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Patient has ‘bloody’ right eye with ulcer, light sensitivity in the left eye
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A 68-year-old Caucasian male was referred from his primary care physician due to blood and ulcer in one eye and light sensitivity in the other. The patient’s wife stated she had noticed the “bloody” right eye for the past 2 weeks. The patient seemed unconcerned with the eye in question, but reported increased light sensitivity in the left eye for the previous 2 to 4 weeks.
The patient gave a meandering and somewhat contradictory history. It was eventually surmised that he had suffered sudden painless loss of vision in the right eye approximately 10 years earlier. He reported seeing an eye doctor at the time, who told him he had suffered a “stroke of the back of the eye.” He reported seeing a second eye doctor at some later date. He claimed this second doctor told him he had glaucoma in both eyes, but no treatment was initiated. No further ocular evaluations had taken place.
Approximately 4 to 5 years after the second examination his right eye became very painful. He refused to see an eye doctor, so his primary care physician prescribed narcotics for the pain. The pain subsided after approximately 6 months.
The patient’s wife said he had a “bloody” right eye for 2 weeks.
Images: Azpiroz L
Classic presentation of dendritic keratitis in the left eye.
The primary reason for seeking eye care at this time was light sensitivity in the left eye for the past 2 to 4 weeks. He attributed these new symptoms to some kind of spillover affect from the eye pain in the right eye. When asked to rate the pain in the right eye from zero to 10, he rated it as a two, but said it varied and approached 10 at times.
The patient’s medical history was positive for congestive heart failure, arrhythmia, high blood pressure, asthma and bruising tendencies in addition to suffering six to eight strokes in the past 10 years. His medications were: amlodipine, carvedilol, furosemide, Vicodin (hydrocodone bitartrate and acetaminophen, Abbott), isosorbide, lisinopril, Pradaxa (dabigatran etexilate mesylate, Boehringer Ingelheim) and pravastatin. He reported a penicillin allergy. His social history was positive for heavy smoking (two packs a day for 25 years) and alcohol consumption on a daily basis for decades.
Best corrected acuities were no light perception in the right eye and 20/40- in the left. Acuities did not improve through pinhole, but a reduction in the photophobia of the left eye was noted. Refraction did not improve beyond pinhole, with a minor hyperopic refractive error. Intraocular pressures were 16 mm Hg OD and 10 mm Hg OS. A superior nasal visual field defect was detected in the left eye by confrontation.
Slit lamp exam of the right eye revealed a mostly white eye with some episcleral vessel engorgement. Corneal vascularization extended 2 mm into the cornea 360 degrees. Microcystic keratitis involved the entire epithelium. A sea fan-like vascular net extended from the anterior chamber angle toward the visual axis along the endothelium and iris surface. A dense fibrovascular exudate extended beyond the corneal vascularization. No view of the angle was possible due to the epithelial edema. A 360-degree posterior synechiae was also present. The lens was completely opacified by a 4+ white cataract.
Evaluation of the left eye was remarkable for a marginal herpetic (herpes simplex virus) dendrite and 2+ nuclear sclerosis of the crystalline lens. Otherwise, the anterior segment appeared unremarkable.
The right pupil failed to dilate, and no view of the posterior segment was achieved. Dilated fundus examination of the left eye revealed a healthy optic nerve, pigment changes of the macula, collateral vessels at the inferior disc margin and inferior to the macula, and attenuated retinal vessels extending inferiorly from the optic nerve. The periphery revealed intraretinal hemorrhages in the inferior temporal quadrant.
Tentative diagnoses would be burnt-out neovascular glaucoma (per intense pain in the past) with subsequent retinal detachment/phthisis bulbi (per no light perception and now normal IOP).
The patient was diagnosed with a blind painful right eye of yet unknown etiology. Branch retinal artery occlusion (BRAO) and HSV dendritic keratitis was diagnosed in the left eye.
Patient management
The patient was prescribed Pred Forte (prednisolone acetate, Allergan) four times per day for pain in the right eye and instructed to continue taking Vicodin as needed. He was prescribed Viroptic (trifluridine, Monarch) every 2 hours while awake for the left eye. He was scheduled for an ultrasound of the right eye and a fluorescein angiogram (FA) of the left eye.
One week later the patient reported decreased pain in the right eye and reduced light sensitivity in the left. Intraocular pressures were now 10 mm Hg OD and 13 mm Hg OS. The HSV dendrite was diminished by 50%. Two weeks later the dendrite had completely resolved, and the Viroptic was discontinued.
One month after initial presentation the cornea remained clear in the left eye. With the continued use of Pred Forte, the patient reported improved comfort of the right eye and a reduction in the need for the use of Vicodin. Results of the ultrasound revealed a nearly completely detached retina in the right eye. FA showed capillary dropout of the inferior retina, delayed filling of attenuated arterioles and the presence of collateral vessels at both the inferior disc margin and inferior macular region, all of which are consistent with an old BRAO in the left eye.
The patient had pigment changes in the macula of the left eye, collateral vessels at the inferior disc margin and inferior to the macula, and attenuated retinal vessels extending inferiorly from the optic nerve.
Going forward, pain management of the right eye may be better attained by enucleation or retrobulbar absolute alcohol injection. A referral to oculoplastics was offered but declined. The patient was asked to continue with the current regimen. The importance of tight blood pressure control to reduce the risk of further vision loss from retinal vasculopathy was discussed, and the patient was asked to return every 6 months to rule out neovascular retinal changes and glaucoma.
Discussion
At the time of presentation, the most important issue was to determine which complaints were associated with an acute condition and which were more chronic in nature. Clearly, the findings in the right eye were longstanding. The left eye showed evidence of both an acute and chronic mechanism. The fundus findings in the left eye gave some insight as to the cause of the chronic presentation in the right eye. It also alerted us to the risk of future vision loss in the left eye.
Results of the ultrasound of the right eye revealed a nearly completely detached retina.
FA showed capillary dropout of the inferior retina, delayed filling of attenuated arterioles and the presence of collateral vessels at both the inferior disc margin and inferior macular region in the left eye.
The history of six to eight strokes in the past 10 years, a review of medications and evidence of an old BRAO in the left eye gave a clue to the possible etiology of the chronic vision loss and eye pain in the right eye. Poorly controlled hypertension led to a central retinal artery occlusion of the right eye 10 years earlier, resulting in a complete, painless loss of vision. An ischemic neovascular glaucoma caused the severe pain that subsided when a complete retinal detachment resulted in a phthisis bulbi.
At this point, pain management and cosmesis are the only considerations for the right eye. The intermittent eye pain could be inflammatory in nature, as the Pred Forte provided some relief, and IOP actually decreased. Ultimately, enucleation or retrobulbar absolute alcohol injection may be necessary to completely relieve the pain. Cosmesis could be improved with a cosmetic contact lens, shell or a prosthetic if the eye is enucleated.
What is the risk of future vision loss in the left eye? Because the BRAO appears chronic, the risk of ischemia from this episode is low at this point. However, if his historically brittle hypertension is not managed, the risk of future vaso-occlusive episodes remains. It is imperative that we communicate both the ocular findings as well as the systemic risks to the primary care physician.
Arterial hypertension, hyperlipidemia, atherosclerosis, arrhythmias, polycythemias and arteritis are some of the systemic conditions that can lead to occlusive events resulting in hemorrhagic and/or ischemic events in the retina and optic nerve. Our job as primary eye care providers is to understand the pathogenesis of these ocular manifestations and communicate our findings to the primary care provider and other specialists. We are also responsible for appropriate ocular monitoring through timely follow up.