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Volume 30, Issue 2, Pages 179-182 (April 2004)


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Acute Viral Myocarditis in the ED Pediatric Patient: Three Case Presentations

Nancy Mecham, APRN, FNPCorresponding Author Information

Nancy Mecham, APRN, FNP, is Clinical Nurse Specialist ED/RTU, Primary Children's Medical Center, Salt Lake City, Utah.

Article Outline

Case presentation No. 1

Case presentation No. 2

Case presentation No. 3

Clinical Manifestations

Pathophysiology

Treatment

Prognosis

Summary

References

Further reading

Copyright

The majority of acute viral myocarditis cases are subclinical and self-limiting in both adults and children. The patient may present with symptoms as common as respiratory distress with tachypnea, retractions, and grunting, or, in its most severe presentation, a seemingly healthy patient can suddenly exhibit a rapidly progressive heart failure, cardiogenic shock, or complex ventricular dysrhythmias. These severe cases are a challenge for the most experienced ED nurse, but when the presentation is in a pediatric patient, the situation takes on aspects that are not faced often in the pediatric setting. Thus, these cases remind us why we need to be prepared to expect the unexpected when caring for a pediatric patient.

Case presentation No. 1 

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An 18-month-old previously healthy girl with no history of congenital heart disease or other major illnesses was brought by her mother to a freestanding urgent care clinic. The child had a 4-day history of upper respiratory tract infection and vomiting. It was noted on her examination that she was clearly ill but awake and alert. She was sent to the neighboring local hospital for laboratory work.

As she arrived back at the urgent care clinic, she suddenly arched her back and went limp and pale. Bag-valve-mask ventilation and CPR were initiated, and she was transferred back to the local emergency department. Her first rhythm on the monitor was a pulseless ventricular tachycardia. She was defibrillated 3 times, given a dose of epinephrine, and after another defibrillation, was noted to be in a narrow complex tachycardia with a pulse. She reverted back to a pulseless ventricular tachycardia within minutes and again was defibrillated and given more epinephrine. A pulseless bradycardia developed and she was intubated and given atropine and lidocaine, with a return to perfusing narrow complex tachycardia at a rate of 140.

During transport by helicopter to a level I pediatric trauma center, she had sluggishly reactive pupils and posturing. She again became bradycardic with a rate in the 30s. CPR was performed and she was given epinephrine times 2 doses with return of a perfusing narrow complex tachycardia in the 150s. Two fluid boluses of 20 mL/kg were given. As the helicopter touched down, she returned to a pulseless ventricular tachycardia. She was defibrillated once as she rolled into the emergency department. With CPR in progress, her initial rhythm was a pulseless electrical activity at 30. Her pupils were fixed and dilated. Her endotracheal tube position was confirmed, another 20 mL/kg bolus was administered, a dose of epinephrine, atropine, and bicarbonate was administered, and blood was drawn for gases and laboratory tests. A perfusing rhythm never returned. She was declared dead 52 minutes after her initial arrest. The patient's postmortem revealed myocardial inflammation consistent with acute viral myocarditis.

Case presentation No. 2 

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A previously healthy 8-year-old boy was at home getting ready for school when he suddenly became pale, limp, and unresponsive. He had a history of having mild “flu-like” symptoms during the previous weekend, but his parents stated that he seemed fine the previous day. He had no significant medical history. His “flu-like” symptoms included low-grade fever, body aches, and a mild cough.

His parents immediately started CPR and called 911. Upon arrival of EMS, he was defibrillated twice, with return of a perfusing rhythm. He was intubated, had peripheral lines placed, and was taken by helicopter to a level I pediatric trauma center. Upon arrival at the emergency department a wide complex tachycardia was noted with a pulse and a rate of 154 and a blood pressure of 80/52. During the next few minutes in the emergency department, infusions of amiodarone, dopamine, and dopatamine were started. He had a capillary refill time of 3 seconds and peripheral pulses of 2.

A pediatric cardiologist was consulted and a stat echocardiogram was completed, which revealed decreased left ventricular function. The patient was transferred to the pediatric intensive care unit (PICU). After a long stay in the PICU that included extracorporeal membrane oxygenation and numerous resuscitations, he was taken off life support 10 days after his initial arrest.

Case presentation No. 3 

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A 12-month-old previously healthy boy brought into the emergency department during the height of the winter respiratory season presented to the triage desk in moderate respiratory distress. He had grunting, costal and subcostal retractions, wheezing, and tachypnea at a rate of 64.

Older children and adolescents are often asymptomatic. The most common predominant symptom, in a severe presentation, is a dysrhythmia, either atrial or ventricular tachycardial fibrillation.

The triage nurse immediately took him back to a room. The patient was given a nebulized bronchodilator respiratory treatment, after a brief assessment by an ED nurse and the ED physician, as a result of his wheezing and respiratory distress. He also was noted to have an oxygen saturation of 84% on room air, and oxygen was administered at 3 L per nasal cannula. Within a few minutes of starting his nebulized treatment, his mental status was noted to be decreasing, his pulses were diminishing, and a blood pressure could not be obtained. A cardiac monitor showed that he was in bradycardia with a rate of 40. CPR was initiated, but his status was unresponsive to any life-saving interventions or pharmacologic therapies. He was pronounced dead in the emergency department 90 minutes after his initial presentation to the triage desk. He was later found to have myocardial inflammation on his postmortem examination.

Clinical Manifestations 

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The manifestations of acute viral myocarditis are, to some degree, age dependent. In young infants, acute viral myocarditis occurs suddenly and with a severe presentation. In toddlers and young children, it is an acute but less severe illness. Older children and adolescents are often asymptomatic. The most common predominant symptom, in a severe presentation, is a dysrhythmia, either atrial or ventricular tachycardia/fibrillation as described in our case studies.1 Patients also can present with palpitations, chest pain, syncope, or signs of acute congestive heart failure, such as dysrhythmias, peripheral vasoconstriction, mottled and cool skin, and diaphoresis.

Often, the patient has a history of a recent upper respiratory infection or “flu-like” symptoms that support the fact that viral infections are the most common cause of an acute myocarditis presentation.1 The most common viral agents indicated in acute viral myocarditis are adenovirus and coxsackievirus.

Some clinical trials have shown improvement in the recovery of left ventricular function in adult patients treated with IVIG. Despite the lack of clinical trials in children, IVIG is standard treatment for pediatric acute viral myocarditis.

Pathophysiology 

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Viral myocarditis is an inflammatory process that affects the myocardium. Although it is the viral infection that is the trigger of acute myocarditis, it is the patient's own inflammatory response to the infection that leads to the myocardial damage.2 In the early stages of the immune response, there are direct effects on the atrial and ventricular myocardium. Later stages of the immune response produce a progressive decompensation that leads to myocardial destruction (cardiomyopathy).3 Recent clinical studies to support this viral trigger with an overzealous immune response concept have resulted in improvements in the treatment of viral myocarditis.3

Treatment 

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The most important aspect in the treatment of children with acute viral myocarditis is early recognition before there is clinical decompensation.2 Supportive care is the mainstay of treatment. Ideally these children should be managed in a pediatric referral center with critical care, cardiology, and cardiovascular surgery capabilities.2 Lethal arrhythmias should be treated according to Pediatric Advanced Life Support and Advanced Cardiac Life Support guidelines. Dopamine or epinephrine are useful with hypotension and decreased cardiac output states.1 However, inotropic agents, including digoxin, should be used cautiously because patients with myocarditis are susceptible to the arrhythmia properties of these agents.1 Digoxin often is used at half normal doses and with caution.2 Children presenting with congestive heart failure should be treated aggressively with inotropic support, afterload reduction, and diuretics.2 For pediatric patients presenting in cardiogenic shock, extracorporeal membrane oxygenation may be indicated. In larger children and adolescents, implantation of the left ventricular assist device has been performed, usually as a bridge to transplantation, which is the treatment of choice with refractory heart failure. Some clinical studies have looked at the use of corticosteroids in the patient with viral myocarditis, but this treatment remains controversial.2 Intravenous immunoglobulin (IVIG) has been used in both adults and children with viral myocarditis. Some clinical trials have shown improvement in the recovery of left ventricular function in adult patients treated with IVIG.2 Despite the lack of clinical trials in children, IVIG is standard treatment for pediatric acute viral myocarditis.2

Prognosis 

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The prognosis for a patient with acute viral myocarditis is related to the age of onset and the patient's response to therapy. As a rough estimate, one third of patients with acute viral myocarditis experience a complete recovery of normal cardiac function, one third improve clinically but show residual cardiac dysfunction, and one third experience chronic heart failure and die or require heart transplantation.2

Summary 

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Respiratory distress can be a common pediatric complaint, but symptoms such as wheezing, grunting, fever, and tachycardia should not always be assumed to be a respiratory illness. Cardiac compromise can mimic respiratory distress. Evaluate the heart rate and rhythm in all pediatric patients with respiratory distress.

if you see children, keep your pediatric critical care skills up to date. Have Pediatric Advanced Life Support and Advanced Cardiac Life Support algorithms and drugs reviewed and practiced in mock codes at least annually.

The presentation of severe acute viral myocarditis in the pediatric patient can be dramatic and test the skills of even the most seasoned pediatric ED nurse. Pediatric patients with acute viral myocarditis can indeed have wide complex ventricular tachycardia, ventricular fibrillation, and pulseless electrical activity.

Finally, no matter what your clinical setting, if you see children, keep your pediatric critical care skills up to date. Have Pediatric Advanced Life Support and Advanced Cardiac Life Support algorithms and drugs reviewed and practiced in mock codes at least annually, if not more frequently.

References 

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1.. 1. In:  Behrman R editors. Nelson textbook of pediatrics. 16th ed. Philadelphia: W.B. Saunders Company; 2000;p. 1431–1435.

2.. 2. Wheeler DS, Kooy NW. A formidable challenge: the diagnosis and treatment of viral myocarditis in children. Crit Care Clin. 2003;19:365–391. Full Text | Full-Text PDF (584 KB) | CrossRef

3.. 3. Levi D, Alejos J. Diagnosis and treatment of pediatric viral myocarditis. Curr Opin Cardiol. 2001;16:77–83. MEDLINE | CrossRef

Further reading 

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Submissions to this column are welcomed and encouraged. Contributions can be sent to one of the following:

Deborah Parkman Henderson, RN, PhD, 1255 Linda Ridge Rd, Pasadena, CA 91103, 310 328-0720 • dhendersn@aol.com

Donna Ojanen Thomas, RN, MSN, 2822 E Canyon View Dr, Salt Lake City, UT 84109, 801 588-2240 • donna.thomas@ihc.com

Salt Lake City, UtahUSA

Corresponding Author InformationReprints not available from the author.

 Section Editors: Donna Ojanen Thomas, RN, MSN, and Deborah Parkman Henderson RN, PhD

PII: S0099-1767(04)00063-7

doi:10.1016/j.jen.2004.01.012


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