Category: Brief Report and Case Report

Red code influenza

Elisa Lainu1, Ilaria Francesca Martino2, Federica Quaglia2, Stefano Perlini1
 
1) Scuola di Specializzazione in Medicina di Emergenza-Urgenza, Università degli Studi di Pavia, Italia 
2) Struttura Complessa Pronto Soccorso Accettazione, IRCCS Policlinico San Matteo, Pavia, Italia 
 

Abstract 

Influenza is usually a self-limiting disease, associated with a low mortality, but it may cause as uncommon as fatal non-respiratory complications: myocardial involvement occurs in up to 12% of influenza and its clinical expression varies from asymptomatic to fulminant myocarditis. 
Most reported cases of acute myocarditis associated with influenza are caused by type A virus. Though, the significance of influenza B virus may have been underestimated. 
We report two clinical cases of acute myocarditis caused by influenza B virus, started with nonspecific flu-like symptoms, rapidly resulting in severe ventricular dysfunction and cardiogenic shock, that needed mechanical hemodynamic support and intensive cares.
In fulminant myocarditis context, a prompt recognition of the clinical state and a multidisciplinary approach are decisive for a positive outcome of the patient. 
 
Key words: Influenza, flu, myocarditis, cardiogenic, shock. 3 

Introduction

Influenza viruses represent the most common etiological agents of human upper respiratory infections: in fact, it is estimated that each year 5% to 10% of adults and 20% to 30% of children globally are infected1
Influenza is usually a self-limiting disease, associated with a low mortality, but it may cause as uncommon as fatal non-respiratory complications, such as myopathy, encephalopathy and myocarditis2. Myocardial involvement occurs in up to 12% of influenza3 and its clinical expression varies from asymptomatic to fulminant myocarditis: this latter fearsome complication is characterized clinically by distinct onset of cardiac symptoms in otherwise young healthy patients after nonspecific flu-like symptoms, rapidly resulting in severe ventricular dysfunction and cardiogenic shock, with a mortality rate up to 30%4.

 

Case reports

Case 1

V.T., woman, 29 years old, came to medical attention in the ED after two syncopale episodes during a flu-syndrome characterized by mild fever and cough from five days and nausea with vomiting the day before. No past medical history. Vital signs: blood pressure 100/70 mmHg, heart rate 88 bpm, peripheral oxygen saturation 100%, afebrile. Only a mild abdominal pain was reported during the physical examination. Blood samples were performed: complete blood count was in normal range, normal renal and liver function tests, mild elevation of reactive C protein (0.61 mg/dl, normal range: 0.00-0.50 mg/dl). After hydration and antiemetic treatment, the patient, as she was clinically stable and felt subjectively better, was discharged with a diagnosis of gastroenteritis. 
The patient reached again the ED the following day for worsening of the abdominal symptoms, with vomiting, diffuse myalgia and additional episode of syncope. On physical examination the patient appeared aware and alert, but looked acutely ill, showing signs of systemic hypoperfusion, cold and dry skin, abdominal tenderness without peritonism; examination of her lungs revealed no pathological findings. The patient’s blood pressure was 100/40 mmHg, she had tachycardia (110 bpm) and a temperature of 35°C. 
Arterial blood gas analysis revealed pH of 7.4, carbon dioxide tension of 27 mmHg, partial pressure of oxygen of 110 mmHg, bicarbonate level of 16.7 mmol/L, lactates 4 mmol/L. Initial laboratory findings revealed normal values of complete blood count, renal and hepatic functions. 
Despite volemic resuscitation with 1000 ml Ringer Acetate and 1000 ml Normal Saline 0.9%, tissue hypoperfusion and hypotension (80/60 mmHg) persisted. 
A transthoracic echocardiography was performed and revealed a moderate pericardic effusion (about 20 mm) with an extremely hypokinetic left ventricle; right ventricular systolic function was normal and no signs of acute pulmonary embolism or cardiac tamponade were noted. Inferior vena cava diameter was 25 mm, without significant inspiratory collapse. 
Additional blood tests revealed cardiac troponin level of 11 ng/ml (normal range < 0.006 ng/ml). Suspecting a cardiogenic shock from acute myocarditis, a consult with Cardiologist and Anesthesiologist was requested. 
During the collegial evaluation, the patient became progressively bradycardic (from 125 to 50 bpm) and a further episode of syncope occurred: a support treatment with catecholamines was started and the patient was moved to the Coronary Intensive Care Unit. 
A second transthoracic echocardiography confirmed severe depression of left ventricular function, with thickening of left ventricle walls, and pericardic effusion without cardiac tamponade.
As severe hypotension and systemic hypoperfusion persisted, the patient underwent right heart catheterization, which revealed a cardiac index of 1 l/min/m2 (normal range 2,5-5 l/min/m2); endomyocardial biopsy and placement of an intra-aortic balloon pump (IABP) were performed, as well. 
Considering the serious clinical situation, the patient was transferred to the Intensive Care Unit and IABP was replaced by the venoarterial extracorporeal membrane oxygenation (ECMO) system. 
During the 11 days of hospitalization in the ICU, 6 of which in ECMO assistance, the hemodynamic state progressively stabilized, as well as the blood tests and the cardiac pump function; the patient was transferred to the ward of Cardiology. 
The virological and serological tests on patient’s nasopharyngeal swab showed positivity for influenza B virus (164700 RNA copies/ml). 5 
After an overall 24 days of hospitalization, the patient was discharged with complete recovery, with diagnosis of acute myocarditis caused by influenza B virus, complicated with cardiogenic shock.

Case 2 

E.G., woman, 36 years old, came to medical attention in the ED for a flu-syndrome characterized by fever (39°C), cough and diffuse myalgia for a week and a syncopale episode the day before. No past medical history. On physical examination the patient appeared aware and alert, hypotensive (blood pressure 80/60 mmHg), tachycardic (heart rate 140 bpm), anuric, with cold skin and signs of hypoperfusion. Cardio-thoracic, abdominal and neurological examinations revealed no pathological findings, as well as chest X-ray. 
A first arterial blood gas analysis revealed only a moderate hyperlactacidemia (lactates 4.2 mmol/l), soon progressed to a severe metabolic acidosis: pH of 7.28, carbon dioxide tension of 13.8 mmHg, partial pressure of oxygen of 100 mmHg, bicarbonate level of 10.9 mmol/L, lactates 11.5 mmol/L. Initial laboratory findings revealed an elevation of reactive C protein (7.74 mg/dl, normal range: 0.00-0.50 mg/dl) and normal values of complete blood count, renal and hepatic functions. Volemic resuscitation was started. 
A transthoracic echocardiography was performed and revealed a severe depression of left ventricular function (FE<10%), with thickening of left ventricle walls, and pericardic effusion without cardiac tamponade. Additional blood tests revealed cardiac troponin level of 0.297 ng/ml (normal range < 0.006 ng/ml), with a progressive increase up to 0.501 ng/ml in the following hours. 
Suspecting a cardiogenic shock from acute myocarditis, a consult with Cardiologist, Cardiothoracic Surgeon and Anesthesiologist was requested.
After the collegial evaluation, considering the serious clinical situation, the patient was admitted to the Intensive Care Unit and underwent endomyocardial biopsy and placement of veno-arterial extracorporeal membrane oxygenation (ECMO) system. Complete virological and serological tests were performed and empiric antibiotic therapy, steroids and catecholamines administered. 
During the hospitalization in the ICU, 6 days of which in ECMO assistance, the patient always remained aware and alert; diuresis promptly resumed and metabolic acidosis normalized. As the hemodynamic state, the blood tests and the cardiac pump function progressively stabilized, the patient was transferred first to the Coronary Intensive Care Unit and then to the ward of Cardiology.
The virological and serological tests on patient’s nasopharyngeal swab showed positivity for influenza B virus (157995 RNA copies/ml) and the endomyocardial biopsy revealed a moderate inflammation state, with a T-lymphocyte and hystio-macrophagic component, with evolutive-reparative aspects of myocarditis. 
After an overall 17 days of hospitalization, the patient was discharged with complete recovery, with diagnosis of acute myocarditis caused by influenza B virus, complicated with cardiogenic shock. 
Two months after discharge, clinical and echocardiographical evaluations confirmed complete recovery of cardiac function. 6  

Conclusion 

Influenza induced cardiogenic shock is extremely rare and most reported cases are due to fulminant myocarditis associated with influenza A virus5. Though, the significance of influenza B virus may have been underestimated, as its infection is generally considered to be mild, with less associated cardiovascular involvement in adults6
The described clinical cases represent, however, examples of acute myocarditis caused by influenza B virus, started with nonspecific flu-like symptoms, rapidly resulting in severe ventricular dysfunction and cardiogenic shock, that needed mechanical hemodynamic support and intensive cares. 
In fulminant myocarditis context, a prompt recognition of the clinical state, a multidisciplinary approach, with the cooperation among Emergency Medicine Doctors, Cardiologists, Anesthesiologists and Cardiothoracic Surgeons, together with an early hemodynamic support, are decisive for a positive outcome of the patient. 7 
References
  1. World Health Organization (WHO). Vaccines against influenza WHO position paper - November 2012. Wkly Epi-demiol Rec 2012; 87:461-76. 
  2. Kuiken T, Taubenberger JK. Pathology of human influenza revisited. Vaccine 2008; 26 (Suppl 4):D59-66. 
  3. Mamas MA, Fraser D, Neyses L: Cardiovascular manifestations associated with influenza virus infection. Int J Cardiol 2008; 130:304-309. 
  4. Dec GW Jr, Palacios IF, Fallon JT, Aretz HT, Mills J, Lee DC, Johnson RA: Active myocarditis in the spectrum of acute dilated ardiomyopathies: clinical features, histologic correlates, and clinical outcome. N Engl J Med 1985; 312:885-90. 
  5. Ukimura A, Ooi Y, Kanzaki Y, Inomata T, Izumi T: A national survey on myocarditis associated with influenza H1N1pdm2009 in the pandemic and postpandemic season in Japan. J Infect Chemother 2013; 19:426–431. 
  6. Paddock CD, Liu L, Denison AM, Bartlett JH, Holman RC, Deleon-Carnes M, Emery SL, Drew CP, Shieh WJ, Uyeki TM, Zaki SR: Myocardial injury and bacterial pneumonia contribute to the pathogenesis of fatal influenza B virus infection. J Infect Dis 2012; 205:895–905.
 

 

 

 

 

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