Case Presentation: A 77 year old male with history significant for mitral valve prolapse presented with constitutional symptoms and leukocytosis for the duration of several weeks. Upon hospital presentation, blood pressure was 90/50 millimeters of mercury (mmHg). Physical exam revealed a systolic murmur. Electrocardiogram revealed sinus rhythm, normal rate, and normal intervals. Most salient laboratory result is a white blood cell count of 19,400 with 2% bands. Computed tomography (CT) scan of the abdomen & pelvis revealed a cystic lesion in the spleen and other small scattered lesions in the spleen and liver. Magnetic Resonance Imaging (MRI) of the abdomen identified the cystic splenic lesion as a hematoma and other lesions as likely embolic infarcts. The patient was started on piperacillin-tazobactam. One blood culture bottle grew coagulase-negative Staphylococcus and the other grew an alpha-hemolytic Streptococcus. Piperacillin-tazobactam was changed to vancomycin and cefazolin. Transthoracic echocardiogram did not show clear evidence of endocarditis, but transesophageal echocardiogram revealed a 5 x 12 millimeter (mm) vegetation on the mitral valve. Antibiotics were changed to ceftriaxone. Surgical management was recommended. Prior to surgery, the patient was noted to have mental status changes, prompting an MRI Brain which revealed a 3 centimeter intraparenchymal hemorrhage and scattered infarcts consistent with septic emboli. Follow-up CT angiography (CTA) of the brain and neck re-demonstrated the MRI Brain findings and also revealed a 3 mm mycotic aneurysm adjacent to the area of hemorrhage, suggesting aneurysmal rupture. Interventional Radiology performed successful coil embolization of the mycotic aneurysm. The patient eventually underwent surgical mitral valve replacement. He was started on a 3 month course of post-operative warfarin for bioprosthetic valve and discharged with a 6 week course of ceftriaxone. He survived without long-term morbidity.
Discussion: Mycotic aneurysms are a known, but less common, complication of infective endocarditis, occurring in less than 5% of cases. A mycotic aneurysm forms when there is infection of the arterial wall, due to bacteremia or direct septic embolization, causing degeneration of the wall and dilatation. In many cases of infective endocarditis, systemic emboli and mycotic aneurysms occur before the patient presents. Mycotic aneurysms tend to be multifocal, and most frequently develop within intracranial arteries, particularly at sites of bifurcation. Intracranial mycotic aneurysms are usually asymptomatic and are often discovered on CTA studies obtained for evaluation of cerebral emboli. Ruptured intracranial mycotic aneurysms should be managed with antibiotics and endovascular or surgical intervention, as there is higher mortality associated with managing ruptured aneurysm with antibiotics alone.
Conclusions: This case highlights the challenging task of prompt recognition of subacute bacterial endocarditis and the feared complication of mycotic aneurysmal rupture. An important skill of the hospitalist is the ability to approach an undifferentiated case, develop a comprehensive plan for workup, and address a wide range of differential diagnoses. In the case of endocarditis, early recognition and intervention is crucial in preventing complications such as septic emboli and mycotic aneurysms.