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Sudden, painless loss of vision
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An 80-year-old Caucasian man presented to the office with a complaint of a sudden and painless loss of vision in the right eye that was initially noticed 2 days prior to his appointment. Entering visual acuity was hand motion in the right eye and 20/20 in the left eye. A review of his medical records showed best-corrected visual acuity at 20/30 in the right eye just 1 month prior to presentation with a diagnosis of early age-related macular degeneration and pigmentary changes. Pupils were equally round and reactive to light and there was no evidence of an afferent pupillary defect. Motility was intact without restriction.
The patient’s medical history was significant for high cholesterol, asthma and arthritis. He reported uneventful cataract surgery approximately 7 years ago. Current medications include 2 mg warfarin, 180 mg diltiazem and 70 mg atorvastatin.
Anterior segment evaluation by slit lamp examination revealed quiet bulbar and palpebral conjunctiva in both eyes; lids and lashes were clear; corneas were clear and intact; anterior chambers were deep and quiet. Intraocular pressures measured via Goldmann tonometry were 13 mm Hg OD and OS.
A dilated fundus examination of both eyes showed well-centered posterior chamber IOLs with minimal posterior capsule opacification. The right fundus is shown in the accompanying image with the corresponding optical coherence tomography image. The left fundus showed a well-perfused optic nerve head and normal retinal vasculature. There were scattered drusen and early pigmentary changes that were stable compared to previous visits.
What’s your diagnosis?
The patient was diagnosed with a large submacular bleed with an associated serous retinal detachment. After counseling and discussion of his condition, he was sent to a retinal specialist for evaluation and treatment. The preoperative and postoperative diagnoses made by the retinologist were neovascular macular degeneration with serous retinal detachment. The patient underwent a pars plan vitrectomy and received subretinal tissue plasminogen activator (TPA), an air-fluid exchange and intravitreal Avastin (bevacizumab, Genentech).
The patient was subsequently seen 1 week after surgery. Vision had improved to counting fingers in the right eye. The gas bubble had nearly resolved, and a large portion of the hemorrhage was displaced inferiorly.
He was seen by the retinologist 3 weeks later, with vision improving to 20/40 in the right eye. Mild peripapillary hemorrhaging still remained, with a significant amount of hemorrhage still displaced inferiorly. The fovea was flat, and the retina remained attached.
Spontaneous development
Submacular hemorrhages may spontaneously develop in the elderly population and most commonly result from choroidal neovascularization. Patients that currently take anticoagulants may have an increased risk of subretinal bleeding. A study by Kiernan and colleagues demonstrated an increased risk of intraocular hemorrhages in patients with neovascular AMD concurrently treated with antiplatelet or anticoagulant therapy.
Visual prognosis for these patients is typically poor, with the potential for significant and permanent visual loss. The visual outcome is especially poor if the hemorrhage is thick, involves the fovea or covers a large area of the macula.
Jeffrey R. Varanelli
Submacular hemorrhages can be categorized by location, size and thickness. The location is classified in relation to the fovea (i.e., subretinal or subretinal pigment epithelium). Small submacular hemorrhages are typically less than 12 disc areas, whereas large are categorized as greater than 12 disc areas. Thin subretinal hemorrhages are typically less than 500 microns thick, while thick hemorrhages have a thickness greater than 500 microns. Small submacular hemorrhages with thin layers of subretinal blood typically have a better prognosis, but subretinal hemorrhages associated with an underlying choroidal neovascular membrane will have a much poorer prognosis on visual recovery.
Damage as a result of subretinal hemorrhages occurs through several mechanisms. Retinal toxicity due to iron from hemoglobin, impaired metabolic exchange between the photoreceptors and the retinal pigment epithelium, as well as fibrin-mediated damage due to clot contraction are all contributory factors. Therefore, early intervention and management of these patients is critical to increase their chances of visual recovery.
Proposed treatments
There are several proposed treatments for submacular hemorrhages that arise from AMD, and controversy surrounds which is most appropriate. Though many options exist, most retinal specialists will typically perform one or more of the following: pars plana vitrectomy, subretinal or intravitreal TPA and anti-VEGF treatment. New studies that look at combining techniques are constantly being evaluated. In determining which procedure or combination of procedures is used, the retinal specialist will make that determination based on causative factors, as well as the size and location of the hemorrhage.
Although no studies exist on the recommended intervention time for optimal clinical outcome, a study by Hattenbach and colleagues showed that patients with hemorrhages that existed for less than 14 days typically had more favorable results after treatment.
A pars plana vitrectomy is an integral part of the treatment regimen. A study by Thompson and Sjaarda looked at patients that presented with submacular hemorrhages and categorized them into two treatment groups: vitrectomy with removal of the submacular hemorrhage complex and vitrectomy with injection of subretinal TPA. They showed that a vitrectomy with removal of the subretinal hemorrhage complex resulted in better visual results.
The patient in this specific case did undergo a core vitrectomy with a trimming of the vitreous skirt. The vitrectomy was performed without incident using 25-gauge instrumentation.
Subretinal TPA is commonly used in these patients as well. This protease enzyme is involved in the cascade of activating plasminogen to plasmin, which will ultimately degrade and dissolve the fibrin clot. The amount of TPA used by the surgeon depends on the size and thickness of the subretinal hemorrhage.
TPA can also be used as an intravitreal injection. Several studies showed improvement in visual acuity when subretinal TPA was combined with a vitrectomy and air/gas exchange. In this particular case, a 41-gauge subretinal cannula was used to infuse the TPA.
Several new perspectives exist on the use of anti-VEGF treatment. A few recent studies have described Avastin monotherapy for treatment, though a study by Treumer and colleagues showed that a pars plana vitrectomy, with concurrent TPA and Avastin, coupled with a fluid-gas exchange, improved visual acuity in most patients. An injection of 0.05 mL of Avastin was used in this patient’s treatment regimen. Ultimately, the patient had a final visual acuity of 20/30 and he continues to function well. He has maintained his current dosage of warfarin but continues to see his cardiologist and have routine blood work on a regular basis.
The goal of treatment in these cases is to ultimately preserve or improve visual acuity while minimizing the chances of vision loss. With the advent of new medications and surgical procedures, the likelihood of visual morbidity is decreased. Prompt referral is critical to improve chances of visual recovery.
References:
Hattenbach LO, et al. Ophthalmology. 2001;108(8):1485-1492.
Haupert CL, et al. Am J Ophthalmol. 2001;131:208-215.
Kiernan DF, et al. Retina. 2010;30(10):1573-1578.
Lewis H. Am J Ophthalmol. 1994;118:559–568.
Shultz RW, et al. Semin Ophthalmol. 2011;26(6):361-371.
Thompson JT, et al. Trans Am Ophthalmol Soc. 2005;103:98-107.
For more information:
Jeffrey R. Varanelli, OD, FAAO, is in private practice and a clinical associate professor at the Michigan College of Optometry. He was awarded the Michigan Optometric Association’s Young Optometrist of the Year in 2004. Dr. Varanelli can be reached at Simone Eye Center, 29245 Ryan Road, Suite 100, Warren, MI 48092; (586) 558-2981; fax: (586) 558-8838; JRVOD@comcast.net.
Edited by Leo P. Semes, OD, a professor of optometry, University of Alabama at Birmingham, and a PCON Editorial Board member. He may be contacted at (205) 934-6773; lsemes@uab.edu.
Disclosure: Varanelli has no financial interests to disclose.