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Review
. 2014 Jul-Sep;26(3):321-6.
doi: 10.5935/0103-507x.20140046.

Fulminant myocarditis associated with the H1N1 influenza virus: case report and literature review

[Article in English, Portuguese]
Maria Lúcia Saraiva Lobo  1 , Ângela Taguchi  1 , Heloísa Amaral Gaspar  1 , Juliana Ferreira Ferranti  1 , Werther Brunow de Carvalho  1 , Artur Figueiredo Delgado  1
Affiliations
Review

Fulminant myocarditis associated with the H1N1 influenza virus: case report and literature review

[Article in English, Portuguese]
Maria Lúcia Saraiva Lobo et al. Rev Bras Ter Intensiva. 2014 Jul-Sep.

Abstract
in English, Portuguese

A case of fulminant myocarditis associated with the H1N1 influenza virus. This case report describes the patient's clinical course and emphasizes the importance of bedside echocardiography as an aid in the early diagnosis and management of children with severe myocardial dysfunction. It also discusses aspects relevant to the treatment and prognosis of fulminant myocarditis. The patient was a female, 4 years and 8 months old, previously healthy and with a history of flu symptoms in the past two weeks. The patient was admitted to the emergency room with signs of hemodynamic instability, requiring ventilatory support and vasoactive drugs. The laboratory tests, chest X-ray and echocardiogram suggested the presence of myocarditis. The test for H1N1 in nasopharyngeal secretions was positive. The patient evolved to refractory cardiogenic shock despite the clinical measures applied and died 48 hours after admission to the intensive care unit. The H1N1 influenza virus is an etiological agent associated with acute myocarditis, but there are few reported cases of fulminant myocarditis caused by the H1N1 virus. The identification of signs and symptoms suggestive of fulminant progression should be immediate, and bedside echocardiography is a useful tool for the early detection of myocardial dysfunction and for therapeutic guidance. The use of immunosuppressive therapy and antiviral therapy in acute myocarditis of viral etiology is controversial; hence,the treatment is based on hemodynamic and ventilatory support. The use of hemodynamic support by extracorporeal membrane oxygenation emerges as a promising treatment.

Caso de miocardite fulminante associada ao vírus influenza H1N1, em que foi descrita a evolução clínica do paciente e enfatizada a importância do ecocardiograma à beira do leito como auxílio no diagnóstico precoce e manejo de crianças com disfunção miocárdica grave, além de terem sido discutidos aspectos relevantes relacionados à terapêutica e ao prognóstico da miocardite fulminante. Trata-se de paciente do sexo feminino, 4 anos e 8 meses, previamente hígida, com história de quadro gripal há 2 semanas. Admitida no pronto-socorro com sinais de instabilidade hemodinâmica, necessitando de suporte ventilatório e drogas vasoativas. Exames laboratoriais, radiografia de tórax e ecocardiograma sugestivos de miocardite. Pesquisa positiva para H1N1 em secreção de nasofaringe. Evoluiu com choque cardiogênico refratário a despeito das medidas clínicas, indo a óbito em 48 horas após admissão na unidade de terapia intensiva. O vírus influenza H1N1 é agente etiológico associado a quadros de miocardite aguda, porém poucos são os casos relatados de miocardite fulminante pelo vírus H1N1. A identificação de sinais e sintomas sugestivos de evolução fulminante deve ser imediata e o ecocardiograma à beira do leito é uma ferramenta útil para detecção precoce de disfunção miocárdica e orientação terapêutica. O uso de terapia imunossupressora, em casos de miocardite fulminante de etiologia viral, é controverso, bem como o de terapia antiviral, de tal forma que o tratamento baseia-se em suporte hemodinâmico e ventilatório. O uso de suporte hemodinâmico, por meio de oxigenação por membrana extracorpórea, aparece como terapia promissora.

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Conflict of interest statement

Conflict of interests: None.

Figures

Figure 1
Figure 1
(A) Chest X-ray after admission showing bilateral alveolar infiltrates. (B) Chest X-ray after admission to the intensive care unit with worsening alveolar infiltration and the presence of invasive devices (tracheal tube and central venous catheter).
Figure 2
Figure 2
(A) Measurement of ejection fraction by M-mode; (B) measurement of cardiac index; (C) apical 4-chamber image showing significant dilation of the left ventricle; (D) presence of significant tricuspid insufficiency by color Doppler. LVDd - left ventricular end-diastolic diameter; LVDs - left ventricular end-systolic diameter; VTI - velocity-time integral; RV - right ventricle; LV - left ventricle; RA - right atrium; LA - left atrium; TI - tricuspid insufficiency.
Figure 3
Figure 3
Macroscopy of the left ventricle. (A) Thickening of the mitral valve. (B) Deposition of yellowish material in the endocardium.
Figure 4
Figure 4
(A) Lymphocytic inflammatory infiltrate in the myocardium with degeneration of some myocytes; (B) interalveolar septum with signs of congestion; (C) alveoli filled with hyaline membranous content.
See this image and copyright information in PMC

Comment in

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