| Prosthetic mitral valve dehiscence caused by infective endocarditis | |
| DOI: 10.5606/e-cvsi.2015.294 | |
| Yüksel Dereli1, Ömer Tanyeli1, Halil İbrahim Erdoğan2, Niyazi Görmüş1 | |
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1Departments of Cardiovascular Surgery, Necmettin Erbakan University, Meram Medical Faculty, Konya, Turkey 2Departments of Cardiology, Necmettin Erbakan University, Meram Medical Faculty, Konya, Turkey |
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| Keywords: Dehiscence; infective endocarditis; prosthetic mitral valve | |
Despite therapeutic advances over the past few decades, prosthetic valve endocarditis remains a life-threatening condition and is
associated with increased significant morbidity and mortality. Prosthetic valve dehiscence caused by endocarditis is one of the most serious
complications of infective endocarditis. In this article, we present a case of acute subtotal dehiscence of prosthetic mitral valve caused
by staphylococcal endocarditis. A 74-year-old female patient presented with fever and breathlessness. She underwent mechanical mitral
valve replacement six years previously for mitral stenosis. Echocardiography confirmed subtotal dehiscence of prosthetic mitral valve.
Staphylococcus capitis was detected in blood cultures. The patient was reoperated successfully. |
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Prosthetic valve endocarditis (PVE) is a life-threatening
condition and has been reported to occur in
1 to 6% of patients.[1] Prosthetic valve dehiscence
(PVD) caused by endocarditis is one of the most
serious complications of infective endocarditis (IE).
If early diagnosis and treatment are not performed,
it may lead to acute decompensation, pulmonary
edema, cardiogenic shock, and death, eventually.
Herein, we present a case of acute subtotal dehiscence
of prosthetic mitral valve after six years caused by
staphylococcal endocarditis. |
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CASE PRESANTATION
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A 74-year-old female patient was admitted to our
clinic with complaints of fever and shortness of breath.
She underwent mitral valve replacement six years ago
for mitral stenosis. The patient had atrial fibrillation.
On physical examination, she had bilateral inspiratory
rales, jugular venous distension, S3 gallop, and
peripheral edema. Laboratory analysis revealed an
increased white blood count (14,000 mm/L), erythrocyte
sedimentation rate (71 mm/hr) and C-reactive
protein (41 mg/L). The international normalized ratio
(INR) was 3.42. The patient was then hospitalized and
three-set blood cultures were drawn. the vegetation of
the mitral prosthetic valve dehiscence, echocardiography
was performed and identified patients with severe
mitral regurgitation (Figure 1). Ampiric antibiotic
therapy was initiated. Staphylococcus capitis (S. capitis)
was detected in blood cultures and antibiotherapy was revised by the culture antibiogram. The patient underwent
one week of antibiotherapy and infection parameters
decreased. The patient was reoperated. During
surgery, subtotal prosthetic mitral valve dehiscence
was observed (Figure 2). Infected valve and annular
vegetations were excised. Bioprosthetic mitral valve
replacement was performed successfully. Figure 1: Preoperative echocardiography, showing prosthetic mitral valve dehiscence. Figure 2: Intraoperative view showing subtotal prosthetic mitral valve dehiscence. |
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Despite advances in medical treatment and surgical
techniques, PVE carries a high mortality risk ranging
from 20 to 80% of affected patients.[1] Early PVE
occurs within the first year of surgery with a risk ratio
of 1 to 3% and is frequently caused by Staphylococcus
epidermidis. Staphylococcal endocarditis has a higher
rate of morbidity and mortality than that caused by
other microorganisms and surgery is usually required.
Pathogens causing late PVE are similar to that of
native valve endocarditis.[2] In our case, PVE developed
six years after surgery and pathogenic microorganism
was reported as S. capitis. Staphylococcus capitis is a subtype of coagulase-negative staphylococci (CoNS) and it is part of the normal flora of the skin of the scalp, face, ears and neck.[3] Rarely, it may present as a significant pathogen causing IE, PVE, and late-onset sepsis. In 2011, Takano et al.,[4] reported four cases of PVE caused by S. capitis which were identified at their hospital over the past two years. The pathogenesis of CoNS is mainly due to their ability to form biofilms on indwelling medical devices which confers tolerance to disinfectants during surgery.[5] Furthermore, prosthetic valve dehiscence is a catastrophic complication of IE. Patients with PVD may have a stable hemodynamic profile or cardiogenic shock. Echocardiography is sufficient for diagnosis. As transthoracic echocardiography has low sensitivity, transesophageal echocardiography recommended for these patients. Recently, three-dimensional echocardiography is the favorite diagnostic method.[6] Treatment of PVD is usually surgical. Inadequate surgical debridement of infected material may result in recurrent PVE. Timing of surgery is of utmost importance for these patients. The success of surgery would increase by stabilizing the hemodynamic and laboratory parameters. In these patients, another important point is the selection of the type of prosthesis. However, Newton and Hunter reported that the choice of the prosthesis, either a bioprosthesis or mechanical valve, had no effect on the rates of recurrence in patients with PVE undergoing surgery.[7] In conclusion, PVE is a rare cause of PVD in late stage. Early diagnosis and treatment is life-saving for this condition.
Declaration of conflicting interests
Funding |
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