[EngO6-3] Influenza-associated septic shock accompanied by septic cardiomyopathy that developed in summer and mimicked fulminant myocarditis
Background: Fulminant myocarditis (FM) and septic cardiomyopathy (SC) are two different disease entities and distinction is important.
Case Presentation: A 34-year-old man was presented to our hospital with shock in September. His blood temperature, pulse rate, blood pressure, and respiratory rate were 39.7°C, 157 bpm, 49/30 mmHg, and 40 breaths/min. Because ECG showed tachycardia with extended ST elevation and a rapid test for influenza A virus was positive, FM was suspected. He was intubated and carried to the ICU, where high-dose vasopressor therapy (noradrenaline up to 0.4γ and vasopressin up to 2 units/hour) was initiated and CRRT was begun. Antimicrobial therapy, including a neuraminidase inhibitor and empiric broad-spectrum antibiotics was administered. Echocardiography showed severe global LV systolic dysfunction (EF, 20%) and LV dilatation (LVDd, 66 mm) without myocardial edema. A right heart catheter examination showed cardiac output of 12.0 L/min (CI 6.16 L/min/m2) which was inconsistent with FM. Additionally, myocardial biopsy findings did not indicate FM. Thus, SC was considered and standard therapy for septic shock was initiated. He was stabilized in first 72 hours without mechanical circulatory support. He was extubated and CRRT were discontinued on 12th hospitalized day. His low LV function was restored and returned to almost normal in following two weeks.
Conclusion: Influenza A infection may cause of septic shock accompanied by SC. It is confusing in clinical appearance of FM, but showed critically different features of FM and it may occur even in not in the epidemic period.
Case Presentation: A 34-year-old man was presented to our hospital with shock in September. His blood temperature, pulse rate, blood pressure, and respiratory rate were 39.7°C, 157 bpm, 49/30 mmHg, and 40 breaths/min. Because ECG showed tachycardia with extended ST elevation and a rapid test for influenza A virus was positive, FM was suspected. He was intubated and carried to the ICU, where high-dose vasopressor therapy (noradrenaline up to 0.4γ and vasopressin up to 2 units/hour) was initiated and CRRT was begun. Antimicrobial therapy, including a neuraminidase inhibitor and empiric broad-spectrum antibiotics was administered. Echocardiography showed severe global LV systolic dysfunction (EF, 20%) and LV dilatation (LVDd, 66 mm) without myocardial edema. A right heart catheter examination showed cardiac output of 12.0 L/min (CI 6.16 L/min/m2) which was inconsistent with FM. Additionally, myocardial biopsy findings did not indicate FM. Thus, SC was considered and standard therapy for septic shock was initiated. He was stabilized in first 72 hours without mechanical circulatory support. He was extubated and CRRT were discontinued on 12th hospitalized day. His low LV function was restored and returned to almost normal in following two weeks.
Conclusion: Influenza A infection may cause of septic shock accompanied by SC. It is confusing in clinical appearance of FM, but showed critically different features of FM and it may occur even in not in the epidemic period.