A 13-year-old boy with a recent diagnosis of ulcerative colitis presented with fever and chest pain to the emergency department. The sharp pain had begun 2 days previous and radiated to his shoulders. It was constant, although it improved with sitting up and leaning forward. On the day before, he had developed a fever to 38.3°C. His past medical history was notable for a diagnosis of ulcerative colitis 2 months before presentation. For this, he was taking mesalamine and rectal hydrocortisone and weaning down on a prolonged course of oral prednisone. On examination, he was noted to be in mild distress, febrile, and tachycardic, with a heart rate of 120 beats per minute. Aside from the tachycardia, his cardiac examination was largely unremarkable. An electrocardiogram revealed diffuse ST elevations in the precordial leads. Blood testing revealed an elevated white blood cell count of 19.1 × 1000 per µL, with 78.9% neutrophils, hemoglobin of 8.3 g/dL, and a platelet count of 628 × 1000 per µL. Troponin T was elevated to 0.46 ng/mL. A rapid bedside cardiac ultrasound was grossly normal. He was admitted to the hospital with a diagnosis of pericarditis and treated with an increased dose of prednisone. Despite this treatment, he experienced rapid clinical deterioration. After considering the broad differential diagnosis, the correct etiology was identified, and steps were taken that led to a swift clinical improvement.

A 13-year-old boy with a recent diagnosis of ulcerative colitis presented to the emergency department at a community hospital with chest pain. The sharp pain had begun 2 days previous and radiated to his shoulders. It was constant, although it improved with sitting up and leaning forward. On the day before presentation, he had developed a fever of 38.3°C. Two weeks previous, he had had a mild respiratory illness and was positive for influenza by using a rapid diagnostic test.

The patient had been diagnosed with ulcerative colitis 2 months before presentation. He was taking mesalamine and rectal hydrocortisone and weaning down on a prolonged course of oral prednisone. He also had a long-standing history of asthma, for which he was on a daily corticosteroid inhaler, montelukast, and an albuterol metered-dose inhaler as needed.

In the emergency department, his vital signs were notable for a temperature of 38.3°C, heart rate of 120 beats per minute, blood pressure of 110/70 mm Hg, and oxygen saturation of 99% on room air. He was in mild distress. His cardiac examination revealed tachycardia, but otherwise a quiet precordium, with regular S1 and S2, and no murmurs, gallops, or rubs. His chest pain was worse when supine and improved when leaning forward. He was warm, well perfused, and with brisk distal pulses. The remainder of his examination was unremarkable.

Dr Asnes, what are your initial thoughts on the diagnosis and management of our patient?

As a pediatric cardiologist, I frequently receive calls about chest pain, although studies in emergency settings demonstrate that <1% of children with this complaint have a cardiac origin of disease.13  A detailed history, physical examination, and electrocardiogram (ECG) are almost always sufficient to suggest a cardiac cause of chest pain.4  Cardiac chest pain typically worsens with exertion and may be associated with syncope, palpitations, or dyspnea. Relevant past medical histories that predispose to cardiac disease include those with past cardiac disease, systemic inflammatory conditions, malignancies, thrombophilia, and myopathies. Finally, a family history of sudden or aborted death, hyperlipidemia, cardiomyopathy, or pulmonary hypertension is also relevant. Abnormalities on the physical examination that would raise suspicion for cardiac disease include fever, tachypnea, abnormal cardiac auscultation (murmur, gallop, and/or distant heart sounds), hepatomegaly, abnormal peripheral pulses, and peripheral edema. ECG changes suggestive of cardiac causes of chest pain include ST-segment changes, T-wave inversions, new conduction delays, ventricular hypertrophy, and, although rarely caught on a single ECG, ventricular ectopy.

Although the classic features of cardiac chest pain are not all seen in this case, the history of fever with chest pain should raise concern for pericarditis and myocarditis. Our patient’s positional chest pain, in particular, the finding of pain that is worse when supine and improves on leaning forward, increases my concern for pericarditis.5,6  A high-pitched and scratchy friction rub may be associated. Finally, I try to determine if the heart sounds are atypically quiet or “distant,” which could suggest a concomitant pericardial effusion, a known complication of pericarditis. Regardless, when there is suspicion for a cardiac source of chest pain, an ECG is a helpful initial study.

There was no friction rub on auscultation. A 12-lead ECG revealed sinus tachycardia with diffuse ST-segment elevations in lead V1 to V6 and PR depressions in lead II (Fig 1).

FIGURE 1

ECG reveals diffuse ST-segment elevations in the precordial leads, with corresponding PR depression.

FIGURE 1

ECG reveals diffuse ST-segment elevations in the precordial leads, with corresponding PR depression.

Close modal

Dr Simmons, what findings are typical on an ECG for pericarditis? How do you make the diagnosis of pericarditis?

Although chest pain and ECG changes are classically thought of to diagnose pericarditis, any 2 of the following 4 features are sufficient to make the diagnosis: (1) characteristic chest pain, typically sharp, pleuritic, and positional; (2) friction rub on auscultation; (3) ECG changes; and (4) new or worsening pericardial effusion.7  With that said, ECG changes are seen in up to 60% of cases of acute pericarditis. The hallmark is a stage I pattern of ST elevation with corresponding PR depression that occurs in the initial hours to days. Stage II occurs over the first week and is marked by normalization of the ST and PR segments. Subsequently, patients may show a subacute stage III pattern with diffuse T-wave inversion. In stage IV, the ECG again normalizes. However, this linear evolution of ECG findings may not occur in all patients because some patients’ ECGs may normalize after stage I.

In children, a common and benign entity that also presents with ST elevations is benign early repolarization (BER). To distinguish between pericarditis and BER, it can help to compare with previous ECGs when the patient is asymptomatic. ST elevations on previous ECGs may be suggestive of BER. Corresponding PR depression does not occur in BER. The other consideration for ST changes on ECG is ischemic heart disease, a rare occurrence in children, but may present as a sequela of Kawasaki disease or coronary anomalies. ST elevations in these cases are often seen with reciprocal ST depression in electrically opposite leads.

In this patient, the classic sharp, pleuritic chest pain combined with ST elevations and corresponding PR depression is sufficient to diagnose pericarditis. There were no reciprocal changes present on ECG. Unfortunately, there were no previous ECGs to compare.

What further evaluation does he need in the emergency department?

When caring for an ill-appearing and tachycardic patient with pericarditis in the emergency department, our goals are to stabilize the patient and establish a safe disposition. In a community setting, without pediatric cardiology or pediatric intensivists readily available, this becomes even more important. Although tachycardia in a patient with pericarditis may be simply because of pain or fever, we should ensure that complications such as constrictive pericarditis, myocarditis, or cardiac tamponade are not present. It would be reasonable to obtain screening laboratories, including a complete blood cell count, basic metabolic panel, inflammatory markers, and a troponin T. Troponin measurement helps to determine if there is myocardial involvement, raising concern for myocarditis. In this patient whose examination revealed a quiet precordium, it would be valuable to perform a bedside focused cardiac ultrasound to evaluate for associated pericardial effusion or grossly abnormal ventricular function; however, qualified ultrasound availability is hospital-dependent. If these are normal, I would favor treating him with a nonsteroidal anti-inflammatory drug (NSAID) to see if his heart rate responds to temperature and pain control. If his heart rate and appearance improve, he may be a candidate for an outpatient course of NSAIDs (although we should ensure that chronic NSAID therapy is not contraindicated from the standpoint of his ulcerative colitis) and referral to cardiology for an echocardiogram and follow-up. Because there are no evidence-based guidelines for the management of pediatric pericarditis, some providers may elect to admit patients with uncomplicated pericarditis to monitor for complications. If his symptoms persist despite our trial of NSAIDs or his laboratory or imaging findings are concerning for associated complications, I would favor sending him to a tertiary care pediatric center for evaluation by a pediatric cardiologist today and overnight monitoring.

The initial laboratory values were notable for an elevated white blood cell count of 19.1 × 1000 per µL, with 78.9% neutrophils and otherwise unremarkable differential, a hemoglobin of 8.3 g/dL, and a platelet count of 628 × 1000 per µL. Troponin T was elevated to 0.46 ng/mL (normal range: <0.01 ng/mL). Inflammatory markers were markedly elevated, with a C-reactive protein at 97.6 mg/L and erythrocyte sedimentation rate at 120 mm per hour. There was no ultrasound capacity at the community site. He was given intravenous ketorolac with improvement in pain, but tachycardia to the 120s persisted. The pediatric cardiology department was contacted, and the patient was transferred to our children’s hospital for further imaging and management. The rapid bedside echocardiogram performed in the pediatric emergency department was grossly normal, without evidence of tamponade.

Dr Asnes, what is the differential diagnosis of pericarditis, and how should we proceed now?

Most commonly, pericarditis is the result of a viral infection or an idiopathic cause, although autoimmune etiologies and malignancy are also on the differential. Given his recent influenza infection, it is reasonable to proceed as if this is virally mediated pericarditis and monitor his response to conventional therapy. The majority of patients with pericarditis may be managed on an outpatient basis. However, this patient remains ill appearing and has vital sign instability, with evidence of myocardial injury. He should be admitted for overnight telemetry and initiation of treatment. He would also benefit from a formal echocardiogram. The accepted first-line treatment of pericarditis is an NSAID, such as ibuprofen, but his anemia in the setting of ulcerative colitis may be a contraindication for antiplatelet agents.8  Corticosteroids are considered second-line therapy because there is a concern for increased risk of disease recurrence. But, given his underlying ulcerative colitis, I suspect that they are likely the best option for management.6,9  The choice to use NSAIDs or corticosteroids for therapy, in this case, should be done in consultation with the gastroenterologists.

He was admitted to the pediatric cardiology general floor and initiated on 5 mg twice daily of prednisone, representing a doubling of the dose he was on for his steroid wean. After discussion with gastroenterology, no further NSAIDs were used in his care. Despite the initiation of treatment, he continued to be febrile and tachycardic overnight with a Tmax of 38.6°C and heart rates ranging from 120 to 150 beats per minute. Findings on a formal echocardiogram obtained the following morning were concerning (Fig 2).

FIGURE 2

Two-dimensional transthoracic echocardiographic short axis of left ventricle with hyperechoic region in the basal inferior and inferolateral segments along with increased posterior wall thickness (yellow arrow), suggestive of myocardial edema.

FIGURE 2

Two-dimensional transthoracic echocardiographic short axis of left ventricle with hyperechoic region in the basal inferior and inferolateral segments along with increased posterior wall thickness (yellow arrow), suggestive of myocardial edema.

Close modal

Dr Karnik, what were these findings, and what do you make of them?

Primarily, we noted a hyperechoic area with increased thickness of the left ventricular (LV) myocardium in the basal inferior and inferolateral segments as compared with the rest of the LV. These changes are suggestive of focal myocardial edema. This region also had decreased contractility, with a globally preserved LV systolic function. The LV cavity size and diastolic function were normal. There was no pericardial effusion. These new echocardiographic findings raise my suspicion for myocarditis, and, perhaps, the clinical picture points toward myopericarditis.

The underlying etiology needs to be considered more thoughtfully. Although the prognosis of pediatric idiopathic or viral pericarditis is good, there is up to 25% morbidity and mortality associated with pediatric myocarditis.6,1012  In otherwise healthy children, the most common provoking agents for myocarditis are viruses, including human herpesvirus 6 and parvovirus B19, followed by enterovirus and adenovirus.11,12  Influenza-associated myocarditis has been reported but is rare.13,14  Another important infectious agent to consider is Trypanosoma cruzi myocarditis, which is responsible for Chagas disease, widespread in Central and South America but unusual in North America.12  Hypersensitivity reactions to drugs are well described, most commonly after exposure to antiepileptics or antibiotics, and should be considered in any patient with a long medication list. Myocarditis can occur secondary to several autoimmune disorders and should be on the differential for a child with inflammatory bowel disease.

An echocardiogram is the imaging modality of choice for initial assessment of ventricular size, wall thickness, function, and pericardial effusion in patients undergoing evaluation for myocarditis. This assessment is crucial to distinguish between fulminant and acute myocarditis.15  Children with fulminant myocarditis are acutely sicker with an increased need for cardiac support but have a favorable prognosis over time.16,17  Despite these uses, echocardiogram is not specific for the diagnosis of myocarditis, and further studies are necessary.12 

The World Health Organization defines myocarditis as an inflammatory disease of the heart and, accordingly, the diagnosis has traditionally demanded endomyocardial biopsy, a procedure that carries the risk of significant complications and has a poor sensitivity.18,19  More recently, cardiac magnetic resonance (CMR) has emerged as a noninvasive tool for which consensus criteria exist to diagnose this disease.12  I would obtain a CMR as soon as possible.

A CMR was obtained the following day to better characterize myocardial involvement. The imaging revealed mildly depressed right ventricular systolic function and severely depressed LV systolic function, with an ejection fraction of 27% and segmental wall motion abnormalities in the LV posterior basal wall. An echocardiogram obtained immediately after the CMR noted an LV ejection fraction of 36%. Also, the patient now had a moderate pericardial effusion. Troponin T was persistently elevated to 0.41 ng/mL. In this period, he developed concomitant hypotension to 90/50 mm Hg and persistent tachycardia in the range of 120 to 130 beats per minute. On physical examination, however, he remained a nontoxic appearing teenager. We auscultated no crackles on lung examination and found no hepatosplenomegaly or peripheral edema. He had warm extremities and easily palpable distal pulses. Because of concern for declining cardiac function, the patient was transferred to the PICU (Fig 3 A–B).

FIGURE 3

A, T2-weighted short axis image showing hyperintensity signal through the lateral wall (yellow arrow) consistent with myocardial edema. B, Pulse sequence inversion recovery image showing patchy diffuse late gadolinium enhancement in the lateral wall (yellow arrow) and a pericardial effusion (**).

FIGURE 3

A, T2-weighted short axis image showing hyperintensity signal through the lateral wall (yellow arrow) consistent with myocardial edema. B, Pulse sequence inversion recovery image showing patchy diffuse late gadolinium enhancement in the lateral wall (yellow arrow) and a pericardial effusion (**).

Close modal

Dr Steele, could you describe the CMR findings?

The benefit of CMR, in comparison with echocardiography, is its ability to perform tissue characterization. CMR allows for identifying tissue edema, hyperemia, and fibrosis, which is helpful for the evaluation of possible myocarditis. The diagnosis of myocarditis by CMR dates from the 2009 Lake Louise Criteria in the myocarditis white paper.20  These diagnostic criteria include the presence of myocardial edema on T2-weighted imaging, presence of hyperemia by T1-weighted imaging, and presence of irreversible cell injury (myocardial fibrosis). Supportive criteria are changes in LV systolic function and the presence of pericardial effusion. If at least 2 of 3 of the tissue characterization sequences are performed, myocardial inflammation can be ruled in or out with 78% accuracy.20  In our patient, the LV systolic function was severely decreased (ejection fraction: 27%), the T2-weighted imaging revealed a high-intensity signal from the anterolateral to the inferolateral wall of the left ventricle, with a signal intensity ratio of myocardial to skeletal muscle of 2.3 (normal: <2) indicating diffuse inflammation (Fig 3A). A postcontrast assessment for fibrosis revealed patchy areas of fibrosis in the same regions as the high-intensity T2 signal (Fig 3B). A pericardial effusion was also noted. These findings represent a positive CMR study for acute myopericarditis.

Dr Asnes, given the new diagnosis of myopericarditis, should our therapeutic plan for this patient change?

This patient’s disease is extensive and progressing at an alarming rate. When he presented to our care, we were suspicious of pericarditis, given his chest pain and ECG findings. Now, the combination of the CMR findings and troponin leak points to significant myocardial involvement. Furthermore, within 48 hours since his presentation, he has had progressive tachycardia with a deterioration of his biventricular function. I agree that he deserves a higher level of care with close monitoring for ventricular arrhythmias and clinical signs of impending hemodynamic collapse. Importantly, biventricular dysfunction is the main predictor of transplant or death in myocarditis. Our treatment should be aggressive and double pronged, focused on supportive care to maintain hemodynamic stability and directed therapy toward the underlying etiology of his myopericarditis.

Dr Canarie, how should we provide supportive care to this patient?

Patients with myocarditis and severely depressed heart function should be treated by a pediatric intensive care and pediatric cardiology team. In this case, although imaging has revealed decreased heart function, our patient has compensated heart failure because there is no evidence of congestive heart failure (an absence of crackles on the lung examination and no peripheral edema). He also has good perfusion, as evidenced by good pulses and warm extremities, despite a low-normal blood pressure. In some cases, inotropic agents, such as dobutamine or milrinone, may be necessary to provide myocardial support, but given our patient’s clinical status, we do not need to pursue this. You do need to be careful, because adrenergic and dopaminergic inotropic agents can increase the risk for arrhythmias, especially in an already inflamed myocardium, and should be used sparingly. This patient needs vigilant monitoring for arrhythmias, which can be fatal in myocarditis. He also requires close monitoring of volume status and end-organ perfusion, with diligent measures of his ins and outs and routine assessments of mental status, pulses, and kidney and liver function.

Dr Asnes, does this patient need pharmacologic heart failure therapy? What does directed therapy in pediatric myocarditis entail?

To support his heart function, we should pursue treatment of heart failure with a choice or combination of angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, aldosterone antagonists, and carvedilol, which should be initiated according to cardiac society guidelines.12 

Directed therapy in pediatric myocarditis remains controversial. Antiviral agents may have efficacy in the early stages of viral myocarditis, but in this case, myocarditis was diagnosed weeks after the suspected viral agent. Intravenous immunoglobulin has been suggested as a therapeutic option, but the evidence is uncertain, with some studies showing improved LV function and mortality and others demonstrating no benefit.21,22  In a Cochrane review of adult and pediatric patients, researchers concluded that routine use cannot be clearly recommended with available data.23  Immunosuppressant agents, such as corticosteroids, have been suggested as another option in acute myocarditis with negative viral study results.6,24  They may be an appropriate therapy for autoimmune-mediated myocarditis. Finally, a review of the literature for associations between the patient’s home medications and myocarditis identified several cases of mesalamine-mediated myocarditis with rapid normalization of heart function after discontinuation of the drug.2528 

Given his rapid deterioration and in consultation with the pediatric gastroenterologists, mesalamine was discontinued. Despite the ambiguity of the evidence, he was treated with 2 g/kg of intravenous immunoglobulin and transitioned to 1 g of intravenous methylprednisolone. He tolerated these infusions well.

Remarkably, within 24 hours of our interventions, his pain improved, his heart rate normalized, and he appeared much more comfortable. An echocardiogram revealed persistent echo brightness in the posterior wall of the LV, but globally normalized systolic function. Troponin T trended down to 0.16 ng/mL. He continued to improve and was discharged the following day, after completing a second day of intravenous methylprednisolone.

Given the history of antecedent viral illness, autoimmune disease, and treatment with a drug associated with hypersensitivity myocarditis, the differential diagnosis of myocarditis in this patient was broad. However, the rapid resolution of symptoms in our patient after discontinuation of mesalamine was classic for mesalamine-mediated myocarditis.

Mesalamine (5-aminosalicylic acid) is a first-line agent in the management of pediatric ulcerative colitis. Although rare, in several case reports, researchers have documented myocarditis as a side effect of this therapy.2528  The mechanism is unclear, but it is thought to be a hypersensitivity reaction, as evidenced by eosinophilic infiltrates in endomyocardial biopsy specimens in patients with suspected disease.27  Further supporting that mechanism, in this case, is the dramatic improvement in cardiac function with the removal of the offending drug, which does not occur with direct cardiotoxicity. Importantly, there are case reports of recurrent symptoms and findings after reintroduction of mesalamine.27  Of note, although tissue eosinophilia may be identified, review of case reports suggests that peripheral eosinophilia within a complete blood cell count may not pe present, as in our patient.26 

Regardless of the mechanism, the mainstay of treatment in hypersensitivity myocarditis is discontinuing the offending agent. Several case reports document normalization of heart function within the 1 to 2 days of doing this. Mesalamine hypersensitivity myocarditis may also be responsive to steroids.

After hospital discharge, patients with myocarditis, irrespective of etiology, should be excluded from competitive athletics and vigorous exercise for at least 6 months because of the association between myocarditis and sudden cardiac death in young athletes.29  Myocarditis represents the third most common cause of sudden cardiac death in this population, behind hypertrophic cardiomyopathy and anomalous coronary artery origin. Return to play can begin after the resolution of arrhythmias and normalization of LV function. Repeat CMR imaging should be obtained at least 4 weeks after the initial diagnosis to determine if the patient will need to follow a chronic course of medical therapy for myocarditis.

Over the course of his 2- and 6-month follow-up CMRs, his heart function improved to normal, and he has tolerated a return to normal activity level. He is doing well and is currently on every 6-week infliximab infusions to treat his ulcerative colitis.

Drs Soma and Simmons contributed to the design and conception of this case presentation, drafted the initial manuscript, and completed initial revisions; Drs Steele and Karnik identified and described representative cardiac images and revised the final manuscript; Drs Canarie, Tiyygura, and Asnes revised the final manuscript; and all authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work.

Dr Simmons’s current affiliation is Presbyterian Medical Group, Albuquerque, NM.

FUNDING: No external funding.

BER

benign early repolarization

CMR

cardiac magnetic resonance

ECG

electrocardiogram

LV

left ventricular

NSAID

nonsteroidal anti-inflammatory drug

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Competing Interests

POTENTIAL CONFLICT OF INTEREST: The authors have no conflicts of interest relevant to this article to disclose.

FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.