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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 8  |  Issue : 6  |  Page : 288-290

Fulminant myocarditis, severe pediatric acute respiratory distress syndrome associated with H1N1 influenza and enteric fever rescued by prone ventilation: A case Report


1 Department of Pediatric Critical Care and Pulmonology, Sri Balaji Action Medical Institute, New Delhi, India
2 Department of Pediatric Critical Care and Pulmonology, Sri Balaji Action Medical Institute; Department of Pediatrics, Shree Aggarsain International Hospital, New Delhi, India

Date of Submission05-Jun-2021
Date of Decision04-Oct-2021
Date of Acceptance14-Oct-2021
Date of Web Publication19-Nov-2021

Correspondence Address:
Dr. Pradeep Kumar Sharma
Flat No 48, Pocket-7, Sector-21, Rohini, New Delhi - 110 086
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpcc.jpcc_44_21

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  Abstract 


H1N1 influenza-associated fulminant myocarditis with pediatric acute respiratory distress syndrome (PARDS) is rare. We report a child of fulminant myocarditis, severe PARDS associated with H1N1 and enteric fever. She rapidly developed severe PARDS and refractory hypoxemia. She was successfully rescued with prone ventilation. Fulminant myocarditis with PARDS can be a manifestation of H1N1 infection. These scenarios pose a tough challenge, especially in resource-limited settings. Although we successfully managed our patient with prone ventilation, success in one case cannot be generalized until more evidence is generated.

Keywords: Fulminant myocarditis, H1N1 influenza, pediatric acute respiratory distress syndrome, prone ventilation


How to cite this article:
Goswami G, Sharma PK, Vinayak N. Fulminant myocarditis, severe pediatric acute respiratory distress syndrome associated with H1N1 influenza and enteric fever rescued by prone ventilation: A case Report. J Pediatr Crit Care 2021;8:288-90

How to cite this URL:
Goswami G, Sharma PK, Vinayak N. Fulminant myocarditis, severe pediatric acute respiratory distress syndrome associated with H1N1 influenza and enteric fever rescued by prone ventilation: A case Report. J Pediatr Crit Care [serial online] 2021 [cited 2021 Nov 27];8:288-90. Available from: http://www.jpcc.org.in/text.asp?2021/8/6/288/330725




  Introduction Top


Fulminant myocarditis is a life-threatening condition causing heart failure and cardiogenic shock. It is mainly caused by viral infections such as Coxsackie B, Adenovirus, Enteroviruses, and Influenza. Diphtheria, Salmonella, Rickettsial fever, and Streptococcus are other important infectious causes of myocarditis.[1] Enteric myocarditis first described in 1884 is a toxic myocarditis seen in 1%–5% of persons with enteric fever.[2] Influenza-associated fulminant myocarditis is rare.[3],[4],[5],[6] During the 2009 pandemic, the prevalence of H1N1-associated myocarditis was 5% (4/80) and 1.4% (n = 838) in two pediatric series, respectively.[5],[6] Incidence of pediatric acute respiratory distress syndrome (PARDS) in H1N1 pneumonia is 20% with 58% mortality.[7] The occurrence of PARDS along with myocarditis in influenza is very rare.[4] We present a case of fulminant myocarditis and severe PARDS rescued by prone ventilation.


  Case Report Top


A 7-year-old girl diagnosed with enteric fever with thrombocytopenia (platelet count 50,000/mm3 and serum Widal TO-1:160, TH-1:160) was admitted at an outlying hospital with fever and loose motions for 6 days. She received intravenous ceftriaxone and oral azithromycin. Platelet count improved to 1 lakh/mm3. However, she continued to have high-grade fever (103°F) and developed generalized anasarca, progressive respiratory distress, and orthopnea. Antibiotics were upgraded to injection meropenem and vancomycin. She was referred on 7th day. On examination, she was conscious, oriented, and thinly built (weight-13 kg). She had orthopnea and respiratory rate – 58/min with subcostal, intercostal, and suprasternal retractions. Heart rate (HR) was 123/min with warm peripheries, normal capillary refill time, and noninvasive blood pressure of 100/60 mmHg. Her saturation (Spo2) on oxygen by mask at 6 L/min was 92%. She had pallor and jugular venous pressure was raised. The abdomen was distended with presence of free fluid and tender hepatomegaly. Chest examination revealed bilateral crepitation and ejection systolic murmur. Complicated enteric fever with myocarditis with congestive heart failure, rickettsial infections, or superadded nosocomial infections was kept as differential diagnosis. She was continued on injection meropenem and vancomycin. Injection doxycycline and injection furosemide were added. She was put on noninvasive ventilation (NIV). The initial venous blood gas revealed pH 7.57, pCo2 25 mmHg, pO2 42 mmHg, lactate 1 mmol/L, and HCO3 22.9 mmol/L. Chest X-ray showed homogenous fluffy shadows in bilateral lung fields with cardiomegaly [Figure 1]. Laboratory investigations revealed that hemoglobin was 8.4 gm/dl, total leukocyte counts: 5750/mm3with 70% neutrophils, 27% lymphocytes, platelet count 2.59 L/mm3, alanine transaminase 47U/L, aspartate transaminase 125U/L, normal serum electrolytes, and normal renal function test. Serum Widal revealed titers of TO 1:80 and TH >1:640. Echocardiography revealed mildly dilated inferior vena cava, global hypokinesia, 15% left ventricular ejection fraction (LVEF), and mild pericardial effusion. Injection dexamethasone (3 mg/kg initial dose, followed by eight doses of 1 mg/kg 6 hourly) was added. Troponin I, troponin T, and creatine kinase-MB were normal. Her clinical condition worsened (HR: 180/min, RR: 60/min with significant work of breathing, SpO2 85%) and she was intubated at 20 h. Pressure control volume guarantee mode of ventilation was used at 100% oxygen, 7 ml/kg of tidal volume (TV), positive end-expiratory pressure (PEEP) of 9 cm H2O, and RR of 24/min. Ventilatory settings were titrated – TV at 5 ml/kg and PEEP 14 cm H2O. Injection milrinone was also started at 0.25 mcg/kg/min. Repeat Chest X-ray showed worsening of lung opacities consistent with PARDS [Figure 1]. However, she continued to remain hypoxemic – SpO2 – 77%–80%, oxygenation index – 40.5, at mean airway pressure – 22 cm, and peak pressure – 31 cm H2O. At this stage, we placed her in the prone position. There were stabilization and improvement (HR: 144/min, oxygen saturation index: 5.3). PEEP and Fio2 were gradually decreased to 10 cm H2O and 40%, respectively. She was made supine after 17 h, and there was mild increase in ventilatory settings. The nasopharyngeal swab polymerase chain reaction was positive for H1N1. Oseltamivir was added. She was extubated to NIV after 7 days. Repeat echocardiography showed good contractility with 60% LVEF. Milrinone was stopped and enalapril was added. NIV was weaned after 5 days, and she was discharged after 21 days of hospitalization with a diagnosis of complicated enteric fever, H1N1 influenza, fulminant myocarditis, left heart failure, and severe PARDS. At 6-week follow-up, she was stable with normal echocardiography.
Figure 1: (a) Chest X-ray on day 1 showing bilateral fluffy shadows mainly perihilar (batwing appearance) and cardiomegaly. (b) Chest X-ray after 20 h revealed confluent, homogenous shadows in bilateral lung field which have progressed in comparison to the previous X-ray

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  Discussion Top


Fulminant myocarditis due to H1N1 is rare and its actual incidence is difficult to predict. Ukimura et al. reviewed 58 cases of myocarditis associated with H1N1 pandemic 2009 worldwide. Out of these, 62% (36/58) were fulminant. Only 14 cases (24%) were <17 years of age. Coexisting pneumonia was seen in 24% (13/58) of cases; however, data on associated acute respiratory distress syndrome are lacking. Extracorporeal membrane oxygenation (ECMO) was required in 21% (12/58) and mechanical circulatory support in 29% (17/58) of cases. A total of 14 (24%) deaths were reported.[4] Acute myocarditis associated with H1N1 pandemic 2009 was reported as an independent risk factor for death in patients <21 years old.[6] Our case had global hypokinesia of the left ventricular wall with poor ejection fraction. She had rapid progression of the disease to severe PARDS. This child was with left ventricular heart dysfunction which was fulfilling all other PARDS criteria.[8] Acute hypoxemia with new chest imaging changes could not be explained by acute left ventricular heart failure or fluid overload. Despite maximum cardiorespiratory support, she had refractory hypoxemia. The optimum therapeutic option at this stage would have been ECMO; however, the same was not available at the author's center. Hence, we decided to prone the child as a rescue measure. Prone ventilation is one of the rescue measures for severe PARDS.[9] Change in lung physiology by prone positioning promotes homogeneous alveolar ventilation leading to improvement in ventilation perfusion matching.[10] However, the role of prone ventilation in patients with associated cardiac compromise is not clear. Prone position reduces right ventricular afterload and increases left ventricular preload and increases cardiac index only in patients who have preload reserve.[10],[11] It also improves cardiac function by increasing myocardial oxygen delivery (improvement in hypoxemia).[10],[11] Clinical assessment of preload reserve in an acutely deteriorating patient is very difficult. In our case, the prone position was probably tolerated because we were able to mobilize lung fluid with furosemide infusion and supported failing heart with milrinone infusion before placing the child in the prone position. Moreover, we did not find any deterioration in cardiac function or hemodynamic status during prone position.

Fulminant myocarditis with PARDS can be a manifestation of H1N1 infection. These scenarios pose a tough challenge, especially in resource-limited settings. Although we successfully managed our patient with prone ventilation, success in one case cannot be generalized until more evidence is generated.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient's legal guardian has given the consent for images and other clinical information to be reported in the journal. The patient's legal guardian understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Dancea AB. Myocarditis in infants and children: A review for the paediatrician. Paediatr Child Health 2001;6:543-5.  Back to cited text no. 1
    
2.
Majid A, Bin Waqar SH, Rehan A, Kumar S. From gut to heart: Havoc in a young patient with typhoid associated cardiomyopathy. Cureus 2019;11:e5049.  Back to cited text no. 2
    
3.
Kalil AC, Thomas PG. Influenza virus-related critical illness: Pathophysiology and epidemiology. Crit Care 2019;23:258.  Back to cited text no. 3
    
4.
Ukimura A, Satomi H, Ooi Y, Kanzaki Y. Myocarditis associated with influenza A H1N1pdm2009. Influenza Res Treat 2012;2012:351979.  Back to cited text no. 4
    
5.
Bratincsák A, El-Said HG, Bradley JS, Shayan K, Grossfeld PD, Cannavino CR. Fulminant myocarditis associated with pandemic H1N1 influenza A virus in children. J Am Coll Cardiol 2010;55:928-9.  Back to cited text no. 5
    
6.
Randolph AG, Vaughn F, Sullivan R, Rubinson L, Thompson BT, Yoon G, et al. Critically ill children during the 2009-2010 influenza pandemic in the United States. Pediatrics 2011;128:e1450-8.  Back to cited text no. 6
    
7.
Töpfer L, Menk M, Weber-Carstens S, Spies C, Wernecke KD, Uhrig A, et al. Influenza A (H1N1) vs non-H1N1 ARDS: Analysis of clinical course. J Crit Care 2014;29:340-6.  Back to cited text no. 7
    
8.
Pediatric Acute Lung Injury Consensus Conference Group. Pediatric acute respiratory distress syndrome: Consensus recommendations from the pediatric acute lung injury consensus conference. Pediatr Crit Care Med 2015;16:428-39.  Back to cited text no. 8
    
9.
Guérin C, Reignier J, Richard JC, Gacouin A, Boulain T, Mercier E, et al. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med 2013;368:2159-68.  Back to cited text no. 9
    
10.
Koulouras V, Papathanakos G, Papathanasiou A, Nakos G. Efficacy of prone position in acute respiratory distress syndrome patients: A pathophysiology-based review. World J Crit Care Med 2016;5:121-36.  Back to cited text no. 10
    
11.
Jozwiak M, Teboul JL, Anguel N, Persichini R, Silva S, Chemla D, et al. Beneficial hemodynamic effects of prone positioning in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2013;188:1428-33.  Back to cited text no. 11
    


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