of substernal chest pain, worse upon breathing. Associated symptoms are subjective fevers, dizziness, sore throat, productive cough of green sputum and myalgias. Denies nausea, vomiting, abdominal pain, rashes, exposure to sick contacts or recent travel.
Physical exam was remarkable for hypotension, mild respiratory distress, tachycardia with no signs of pulsus paradoxus. Labs were notable for elevated troponin of 0.404 ng/mL. Initial 12-lead ECG was sinus tachycardia at 100 bpm, low voltage without electrical alternans, no ST elevations present.
Due to her hemodynamic status, she was admitted to MICU, where she was treated for septic shock with vancomycin and cefepime, received tamiflu, colchicine and ibuprofen for possible myopericarditis and was maintained on pressors. Bedside echo confirmed large sized pericardial effusion with right ventricular free wall collapse consistent with tamponade physiology. Cardiology performed pericardiocentesis in which 500 cc of serous fluid was removed and consisted of 19 WBC/uL, 46% neutrophils and 36% lymphocytes with negative culture. ESR was 2 mm/hr and CRP was 1.1 mg/dl. Further testing included: Quantiferon TB gold, Adenovirus, M. Pneumoniae IgM, Echovirus, Parvovirus B19 IgM, Coxsackie A/B, acute hepatitis panel, urinalysis, urine legionella, HIV, and CMV IgM that were all negative. TSH level was normal. ANA was low positive and DSDNA AB IgG negative. Influenzae A virus culture resulted and was positive. Finallly, her diagnosis was found to be myopericarditis from influenzae A. Eventually patient was tapered off of pressors with complete resolution of symptoms and transferred to general medical service and then one week after admission she was discharged with cardiology follow up.
Discussion:
Influenza is a known cause of myopericarditis. To diagnose myopericarditis, there must be presence of acute pericarditis in addition to at least one of the following: elevation in serum cardiac biomarkers or evidence of myocardial inflammation by cardiac magnetic resonance or new LV systolic dysfunction on echo. The majority of the literature describing influenza myopericarditis comes from case reports. One such example is a case series of 5 Japanese patients with influenza myocarditis, in which cardiac involvement typically occurred between 4 and 9 days after the onset of influenza symptoms with worsening dyspnea being the most common symptom. In this case series, all the patients had elevated CK-MB and LV dysfunction. Influenza can also cause fulminant myocarditis; in which patients present with severe LV dysfunction and endomyocardial biopsy shows multiple foci of active inflammation and necrosis.
Conclusions:
There are no specific therapies that have been proven to improve outcomes in influenza myocarditis and the mainstay of treatment appears to be supportive.