Case report

Our patient was a 30-year-old woman. She had been followed up with depot penicilline parenteral antibiotherapy until the age of 18 since she had had acute rheumatic fever when 4 years old. Three months ago she started to suffer from swelling and pain at the joints of her hands and feet. Speech disturbances were added to her complaints afterwards and she was admitted to an institution with a diagnosis of infective endocarditis. She was then followed up by applying a combined antibiotherapy protocol. She was referred to our Cardiology Clinic for more advanced investigation and therapy. Her transthoracic echocardiography (TTE) revealed severe aortic regurgitation, severe mitral stenosis (MVA=1.6cm ² ) and a vegetative mass of 0.8x0.8 cm on the right coronary cusp of the aortic valve.Pulmonary arterial pressure was 45 mmHg.She was in New York Heart Association (NYHA) functional class III at presentation. Cranial MR imaging showed septic emboli in the distal branches of the left middle cerebral artery (MCA) and associated perilesional contrast enhancement supporting the diagnosis of focal abscess formation. An ovoid collection of 3 cm with central necrosis and peripheral contrast enhancement was observed. This lesion was consistent with left fronto-temporal infarcted area involving both cortex and white matter and an abscess developing on this ground. A control MR imaging was held 6 weeks later demonstrating near-total shrinkage of the abscess (Figure A).

Figure 1

Figure a

Our patient was consulted with the Neurosurgery Clinic repeatedly. Neither an immediate nor an elective surgery was planned. Neurology Clinic recommended the maintenance of prophylactic anticonvulsive therapy since this abscess was located at left parietal region next to the cortex. After completion of the parenteral antibiotherapy protocol and follow-up by both Cardiology and Neurology Clinics, our case was taken to the operating room electively.

She was operated under endotracheal general anesthesia and in supine position.Following a median sternotomy, pericardium was opened longitudinally. After heparinization, extra-corporeal circulation was established between the venae cavae and the ascending aorta. A cross clamp was placed on aorta and by antegrade intermittent isothermic blood cardioplegia from aortic root,cardiac arrest was established.Hypothermia was moderate (28ºc). A vent was placed via the right superior pulmonary vein.Standard left atriotomy was made from interatrial junction.The mitral valve is approached via a standard left atriotomy parallel to the interatrial sulcus. Cooley's retractor was positioned for optimal exposure.The entire valvular apparatus was carefully examined in order to assess the feasibility of reconstructive surgery and to plan the operative technique. The valvular apparatus was then mobilized as an entire unit with a nerve hook in order to assess tissue flexibility and to identify leaflet restriction. There was a severe mitral stenosis(Figure 1).

Figure 2

Figure 1

The bilateral comissures were incised while leaving one millimeter of valvular tissue intact as in the normal anatomy. The underlying chordae and papillary muscles were then incised accordingly. After this step we performed bilateral segmental annuloplasty. This procedure may also be used to achieve better approximation of leaflet tissue with the placement of mattress stitches at the commissures (Figure 2).

Figure 3

Figure 2

We tested the valve competence after this step on observing valve closure while the left ventricular cavity was filled with saline solution. There wasn't saline regurgitation. Valve competence and closure were excellent.

Following aortotomy we explored that right coronary leaflet contained a vegetative mass of 1x1 centimeter in diameter.

Figure 4

Figure 3

Native aortic valve was resected. We performed an AVR (21 no St Jude bileaflet mechanical valve) with separate sutures. No additional problem was seen postoperatively and he was discharged on 9 ^th postoperative day with surgical cure and outpatient clinic follow was recommended. She is still symptom-free and the valve functions are good in control TTE.

Comments

Cerebrovascular events complicate the management of infective endocarditis(₁). Neurological complications are very frequent in patients with infective endocarditis (20-40 %)(₂). The neurologic syndrome often is the presenting feature. The most frequent neurologic complication is cerebral ischemia. In these patients and those with intracranial hemorrhage, a heart murmur as well as systemic signs of inflammation point to endocarditis. The encephalopathy in endocarditis is mostly due to cerebral infarction. In bacterial meningitis and brain abscess an uncommon isolate arouses suspicion (₃).

Emboli are important not only in terms of the direct morbidity and mortality they cause via cerebral infarction, but also because of their role in the causation of mycotic aneurysms, brain abscesses, and abnormal CSF formulae. Macroscopic brain abscess is a rare complication of bacterial endocarditis. Miliary microscopic abscesses are more common than larger abscesses, particularly in patients with acute disease and miliary infection in other organs of the body (₄).

Two factors affect the incidence of neurologic complications (NC): first, the location of endocarditis with 76% of NC in mitral valve endocarditis compared with 37% in other cases , and second the infecting organism: 71% of NC in staphylococcus aureus endocarditis versus 45% in endocarditis with other bacteria(₅).

About the study of Eishi et al; in 181 patients with cerebral complications, organisms were detected as follows: gram-positive cocci in 133 (73.5% [Streptococcus in 85, Staphylococcus in 32]), gram-negative in 18 (9.9%), fungus in 11 (6.1%), and unknown in 64.6%, cerebral bleeding in 31.5%, cerebral abscess in 2.8%, and meningitis in 1.1%(₆).

In these patients it is unclear at what time a valve replacement should be performed(₂). Neurologic complications interfere with the timing of the valve replacement. Cases of successful valve replacement within 4 weeks after intracranial hemorrhage have been reported, but it is recommended to postpone it for 4-6 weeks(₃).

Mortality is increased in patients with neurologic manifestations. A neurologic event per se may constitute an indication for surgical treatment(₇). Valve replacement within the first four weeks after intracranial hemorrhage has been reported to be successful only in individual cases. The risk of deteriorating declines later to 15%. Only selected patients with intracranial hemorrhage and progressive heart failure might benefit from valve replacement within the first four weeks(₂).

The data of the study of Eishi suggest that cardiac operations can be done safely 4 weeks after cerebral infarction, and if the delay is more than 2 weeks, the exacerbation rate will be around 10%. The risk of progression of cerebral damage is still significant 15 days and even 4 weeks after cerebral hemorrhage(₆). Medical records suggest that early cardiosurgical intervention, if necessary, needs at least 2-3 weeks of preceding chemotherapy(₁). In patients with neurologic complications the mortality was significantly higher among those treated with antibiotics alone as compared with those treated surgically (₇).

Hospital mortality rate and an exacerbation rate of cerebral complications, including related death, according to the interval from onset of cerebral infarction to cardiac surgery. A significant correlation existed between the interval and the exacerbation of cerebral complications .Preoperative risk factors affecting exacerbation of cerebral complications were as follows: (i) severity of cerebral complications , (ii) intervals ,and (iii) uncontrolled congestive heart failure as indications for cardiac surgery(₆).

Correspondence to

Doç. Dr. Ufuk YETKIN, 1379 Sok. No: 9,Burç Apt. D: 13 - 35220, Alsancak – IZMIR / TURKEY Tel: +90 505 3124906 , Fax: +90 232 2434848 e-mail:ufuk_yetkin@yahoo.fr