CME REVIEW ARTICLE

Myocarditis Mark A. Pettit, MD,* Alex Koyfman, MD,† and Mark Foran, MD‡ Abstract: Myocarditis is an inflammatory disease of the heart that can cause devastating disease in otherwise healthy children. Inciting agents such as viral infection cause direct damage to the myocardial cells, which triggers an inflammatory response that enhances myocardial toxicity and associated morbidity. Severe cases typically present with respiratory distress and cardiovascular collapse, whereas subclinical cases are unnoticed by the medical community. The initial workup in suspected cases should include an electrocardiogram, chest radiograph, and cardiac troponin T. Treatment is concentrated on hemodynamic stabilization with optimization of heart failure management, dysrhythmia protocol, and supportive therapy. The purpose of this review was to provide the emergency medicine practitioner a concise and current review of the basic pathophysiology as well as a functional and evidence-based approach to the diagnosis and treatment of myocarditis in the pediatric population. Key Words: myocarditis, heart failure, dysrhythmia, cardiac, acute (Pediatr Emer Care 2014;30: 832–838)

shock leading to death. The true incidence of the disease is not known, partly owing to the lack of a readily available sensitive and specific diagnostic test. Consequently, epidemiologic figures are largely derived from pediatric autopsy studies. Weber et al3 revealed histologically confirmed myocarditis in almost 2% of all pediatric deaths at autopsy in a retrospective review at a British tertiary center. The findings in cases of sudden pediatric deaths are even more staggering: Neuspiel and Kuller4 demonstrated evidence of myocarditis in 27% of infants and children who died suddenly in nontraumatic situations. Early recognition of the clinical features and a high level of suspicion are required to make the appropriate diagnostic and management decisions. With supportive therapy and cardiovascular stabilization, generally favorable outcomes can be expected even in the most severe cases.1 After this activity, the reader will be able to understand the basic mechanisms of the pathophysiology of myocarditis, characterize the clinical features of myocarditis, and manage pediatric patients diagnosed with myocarditis.

TARGET AUDIENCE This CME activity is intended for pediatric emergency medicine practitioners.

LEARNING OBJECTIVES After completion of this CME article, the reader should be better able to: 1. Describe the pathophysiology of myocarditis. 2. Identify the clinical features consistent with the diagnosis of myocarditis. 3. Initiate or take part in the management of critically ill patients with myocarditis. Myocarditis is characterized by inflammation of the myocardium that causes cardiac dysfunction. It is a rare yet underrecognized disease, despite the fact that it contributes significantly to the morbidity and mortality of pediatric populations.1 Because of the eclectic assortment of causative agents and host immune factors, patients may present clinically at many different points on the disease spectrum.2 On one end of the continuum, subclinical cases often self-resolve and go unnoticed by the medical community, whereas fulminant myocarditis can present with cardiogenic Emergency Medicine Resident Physician (Pettit), *Department of Emergency Medicine, Christiana Care Health System, Newark, DE; Emergency Medicine Attending Physician, Assistant Professor of Emergency Medicine (Koyfman), †Division of Emergency Medicine, University of Illinois College of Medicine at Peoria, OSF Saint Francis Medical Center, Peoria, IL; and Emergency Medicine Attending Physician, Assistant Professor of Emergency Medicine (Foran), ‡Department of Emergency Medicine, NYU School of Medicine, Bellevue Hospital Center, New York, NY. The authors and staff in a position to control the content of this CME activity and their spouses/life partners (if any) have disclosed that they have no financial relationships with, or financial interest in, any commercial organizations pertaining to this educational activity. Disclosure: The authors declare no conflict of interest. Reprints: Alex Koyfman, MD, Department of Emergency Medicine, 5323 Harry Hines Blvd, MC 8579 Dallas, TX 75390-8579 (e‐mail: [email protected]). Copyright © 2014 by Lippincott Williams & Wilkins ISSN: 0749-5161

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PATHOPHYSIOLOGY There has been a considerable number of inciting agents implicated in the development of myocarditis, including infection, cardiotoxins, drug hypersensitivity, and rheumatologic disease.2 Viral infection is believed to be the most prevalent cause of myocarditis in the pediatric population, although specific epidemiologic data are lacking. In an analysis of 50 pediatric endomyocardial biopsies with the diagnosis of myocarditis, findings of polymerase chain reaction testing were positive in 40% of the samples, with enterovirus, adenovirus, and parvovirus being the most commonly amplified, followed by Epstein-Barr virus and influenza.5 Because of the complications associated with endomyocardial biopsy, serologic testing and polymerase chain reaction of blood samples have been used as a surrogate detection strategy for viral agents.6,7 Bacterial, fungal, and parasitic infections have also been described in the literature, although they are much less common.4 Researchers have illustrated the pathogenesis of viral myocarditis in 3 separate phases using murine models: acute, subacute, and chronic. Once the virus infects a susceptible host, the first step in the acute phase is entry into the myocardial cells, accomplished via surface receptors and coreceptors such as a common receptor for Coxsackie B and adenovirus types 2 and 5.8 Upon entry, myocyte injury may occur as a result of direct viral damage via inflammation and necrosis. This is exemplified by the discovery that certain enteroviruses can cleave dystrophin with viral protease 2A, predictably causing deleterious effects on the cardiac myocytes.9 Ushering in the subacute phase, host inflammatory factors and mediators are activated both directly and indirectly by the virus such as with the Coxsackie B virus, which directly upregulates toll-like receptor 4 on mast cells, activates macrophages, and induces cytokine production.10 The combined effects of direct viral damage, apoptosis, cytokine production, and induction of cytotoxic T cells cause myocyte destruction. The peak in severity occurs approximately 7 to 14 days after initial infection, which explains why many patients may present with a viral prodrome weeks or even months before becoming clinically symptomatic.10 Finally, in the chronic phase, the host's immune system is exposed to the previously intracellular viral antigens, facilitating antibody Pediatric Emergency Care • Volume 30, Number 11, November 2014

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production. Although the host's immune response serves to clear the virus, certain viruses also share epitopes with the myosin protein of cardiac myocytes, causing cross-reactivity.11 This molecular mimicry, in addition to the persistence of cytokines in the chronic phase, may produce ongoing myocyte damage and a negative inotropic effect on the heart. Because of the variability of direct myocyte damage in the acute phase and the host immune response in the subacute and chronic phases, the severity and longevity of cardiac dysfunction and, thus, clinical presentation are similarly variable. Although this concise discussion of viral pathogenesis is not representative of all the mechanisms of various etiologies of myocarditis, it does provide a general overview for the clinician.

Myocarditis

DIAGNOSIS

There are no pathognomonic findings on an electrocardiogram of a patient with myocarditis, although it is rare to be read as normal. In the sample of Durani et al,12 100% of patients had an abnormal electrocardiographic result, with the most common abnormality being sinus tachycardia. Dysrhythmias seen in myocarditis include supraventricular and ventricular tachycardia; conduction abnormalities include atrioventricular or intraventricular blocks.17 Pseudoinfarct patterns with ST segment elevation/depression, Twave inversion, or Q waves have also been described, prompting an acute coronary syndrome workup in selected cases.17 Laboratory studies have variable utility in the diagnostic workup of myocarditis. Inflammatory markers such as complete blood count, c-reactive protein, and erythrocyte sedimentation rate may suggest an inflammatory process but are generally considered unhelpful owing to their poor specificity.12 Microbiologic culture data may identify the specific causative pathogen from blood, respiratory, urinary, and rectal cultures, although the causative agent is unrecognized in the majority of cases. Cardiac enzymes, which become elevated secondary to the necrosis of the myocardial cells, are considered to be the most useful of the laboratory studies in the initial workup. A recent retrospective review by Eisenberg et al18 found that, at a cutoff of 0.01 ng/mL, cardiac troponin T had a sensitivity of 100% and a specificity of 85% with a negative predictive value of 100% for the diagnosis of myocarditis in children with no prior cardiac disease. On the basis of these findings, a cardiac troponin T of less than 0.01 ng/mL in a child without preexisting cardiac disease rules out the diagnosis of myocarditis. Imaging modalities such as radiographs, echocardiography, and cardiac magnetic resonance imaging (MRI) can help to further focus the differential in the diagnostic workup. An abnormal finding of chest radiograph was found in as many as 90% of cases, with cardiomegaly and pulmonary edema as the most common findings.12 Echocardiographic result, which was abnormal in 98% of patients, may identify wall motion or valvular abnormalities, lending further prognostic data to the physician.12 Although frequently abnormal, neither a chest radiograph nor echocardiography have findings specific for the diagnosis of myocarditis. As a result, cardiac MRI is gaining support as the criterion standard of the future owing to its impressive sensitivity and specificity as well as its ability to assist in localization to optimize endomyocardialbiopsy.19,20 Although the discussed testing modalities have variable findings in myocarditis and only modestly contribute to ruling in the diagnosis, they help to rule out important diseases in the differential. By eliminating diseases such as acute coronary syndrome, structural abnormalities, pneumonia, pulmonary embolism, Kawasaki disease, esophageal rupture, and aortic dissection, the clinician can focus the diagnosis and begin appropriate treatment.

Many still consider the diagnostic criterion standard to be endomyocardial biopsy, which carries the risks for cardiac perforation and valvular damage.15 The procedure has a sensitivity of only 33%, and risks are magnified in pediatric patients because of anatomic characteristics.12 The Dallas Criteria was designed as an identification and classification system for endomyocardial biopsy in the late 1980s, largely relying on inflammatory cell infiltrate and myocardial necrosis as indicators of disease.16 Biopsy remains in use today because it may help to improve the yield of molecular analysis techniques such as polymerase chain reaction. However, recent literature continues to demonstrate its poor utility and predictive value.15 Because of the risks and ambiguous utility of biopsy, considerable emphasis has been placed on less-invasive testing modalities. As a result, diagnosis generally depends on classic clinical findings and supportive noninvasive testing rather than confirmatory biopsy results.

Because of the variable etiology of myocarditis, the formulation of a comprehensive treatment plan to cover the entire spectrum of causative agents is difficult. In addition, the low incidence of clinically symptomatic myocarditis has limited the evidence base for treatments for this condition. Consequently, current treatment recommendations are largely based on clinical experience and consensus opinion rather than empiric evidence. The initial management of myocarditis is centered on supportive therapy and cardiovascular stabilization by treating associated heart failure and dysrhythmias. The severity of symptoms and diagnostic findings dictates the extent of treatment: outpatient follow-up may be preferred in mildly symptomatic cases, whereas transfer to a pediatric intensive care unit may be required for more

CLINICAL FEATURES Myocarditis may present initially with mild prodromal symptoms such as dyspnea, cough, emesis, irritability, poor feeding, diarrhea, myalgias, or fever. A retrospective review of pediatric patients with myocarditis by Durani et al12 grouped presenting symptoms by system with respiratory (32%), cardiac (29%), hypoperfusion/shock (23%), Kawasaki-related (10%), and gastrointestinal (7%) being the most common. Respiratory distress (47%) was the most common presenting symptom in patients younger than 10 years old, whereas chest pain was exceedingly uncommon.12 Cardiovascular symptoms tend to predominate 7 to 14 days after the inception of the prodrome, with the dyspnea, edema, or weakness of heart failure and the palpitations or syncope of dysrhythmias being the most closely associated with admitted pediatric patients found to have myocarditis.13 In the most devastating cases, myocarditis and resulting dysrhythmias have been implicated in sudden death, although the incidence of such cases can only be estimated from autopsy studies.14 Physical examination findings may be similarly variable when compared with historical features, ranging from subtle abnormalities to overt cardiogenic shock. In the same retrospective study, an abnormal respiratory examination with tachypnea, grunting, retractions, or abnormal breath sounds was found to be the most common physical examination finding (68%), followed by tachycardia (58%). Other findings in the pediatric population include lethargy (39%), hepatomegaly (36%), a new murmur or gallop (32%), fever (30%), hypotension (23%), pallor (19%), peripheral edema (16%), and cyanosis/hypoxia (10%).12 With nonspecific historical clues and physical examination findings on presentation, patients are often misdiagnosed initially and require multiple medical contacts for the appropriate diagnosis to be made.

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TREATMENT

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invasive hemodynamic monitoring. When appropriate, medical therapy should be initiated with antiarrhythmics, vasodilators, inotropes, and diuretics in the acute setting with the assistance of a pediatric cardiologist.21 In the subacute setting, providers may opt for angiotensin-converting enzyme inhibitors and cardiac glycosides with caution before initiating anticoagulation and β-blockers after stabilization is achieved.21 If a specific bacterial or fungal pathogen is identified or strongly suspected, antimicrobial therapy should be instituted. In murine models of acute viral myocarditis, non-steroidal anti-inflammatory drugs (NSAIDs) paradoxically increased inflammation and mortality when compared with placebo, although it is difficult to extrapolate these data.22,23 As a result of the animal data, NSAIDs are not recommended in the treatment of severe cases, but they may still play a role in outpatient management. Physical activity should be restricted to prevent further cardiovascular stress, and in cases of continued cardiovascular collapse, mechanical ventilation is preferred to remove the metabolic demands of respiration.24 Because of the demonstrated contribution of the host’s immune system to the pathogenesis of myocarditis, immunomodulating and immunosuppressive therapies have been a targeted area of research. In a small study of pediatric patients with presumed myocarditis, Drucker et al25 demonstrated that patients treated with high dose (2 g/kg) of intravenous immune globulin for 24 hours were more likely to achieve a normal left ventricular ejection fraction at 1 year. In addition, there was a trend toward improved survival, although it was not statistically significant.25 These findings have yet to be replicated in future studies, and further pediatric data are lacking. In the adult population, McNamara et al26 demonstrated that intravenous immune globulin failed to improve left ventricular ejection fraction when compared with controls at 6 and 12 months.25 The literature regarding alternative immunosuppressive regimens is similarly conflicted. Prednisone and either cyclosporine or azathioprine were not statistically different compared with the control group when Mason et al27 analyzed their effect on left ventricular ejection fraction and survival. A number of limitations restrict the applicability of this study, including the small percentage of pediatric patients enrolled, the hard outcomes of ejection fraction and survival, the sparse number of patients presenting with fulminant myocarditis, and the fact that the Dallas Criteria may not appropriately identify patients who would benefit the most from immunosuppression. The best supporting literature can be found in the treatment of giant cell myocarditis, as Cooper et al28 demonstrated that survival in the treatment group was 12.3 months compared with 3 months in the control group. Although small case series have demonstrated histologic and hemodynamic improvement with corticosteroids, azathioprine, and cyclosporine, these findings have not been validated.29,30 In summary, the conflicting literature currently available suggests that therapies targeting the immune system may play a role in treatment, but further research needs to be performed to clarify their utility. If clinical deterioration progresses in the setting of optimal heart failure and arrhythmia management, the literature has demonstrated a role for circulatory support. Left ventricular assist devices, intra-aortic balloon pumps, and extracorporeal membrane oxygenation may be used as a last-resort bridge therapy to resolution or cardiac transplantation.31,32

CONCLUSIONS Myocarditis is a rare but potentially devastating disease that can strike otherwise healthy children. Most pediatric cases of myocarditis are mildly symptomatic or asymptomatic children who may not present clinically. In these instances, without signs

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or symptoms to suggest heart failure, little, if any, workup is required and they may be followed as an outpatient. However, the diagnosis of myocarditis must be considered by the emergency medicine practitioner in any case of suspected or confirmed acute heart failure in the absence of prior cardiac disease, especially if there is an associated history of a viral prodrome. The initial workup should include an electrocardiogram, chest radiograph, and cardiac enzymes, the latter of which may be used to rule out the diagnosis of myocarditis. Echocardiography should be used to evaluate for ventricular function and for other causes of heart failure if the clinical presentation is severe enough to warrant admission. The use of cardiac MRI, endomyocardial biopsy, and molecular techniques is generally limited to refractory cases or research purposes. Initial treatment in the emergency department should be focused on hemodynamic stabilization and supportive therapy. Both NSAIDs and corticosteroids may be considered in stable patients as outpatient therapy, although there is little evidence to support their use. Non-steroidal anti-inflammatory drugs should most likely be avoided in severely ill patients requiring intensive care on the basis of animal model data. Finally, intravenous immunoglobulin should be considered in patients requiring hospital admission, and immunosuppression should be reserved for cases with a confirmed or suspected autoimmune etiology. The ultimate disposition of these patients depends on the overall clinical picture, although those with myocarditis-induced heart failure should be admitted to the intensive care unit for further hemodynamic monitoring. Although recent discoveries have augmented the understanding of the pathophysiology, diagnosis, and treatment of myocarditis, there are many opportunities for advancement. Future research should be aimed at improving diagnostic tools and algorithms, strengthening the evidence base for exiting treatments, and identifying novel therapies that improve outcomes of the disease. REFERENCES 1. Amabile N, Fraisse A, Bouvenot J, et al. Outcome of acute fulminant myocarditis in children. Heart. 2006;92:1269–1273. 2. Cooper L. Myocarditis. N Engl J Med. 2009;360:1526–1538. 3. Weber MA, Ashworth MT, Risdon RA, et al. Clinicopathological features of paediatric deaths due to myocarditis: an autopsy series. Arch Dis Child. 2008;93:594. 4. Neuspiel DR, Kuller LH. Sudden and unexpected natural death in childhood and adolescence. JAMA. 1985;254:1321–1325. 5. Calabrese F, Carturan E, Thiene G. Cardiac infections: focus on molecular diagnosis. Cardiovasc Pathol. 2010;19:171–182. 6. Pophal SG, Sigfusson G, Booth KL, et al. Complications of endomycardial biopsy in children. J Am Coll Cardiol. 1999;34:2105–2110. 7. Calabrese F, Rigo E, Milanesi O, et al. Molecular diagnosis of myocarditis and dilated cardiomyopathy in children: clinicopathologic features and prognostic implications. Diagn Mol Pathol. 2002;11:212–221. 8. Bergelson JM, Cunningham JA, Drouguett G, et al. Isolation of a common receptor for Coxsackie B virus and adenoviruses types 2 and 5. Science. 1997;275:1320–1323. 9. Badorff C, Lee GH, Lamphear BJ, et al. Enteroviral protease 2A cleaves dystrophin: evidence of cytoskeletal disruption in an acquired cardiomyopathy. Nat Med. 1999;5:320–326. 10. Fairweather D, Frisancho-Kiss S, Rose NR. Viruses as adjuvants for autoimmunity: evidence from Coxsackievirus-induced myocarditis. Rev Med Virol. 2005;15:17–27. 11. Li Y, Heuser JS, Cunningham LC, et al. Mimicry and antibody-mediated cell signaling in autoimmune myocarditis. J Immunol. 2006;177: 8234–8240.

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12. Durani Y, Egan M, Baffa J, et al. Pediatric myocarditis: presenting clinical characteristics. Pediatrics. 2007;27:942–947.

23. Khatib R, Reyes MP, Smith F, et al. Enhancement of coxsackie B4 virulence by indomethacin. J Lab Clin Med. 1990;116:116–120.

13. Ramamurthy S, Talwar KK, Goswami KC. Clinical profile of biopsy proven idiopathic myocarditis. Int J Cardiol. 1993;41:225–232.

24. Burch GE. Prolonged bed rest in the management of patients with cardiomyopathy. Cardiovasc Clin. 1972;4:375–387.

14. Drory Y, Turetz Y, Hiss Y, et al. Sudden unexpected death in persons less than 40 years of age. Am J Cardiol. 1991;68:1388–1392.

25. Drucker NA, Colan SD, Lewis AB, et al. Gamma-globulin treatment of acute myocarditis in the pediatric population. Circulation. 1994; 89:252.

15. Baughman KL. Diagnosis of myocarditis: death of Dallas criteria. Circulation. 2006;113:593–595. 16. Aretz HT, Billingham ME, Edwards WD, et al. Myocarditis: a histopathologic definition and classification. Am J Cardiovasc Pathol. 1987;1:3–14. 17. Punja M, Mark DG, McCoy JV, et al. Electrocardiographic manifestations of cardiac infectious-inflammatory disorders. Am J Emerg Med. 2010;3: 364–377. 18. Eisenberg MA, Green-Hopkins I, Alexander ME, et al. Cardiac troponin T as a screening test for myocarditis in children. Pediatr Emerg Care. 2012; 28:1173–1178. 19. Marholdt H, Goedecke C, Wagner A, et al. Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology. Circulation. 2004;109:1250–1258. 20. Olimulder MA, van Es J, Galjee MA. The importance of cardiac MRI as a diagnostic tool in viral myocarditis-induced cardiomyopathy. Neth Heart J. 2009;17:481–486. 21. Maisch B, Pankuweit S. Current treatment options in (peri)myocarditis and inflammatory cardiomyopathy. Herz. 2012;6:655–656. 22. Costanzo-Nordin MR, Reap EA, O'Connell JB, et al. A nonsteroid anti-inflammatory drug exacerbates Coxsackie B3 murine myocarditis. J Am Coll Cardiol. 1985;6:1078–1082.

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26. McNamara DM, Holubkov R, Starling RC, et al. Controlled trial of intravenous immune globulin in recent-onset dilated cardiomyopathy. Circulation. 2001;103:2254–2259. 27. Mason JW, O'Connell JB, Herskowitz A, et al. A clinical trial of immunosuppressive therapy in myocarditis. N Engl J Med. 1995;333: 269–275. 28. Cooper LT, Berry GJ, Shabetai R. Idiopathic giant-cell myocarditis—natural history and treatment. N Engl J Med. 1997;336: 1860–1866. 29. Balaji S, Wiles HB, Sens MA, et al. Immunosuppressive treatment for myocarditis and borderline myocarditis in children with ventricular ectopic rhythm. Br Heart J. 1994;72:354–359. 30. Camargo PR, Snitcowsky R, da Luz PL, et al. Favorable effects of immunosuppressive therapy in children with dilated cardiomyopathy and active myocarditis. Pediatr Cardiol. 1995;16:61–68. 31. Farrar DJ, Holman WR, McBridge LR, et al. Long-term follow-up of Thoratec ventricular assist device bridge-to-recovery patients successfully removed from support after recovery of ventricular function. J Heart Lung Transplant. 2002;21:516–521. 32. Moloney ED, Egan JJ, Kelly P, et al. Transplantation for myocarditis: a controversy revisited. J Heart Lung Transplant. 2005;24:1103–1110.

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CME EXAM INSTRUCTIONS FOR OBTAINING AMA PRA CATEGORY 1 CREDITSTM Pediatric Emergency Care includes CME-certified content that is designed to meet the educational needs of its readers. An annual total of 12 AMA PRA Category 1 CreditsTM is available through the twelve 2014 issues of Pediatric Emergency Care. This activity is available for credit through February 15, 2015.

CME EXAMINATION November 2014 Please mark your answers on the ANSWER SHEET. Myocarditis, Pettit et al 1. What is the most common electrocardiographic abnormality encountered in myocarditis? A. Left bundle branch block B. Second-degree atrioventricular block C. Ventricular tachycardia D. Sinus tachycardia

4. Which of the following physical examination findings are most commonly associated with myocarditis? A. Abnormal respiratory examination B. New murmur/gallop C. Hypoxia/cyanosis D. Fever

2. How long after the initial prodrome do symptoms tend to peak in a patient with myocarditis? A. 21 days

5. Which of the following mechanisms is believed to contribute to the pathogenesis of myocarditis? A. Direct myocardial damage B. Host inflammatory response C. Both A and B D. Neither A nor B

3. A 14-year-old adolescent boy with no prior cardiac history presents to the emergency department with severe shortness of breath and generalized weakness that has progressed for the past 2 to 3 weeks. He was previously seen at an urgent care facility, diagnosed with an upper respiratory infection, and did not improve on a 5-day course of antibiotics. He notes difficulty in breathing when lying flat and swollen ankles. In the emergency department, he is tachypneic, tachycardic, and hypoxic on room air. Which test can be used as a screen to rule out the diagnosis of myocarditis? A. complete blood count B. Troponin T C. Chest x-ray D. erythrocyte sedimentation rate

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Myocarditis

ANSWER SHEET FOR THE PEDIATRIC EMERGENCY CARE CME PROGRAM EXAM November 2014 Please answer the questions on page 838 by filling in the appropriate circles on the answer sheet below. Please mark the one best answer and fill in the circle until the letter is no longer visible. To process your exam, you must also provide the following information: Name (please print): ___________________________________________________________________________________________ Street Address _______________________________________________________________________________________________ City/State/Zip _______________________________________________________________________________________________ Daytime Phone ______________________________________________________________________________________________ Specialty ___________________________________________________________________________________________________

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Your completion of this activity includes evaluating them. Please respond to the following questions below. Please rate this activity (1 - minimally, 5 - completely) Was effective in meeting the educational objectives Was appropriately evidence-based Was relevant to my practice Please rate your ability to achieve the following objectives, both before this activity and after it: 1 (minimally) to 5 (completely) Pre 1. Describe the pathophysiology of myocarditis. 2. Identify the clinical features consistent with the diagnosis of myocarditis. 3. Initiate or take part in the management of critically ill patients with myocarditis.

1 2 3 4 5











Pre 1 2 3 4 5 1 2 3 4 5



















How many of your patients are likely to be impacted by what you learned from these activities? ○ 80% Do you expect that these activities will help you improve your skill or judgment 1 2 3 4 5 within the next 6 months? (1 - definitely will not change, 5 - definitely will change)



How will you apply what you learned from these activities (mark all that apply): In making treatment decisions ○ In diagnosing patients ○ As a foundation to learn more ○ In monitoring patients ○ In educating patients and their caregivers ○ In educating students and colleagues ○ To confirm current practice ○ As part of a quality or peformance improvement project ○ For maintenance of licensure ○ For maintenance of board certification ○ To consider enrolling patients in clinical trials ○ Other ______________________________________________________________________________________________________ Please list at least one strategy you learned from this activity that you will apply in practice: How committed are you to applying these activities to your practice in the ways 1 2 3 4 5 you indicated above? (1 - minimally, 5 - completely)



Did you receive any bias for or againts any commercial products or devices? Yes No

If yes, please explain: How long did it take you to complete these activities? _______ hours _______ minutes What are your biggest clinical challenges related to pediatric emergency care? [ ] Yes! I am interested in receiving future CME programs from Lippincott CME Institute! (Please place a check mark in the box ) Mail by February 15, 2015 to Lippincott CME Institute, Inc. Wolters Kluwer Health Two Commerce Square 2001 Market Street, 3rd Floor Philadelphia, PA 19103

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CME EXAM ANSWERS Answers for the Pediatric Emergency Care CME Program Exam Below you will find the answers to the examination covering the review article in the August 2014 issue. All participants whose examinations were postmarked by November 15, 2014 and who achieved a score of 80% or greater will receive a certificate from Lippincott CME Institute, Inc.

EXAM ANSWERS August 2014 1. 2. 3. 4. 5.

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A C D D A

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Myocarditis.

Myocarditis is an inflammatory disease of the heart that can cause devastating disease in otherwise healthy children. Inciting agents such as viral in...
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