Transient Central Retinal Artery Occlusion Research Articles

The great escape- preserved cilioretinal artery with transient central retinal artery occlusion following snake bite

A 24-year female sustained a snake bite on the lateral side of the left ankle, followed by localized pain and blurring of vision in right eye. Her best corrected visual acuity was 20/20 in the both eyes. Relative afferent pupillary defect was noted in right eye. Fundus examination of right eye showed clear media, normal optic disc and retinal whitening with sparing of small area on macula, temporal to disc with small cilioretinal artery, suggestive of central retinal artery occlusion (CRAO) with presence of cilioretinal artery sparing. Ophthalmic manifestations following a snake bite are uncommon and can arise through diverse mechanism such as hematotoxicity from the snake bite, resulting in CRAO. Although CRAO following snake bite has been reported, we present a very rare case of snake bite induced transient CRAO with presence of spared cilioretinal artery.

Bilateral central retinal artery occlusion: Endovenous and intra-arterial thrombolysis in a patient with a subsequent diagnosis of antiphospholipid antibody syndrome

Bilateral central retinal artery occlusion: Endovenous and intra-arterial thrombolysis in a patient with a subsequent diagnosis of antiphospholipid antibody syndrome

A rare presentation of vasculotoxic and neurotoxic ophthalmic manifestations of snakebite

Every year, a substantial number of snakebite cases are reported worldwide, more so from tropical countries. Although the fatality rate is quite low, it is nonetheless considered a medical emergency in view of the possible hematological, neurological, cardiac, and renal complications. The snake venom injected into the body contains a multitude of compounds that are responsible for their multisystem involvement. However, ocular complications following a snakebite are seldom reported in the literature. Our case report deals with the occurrence of transient central retinal artery occlusion and toxic neuritis soon after a snakebite.

Transient central retina artery occlusion in patients undergoing intravitreal anti vegf injections.

To evaluate the occurrence of transient central retinal artery occlusion following intravitreal anti-vascular endothelial growth factor injection. Prospective, observational study of 807 patients (807 eyes) who were given intravitreal injections of ranibizumab or aflibercept to treat any cause of retinal vascular diseases between 1 January 2017 and 30 November 2018 at the Federal Fluminense University Hospital in Niteroi, and a private facility in Rio de Janeiro, Brazil. Patients who did not present transient central retinal artery occlusion were excluded. Among 4069 injections, only 18 patients (0.44%) presented transient central retinal artery occlusion, 14 mild cases (77.7%), and 4 severe cases (22.3%). The clinical factors associated with more severe cases of transient central retinal artery occlusion were the duration of the transient central retinal artery occlusion (p = 0.001), number of prior injections (p = 0.01), and a positive carotid Doppler test (p = 0.01). Twelve cases (66.6%) had positive carotid artery obstruction (atheroma plaque size ≥70%) while 6 cases (33.3%) had negative carotid artery obstruction (atheroma plaque size <70%). The age group >60 years old (p = 0.06), cup/disc ratio >0.6 (p = 0.06), and pseudophakic lens status were also factors with association with transient central retinal artery occlusion, although did not meet criteria for statistical significance. The only patient who experienced a recurrent episode of transient central retinal artery occlusion had diabetic macular edema, positive carotid Doppler test, and cup/optic disc ratio >0.6. Transient central retinal artery occlusion is a rare adverse event that can appear in patients with retinal vascular disease receiving anti-vascular endothelial growth factor therapy. The atheroma plaque size and the number of prior injections can be associated with the severity of the event.

CRAO in Moyamoya Syndrome Associated With Southampton Hemoglobinopathy

The authors present the first case of central retinal artery occlusion (CRAO) resulting from moyamoya syndrome secondary to Southampton hemoglobinopathy. A 12-year-old Hispanic girl with a history of Southampton hemoglobinopathy with moyamoya syndrome presented with amaurosis fugax in her left eye that resolved within hours except for an inferior paracentral scotoma. She had left ophthalmic artery occlusion on magnetic resonance angiogram. Seven months later, spectral-domain optical coherence tomography showed diffuse inner retinal thinning. She was diagnosed with transient CRAO. The authors conclude that CRAO can result from moyamoya syndrome secondary to an underlying hemoglobinopathy. Multimodal imaging demonstrated residual inner retinal injury despite reperfusion. [Ophthalmic Surg Lasers Imaging Retina. 2019;50:e166-e170.].

Is Management of Central Retinal Artery Occlusion the Next Frontier in Cerebrovascular Diseases?

Central retinal artery occlusion (CRAO) is a medical emergency that, if not treated, may result in irreversible loss of vision. It continues to be an important cause for acute painless loss of vision. Amaurosis fugax or “transient CRAO” has long been considered an equivalent of transient cerebral ischemic event. Animal models, in addition to data from retrospective and randomized clinical studies, provide valuable insights into the time interval for irreversible retinal ischemia. Subset analyses from 2 large studies of patients with CRAO show benefit from treatment with thrombolysis within 6 hours from symptoms onset. Significant workflow improvements after the intra-arterial therapy trials for acute ischemic stroke have occurred world over in last 5 years.Patients with CRAO are uniquely suited to receive maximum benefits from the changes in workflow for treatment of patient's acute ischemic stroke. Just as in clinical triage of acute ischemic stroke, correct and timely diagnosis of patients with CRAO may help in preventing visual loss. The approach to acute ocular ischemia should mimic that used for acute brain ischemia. Comprehensive stroke centers would be ideal triage centers for these patients in view of availability of multidisciplinary participation from vascular neurology, neuroendovascular surgery, and ophthalmology.Time is Retina!

Transient central retinal artery occlusion after sub-tenon's anaesthesia: Is it a safe technique?

Transient central retinal artery occlusion after sub-tenon's anaesthesia: Is it a safe technique?

Polycythemia causing posterior segment vascular occlusions

A 44-year-old male patient presented with features suggestive of transient central retinal artery occlusion (CRAO) followed by permanent CRAO and lateral posterior ciliary artery occlusion. He had diagnostic features of polycythemia vera (PV). When presented for the first time, the patient had features of ocular ischemia such as ocular pain, conjunctival congestion, and retinal opacification but with normal arm-to-retina time and normal arteriovenous transit time. During the second presentation, he had ocular pain, congested conjunctiva, retinal opacification, cherry red spot with box-carrying of retinal vessels, and choroidal infarct (Amalric's sign). He had lost light perception in that eye. Patients with polycythemia are prone to multifocal vascular occlusions and this can be the presenting feature in PV. A timely diagnosis and prompt management can prevent these repeated thromboembolic occlusive episodes.

Ocular vascular occlusive disorders: natural history of visual outcome.

Ocular vascular occlusive disorders collectively constitute the most common cause of visual disability. Before a disease can be managed, it is essential to understand its natural history, so as to be able to assess the likely effectiveness of any intervention. I investigated natural history of visual outcome in prospective studies of 386 eyes with non-arteritic anterior ischemic optic neuropathy (NA-AION), 16 eyes with non-arteritic posterior ischemic optic neuropathy, 697 eyes with central retinal vein occlusion (CRVO), 67 eyes with hemi-CRVO (HCRVO), 216 eyes with branch retinal vein occlusion (BRVO), 260 eyes with central retinal artery occlusion (CRAO), 151 eyes with branch retinal artery occlusion (BRAO) and 61 eyes with cilioretinal artery occlusion (CLRAO). My studies have shown that every one of these disorders consists of multiple distinct clinical sub-categories with different visual findings. When an ocular vascular occlusive disorder is caused by giant cell arteritis, which is an ophthalmic emergency, it would be unethical to do a natural history study of visual outcome in them, because in this case early diagnosis and immediate, intensive high-dose steroid therapy is essential to prevent any further visual loss, not only in the involved eye but also in the fellow, normal eye. In NA-AION in eyes seen ≤2 weeks after the onset, visual acuity (VA) improved in 41% of those with VA 20/70 or worse, and visual field (VF) improved in 26% of those with moderate to severe VF defect. In non-ischemic CRVO eyes with VA 20/70 or worse, VA improved in 47% and in ischemic CRVO in 23%; moderate to severe VF defect improved in 79% in non-ischemic CRVO and in 27% in ischemic CRVO. In HCRVO, overall findings demonstrated that initial VA and VF defect and the final visual outcome were different in non-ischemic from ischemic HCRVO - much better in the former than the latter. In major BRVO, in eyes with initial VA of 20/70 or worse, VA improved in 69%, and moderate to severe VF defect improved in 52%. In macular BRVO with 20/70 or worse initial VA, it improved in 53%, and initial minimal-mild VF defect was stable or improved in 85%. In various types of CRAO there are significant differences in both initial and final VA and VF defects. In CRAO eyes seen within 7 days of onset and initial VA of counting fingers or worse, VA improved in 82% with transient non-arteritic CRAO, 67% with non-arteritic CRAO with cilioretinal artery sparing, 22% with non-arteritic CRAO. Central VF improved in 39% of transient non-arteritic CRAO, 25% of non-arteritic CRAO with cilioretinal artery sparing and 21% of non-arteritic CRAO. Peripheral VF improved in non-arteritic CRAO in 39% and in transient non-arteritic CRAO in 39%. In transient CRAO, finally peripheral VFs were normal in 93%. In non-arteritic CRAO eyes initially 22% had normal peripheral VF and in the rest it improved in 39%. Final VA of 20/40 or better was seen in 89% of permanent BRAO, and in 100% of transient BRAO and non-arteritic CLRAO. In permanent BRAO eyes, among those seen within 7 days of onset, central VF defect improved in 47% and peripheral VF in 52%, and in transient BRAO central and peripheral VFs were normal at follow-up. My studies showed that AION, CRVO, BRVO, CRAO and BRAO, each consist of multiple distinct clinical sub-categories with different visual outcome. Contrary to the prevalent impression, these studies on the natural history of visual outcome have shown that there is a statistically significant spontaneous visual improvement in each category. The factors which influence the visual outcome in various ocular vascular occlusive disorders are discussed.

Reply: ‘Central retinal artery occlusion and cerebral stroke’

Sir, We are grateful to Dr McLeod1 for the interest that he has shown in our paper.2 Rather, then there being a conspiracy to increase the confusion within central retinal artery occlusion (CRAO), our study demonstrates that the disease is incompletely understood. In particular, we disagree with Dr McLeod that the retinal penumbra lasts for more than 24 h. Retinal and cerebrovascular ischaemia share a number of common pathophysiological features and is reflected by the recent extended definition of stroke involving retinal as well as cerebral ischaemia.3 In vitro experiments show that when neuronal cells are deprived of oxygen, that within 5 s, there is evidence of neuronal dysfunction. Within 10 s, cell death occurs. The elegant experiment of Astrup et al4 demonstrated that the penumbra is a function of collateral perfusion and that if there was no resolution of the occlusion, then eventually the penumbra would fail, and infarction would be permanent. In cerebral stroke using perfusion imaging, various groups have demonstrated that the ischaemic penumbra may persist beyond 24 h. However, randomised controlled trials of reperfusion therapy in acute stroke have demonstrated on that in the majority of individuals, the ischaemic penumbra only extends out to 4.5 h and at maximum, 6 h.5, 6 The misperceptions that the retinal penumbra persists for 24 h, initially backed up by observational data, led to the design of two randomised controlled trials that recruited individual with central retinal artery occlusion of beyond 6 h. The EAGLE study recruited subjects up to 19 h of symptom onset,7 while our group conducted a randomised controlled trial of intravenous tPA given to individuals within 24 h of symptom onset.8 Both of these randomised controlled trials were negative studies, however, a signal was seen in individuals who receive tPA within 6 h of symptom onset.8 This mirrors the retinal tolerance time demonstrated in Hayreh's animal experiments of 4 h.9 Conversely, if the thrombus that initially caused a retinal artery occlusion resolves such that retinal perfusion is restored, then the symptoms will be invariably improved leading to a transient central retinal artery occlusion. Nevertheless, we agree with Dr McLeod that the classical clinical features of central retinal artery occlusion remain more or less the same, but that various findings may give a clue as to the time of the onset or alternatively the presence of partial occlusion. These are important points given that for randomised controlled trials on the treatment of CRAO are to succeed, then individuals need to be recruited within the shortest time possible.

Unusual visual loss after snakebite

Snakebites are endemic in some parts of Thailand, being associated with several complications. Ocular disturbances are uncommon, except in cases of corneal or conjunctival injury, when the eye is directly exposed to the snake venom. The present study presents a case of combined ophthalmic artery occlusion and transient central retinal artery occlusion with macular ischemia after a Russell's viper bite.

Transient Central Retinal Artery Occlusion Following Viperine Snake Bite

Transient Central Retinal Artery Occlusion Following Viperine Snake Bite

Transient Central Retinal Artery Occlusion Following Viperine Snake Bite—Reply

Transient Central Retinal Artery Occlusion Following Viperine Snake Bite—Reply

FUNDUS CHANGES IN CENTRAL RETINAL ARTERY OCCLUSION

To investigate systematically the ophthalmoscopic fundus findings associated with central retinal artery occlusion (CRAO). The study included 240 consecutive patients (248 eyes) with CRAO. The eyes underwent detailed fundus evaluation and stereoscopic color fundus photography at initial and follow-up visits. Patients without evidence of giant cell arteritis were advised to have carotid Doppler imaging and echocardiography to determine the source of emboli. CRAO was classified into 3 types: permanent CRAO (175 eyes), permanent CRAO with cilioretinal artery sparing (35 eyes), and transient CRAO (38 eyes). In the three types of CRAO, acute-phase and late-phase changes in the retina, optic disk, and retinal vessels were evaluated. The main findings during the initial examination in our clinic for permanent CRAO were retinal opacity in the posterior pole (58%), cherry-red spot (90%), box-carring (19%), retinal arterial attenuation (32%), and optic disk edema (22%) and pallor (39%). The most frequent findings identified at the late stage, based on survivorship curves, were optic atrophy (91%), retinal arterial attenuation (58%), cilioretinal collaterals (18%), and macular retinal pigment epithelial changes (11%). Compared with permanent CRAO, permanent CRAO with cilioretinal artery sparing was associated with a lower incidence of all macular and optic disk abnormalities. For transient CRAO, the incidence of initial findings varied greatly compared with the other types. Intraarterial emboli were observed in 20% of patients. Carotid Doppler evaluation identified carotid vascular plaques in 67% of patients tested and hemodynamically significant (>50%) obstruction in 32%. Four percent of CRAOs presented with simultaneous bilateral onset. The type and incidence of fundus findings at the initial visit and in the late phase of CRAO vary by its type. This study confirms that retinal opacity is predominantly evident in the posterior retina, that optic disk findings at presentation are common, that CRAO associated with normal-appearing retinal vessels and/or optic disk is not rare, and that observation of emboli is infrequent. Clinicians should be aware of the various presentation findings during the acute and late stages of CRAO and its various types. A complete picture of CRAO is provided by combined information of our clinical and experimental studies of CRAO.

Vitreous and retinal amino acid concentrations in experimental central retinal artery occlusion in the primate.

Vitreous and retinal amino-acid concentrations were evaluated in a primate model of central retinal artery occlusion (CRAO) to study the role of glutamate excitotoxicity in acute retinal ischaemia. Unilateral, acute CRAO was produced by temporary clamping of the central retinal artery for 190 min in four elderly rhesus monkeys. Fundus photography, fluorescein angiography, and electroretinogram were performed before and during CRAO, and after unclamping the artery. Vitreous samples were obtained before and after CRAO in both eyes, and analysed for 13 amino-acid concentrations using high-pressure liquid chromatography. The animals were killed 350 min after retinal reperfusion, and the retinal tissue was submitted for amino-acid analysis. In all four eyes, the macula showed the 'cherry red spot'. The CRAO was confirmed by fluorescein angiography and decreased b-wave on electroretinogram. Retinal histology confirmed ischaemic changes in the inner retina. Changes in all 13 vitreous amino-acid concentrations after CRAO (including glutamate) were not significantly different between study and control eyes (P = 0.09 to 0.82). All retinal amino-acid concentrations (including glutamate) were not significantly different between two eyes (P = 0.07-0.93). In the primate model of acute inner retinal ischaemia induced by transient CRAO, we were unable to detect significantly elevated concentrations of vitreous and retinal glutamate. Our primate model has the advantage of closely modelling the CRAO in humans. Further basic and clinical studies are needed to elucidate the role of glutamate excitotoxicity in retinal ischaemia.

Ocular side effects and complications of intravitreal triamcinolone acetonide injection

With the advent of intravitreal triamcinolone acetonid injections major focus was assigned to potential ocular side effects. The current discussion is dominated by the potential cytotoxicity of particular biologically incompatible components. Those are regarded as substantial pathogenetic factor of the sterile pseudoendophthalmitis that seems to be avoidable by meticulous purification of the commercially available preparations. Even sustained subretinal or epiretinal deposits disclosed no signs of retinal toxicity. Major ocular side effects comprise temporary corticosteroid glaucoma and progressive cataract formation. Infectious endophthalmitis represents a rare but serious complication that might be set into critical context with hygienic surgical standards applied. Due to steroid-induced immune suppression clinical signs of inflammation might be masked and a proper diagnosis delayed. Other rare complications reported include a transient central retinal artery occlusion, conjunctival ulcerations, retinal detachment and potential reactivation of a cytomegalovirus retinitis. In conclusion, ocular side effects and complications show a wide variety of clinical signs and underlying causal mechanisms. However, the consequences are mostly temporary and show a good response to therapeutic intervention.

Central retinal artery occlusion.: Retinal survival time

Purpose. To investigate the retinal survival time following central retinal artery occlusion (CRAO). Methods. In 38 elderly, atherosclerotic and hypertensive rhesus monkeys, transient CRAO (varying from 97 to 240 min) was produced by temporarily clamping the CRA at its site of entry into the optic nerve. Stereoscopic color fundus photography, fluorescein fundus angiography, electroretinography (ERG), and visual evoked potential (VEP) recording were performed before and during CRA clamping, after unclamping, and serially thereafter. After unclamping of the CRA, the animals were followed for variable lengths of time (median duration 8·14 weeks). Finally, the eyes and optic nerves were examined histologically. The data on ERG changes were analyzed in the following four time frames: (1) baseline before CRA clamping, (2) during CRA clamping, (3) immediately after unclamping, and (4) at the end of follow-up. Duration of CRAO was divided into four groups: 97, 105–120, 150–165, and ≥180 min. Results. A ‘negative ERG’ appeared during CRA clamping. With removal of the CRA clamp, there was b-wave recovery, with differential rates of recovery of ERG-eyes with shorter CRAO recovered sooner than those with longer occlusion. On removal of clamp, recovery was seen in scotopic 24 dB b-wave, photopic 0 dB single flash b-wave and 30 Hz flicker, with the b/a ratio of the combined rod and cone response and selective rod response showing statistically significant differences amongst the shorter and longer periods of CRAO. A delayed normalization of the depressed b/a ratio immediately after CRA reperfusion may indicate high-grade ischemic damage. At the final follow-up test session, no clear-cut derangement of any ERG parameter was seen for any group, with subtotal b-wave amplitude recovery for all groups. Longer CRAO produced incomplete VEP recovery. On histology, in the macular retina, eyes with CRAO for 97 min showed practically no damage, but duration of CRAO was found to be significantly associated with the amount of damage in the ganglion cell layer ( p=0·009) and inner nuclear layer ( p=0·017). Outer nuclear and plexiform layers and photoreceptors showed no damage at all with CRAO. There was no significant association of the ERG measures and histologic changes with any of the residual retinal circulation variables. Conclusions. Our electrophysiologic, histopathologic and morphometric studies showed that the retina of old, atherosclerotic, hypertensive rhesus monkeys suffers no detectable damage with CRAO of 97 min but above that level, the longer the CRAO, the more extensive the irreversible damage. The study suggests that CRAO lasting for about 240 min results in massive irreversible retinal damage.

Transient central retinal artery occlusion after posterior sub-Tenon's anesthesia

Two cases of transient central retinal artery occlusion were observed preoperatively after uneventful sub-Tenon's infusion of local anesthetic for cataract surgery and intraocular lens implantation. In these eyes, the retinal circulation reperfused spontaneously before surgery and there were no visual sequelae. A third case was observed in an eye after strabismus surgery with sub-Tenon's anesthesia. The patient was left with profound visual loss in this eye. The cause of this complication is unknown, but possible factors include mechanical pressure from the bolus of the anesthetic solution or localized vasoconstriction from the anesthetic, producing a decrease in ocular blood flow. Suggestions to avoid this problem include not inserting the cannula too posteriorly, not injecting forcibly against resistance, and using the minimum volume of anesthetic possible.

Association for Research in Vision and Ophthalmology (ARVO) Annual Meeting, April 29???May 4, 2001

Association for Research in Vision and Ophthalmology (ARVO) Annual Meeting, April 29???May 4, 2001

Abstracts of literature

Abstracts of literature