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Viral Myocarditis in Children

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Financial Disclosures
None reported.

This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:

1. Identify which population is at most risk of death as the result of myocarditis
   
2. Identify the mechanism that results in morbidity and mortality in children with myocarditis
   
3. Discuss the signs and symptoms of myocarditits in children
   
4. Describe the treatment of patients with myocarditis
   

Corresponding author: Tammy L. Uhl, RN, MSN, CCRN, CCNS, Brenner Children’s Hospital, Wake Forest University Baptist Medical Center, Medical Center Blvd, Winston-Salem, NC 27157 (e-mail: tuhl{at}wfubmc.edu).

Although myocarditis severe enough to be recognized is rare, it is the most common cause of heart failure in otherwise healthy children.⁴ In both children and adults, most cases are subclinical; thus, the true incidence of myocarditis in children is unknown.^2,5–7 Unfortunately, the clinical features of myocarditis can vary widely, and often no cardiac signs or symptoms occur, complicating recognition. For children in whom the diagnosis is suspected or cardiovascular compromise is severe enough to require admission to the pediatric intensive care unit (PICU), critical care nurses are an essential component in determining management, care, and outcomes. In this article, I describe the etiology of viral myocarditis in children, potential insidious clinical features, pathophysiology of the disease, and critical care management.

	Case 1

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A.J., a previously healthy 3-year-old boy, was brought to the emergency department because his body temperature was 40.5°C. During the previous week, he had had some nasal discharge and a mild, nonproductive cough. He had no history of increased work of breathing, rashes, or diarrhea. One day before the visit to the emergency department, he had been vomiting and had been unable to tolerate anything by mouth.

On arrival in the emergency department, A.J. appeared ill but was alert and in no marked distress. Vital signs were heart rate, 162/min; respirations, 26/min; and oxygen saturation, determined by pulse oximetry, 99% on room air. No murmur or gallop was noted; capillary refill was brisk with 2+ peripheral pulses and warm extremities. Breath sounds were clear bilaterally. He appeared mildly dehydrated with tachycardia, mildly sunken eyes, and tacky mucous membranes.

Routine blood tests were done. Electrolyte levels were normal except for a carbon dioxide level of 18 mEq/L, an anion gap of 23 mEq/L, and a serum urea nitrogen level of 21 mg/dL (to convert to millimoles per liter, multiply by 0.357), consistent with dehydration. A complete blood cell count revealed a white blood cell count of 26900/µL, a hemoglobin level of 12 g/dL, a hematocrit of 35.9%, and a platelet count of 321000/µL. A differential count was not completed.

Approximately 15 minutes after his initial examination, A.J. received two 20 mL/kg intravenous boluses of normal saline and was given something to eat, which he tolerated well. Because his parents were comfortable with observing the child at home and expressed full understanding of the signs of dehydration, A.J. was readied for discharge.

While the discharge papers were being completed, A.J. suddenly became unresponsive and apneic. Bag-valve -mask ventilation was begun, and subsequently he was pulseless. Cardiopulmonary resuscitation was initiated. After a prolonged attempt at resuscitation, he was pronounced dead. Postmortem examination revealed myocarditis of probable viral origin.

	Case 2

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K.M., a 5-year-old boy with a history of asthma, was brought to the emergency department because he had fainted. After the syncopal episode, he had shortness of breath and tachypnea. Approximately 4 days before this visit to the emergency department, he had had gastroenteritis with vomiting and diarrhea that resolved. Findings on a physical examination were unremarkable except for bilateral wheezing and increased work of breathing. He was given several albuterol nebulizers for a suspected exacerbation of asthma. A chest radiograph revealed bilateral infiltrates thought to be consistent with Mycoplasma pneumonia. He was given azithromycin and was transferred to a tertiary care center for closer observation.

On arrival in the PICU, his respiratory status continued to deteriorate. He was markedly tachypneic. Oxygen saturations were 86% to 91% on a 100% nonrebreather mask. Continuous albuterol was begun, but his pulmonary status did not change. Auscultation revealed diminished breath sounds at the bases bilaterally, no wheezing, and no murmur but a gallop. A repeat chest radiograph revealed pulmonary edema and cardiomegaly. After the repeat radiograph and continuing respiratory deterioration, he was intubated and mechanical ventilation was started. Within minutes of intubation, clinically significant unifocal premature ventricular contractions and hypotension (50–60/20–30 mm Hg) developed. He was given a lidocaine bolus, and continuous infusions of both lidocaine and epinephrine were started. Laboratory studies revealed a white blood cell count of 7300/µL, a hemoglobin level of 11.1 g/dL, a platelet count of 103000/µL, and unremarkable electrolyte levels. An echocardiogram showed markedly decreased left ventricular function with an ejection fraction of 10% to 14% and diminished right ventricular function. Neither structural abnormalities nor pericardial effusion was seen. A 12-lead electrocardiogram showed a normal sinus rhythm with frequent premature ventricular contractions and nonspecific T-wave abnormalities (Figure 1). The diagnosis was acute myocarditis with severe cardiomyopathy. Because of the continued deterioration in K.M.’s condition, inability to oxygenate, and worsening cardiac function, extracorporeal membrane oxygenation (ECMO) was started.

View larger version (133K): [in this window] [in a new window]   Figure 1 K.M.’s electrocardiogram on admission to the pediatric intensive care unit shows sinus tachycardia, frequent unifocal premature ventricular contractions, and nonspecific T-wave abnormality.

	Incidence and Prevalence

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Myocarditis appears to be more common in children than in adults.⁸ Its true incidence, however, is unknown; it is thought that subclinical cases ("silent" myocarditis) occur much more often than do severe cases. Many cases are unrecognized because of the wide range of signs and symptoms and, in some patients, the complete lack of clinical findings.^8,9 In a postmortem study of children who died without a history suggestive of myocarditis, researchers found evidence of active or healed myocarditis in 17 of 138 cases (12.3%).^8,10 Of the 17 cases, 15 occurred in children who died suddenly. In postmortem studies in adults, myocardial inflammation occurred in 1% to 9%.⁸

	Etiology

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The most common form of myocarditis, endemic in both rural Central and South America, is Chagas’ disease, caused by the parasitic protozoan Trypanosoma cruzi. In North America, viral infections cause most cases of myocarditis. Enteroviruses, most importantly coxsackievirus B, are the most frequently reported cause of epidemics of viral myocarditis in children.^5,11–13 However, more recent reports^9,14,15 indicated that adenoviral infection is as common a cause as enteroviral infection is, if not more so. Rarely, bacteria, fungi, protozoa, parasites, and rickettsiae are causative agents. Myocarditis has also been associated with immune-mediated diseases, collagen vascular diseases, and toxins (Table 1).

	Epidemiology

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Age plays a marked role in prevalence. During the neonatal period, myocarditis is usually abrupt, severe, and often fatal, with mortality as high as 75%.^11,12 Infants infected with coxsackievirus B during the first year of life have a high incidence of myocarditis. Myocarditis has been linked to sudden infant death syndrome, because inflammatory infiltrates have been found on autopsies of some victims.² Incidence increases again during late childhood and adolescence; the myocarditis usually has a delayed onset and patients recover.⁷

Male predominance has been noted with coxsackievirus B heart disease, particularly in adolescents and adults. In these age groups, two-thirds to three-quarters of patients with myocarditis are male.⁷ Male predominance has also been reported with coxsackievirus A myocarditis and poliomyelitis. Whether or not differences between the sexes occur in other viral infections is unknown.⁷

	Pathophysiology

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Although viral infection is the most common initiator of acute myocarditis, the subsequent autoimmune response plays a lead role in myocyte injury.^7,8,11,15,17 The principal mechanism of myocardial damage is not just viral replication; it includes cell-mediated immunological reactions.

The pathophysiology of myocarditis has been studied in mice infected with a cardiotropic virus, such as coxsackievirus B. After systemic infection, the virus enters the myocyte, where it replicates in the cytoplasm of the cell. Some replicated viruses then enter the interstitium and are phagocytized by activated macrophages.^3,8 Macrophage activation is due to both viral particles in the interstitium and the release of interferon by natural killer (NK) cells. The release of interferon is followed by release of proinflammatory cytokines (interleukins 1β and 2 and tumor necrosis factor ). When activated by interleukin 2, NK cells eliminate virally infected myocytes and inhibit virus replication^11,18,19 (Figure 2). The significance of the action of NK cells in the pathogenesis of the disease is well established; in animals depleted of NK cells before infection, a more severe myocarditis develops.⁸

View larger version (63K): [in this window] [in a new window]   Figure 2 Pathophysiology of myocarditis.

Unlike NK cells, T cells may contribute to damage in both infected and noninfected myocytes.^5,11,20 Activation of T cells results in accumulation of macrophages within the myocyte and production of cell-mediated cytotoxic effects.^7,11 Although T cells can lyse virus-infected myocytes, the accumulation of macrophages and the concomitant cytotoxic effects create a fine balance between viral clearance and myocyte damage.⁸ Adding to myocyte injury, lysis by T cells is indiscriminate; it occurs in both infected and noninfected cells.^7,11 The result is necrosis of healthy as well as infected myocytes. Therefore, a percentage of myocardial damage comes from "friendly fire," specifically the patient’s own immune response.

Permanent myocardial damage can be the end result of myocarditis. Such damage is thought to be due to an overaggressive immunological activation in which persistent T-cell infiltration leads to long-term tissue destruction and subsequent dilated cardiomyopathy.^8,18 Infection with enteroviruses plays a major role in chronic forms of dilated cardiomyopathy.^21,22

	Clinical Manifestations and Diagnosis

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Myocarditis is classified as fulminant, acute, or chronic. Fulminant myocarditis is preceded by a viral prodrome that is followed by sudden onset of severe hemodynamic compromise. Acute myocarditis has a less distinct onset and, initially, less severe compromise but is followed by a worse outcome than fulminant myocarditis. McCarthy et al²³ found that adults with fulminant myocarditis had excellent long-term survival, whereas patients with acute myocarditis had progressive failure that led to death or the need for a heart transplant. Chronic myocarditis can be defined as persistent (lasting >3 months), recurrent, and latent.²³

Diagnosing myocarditis in children can be challenging. Not only can children have a wide range of nonspecific signs and symptoms, but depending on cognitive development, they may not be able to communicate their symptoms. Despite a variety of invasive and noninvasive studies, myocarditis is a presumptive diagnosis based on history and clinical features.^5,8

	History

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Clinical features of viral myocarditis are affected by age, sex, and the child’s baseline health status. These variables affect the balance between pathogen clearance and degree of inflammation.^3,11,12 Older children may have a history of upper respiratory infection; infants may have anorexia, vomiting, and lethargy.¹² Often, signs and symptoms are nonspecific or may resemble the signs and symptoms of relatively common diagnoses in children, including bronchiolitis, pneumonia, failure to thrive, and gastroenteritis.^5,9

Both cases described earlier had the potentially insidious manifestations of viral myocarditis. In the first case, the signs and symptoms suggested benign gastroenteritis with slight dehydration, a situation that is not unusual in toddlers and pre-school children. K.M., who had a history of gastroenteritis, also had syncope, wheezing, and increased work of breathing. His history of asthma confounded his clinical features. Consequently, he initially received treatment for an exacerbation of asthma.

Older children may have chest pain (the sole symptom in some patients).²⁴ Some have abdominal pain. Atypical manifestations such as syncope (K.M.), seizures, and sudden death also have been reported.^2,6 A more focused cardiac examination when no signs of congestive heart failure occur may be prompted by patients’ reports of chest pain, dyspnea, exercise intolerance, or fatigue. Tachycardia of unknown origin in an otherwise healthy child may be an ominous sign. Newborns and infants, unlike older children, are more likely to have circulatory shock.¹²

When myocarditis is suspected, a thorough history is imperative for identifying possible causes. Parents should be asked about exposures to potential infectious agents, pharmacological agents that can cause myocardial inflammation, and toxins, including illicit drugs (eg, cocaine). Immunization status should be obtained because several infectious diseases of childhood (diphtheria, poliomyelitis) are potential causes.

	Physical Examination

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During episodes of cardiac compromise, neurohormonal responses activate the sympathetic nervous system and the renin-angiotensin-aldosterone system, resulting in improved contractility, increase in heart rate, vasoconstriction, and fluid and sodium retention. Tachycardia out of proportion for age is common in children with myocardial compromise as the heart attempts to compensate for inadequate oxygen delivery to the tissues. Vasoconstriction occurs to improve preload and maintain blood pressure. This decrease in peripheral perfusion is manifested as cool extremities, described by level of coolness (eg, cool to midcalf, cool to knee), quality of pulses, capillary refill time (compromise considered at >3 seconds with the extremity at the level of the heart), decreased urine output (<1 mL/kg per hour), and changes in mental status.^25,26 Pulse quality is characterized by using the 0 to 4 pulse intensity scale (0 = no pulses detected, 4 = bounding).²⁶ Extremities may appear mottled or pale. Despite these alterations in perfusion, it must be emphasized that vasoconstriction in children will maintain a blood pressure within a normal range for age even when tissue perfusion is inadequate. Hypotension is considered not only a late finding of cardiac failure but also an ominous one.²⁷

Often, an S₃ (ventricular gallop) occurs because of rapid filling of a non-compliant, poorly contracting left ventricle. Murmurs are less common, although a soft systolic murmur may be heard if mitral or tricuspid insufficiency is present.¹² Heart sounds may be muffled if concomitant pericarditis is present.¹¹ Rhythm irregularities may be detected, especially supraventricular tachycardia or ventricular ectopic beats as with K.M.

Tachypnea is a common sign of myocardial failure in children. Tachypnea is the result of pulmonary edema due to left ventricular failure.²⁶ Clinical findings can include wheezing, a cough, grunting, nasal flaring, and intercostal retraction. Older children may report orthopnea or inability to catch their breath. Cyanosis is rare. Rales are typically a late sign of pulmonary congestion and may not occur at all in infants.²⁶

Hepatomegaly, an indication of venous congestion, may or may not occur. Liver tenderness or absence of a firm edge on palpation below the right costal margin may indicate liver engorgement. Clinical findings of viral myocarditis are summarized in Table 2.

	Diagnostic Evaluation

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	Chest Radiography

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	Electrocardiography

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Although not diagnostic, findings on an electrocardiogram are rarely normal in patients with myocarditis.^5,12 Some children have such mild illness that a conduction disturbance on an electrocardiogram is the only abnormal finding.¹¹ Sinus tachycardia is a common finding with myocarditis.¹² Low-voltage QRS complexes, ST-T wave abnormalities, or prolonged QT interval may be apparent.^5,11,12 Left ventricular hypertrophy with repolarization changes (strain) is typical. Complete atrioventricular block has also been described.^9,11 Occasionally, evidence of myocardial infarction is seen.¹²

	Echocardiography

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Findings on echocardiograms are rarely normal in patients with myocarditis. As with K.M., impaired left ventricular function with dilatation of 1 or more chambers is typical. K.M.’s echocardiogram showed poor left ventricular systolic function, with dilatation and slightly diminished right ventricular function. In the absence of any structural abnormalities, these findings help establish the diagnosis.^11,12 Generally, right ventricular function is less compromised than is left ventricular function; atrioventricular valve regurgitation may occur. Occasionally, left ventricular thrombi are found.¹²

	Laboratory Studies

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Historically, despite its limited sensitivity and specificity and its inherent risks, endomyocardial biopsy has been the reference standard for diagnosing viral myocarditis.^2,15,20 Nevertheless, for several reasons, endomyocardial biopsy is used less often in children than in adults.⁹ First, biopsy can be associated with significant sampling error.^24,28 Several tissue specimens (5 or more) are needed because of the focal nature of the disease; many clinicians think that biopsy leads to underestimation of the presence of the disease.^24,28 Second, borderline myocarditis can result in little to no evidence of myocyte destruction.¹ Third, expert interpretation can vary, including variance with other markers of viral infection.^2,8,24,28 Because of the possibility of false-negative results, lack of an endomyocardial biopsy positive for myocarditis does not rule out this disease.

For K.M., findings on endomyocardial biopsy on hospital day 8 confirmed the diagnosis. Tissue specimens from the right ventricle had intact myocytes with small foci of lymphocytic infiltrates and extensive areas of myocyte destruction with organizing fibrosis and infiltrates of inflammatory cells most consistent with myocarditis.

Recently, use of less invasive means of diagnosing myocarditis in children has been emphasized.² Use of polymerase chain reaction (PCR) and in situ hybridization has increased the sensitivity for diagnosing viral myocarditis.^3,5,13,19,29 Tracheal aspirates for PCR analysis in intubated children are useful for detecting viral genomes in children with or without myocarditis. Akhtar et al³⁰ reported that PCR of tracheal aspirates had a sensitivity of 100% for predicting the results of PCR of endomyocardial biopsy specimens, albeit for a small (n = 10) sample size. Although a tracheal aspirate positive for virus is not diagnostic for myocarditis itself, PCR of tracheal aspirates may provide a safer means of identifying a viral cause for illness in children with cardiac decompensation of unknown origin.³⁰

Serological studies may reveal an elevation in myocardial enzyme levels (creatine kinase, normal value 25–190 IU/L [to convert to microkatals, multiply by 0.0167]; MB isoenzyme of creatine kinase, normal value <12% of creatine kinase).¹² In children, the level of cardiac troponin T is a more sensitive indicator of myocardial damage than are myocardial enzyme levels.^5,12,26 In healthy children, cardiac troponin levels are typically less than the detection level (<0.02 ng/mL). Lauer et al³¹ reported that 35% of patients with suspected myocarditis also had elevated levels of cardiac troponin; among those, 98% had viral myocarditis confirmed histologically.

Other nonspecific laboratory studies may aid in the diagnosis of viral myocarditis. Elevations in sedimentation rate (>20 mm/h) and level of C-reactive protein (>0.05 mg/dL; to convert to nanomoles per liter, multiply by 9.524) may occur. A normal sedimentation rate, however, does not rule out myocarditis. Viral studies may reveal enteroviral or adenoviral antibodies, Esptein-Barr virus, cytomegalovirus, or a 4-fold increase in the level of immunoglobulin G but do not definitively establish causation.^3,5,20 Levels of immunoglobulin G antibodies to Epstein-Barr virus nuclear antigen were elevated in K.M. PCR may also be used to detect viral genomes.

Elevation in white blood cell count with predominance of lymphocytes may suggest viral causes of myocarditis. Cultures of blood, stool, cerebrospinal fluid, or nasopharyngeal secretions are less specific than cultures of tracheal aspirates; Martin et al¹³ found that cultures showed growth in only 27% of children with viral myocarditis.

	Critical Care Management

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Care of children with clinical features consistent with myocarditis depends on the severity of myocardial dysfunction. Management is designed around supportive measures rather than being aimed at a causative agent. Maintenance of cardiac output with aggressive support of cardiac function is essential. Such support includes initiation and monitoring of inotropic therapy, afterload reduction, arrhythmia management, and adequate tissue oxygenation. Respiratory support may require intubation and mechanical ventilation. Fluid management may include both administration of fluid boluses and diuretic therapy. Monitoring of and interventions to prevent complications should be ongoing.

	Inotropic Support

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When cardiac output is inadequate, a rapid acting inotropic agent is administered.^11,12,26 Inotropic agents are administered cautiously because the myocardium is irritable and use of inotropic agents can instigate and/or worsen arrhythmias. One inotropic agent or a combination of such agents, including dopamine, dobutamine, and milrinone, can be administered (Table 4).

Dopamine has both inotropic and vasopressor properties and is useful in patients who are in shock with cardiac dysfunction and associated mild to moderate hypotension. Dopamine is not routinely used to tidal volume (pressure ventilation), a decrease in oxygen saturation, and asymmetric chest rise. If the tube migrates into the right main bronchus, the child should immediately be placed back in the previous position and reassessed. Breath sounds should be assessed after any change in body position.

Neck extension increases airway length, potentially causing unintentional extubation because the uncuffed tube can easily pass upward through the vocal cords. Immediate respiratory distress, decrease in oxygen saturation, marked decrease in or undetectable end-tidal carbon dioxide levels, grunting, or vocalization can indicate possible inadvertent extubation. If dislodgement of the endotracheal tube into the esophagus is suspected, the tube should be removed and bag-valve-mask ventilation performed until reintubation or effective spontaneous breathing occurs.

Although a common practice in intensive care units, endotracheal suctioning should not be performed routinely.⁴⁴ Suctioning can be associated with complications, including hypoxemia, bradycardia, atelectasis, and dysrhythmias. Suctioning should be done on an as-needed basis rather than routinely. Indications for suctioning include increase in airway pressure, decrease in tidal volume, decrease in oxygen saturation, visualization of secretions in the tube, development of rhonchi, and coughing. Hyperoxygenation may or may not be required before suctioning, depending on the child’s arterial oxygenation and tolerance to the procedure. The catheter should not be deeper than the end of the endotracheal tube. Catheters inserted to the point of resistance (carina) cause tissue inflammation and damage.⁴⁵ Instillation of normal saline for lavage should be avoided because that practice is not supported by research and may actually be harmful.^44,45

Routine bedside nursing interventions such as dressing changes, bathing, weighing, and repositioning all significantly increase tissue oxygen consumption. Delay in carrying out these procedures may be necessary. Conversely, some or all of these activities may be clustered if tolerated in order to allow longer periods of rest.

Fever increases oxygen consumption 10% for each 1°C elevation in body temperature. Although not all fever is "bad," treatment of fever is recommended in children with cardiopulmonary disease. Attempts should be made to maintain normothermia.²⁶ Unless contraindicated, antipyretics (acetaminophen, ibuprofen) should be administered. Fever reduction can also be attempted with external cooling, usually by sponging with tepid water.

Pain and anxiety significantly increase oxygen demand and consumption and cause considerable distress for children in the PICU. Assessment and management of pain and anxiety should be ongoing.

	Arrhythmias

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Heart rate and rhythm require monitoring. Arrhythmias are a significant life-threatening complication of myocarditis.²⁴ Development of bradycardia or tachyarrhythmias is unlikely to be tolerated and requires immediate recognition and treatment.

Infants and small children depend on heart rate for adequate cardiac output because stroke volume is relatively fixed; in young children, bradycardia can rapidly diminish cardiac output. Because chronotropic drugs can induce ventricular tachycardia in patients with viral myocarditis, cardiac pacing is the preferred treatment for life-threatening bradyarrhythmias, including atrioventricular block.²⁵

Transcutaneous or transthoracic pacing is a noninvasive procedure that can be done rapidly. Two electrodes are placed on the patient with the anterior electrode in the V₂ to V₅ position and the posterior electrode under the scapula to the left of the spine. Electrode adherence should be checked frequently, especially if the child is diaphoretic. If needed for prolonged periods, electrodes should be changed a minimum of every 24 hours to maintain effectiveness of the contact gel.

For ongoing bradyarrhythmias, invasive pacing should be considered. Transvenous leads are placed percutaneously via a large vessel into the right atrium or ventricle. Leads are stiff; nurses must be alert for indications of ventricular perforation, including cardiac tamponade. An extra battery should be kept at the bedside of any patient who is pacemaker dependent. Hospital policy should be followed when caring for the insertion site and catheter.

Sidebar As a general rule, for children more than 1 year old, estimated systolic blood pressure norms can be calculated as follows:

 

Conversely, an excessively rapid heart rate will decrease ventricular filling time, resulting in inadequate preload and subsequent cardiac output. Tachycardias also result in inadequate coronary artery filling time. Coronary arteries fill and perfuse the myocardium during diastole; the faster the heart rate, the shorter is diastole, leading to a decrease in myocardial oxygen supply during a time of increasing consumption.

Differentiation between sinus tachycardia and supraventricular tachycardia is critical. Typically, sinus tachycardia is heart rate greater than 140/min in children, greater than 160/min in infants, and varies from beat to beat. Heart rate generally remains less than 200/min. Sinus tachycardia can be the result of a variety of factors, including fear, anxiety, fever, pain, intravascular dehydration, and marked vasodilatation. Sinus tachycardia will resolve, or partially resolve, with resolution of the inciting factor.

Supraventricular tachycardia is an extremely rapid heart rate (200–280/min); is unresponsive to resolution of fever, pain, hypovolemia, and so on; and has no beat-to-beat variability. Rates of sinus tachycardia and supraventricular tachycardia can overlap, making determination of the type of tachycardia difficult. A 12-lead electrocardiogram may be necessary to differentiate between the two. Once supraventricular tachycardia has been established, rapid treatment with adenosine in the patients with stable hemodynamic status or cardioversion in patients with unstable hemodynamic status is performed. A defibrillator should remain near any child who has myocarditis or recurring supraventricular tachycardia.

	Hemodynamic Monitoring

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With invasive hemodynamic monitoring, physiological variables specific to cardiovascular function can be monitored and, when coupled with clinical examination, the results provide data for sound clinical decision making.

Arterial Pressure.
Continuous blood pressure monitoring via an arterial catheter is preferred in children with severe cardiac dysfunction, particularly those who require infusions of vasoactive agents. Non-invasive measurements may be inaccurate or impossible to obtain because of impaired peripheral perfusion and vasoconstriction. Arterial catheters can be placed peripherally (radial artery) or centrally (femoral artery) and provide a dynamic picture of systolic, diastolic, and mean blood pressures. Because evaluations of interventions and their effectiveness will be based partly on invasive measurement of blood pressure, care must be taken to ensure accuracy of readings. Routinely inspecting for proper transducer placement (phlebostatic axis), zeroing the transducer a minimum of once a shift, inspecting for and eliminating air bubbles in the system, and using noncompliant pressure tubing will help ensure accurate measurements.

Normal blood pressure in children is dependent on age and size²⁷ (see Sidebar). As previously noted, however, children with myocarditis can maintain a blood pressure within normal limits for age until very late in the disease. No single clinical parameter should determine critical care interventions, and this rule is particularly true for blood pressure, unless hypotension is present. Adequacy of tissue perfusion is determined by analysis of clinical findings on bedside examination along with blood pressure.

The extremity distal to the arterial catheter should be assessed at least once a shift to monitor for any compromise in perfusion related to catheter placement. Extremity coolness, color changes, delayed capillary refill, and diminishing pulse quality can indicate inadequate perfusion. Numbness, tingling, and motor deficit can also be indicators of impaired circulation. Development or change in any one or more of these variables requires immediate attention and potentially removal of the catheter.

Central Venous Pressure.
Central venous pressure (CVP) or right atrial monitoring provides a continual reflection of intravascular volume status and is a good determinant of right ventricular end-diastolic volume, or preload. CVP should be interpreted along with other measures of cardiac function (heart rate, peripheral perfusion, urine output). In critically ill children, the absolute value is not as important as serial measurements and changes in response to interventions.

CVP monitoring should be done via the distal lumen of the catheter. Monitoring can be continual or intermittent, depending on availability of intravenous access. If the distal lumen is being used for continuous intravenous administration of fluids and/or drugs, CVP should be assessed a minimum of once an hour and after any administration of fluid boluses or diuresis. When intermittent CVP monitoring is used, care must be taken to ensure that no cardiotonic medications are infused through the distal port. If such infusions are used, turning the stopcock for pressure readings causes a disruption in the delivery of medication and potential hemodynamic compromise. Ideally, infusions of inotropic or vasoactive agents should be given through the medial or proximal lumen only.

Normal CVP values can vary widely in infants and children, depending on age, disease, concomitant conditions, and critical care therapies. In healthy infants, normal values can range from –2 to +4 mm Hg, from 4 to 8 mm Hg in those with congenital heart disease, and from 2 to 6 mm Hg in those with respiratory disease requiring mechanical ventilation. In this age group, measurements above 8 mm Hg are generally indicative of myocardial dysfunction or high intrathoracic pressure.⁴⁶ In older children without underlying disease, a CVP range of 2 to 6 mm Hg is considered normal. Values can vary markedly and should be interpreted along with the child’s underlying disease state, concomitant conditions, and critical care therapies.

CVP measurements do not stand alone and must be considered in context of the entire clinical picture. Any changes in intrathoracic pressure will affect CVP values; spontaneous respirations decrease CVP, whereas increased intrathoracic pressure increases CVP. Values lower than expected may or may not indicate hypovolemia; high CVP values may or may not indicate hypervolemia. Elevated CVP values may also occur in patients receiving positive pressure ventilation and with the addition of positive end-expiratory pressure. Conditions that increase pulmonary vascular resistance (hypothermia, hypoxemia, acidosis, severe respiratory disease, underlying pulmonary hypertension) also increase CVP. High CVP values do not necessarily reflect cardiac disease but may be an indication of elevated right ventricular end-diastolic pressure, suggesting right ventricular dysfunction.²⁶ Variables that affect interpretation of CVP values must be considered when therapies are determined.

Complications of central venous catheters include bloodstream infection (increased risk with multilumen catheters), venous thrombosis, thrombophlebitis, and catheter occlusion. Routine maintenance of the catheter and insertion site should be done per hospital policy.

Pulmonary Artery Pressure.
Pulmonary artery catheters can provide valuable information in children with cardiopulmonary failure. The ability to measure pulmonary artery pressures, cardiac output/index, and systemic and pulmonary vascular resistance can provide important data for directing therapies. However, because of potential complications, pulmonary artery catheters tend to be used less often in children than in adults. Pulmonary artery catheters are therefore indicated only when the additional data obtained will enhance clinical decision making.²⁶

	Comfort

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Several pain intensity scales for children are available; determining which scale to use is based on the child’s age and/or ability to communicate. Self-reporting scales can be used with children who are able to express their level of pain. The faces scale is a visual scale that provides facial expressions varying from no pain (smiling) to worst pain (deep frown, crying). The child is asked to choose the facial expression that best reflects his or her pain. The pain intensity scale is a numerical scale from 1 to 10, with 1 = no pain and 10 = severe pain. It is used with older children who understand the concept of rank and order. For infants, scales designed for assessment of postoperative pain are available; these scales may or may not provide adequate assessment of other types of pain; thus subjective assessment by nurses within the context of the clinical situation is critical.

In children who are unconscious, are sedated, or require mechanical ventilation, observational scales are used. Unfortunately, these tools are not effective for assessing pain in children with chemically induced paralysis because the tools require scoring of alertness and physical movement. For children with neuro-muscular blockade, bedside nurses must maintain a keen sense of awareness as to whether, given the severity of illness and the treatments in use, it is reasonable to expect that a child is experiencing pain and, if so, to treat the child accordingly.

For severe pain, opioids (morphine, fentanyl, dilaudid) remain the most commonly used class of analgesics. Children receiving opioids should be monitored not only for effectiveness of therapy but also for respiratory depression, particularly if they are dependent on spontaneous breathing, with or without mechanical ventilation. Hypotension can also occur after administration of opioids. Dosing can be adjusted accordingly, or regimens can be revised to minimize side effects. Acetaminophen, ketorolac, and ibuprofen (if not contraindicated) can be used for mild to moderate pain or as adjunct therapy in addition to opioids.

Anxiety in children is often expressed as agitation. Assessing agitation can be especially challenging. Agitation is a means of communicating physical and/or mental discomfort; many children in the PICU cannot communicate their needs. Nurses must systematically review and rule out any internal, external, or environmental factors that may be causing or contributing to agitation.

Anxiety and/or distress not relieved with comfort measures (repositioning the child, having a parent at the bedside, or quieting the environment) are typically treated with sedatives and anxiolytics (lorazepam, midazolam). These medications alleviate agitation and can provide tolerance of invasive procedures and intensive care therapies. Additionally, these medications provide a lack of awareness, and subsequent memory, of what can be an extremely frightening experience.

The need for chemically induced paralysis must be assessed on an individual basis. Although some children maintain ventilator synchrony with sedation and analgesia alone, others may require neuromuscular blockade to achieve synchrony. Neuromuscular blocking agents can be given intermittently or as a continuous infusion. Before a chemical paralytic agent is administered, patency of the airway and adequacy of sedation and analgesia must be established. Neuromuscular blockade should never be used without concomitant administration of an opioid and/or an anxiolytic, whether the paralytic agent is given as a one-time dose or as a continuous infusion. Train-of-4 monitoring should be routinely assessed for all children receiving continuous infusions of chemical paralytics, and dosing should be titrated to the ordered level of neuromuscular blockade.

	Acquired Infection

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Hospital-acquired infections are a constant threat for any critically ill child in the PICU. Acquired nosocomial infection coupled with extreme severity of illness in a child with myocarditis significantly increases morbidity and mortality. Nurses’ diligence in preventing and monitoring for infection is essential.

Within hours of admission, hospital-associated bacteria can be detected on skin and in the respiratory and genitourinary tracts.⁴⁵ Invasive devices, antibiotic use, and/or critical care procedures increase the risk of bacterial invasion. Some of the highest rates of hospital-acquired infection occur in PICUs; bloodstream infection and ventilator-associated pneumonia are the most common.⁴⁵

Fever is often the first sign of infection in children; however, infants often have decreases in body temperature because of the immaturity of the brain’s temperature-regulating center. Monitoring of temperature changes in this age group can be complicated by the use of radiant warmers, designed to maintain normothermia. Radiant warmer temperature is adjusted according to an infant’s skin temperature; consequently, decreases in body temperature related to infection may be masked. Although skin temperature is continuously monitored in infants under a radiant warmer, core body temperature should be monitored a minimum of once an hour, if not continuously, in all age groups.

White blood cell count with a differential count should be assessed closely. Leukocytosis (elevation) or leukopenia (decrease) develop in children with infection, depending on age. A normal total white blood cell count is 5000 to 10 000 cells/µL but varies depending on the age of the child; the younger the child, the higher the upper range limit. Monitoring trends is as important as getting absolute counts.

The differential count provides the percentage of each subset of white blood cells (eosinophils, neutrophils, basophils, monocytes, and lymphocytes) and can aid in differentiating the type of infection. In older infants and children, a "shift to the left," or an excess of immature neutrophils (bands), usually indicates bacterial infection. An increase in the number or percentage of bands along with fever may warrant further workup (eg, blood cultures for detection of secondary bacterial infection). Coagulase-negative staphylococci are the most common cause of nosocomial bloodstream infections in the PICU.⁴⁵ Unlike older children, young infants commonly have neutropenia when infected because of their small storage pools and inability to produce white blood cells at a fast rate.

Pulmonary secretions should be monitored for changes in viscosity, color, and amount. Changes in the character of the secretions along with evidence of new pulmonary infiltrates may indicate the development of ventilator-associated pneumonia (the second most common hospital-acquired infection in PICUs) in intubated patients.⁴⁵ Although nosocomial urinary tract infections occur less often than do acquired bloodstream or pulmonary infections in children, urine should be routinely examined for color, odor, and changes in opacity, particularly if a child has a urinary catheter in place.

Any invasive catheter is a potential source of infection. Insertion sites should be routinely inspected for edema, redness, and drainage. Although central venous catheters are not routinely changed in children, signs of infection at the site may warrant removal of the catheter. Factors increasing the risk for bloodstream infection include multilumen catheters, repeated catheterizations, and certain types of dressing. In order to minimize risk of infection, catheters should be manipulated as little as possible and should be removed as soon as they are no longer needed.

Immobility and alteration in tissue perfusion increase the potential for skin breakdown. Skin should be kept free from exposure to moisture and secretions; moisture-barrier products can be applied to the perineal area. Application of topical moisturizers, with avoidance of products containing perfume or alcohol, aids in maintaining skin hydration. Mouth care, a minimum of every 8 hours, helps keep oral mucosa clean and moist. In children without a blink response (chemically paralyzed) or with incomplete lid closure, the eyes should be kept moist with artificial tears and/or lubricant as needed. Frequent turning (as tolerated), alleviation of pressure points on bony prominences (use of pillows, stuffed animals), and alternating pressure points related to mechanical devices (oxygen saturation probes, blood pressure cuffs, electrodes) should be performed on a routine basis. Air mattresses or rotating beds can also be used to prevent skin breakdown. Any evidence of altered skin integrity should be immediately addressed.

	Family Support

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As with all children admitted to the PICU, the bedside nurse has an essential role in providing ongoing support and education to the patient’s family. Emergent admission to the PICU creates feelings of overwhelming shock and disbelief associated with helplessness.^47,48 The possibility of death is real and frightening. Adding to parental stress is alteration in the parental role, that is, loss of control and/or ability to care for their child. Alteration in parenting and disruption of the parent-child relationship are deemed the most stressful characteristics of a PICU admission.⁴⁷

Use of the Nursing Mutual Participation Model of Care can help nurture a trusting environment, establish effective communication patterns, and limit parental powerlessness.⁴⁶ This model of nursing care focuses on the individuality of parental stress, recognizing that nurses’ perception of parental stress and actual parental stress may differ greatly. Nursing interventions to alleviate stress must be individualized to each family and, indeed, to individuals within the family. Generic interventions, although well intended, may not be helpful. Identification of individual coping mechanisms and appropriate nursing interventions are critical to enabling parental adjustment to the PICU.⁴⁷

The Nursing Mutual Participation Model of Care also recognizes and supports the value of parenting, parent-child connectedness, and the development of nurse-parent partnerships in caring for a critically ill child. Nurse-parent partnerships develop as nurses empower parents to maintain the parental role to the fullest extent possible during a child’s critical care course. Such empowerment is done in many ways, including (1) providing concise, consistent information that enables parents to participate in decision making and daily goal setting; (2) role modeling activities traditionally done by nurses but that parents can participate in or lead; (3) providing anticipatory guidance to aid parents in distinguishing what is "expected" from what is "unexpected" during the PICU course; and (4) providing options (step out or stay) during procedures and treatments. Parents of a critically ill child are still parents; providing care supportive to their individual needs and enabling parenting activities will establish a therapeutic nurse-parent relationship, in the hope of making the experience as a parent of a critically ill child as positive an experience as possible.⁴⁷

	Prognosis

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The survival rate in children and adults with myocarditis is approximately 80%.⁴⁶ Lee et al¹⁰ found that patients who died almost always did so within the first few hospital days. Survival after 72 hours in patients not requiring ECMO is as high as 97%.¹⁰ Some centers have had a 1-year survival rate of 80% in children who required mechanical circulatory support.²

Unfortunately, survival to discharge does not imply full recovery. Although Lee et al found that recovery of ventricular function without the need for ongoing cardiac medications or restrictions in physical activity was the norm, some evidence suggests that myocarditis can progress to dilated cardiomyopathy.¹⁰ Viral persistence in the myocardium has been associated with progressive impairment of left ventricular function and is predictive of adverse outcomes.^9,49 Progression from myocarditis to dilated cardiomyopathy is further supported by the finding of a coxsackievirus B–adenovirus receptor gene present in larger amounts in the myocardium of patients with dilated cardiomyopathy than in healthy hearts.⁵⁰ The discovery of this receptor also suggests a role in not only the viral origin of myocarditis but also the occasional "familial" case of myocarditis.¹⁵ Survival in children with dilated cardiomyopathy ranges from 60% to 70% at 1 year to 34% to 56% at 5 years. Gagliardi et al³⁶ reported that in children with dilated cardiomyopathy, the first 2 years after diagnosis are the most crucial.³⁶ Favorable events (nearly complete recovery) and worse outcomes (death or need for a transplant) occur during this period.

For children with residual myocardial dysfunction at discharge, diuretics and afterload reducers are considered first-line agents. Diuretics are used for congestive heart failure of any cause because they reduce respiratory signs and symptoms associated with heart failure.³³ Thiazides (diuril, hydrochlorothiazide) are often used; the addition of spironolactone may obviate potassium supplementation. Angiotensin-converting enzyme inhibitors (captopril and enalapril) may also improve chronic signs and symptoms²⁴ (Table 8).

Beta-blockade may improve outcome in children with dilated cardiomyopathy. Carvedilol, a non-selective β-blocker used in adults, has been examined as an adjunct therapy for management of heart failure in children. Carvedilol may improve congestive heart failure through several mechanisms, including decreased heart rate leading to improved myocardial oxygen consumption and enhanced coronary artery blood flow, improvement in left ventricular ejection fraction, and reduction in neurohormonal vasoconstrictor systems. Carvedilol may also prevent ventricular arrhythmias and sudden death.

Use of carvedilol in children remains controversial. Bruns et al⁵¹ studied the use of carvedilol in 46 children with heart failure in 6 different centers and found improvement in left ventricular function and overall signs and symptoms in 67%. Schwartz and Wessel³³ also examined use of carvedilol in children with heart failure and found no statistically significant effect; left ventricular ejection fraction improved in both the carvedilol and the placebo groups. Although carvedilol is effective in reducing mortality in adults, more research into the use of carvedilol is needed in children with heart failure.

Transplantation is sometimes the only option for children with significant cardiac failure or dilated cardiomyopathy due to myocarditis. Preferably, children are not put on a list for transplantation until they have progressed to the chronic phase of the disease, because recovery is possible in even the most severe cases.² Transplantation may, however, be considered an option for a child who requires ECMO for more than 10 days and has no clinical signs of improvement.³⁸

	Conclusion

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Viral myocarditis remains an uncommon but challenging illness. In children, the initial signs and symptoms are often those of common pediatric illnesses and without any obvious cardiac signs. Adding to the challenge is the potential inability of the child to convey precise symptoms or describe location or intensity of pain or discomfort. A history of asthma or congenital heart disease can skew the clinical picture. Although few children actually have viral myocarditis diagnosed and require admission to the PICU, practitioners must maintain a heightened sense of awareness for the "zebra in the herd of horses." Concomitantly, for any previously healthy child with sudden cardiogenic shock, myocarditis must be included in the differential diagnosis.

Most children with myocarditis recover without requiring admission to the PICU; only a small percentage progress to development of significant cardiopulmonary compromise that requires intensive cardiopulmonary support and monitoring. Critical care management is aimed at supportive rather than curative measures and depends on the severity of myocardial dysfunction. The most common techniques used in the PICU for children with cardiovascular compromise or collapse include invasive hemodynamic monitoring, infusions of inotropic agents, antiarrhythmics, afterload reducers, mechanical ventilation, prevention of complications, and, when a child is unresponsive to ordinary PICU therapies, extracorporeal life support.

	References

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