Asian Cardiovasc Thorac Ann 2006;14:e111-e112
© 2006 Asia Publishing EXchange Ltd
Acute Fulminant Myocarditis after Diphtheria, Polio, and Tetanus Vaccination
Shye-Jao Wu, MD,
Shen Sun, MD,
Jiun-Yi Li, MD,
Po-Yuan Hu, MD,
Chen-Yen Chien, MD
Division of Cardiovascular Surgery, Department of Surgery, MacKay Memorial Hospital, Taipei, Taiwan
For reprint information contact: Shye-Jao Wu, MD Tel: 886 2 2543 3535 Fax: 886 2 2543 3642 Email: wsj003{at}med-assn.org.tw, Department of Surgery, MacKay Memorial Hospital, No.92, Section 2, Chung-Shan North Road, Taipei 104, Taiwan.
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ABSTRACT
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We report an infant case of acute fulminant myocarditis which occurred after administration of a diphtheria, polio, and tetanus vaccination. Fever and dyspnea developed after the vaccination. Extracorporeal membrane oxygenation was used for intractable cardiogenic shock. The patient survived the extracorporeal support, but poor ventricular contractility recurred 2 months later and she died while waiting for heart transplantation.
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INTRODUCTION
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While there are various causes of acute myocarditis, cardiovascular complications after vaccinations are rare,1–4 and have only been reported sporadically. We report a case of acute fulminant myocarditis after triple vaccination against diphtheria, polio, and tetanus in an infant.
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CASE REPORT
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A previously healthy 8-month-old female baby, body height 67cm and body weight 8.0kg, suffered from fever (38.3°C) 12 hours after she received triple vaccination against diphtheria, polio, and tetanus. Dyspnea occurred 3 days later. She presented with poor activity, persistent dyspnea with subcostal retraction and skin mottling 5 days later. There was no prior history of adverse reactions to previous diphtheria, polio, and tetanus vaccinations, or other vaccinations. Body temperature was 37.7°C. Breathing sounds revealed rales bilaterally. Laboratory examinations showed white blood cell count 23.9x 109·L–1 with neutrophils 41%, lymphocytes 54% and eosinophils 1.5%; C-reactive protein 0.89 mg·dL–1, troponin-I 0.69 ng·mL–1, creatine kinase 83 U·L–1, and CK-MB fraction 16.7 U·L–1 (Table 1
). Polymerase chain reaction studies failed to demonstrate evidence of enteroviral ribonucleic acid. Chest roentgenography revealed cardiomegaly with pulmonary congestion. Echocardiography showed a left ventricular ejection fraction of 38% (Table 2).
Clinical conditions deteriorated rapidly. Endotracheal intubation was performed immediately after admission. Blood pressure dropped to 60/26 mm Hg and heart rate increased to 210 beats·min–1 two hours after admission. An intravenous infusion of inotropic agents was given for unstable hemodynamics. Ventilator support and high doses of inotropic support (dopamine 20 µg·kg–1·min–1, dobutamine 20 µg·kg–1·min–1, epinephrine 2 µg·kg–1·min–1, milrinone 0.5 µg·kg–1·min–1) failed to maintain adequate hemodynamics and oxygenation. Severe metabolic acidosis (pH 6.843, PaCO2 20.6 mm Hg, PaO2 307.9 mm Hg, bicarbonate 3.5 mmol·L–1, base excess –30 mmol·L–1) persisted. About 3 hours after admission, venoarterial-mode extracorporeal membrane oxygenation (ECMO) was used for intractable cardiogenic shock. ECMO setup was via a right neck approach. Cardiac catheterization or endomyocardial biopsy was not attempted due to the patient’s poor general condition. Total ECMO support time was 159 hours. The endotracheal tube was removed 7 days after cessation of ECMO, and the inotropic agents were tapered off gradually. Repeated echocardiography showed an improved left ventricular ejection fraction of 51%. Bacterial and viral cultures performed on admission showed no growth of pathogens. Digoxin 40 g·day–1 and furosemide 16 mg·day–1 were prescribed.
However, poor ventricular contractility recurred 2 months after the initial episode of acute fulminant myocarditis. Digoxin 80 g·day–1, furosemide 32 mg·day–1, and captopril 7.5 mg·day–1 were prescribed for congestive heart failure. Cardiac catheterization showed patent coronary arteries and a left ventricular ejection fraction of 14%. Endomyocardial biopsy was still not attempted due to poor general condition. The patient died while waiting for heart transplantation.
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DISCUSSION
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Vaccinations are usually well tolerated and vaccination-related myocarditis has rarely been reported.1–4 The possible mechanisms of myocarditis after vaccination are infective myocarditis and hypersensitivity myocarditis. Infective myocarditis is an infective disease entity. However, in this case virological and bacterial study findings were negative for bacteria, Coxsackie virus, and other enteroviruses. Serologic studies also failed to show elevation of IgM level of viruses. Additionally, there were no associated symptoms of diphtheria, polio, and tetanus virus. Therefore infective myocarditis coincidental, or related, to the vaccination was not likely in our patient.
Hypersensitivity myocarditis is an inflammatory status of the myocardium, usually related to drug allergy.5,6 Hypersensitivity myocarditis due to vaccination has been reported sporadically.1–4 Occurrence of early fever after vaccination, negative results of microbial culture and the absence of associated symptoms for diphtheria, polio, and tetanus favor the diagnosis of hypersensitivity myocarditis. However, there was no definite evidence to support a causal link between the administration of vaccines and myocarditis. Repeated antigen injection is a well-established provocation test to substantiate a causal relationship, however this in itself raises ethical dilemmas.
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REFERENCES
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ABSTRACT
INTRODUCTION
