Pulmonary valve endocarditis: a case report

P. Vijay Shekar1,*, D. Senguttuvan2

1Department of Cardiology, Kauvery HeartCity, Trichy, Tamilnadu, India

2Department of Paediatrics, Kauvery Hospital, Trichy, Tamilnadu, India

*Correspondence: Tel.: +91 96864 69004; email: [email protected]

Abstract

Background: Pulmonary valve endocarditis is a very rare clinical scenario accounting for 1.5% of all infective endocarditis cases.

Case presentation: We report a case of pulmonary valve endocarditis, who presented with fever and pulmonary regurgitation murmur, and was successfully treated with appropriate antibiotics.

Conclusion: A high index of suspicion is required for the diagnosis of pulmonary valve endocarditis. Serial imaging and close follow up is required in such patients.

Keywords: Infective endocarditis, Pulmonary valve, Right sided endocarditis

Background

Right sided infective endocarditis is uncommon. Infective endocarditis involving the pulmonary valve is a rare occurrence. Isolated infective endocarditis involving the pulmonary valve in the absence of risk factors is an extremely rare scenario. With only sporadic case reports, management strategies of such patients remain unclear. The case highlights the importance of high index of clinical suspicion and serial imaging to establish such uncommon diagnosis.

Case Presentation

A 15-years-old boy, presented with complaints of fever of five days’ duration. After initial evaluation, in the view of suspected sepsis and unidentified source, patient was started on antibiotics (cefoperazone + sulbactam) elsewhere. In view of worsening clinical status, patient was referred to us for further treatment.

On admission, patient was dyspnoeic and tachypneic at rest. High grade fever (102.2°F) was documented at the time of admission. Blood pressure was 100/60 mm Hg with heart rate of 120 per min. On auscultation, an early diastolic murmur was heard at the base.

Patient underwent a transthoracic echocardiogram, which showed a hyper echoic freely mobile structure attached to the pulmonary valve, suggestive of vegetation (Fig. 1a and b). The vegetation

pulmonary-valve-endocarditis-image-a
pulmonary-valve-endocarditis-image-b

is seen moving into pulmonary artery during systole and right ventricle (RV) outflow tract in diastole.

Fig. 1a and b. Transthoracic echo parasternal short axis view (aortic valve level) shows hyperechoic lesion attached to the pulmonary valve. The hyperechoic lesion is seen freely moving into the pulmonary artery (a) and into the right ventricular outflow tract (b) during each cardiac cycle.

Mild to moderate pulmonary regurgitation was noted (Fig. 2), suggesting the possibility of infective endocarditis of pulmonary valve. Other valves and chambers were normal. Left and right ventricular function were normal. Mild pericardial effusion was present.

Blood investigations including blood cultures were sent. Patient’s antibiotics were escalated to Vancomycin along with cefoperazone/sulbactam. Patient’s clinical status improved with complete resolution of fever spikes within the next 48 hours. Blood cultures were negative. Antibiotics were continued for a period of six weeks.

Repeat ECHO after two weeks and six weeks showed complete resolution of the vegetation and residual mild pulmonary regurgitation (Fig. 3).

Discussion

Right sided endocarditis is less common than left sided endocarditis, accounting for 5–10% of cases. Pulmonary valve endocarditis is an extremely rare entity, accounting for 1.5–2% of endocarditis cases [1,6]. Only 70 case reports of pulmonary valve endocarditis have been reported in literature between 1979 and 2013 [1–4].

Pulmonary valve endocarditis, though has been reported to affect normal and abnormal valves is uncommon due to the following factors: endothelial lining and vascularity of the pulmonary valve, lower pressures of the right sided chambers and lower oxygen content of the right sided chambers [1,5]

pulmonary-valve-endocarditis-fig-2 Fig. 2. Continuous wave Doppler across the pulmonary valve shows moderate pulmonary regurgitation.

pulmonary-valve-endocarditis-fig-3 Fig. 3. Follow up transthoracic echo image (parasternal short axis view) demonstrating complete resolution of vegetation.

Risk factors for pulmonary valve endocarditis include indwelling catheters, iv drug abuse, alcoholism, sepsis, renal or liver transplant, immunosuppressive therapy, recent bowel surgery, gonorrhoea, underlying congenital heart disease, male gender, dental extraction and angiodysplasia [2]. Most common organisms reported are Staphyloccoccus aureus, Coagulase negative Staphylcocci and Streptococci [2].

The most common mode of presentation of pulmonary valve endocarditis is with fever and pulmonary symptoms (cough, dyspnoea, hemoptysis). The pulmonary symptoms are attributable to septic emboli. Pulmonary regurgitation results in an early diastolic murmur.

Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) are the usual modalities to establish diagnosis with good diagnostic yield with TTE (> 90%), due to the anterior location of the pulmonary valve [2]. Antibiotics are the mainstay of treatment, whereas surgery is reserved for valvular regurgitation resulting in acute heart failure, the presence of multi-drug resistant organisms or fungi, IE complicated by heart block or abscess formation, persistent bacteremia or recurrent emboli despite appropriate antibiotic therapy, and severe regurgitation with mobile vegetation >10 mm [6].

Our patient presented with fever and pulmonary regurgitation. There were no identifiable risk factors in our patient. Blood cultures were negative, however patient responded to the empirical anti biotic therapy of six weeks’ duration. Patient was followed up with TTE, which showed good resolution of vegetation and pulmonary regurgitation.

Conclusion

Isolated pulmonary valve endocarditis, without predisposing factors is an extremely rare entity. A high index of suspicion and echocardiography is necessary to establish diagnosis in such cases. The rarity of presentation accounted for diagnostic and therapeutic challenge, which was successfully treated.

Acknowledgements

We thank Dr. Suresh Venkita and Dr. R. Prabhaharan who helped us in preparing the manuscript.

Author contributions

P. Vijay Shekar and D. Senguttuvan were involved in diagnosis and treatment of the patient. P. Vijay Shekar drafted and edited the manuscript.

Competing interests

The authors have no competing interest to declare.

References

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