Central retinal artery occlusion and central retinal vein occlusion in contralateral eye Oclusão da artéria central da retina com oclusão da veia central em olho contralateral

The case of a 55-year-old male who presented central retinal vein occlusion with marked macular ischemia in left eye is reported. Despite the intervention with sustained-release dexamethasone polymer injection and other clinical measures, the visual acuity was severely reduced in left eye. After 8 months, he returned to the emergency with acute visual loss of 2 hours of progression in right eye due to a central retinal artery occlusion, sparing only the territory of the cilioretinal artery. Patient underwent clinical maneuvers with anterior chamber paracentesis and intravenous injection of tissue plasminogen activator. Fluorescein angiography immediately after the procedures showed recanalization, but despite arterial vasodilation, no complete recanalization was observed after 24 hours. The patient developed retinal atrophy.


INTRODUCTION
Central retinal artery occlusion (CRAO) presents with sudden, severe, painless and usually unilateral loss of vision. Analogous to ischemic cerebral stroke, it is often caused by thromboembolic events due to ipsilateral carotid artery disease, primarily related to atherosclerotic plaques. (1) It is one of the ocular conditions requiring urgent treatment, since patients may have comorbidities and the associated mortality rate is high. (2,3) Obstruction reveals ischemic whitening at the posterior pole, which may spare the papillomacular bundle in cases where the cilioretinal artery irrigates this region. (4,5) Regarding venous occlusion, an increase in retinal venous pressure is expected and blood flow is reduced. The mechanism of obstruction is not well established, but it is believed to be caused by either thrombosis or mechanical compression in the lamina cribosa. (6) Some findings, such as intraretinal hemorrhages and vessel tortuosity, are characteristic of this condition. (6,7) In both cases, impaired visual acuity is closely linked to severity of ischemia and foveal involvement, and sudden loss of vision is more common. (1,7) The present study aimed to elucidate a clinical case of a patient presenting central retinal vein occlusion (CRVO) and CRAO in the contralateral eye. .

CASE REPORT
A 55-year-old white hypertensive male patient on bisoprolol 5 mg/day and losartan 50 mg/day, presented visual acuity (VA) of 20/20 in the right eye (RE) and 20/400 in the left eye (LE). The low VA was secondary to a CRVO in LE with severe ischemic component one week before (Figure 1). Treatment was initiated with intravitreal injection of Ozurdex®, peripheral vasodilator, ocular hypotensive agent, and retinal photocoagulation in ischemic areas, according to fluorescein angiography (AGF).
Laboratory tests showed only an increase in low-density lipoprotein (LDL; 295 mg/dL), with no other major changes. Carotid Doppler showed bilateral atheroma with no hemodynamic changes. In addition, blood pressure of 190/110 mmHg was measured due to poor adherence to systemic antihypertensive treatment. Losartan was replaced by clonidine hydrochloride 0.1 mg, and rosuvastatin 20 mg was initiated, which normalized blood pressure control to 130/80 mmHg.
Despite the measures taken, the patient evolved with severe low VA secondary to retinal atrophy, as confirmed by the optical coherence tomography (OCT) (Figure 2). After 8-month progression, the patient came to the emergency room complaining of loss of VA in the RE, two hours before. The examination revealed CRAO (Figure 3), with preservation of the territory of cilioretinal artery. At this time, ocular paracentesis was performed, followed by compression/decompression massage on the eyeball, endovenous tissue plasminogen activators (tPA) injection, arterial vasodilator (Sustrate®), and fundus fluorescein angiography (FFA) to verify arterial flow, in which it was possible to observe there was already arterial flow ( Figure  3). After 24 hours, the condition improved, but CRAO persisted ( Figure 4).
Due to time elapsed, it was decided to observe the risk of neovascular glaucoma and order screening laboratory tests for rheumatic and hematological diseases; the results were negative. At this time, it was also found the patient was not regularly using antihypertensive medication. pathophysiology has not been fully understood yet. It is believed the condition is due to thromboembolic occlusion in the region of the lamina cribosa, but can also be caused by mechanical compression of the vein at the same place, secondary to increased intraocular pressure. (6) Fundus examination shows intraretinal hemorrhages (dot blot and flame-shaped) in the four quadrants, associated with increased venous caliber and tortuosity. (6) The prognosis is related to the occurrence of vision loss due to macular edema, intraretinal hemorrhage, and ischemia, leading to neovascularization. (9) The control of factors associated with arterial occlusion may be crucial, preventing the onset of cerebral ischemic disease or ischemic cardiomyopathy, (2,5,10) which may appear in the first and second week, when upon examination. (8) Thus, rapid and accurate diagnosis of the condition involved is important to prevent mortality. Classical retinal findings on fundus examination include retinal edema, cherry red spot, retinal arteriolar attenuation, and slow segmental blood flow in retinal arterioles. (4,5) Based on etiology and characteristics, CRAO can be classified into four types: non-arteritic CRAO; non-arteritic CRAO with cilioretinal artery sparing; transient non-arteritic CRAO; and arteritic CRAO. (5) The incidence of presence of cilioretinal artery is variable, and may reach up to 33%. (4) In the present case, the final acuity associated with tubular vision occurred largely due to blood flow maintained by irrigation of this artery. The presence of this artery is a positive prognostic factor. (4) Ocular compression/ decompression and paracentesis maneuvers as first measures in treatment of CRAO, in addition to use of pharmacological agents, such as urokinase and streptokinase, have been reported, as well as intravenous tPA. (11) All of these models are employed at the interval between occlusion and treatment initiation, which should not exceed 6 hours. (11) Central retinal vein occlusion can be classified according to tissue perfusion status by fluorescein angiography (FA) as ischemic or non-ischemic. (6,7,9) Moreover, it is well known that over 75% of CRVOs are non-ischemic, and 34% of those cases converted to ischemic form during follow-up. Furthermore, up to 60% of eyes with ischemic CRVO developed neovascularization, with neovascular glaucoma developing in some cases. (9) Systemic findings found in CRAO combined with CRVO include diabetes, hypertension, dyslipidemia, as well as inflammatory, coagulation and tumoral disorders. (12,13) Recently, high factor VIII indices have been associated with venous thromboembolism in cases of combined venous and arterial  In 6-month follow-up of the condition in RE, there was a complete vascular recanalization, with no glaucoma associated, but atrophy of the retinal inner layers on OCT ( Figure 5).

DISCUSSION
As from the initial description by Graefes, in 1859, (8) CRAO has been one of the few ocular conditions absolutely urgent, usually accompanied by comorbidities, and a high five-year mortality rate. (2,3) Arterial occlusion is a rare condition, with an estimated incidence of 8.5 cases per 100,000 inhabitants, usually secondary to fatty embolus from the internal carotid artery, and it presents as sudden and painless visual field loss. (4)(5)(6) The CRVO has an estimated prevalence of 0.4% and its occlusions, (13) but they were not present in this patient. Carotid Doppler ultrasound and echocardiography are important ancillary tests to order and elucidate etiology of the cases. (4,5) The finding of atheromatous plaques on carotid ultrasound is more relevant than the presence of hemodynamic changes. (4) In CRVO, the most common treatments are intravitreal injection of anti-VEGF, such as ranibizumab and aflibercept, or intravitreal dexamethasone implant, such as Ozurdex®. All of those treatments are approved by Food and Drug Administration (FDA). (14) Ozurdex® was chosen in this case since it seems to have significant beneficial effects in improving venous engorgement, retinal hemorrhage and disc swelling. (9,15) Considering most negative ancillary tests and presence of bilateral atheroma in carotid arteries, we believe the bilateral ocular findings of our patient were probably a consequence of non-controlled comorbidities, such as hypertension and dyslipidemia. Also, it is important to emphasize the patient is also at risk for ischemic events after treatment, largely because atherosclerotic disease is the primary underlying diagnosis of his condition. (1)