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Retinal plaque ring found in elderly man
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Leo P. Semes
An 83-year-old white male presented for a routine eye exam. He complained of difficulty reading with his current glasses. His ocular history was significant for a resolved Hollenhorst plaque in his right eye in 2008 and a resolved flame-shaped retinal hemorrhage in his left eye in 2006.
The patient had an extensive medical history including two previous cerebral vascular accidents, memory loss, atrial fibrillation, benign prostatic hypertrophy, vertigo, hyperlipidemia, sleep apnea, chronic obstructive pulmonary disease, ventricular tachycardia, congestive heart failure, hypertension and coronary atherosclerosis. As can be expected, the patient was on numerous medications.
Plaque is inferior temporal to the disc with hemorrhages along the venous arcade.
Close-up of plaque showing segmentation of the arteriolar blood column, attenuation of the vein proximal and dilation of the vein distal to the occlusion.
Images: Sellechio JC
The patient’s entering visual acuity with his habitual glasses was 20/20 in the right eye and 20/25 in the left. Pupillary function was normal with no afferent pupillary defect. Extraocular muscle motility was smooth and accurate. Confrontation visual fields were full to finger counting. Biomicroscopic evaluation was remarkable only for early to moderate nuclear and cortical cataracts in each eye. Goldmann applanation tonometry measured 11 mm Hg in his right eye and 9 mm Hg in his left eye.
Upon dilated examination of the right eye, the vitreous was clear, the optic nerve head appeared well perfused with a cup-to-disc ratio of 0.30, and there was mild pigment mottling of the macula. The vasculature appeared normal with no apparent emboli. The peripheral retina was flat and intact.
In the left eye, a prominent Weiss ring was visible. The optic nerve head appeared well perfused with a cup-to-disc ratio of 0.30, and there was mild pigment mottling of the macula. The peripheral retina was flat and intact. Observation of the retinal vasculature revealed a whitish-yellow plaque within the inferior branch of the first bifurcation of the inferior temporal retinal arteriole as it crossed the inferior temporal retinal venule. There was segmentation of the arteriolar blood column distal to the plaque, with apparent reperfusion by collateral vessels at two subsequent locations. Scrutiny of the venule showed that it was dilated distal to the initial arteriolar crossing and attenuated proximal to the crossing. Several intraretinal blot hemorrhages were present following the curve of the arcade from this point.
What’s your diagnosis?
Retinal plaque
We diagnosed the patient with combined branch retinal artery occlusion (BRAO) and branch retinal vein occlusion (BRVO).
Source: Sellechio JC, Baskin EG
Source: Sellechio JC, Baskin EG
BRAO generally presents as a painless, abrupt loss of part of the visual field in one eye. The patient may report a recent history of amaurosis fugax or other visual disturbance. The patient’s entering visual acuity depends on the location of the occlusion and the extent of the blockage of retinal arterial blood flow. Ophthalmoscopically, there may be a visible embolus within a retinal arteriole. Initially, there may be superficial whitening of the retina along the distribution of the affected branch artery, an indication of acute edema of the inner retinal layers. Other signs may include arteriolar narrowing, segmentation of the blood column and occasional cotton-wool spots. BRAO most often occurs in the superior temporal arcades.
A BRAO results from an embolus dislodged from elsewhere in the cardiovascular system that travels through the circulation until encountering a vessel within the retina that is too narrow for it to pass through. The accompanying table lists some common reported etiologies of emboli.
Common types
The three most common types of emboli are cholesterol (Hollenhorst), calcium and platelet-fibrin. Hollenhorst plaques tend to be discrete, refractile and yellowish and are often observed at vessel bifurcations. They may indicate carotid artery disease. Platelet-fibrin plaques may also originate from the carotid arteries and tend to be dull in color and elongated within the vessel. Calcium plaques commonly originate from cardiac valves and are white.
In working up a patient with a BRAO, blood pressure should be measured at the time of examination and appropriate measures should be taken if malignant hypertension is present. Laboratory testing is usually indicated, as is cardiovascular testing such as EKG, echocardiography and carotid duplex Doppler ultrasound. A fluorescein angiogram can be obtained to confirm the diagnosis. The optometrist’s most common course of action is to promptly notify the patient’s primary care provider of the findings and consider referral to a retina specialist.
There is no documented effective treatment for BRAO. Any underlying cardiovascular disease should be treated and the patient should be re-evaluated in 3 to 6 months for progression. Neovascularization is a rare complication.
Unlike the embolic closure of an artery in BRAO, BRVO is caused by compression of a venule by an overlying arteriole diseased by hypertension, arteriosclerosis or diabetes. Similar to BRAO, patients with BRVO usually present with a complaint of unilateral vision loss. Retinal examination will reveal superficial hemorrhages along the affected retinal vein that generally respect the horizontal raphe. Other signs may include retinal edema, cotton-wool spots, retinal neovascularization and vitreous hemorrhage. The occluded vein will appear dilated and tortuous and the adjacent artery may be narrowed. The differential diagnosis of BRVO should include diabetic retinopathy and hypertensive retinopathy. These conditions will usually present bilaterally, and the hemorrhages may cross the horizontal raphe.
Work-up
The work-up for BRVO may include laboratory and imaging studies. The findings of the Branch Vein Occlusion Study (BVOS) suggest that extensive laboratory testing in patients with typical BRVO is unnecessary. Certain lab tests may be useful in atypical cases such as bilateral BRVO, in young patients or in patients with personal/family history of thromboembolism.
Fluorescein angiography may be performed to look for macular edema or ischemia if the patient’s vision remains decreased 3 months after the occlusion. Optical coherence tomography also offers useful information in the follow-up of patients with macular edema secondary to BRVO.
Treatment
Medical treatment of BRVO has been shown to be generally ineffective. Complications including macular edema as well as the sequelae from retinal neovascularization such as vitreous hemorrhage, tractional retinal detachment and neovascular glaucoma can all lead to vision loss.
Several surgical and laser procedures, as well as injections of a vascular endothelial growth factor inhibitor such as Avastin (bevacizumab injection, Genentech) or Lucentis (ranibizumab injection, Genentech) are available for treatment of macular edema or neovascular complications. If macular edema is present, the patient may benefit from laser photocoagulation in a grid pattern. This treatment is not offered in the case of macular ischemia.
As for prognosis, Rehak and Rehak reported that 53% of eyes suffering BRVO will ultimately obtain 20/40 or better visual acuity, 25% have best corrected visual acuity between 20/50 and 20/100, and 22% have vision 20/200 or worse. The more distal to the optic nerve the occlusion occurs, the better the visual prognosis.
Our patient’s management
Source: Sellechio JC, Baskin EG
In the case of our patient, it would appear that he suffered both a BRAO and BRVO. Nicolo and colleagues and Conway and colleagues reported combined BRAO and BRVO occurring in hepatitis and HIV patients. These appear to be caused by immune complexes or inflammation. In our case, it is likely that the precipitating event was the embolus within the inferior branch of the first bifurcation of the inferior temporal retinal arteriole causing BRAO. Unfortunately, the occlusion occurred precisely at the point where the arteriole crosses the underlying inferior temporal retinal venule, causing compression and ultimately partial occlusion of the venule. In a case such as this, a combined work-up for BRAO and BRVO would be indicated.
Our patient had an extensive cardiovascular history and was being followed closely by his primary care provider and cardiologist, who were both notified, and required no further work-up initiated by the eye clinic. The patient was scheduled to follow up with us in 2 to 3 months. Regrettably, the patient passed away prior to his follow-up.
References:
- Branch Vein Occlusion Study Group. Argon laser photocoagulation for macular edema in branch vein occlusion. The Branch Vein Occlusion Study Group. Am J Ophthalmol. 1984;98(3):271-282.
- Conway M, Tong, P, Olk RJ. Branch retinal artery occlusion (BRAO) combined with branch retinal vein occlusion (BRVO) and optic disc neovascularization associated with HIV and CMV retinitis. International Ophthalmology. 1995;19:249-252.
- Hayreh SS, Podhajsky PA, Zimmerman MB. Branch retinal artery occlusion: natural history of visual outcome. Ophthalmology. 2009;116(6):1188-1194.
- Nicolo M, Artioli S, La Mattina GC, et al. Branch retinal artery occlusion combined with branch retinal vein occlusion in a patient with hepatitis C treated with interferon and ribavirin. Eur J Ophthalmol. 2005;15:811–814.
- Nowak RJ, Amin H, Robeson K, Schindler JL. Acute central retinal artery occlusion treated with intravenous recombinant tissue plasminogen activator [published online ahead of print February 18, 2012]. J Stroke Cerebrovasc Dis. Accessed May 10, 2012.
- Rehak J, Rehak M. Branch retinal vein occlusion: pathogenesis, visual prognosis and treatment modalities. Curr Eye Res. 2008;33(2):111-131.
For more information:
- John C. Sellechio, OD, is a staff optometrist at the VA Medical Center in Providence, R.I., and is in private practice in Warwick, R.I. He is an affiliated clinical professor of optometry with both the New England College of Optometry and the Illinois College of Optometry. He can be reached at VAMC Providence Eye Clinic, 623 Atwells Ave., Providence, RI 02909-2472; (401) 273-7100; john.sellechio@va.gov.
- Elina Goman Baskin, OD, is a staff optometrist at the VA Medical Center in Providence, R.I., and is in private practice in Providence and Attleboro, Mass. She is an affiliated clinical professor of optometry with both the New England College of Optometry and the Illinois College of Optometry. She can be reached at VAMC Providence Eye Clinic; elina.goman-baskin@va.gov.
- Edited by Leo P. Semes, OD, a professor of optometry, University of Alabama at Birmingham and a member of the Primary Care Optometry News Editorial Board. He may be contacted at lsemes@uab.edu.