Case Report: Subacute Bacterial Endocarditis Presenting with Decreased Visual Acuity and Intraretinal Hemorrhage
ALLISON ANGELILLI, MD and JASON S. SLAKTER, MD
This is a case of subacute bacterial endocarditis presenting with mildly decreased visual acuity (VA), symptoms of posterior vitreous detachment, vitreous inflammation, and intraretinal hemorrhage.
Case history presentation: A 67-year-old woman was referred for symptoms of floaters and 3 weeks of mildly decreased VA in the right eye. The patient denied a history of eye disease, surgery, and trauma; and she had not experienced pain, redness, or photopsia. Her medical history was significant for labile hypertension (blood pressure 138/95 in the office). In addition, the patient reported a mild febrile illness with malaise and dysuria during the 3 weeks prior to presentation.
Figure 1. A normal appearing optic nerve and several scattered intraretinal hemorrhages along the superior arcade of the right eye.
Figure 2. A rare cell in the vitreous and scattered intraretinal hemorrhages superiorly, as well as in the perimacular area of the left eye.
Examination: The patient had a VA of 20/60 in the right eye and 20/40+ in the left eye in a dilated state. The IOP was 10 mm Hg bilaterally and external examination was normal. Slit lamp examination revealed a quiet anterior segment in both eyes with no evidence of inflammatory cells. The anterior vitreous; however, showed 1+ cells in the right eye and a rare cell in the left eye.
Fundus examination of the right eye demonstrated a normal appearing optic nerve and several scattered intraretinal hemorrhages along the superior arcade (Figure 1). There was a posterior vitreous separation with cellular debris on the vitreous face and within the formed vitreous. In the left eye there was a rare cell in the vitreous and scattered intraretinal hemorrhages superiorly and in the perimacular area (Figure 2). No vitreous separation was noted in the left eye. Neither eye demonstrated neovascularization, periphlebitis, subretinal exudation, peripheral tears, breaks, holes, or detachments.
B-scan ultrasound examination confirmed the vitreous separation in the right eye. Fluorescein angiography was notable for blocked fluorescence by scattered hemorrhages.
Due to the presence of the vitreous cells and debris, the patient was referred for laboratory testing. Serum chemistry, PPD, angiotensin-converting enzyme level, and RPR were within normal limits. The erythrocyte sedimentation rate was mildly elevated at 45 mm, and the white blood count was 11300 with a significant left shift. At this time the patient revealed that she had been diagnosed with a heart murmur and had undergone dental work 4 weeks prior to presentation for which she had taken antibiotic with clindamycin. An echocardiogram revealed a 2-cm, mitral valve vegetation.
Treatment: The patient underwent emergent mitral valve replacement and was treated with 6 weeks of intravenous gentamycin and vancomycin. Eight weeks after presentation the patient's VA was 20/25 in the right and 20/20 in the left, she denied symptoms of floaters and exam showed resolution of vitreous inflammation and resolution of hemorrhages bilaterally.
Discussion: The patient likely developed this condition as a result of colonization of a previously damaged mitral valve endothelium secondary to transient bacteremia in spite of prophylactic therapy. This subacute process manifested as mild constitutional symptoms, mildly decreased VA, and floaters.
The majority of ophthalmic manifestations of bacterial endocarditis result from microembolization of bacteria or debris from the damaged valve into the retinal and choroidal circulations.1-4 The ocular findings in this patient can best be understood as the result of multiple microscopic emboli to the retinal circulation causing retinal hemorrhage and a vitreous inflammatory response leading to a mild decrease in VA. The symptomatology and excellent visual outcome speak against a diagnosis of bacterial endophthalmitis although the patient was treated with ciprofloxacin prior to this examination, which may have prevented a more obvious presentation of endophthalmitis. Unlike the majority of reports of patients with ocular involvement in bacterial endocarditis, this patient had minimally decreased VA and her primary complaint of floaters may have been unrelated to the underlying diagnosis.
Conclusion: This case demonstrates the necessity of a high index of suspicion in a patient with minimal vitreous inflammation in the setting of a preceding febrile illness and highlights the importance of the ophthalmic exam in detecting this serious condition.
1. Reese LT, Shafer D. Retinal embolization from endocarditis. Ann Ophthalmol. 1978;10:1655-1657.
2. Munier F, Othenin-Girard P. Subretinal neovascularization secondary to choroidal septic metastasis from acute bacterial endocarditis. Retina. 1992;12:108-112.
3. Magone MT, Lustbader JM, Cupples HP. Endogenous endophthalmitis as the initial presentation of a left ventricular mass causing embolic showers. Retina. 2002;22:640-641.
4. Schocket S, Braver D. Cilioretinal artery occlusion in a patient with suspected subacute bacterial endocarditis. South Med J. 1970;63:1-4.
From Vitreous Retina Macula Consultants of New York, New York, NY. None of the authors has financial interest in the information presented in this article.