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I. CASE HISTORY A. Patient Demographics: 78 Year Old White Male B

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I. CASE HISTORY A. Patient Demographics: 78 Year Old White Male B I. CASE HISTORY a. Patient Demographics: 78 year old white male b. Chief Complaint: Patient presents for comprehensive eye examination to transfer eye care to the VA from an outside private provider. Patient originally contacted the clinic because he would like refills on his drop medication. No visual complaints with current correction. Patient reports that he has seen a “black line that looks like a hair” in his vision for 3 weeks. Denies flashes, floaters, other changes in vision. c. Ocular, Medical history: i. Chronic Open Angle Glaucoma OD ii. Uveitis associated with adverse reaction to Lumigan OD iii. Essential Hypertension, Atrial fibrillation, Obstructive Sleep Apnea d. Ocular Surgical History i. PCIOL w/ PHACO OD (11/2011), YAG Capsulotomy OD (2013), PCIOL w/ PHACO OS (12/2014), SLT OD (7/2015) e. Ocular medications i. Pred Forte BID OD (last dose: this morning), Cyclopentolate BID OD (last dose: 1 month ago), Cosopt BID OD (last dose: 1 month ago) f. Systemic Medications i. Lisinopril 5mg QD PO, Warfarin 5mg QD PO II. Pertinent Findings a. Clinical i. Entering Visual Acuity OD 20/50-1, PH 20/40+1; OS 20/20 ii. Confrontation Fields: mildly restricted 360, greater difficulty with superior and nasal field OD, FTFC OS iii. Pupils: EERL, 3+ reactivity OU, 2+ APD OD iv. Manifest Refraction: OD -0.25 – 1.00 x 045 VA 20/40+1 OS plano VA 20/20 v. Lids/Lashes: clear OU vi. Cornea: clear OU vii. Conjunctiva: one large dilated blood vessel temporally OD, clear OS viii. Anterior Chamber: OD deep with 1+ cells and flare, OS deep and quiet ix. Iris: peripupillary rubeosis OD, clear and flat OS x. Tonometry (Perkins Applanation): OD 22mmHg, OS 15mmHg xi. Ant Vitreous: OD pigmented cells, OS clear xii. Media: OD vitreous hemorrhage inf obscuring view of retina, OS Syneresis xiii. Optic Nerve OD: 0.85/0.90, thin rim 360, OS: 0.75/0.80, pink distinct rim tissue xiv. Macula: clear OU xv. Vessels: 2/3, normal OU xvi. Periphery: OD vitreous hemorrhage obscuring view of inf periphery, flat without holes, tears, or detachments OU; OD scleral depressed 360 b. Humphrey Visual Field 24-2: OD unreliable secondary to high false positives; overall depression most dense superiorly and nasally, OS questionable reliability secondary to fixation losses; superior defects possibly indicative of superior arcuate. c. Fluorescein Angiography: OD Iris leakage. Delayed filling. Scattered RPE staining. No leakage of disc or periphery. Patchy blockage from VH. OS normal iris, no posterior leakage. III. Differential Diagnosis a. Etiologies of Vitreous Hemorrhage: i. Neovascularization secondary to Proliferative Diabetic Retinopathy, Exudative Age- Related Macular Degeneration, Central Retinal Vein Occlusion, Ocular Ischemic Syndrome, Sickle Cell Retinopathy ii. Hemorrhagic Posterior Vitreous Detachment iii. Trauma, closed or open globe b. Hemorrhagic posterior vitreous detachment was ruled out by careful examination of the fundus with scleral depression OD. Presence of rubeosis OD makes neovascularization the most likely etiology of the vitreous hemorrhage; ocular ischemic syndrome is determined as the underlying cause due to the pathognomonic delay in transit times on fluorescein angiography, and the medical history lowers suspicion for disease states such as diabetes. IV. Diagnosis and Discussion a. Fluorescein Angiography is critical in the diagnosis of ocular ischemic syndrome in this case due to the leakage of iris vessels and delayed filling OD. b. Carotid ultrasound confirms suspicion of carotid disease and reveals >70% stenosis of the right internal carotid artery and 50-69% stenosis of left internal carotid artery c. Ocular Ischemic Syndrome is typically a unilateral condition characterized by decreased blood supply to the retrobulbar vessels and reversal of blood flow in the ophthalmic artery. Ischemia of the retina may manifest anteriorly as iris neovascularization or an anterior chamber reaction (cells and/or flare). Ischemia may present in the posterior segment as arterial attenuation, intra-retinal hemorrhages, retinal neovascularization, cotton wool spots, or macular edema. Patients typically experience loss of vision from macular edema or vitreous hemorrhage, ocular pain, or may be completely asymptomatic. d. Diagnosis of the case is confounded by previous diagnosis of Lumigan-associated uveitis OD, so the anterior chamber reaction exhibited by the patient may be a result of ocular ischemic syndrome or a lingering inflammatory reaction. The relatively high pressure OD is likely due to the patient’s non-compliance with glaucoma medication. e. Vitreous hemorrhage obscuring the view of inferior retina makes it difficult to rule out a peripheral retinal tear or break as the etiology. Additionally, the patient exhibited no symptoms of transient ischemic attack or unilateral vision loss and is in fact completely asymptomatic excluding the new onset “hair in vision” that was elicited during HPI. V. Treatment, management a. Pt was referred to ophthalmology and subsequently injected with Eyelea OD. Pt is currently scheduled for a one month follow up to monitor for resolution of neovascularization. A vascular surgery consult has been ordered to address the patient’s carotid artery stenosis. VI. Conclusion a. Ocular Ischemic Syndrome may present in an asymptomatic patient with minimal risk factors. A careful anterior segment evaluation is critical in all patients with a vitreous hemorrhage of unclear etiology to rule out iris neovascularization, and fluorescein angiography is indicated to confirm the diagnosis of ocular ischemic syndrome. Iris neovascularization is present in 20% of patients with ocular ischemic syndrome, and prompt diagnosis may save the patient’s vision and life. Carotid Ultrasound is indicated to rule out carotid stenosis and prompt referral to ophthalmology is necessary for treatment of any neovascularization or macular edema. A vascular consult is also warranted to address any potential treatment or surgical options for the patient’s carotid artery stenosis. VII. Literature Cited a. Mendrinos, E et al. Ocular Ischemic Syndrome. Survey of Ophthalmology. 2010; 55(1):2-34. b. Terelak-Borys B et al. Ocular Ischemic Syndrome – a systematic review. Medical Science Monitor. 2012;18(8):138-144. c. Yung K et al. Clinical Features of Ocular Ischemic Syndrome and Risk Factors for Neovascular Glaucoma. Korean Journal of Ophthalmology. 2017; 31(4): 343–350. .
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