A 16 year‐old male with cystic fibrosis presented with chest pain. He had not been feeling well for two weeks, but attributed his dry cough and mild malaise to his usual allergy symptoms. On the day of presentation, he developed acute, central chest pain that was worsened with taking a deep breath, as well as increased fatigue, subjective fevers, mild nausea, and a headache. There was no sputum production, hemoptysis, rhinorrhea or wheezing. Historically, his cystic fibrosis symptoms had been gastrointestinal, and he had not been hospitalized for pulmonary symptoms in three years. Regular treatments included dornase alpha, cetirizine, and chest physiotherapy, as well as vitamin K and pancreatic enzyme replacement.
Physical examination revealed an uncomfortable, but well‐appearing young man, who was febrile at 38.3 C, with regular tachycardia at a rate of 115, and a respiratory rate of 20. Respirations were shallow, and deeper inspiration evoked pain, though there was no increased work of breathing, crackles or wheezes. Cardiac exam demonstrated normal heart sounds without murmurs, gallops or rubs. There was no digital clubbing, sinus tenderness, or nasal polyps.
Chest radiograph showed mild hypoinflation and streakiness suggestive of viral infection or atelectasis. Basic chemistries and complete blood count were normal. Sputum and blood cultures were obtained. Emergency department phone consultation with a pulmonologist resulted in starting intravenous and inhaled antibiotics for a presumed cystic fibrosis pulmonary exacerbation given his fever, chest pain, pleurisy and radiographic findings.
The patient was admitted to the hospitalist service and chest pain persisted. Additional history revealed that the patient had played 36 holes of golf the day prior to presentation without dyspnea. Physical exam then demonstrated that chest pain improved with sitting forward. With this information, an EKG was obtained that demonstrated diffuse ST segment elevation, consistent with pericarditis. Troponin levels were elevated and an echocardiogram revealed a bright pericardium without effusion and normal heart function without restriction. Ibuprofen resulted in improvement in chest pain. Antibiotics were discontinued and the patient was discharged home with a diagnosis of acute myopericarditis, treatment with NSAIDs, and close follow‐up. He was playing competitive golf again within 2 months without any residual symptoms.
Chest pain is commonly encountered by pediatric hospitalists and the above presentation is classic for acute myopericarditis, albeit in a patient with co‐morbidities that led to an erroneous initial diagnosis. Acute myopericarditis is most often viral or idiopathic and diagnosis is established by history and physical exam and confirmed with EKG, cardiac biomarkers and echocardiogram. Treatment is primarily with non‐steroidal anti‐inflammatories in patients with preserved heart function. Prognosis is excellent, with most patients achieving a full recovery. Additonally, this case demonstrates the dangers of anchoring too readily to co‐morbid conditions when establishing a diagnosis.
Pediatric hospitalists must maintain a broad differential diagnosis and not anchor too early when approaching adolescents with chest pain. History and physical exam techniqes are vital to making the correct chest pain diagnosis. An EKG, cardiac biomarkers and echocardiography are essential to confirm and further characterize acute myopericarditis.
To cite this abstract:Hobbs R. On Second Exam: Forward to a Diagnosis Chest Pain in an Adolescent with Cystic Fibrosis. Abstract published at Hospital Medicine 2014, March 24-27, Las Vegas, Nev. Abstract 269. Journal of Hospital Medicine. 2014; 9 (suppl 2). https://www.shmabstracts.com/abstract/on-second-exam-forward-to-a-diagnosis-chest-pain-in-an-adolescent-with-cystic-fibrosis/. Accessed March 28, 2020.