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Retinal arterial occlusion remains a difficult clinical entity to manage. Treatment can best be categorized as conservative (ocular massage, pharmacologic, anterior chamber paracentesis) and invasive (catheterization of the proximal ophthalmic artery through the femoral artery with the infusion of thrombolytic agents). Most reports remain anecdotal due to its low incidence (0.85/100,000/y).
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 > or = 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.
INTRODUCTION: High plasma lipoprotein (a) concentration is an independent risk factor for atherosclerosis and thrombosis. PATIENTS: We present the cases of two young women, one with central retinal artery occlusion and the other with branch retinal artery occlusion. Case 1: A 32-year-old woman was seen in our clinic complaining of a sudden decrease in visual acuity to 1/50 with a central visual field defect in the right eye. The fundus examination revealed an occlusion of the central retinal artery, which was confirmed by fluorescein fundus angiography. Thorough systemic evaluation showed no signs of cardiovascular disease, no coagulation abnormalities, and no clinical or biological evidence of a systemic disorder. On the other hand, hypercholesterolemia and elevated levels of lipoprotein (a) were detected. Case 2: A 35-year-old woman consulted complaining of a visual field loss in the left eye without reduction of visual acuity. Fundus examination and angiography showed the occlusion of the temporal-superior branch artery. A detailed systemic work-up revealed a pseudo-bicuspid aortic valve and high lipoprotein (a) levels. CONCLUSION: These two cases emphasize the importance of a thorough systemic evaluation of young adults with a retinal artery occlusion. High plasma lipoprotein (a) concentration is a risk factor which should not be neglected.
BACKGROUND: To date, no satisfactory therapy has become available for patients with acute central retinal artery occlusion (CRAO) or branch retinal artery occlusion (BRAO). Enhanced external counterpulsation (EECP) is a new noninvasive procedure that increases perfusion of inner organs. In the current study, the authors measured the impact of EECP on reperfusion in ischemic retinal tissue. METHODS: In a prospective, randomized study, 20 patients with CRAO or BRAO were included. Ten patients were given hemodilution therapy and 2 hours of EECP, and 10 patients were given regular hemodilution therapy only. Quantification of changes in retinal perfusion was carried out by means of scanning laser Doppler flowmetry (in arbitrary units). RESULTS: Enhanced external counterpulsation caused no observable adverse events. A significant increase in perfusion occurred immediately after EECP in the ischemic retinal areas (57 +/- 19 arbitrary units versus 99 +/- 14 arbitrary units). In contrast, no change was measured in the group not treated with EECP (83 +/- 19 arbitrary units versus 89 +/- 44 arbitrary units). Forty-eight hours later, a significant increase in perfusion could be shown in the ischemic retina of both groups, and no significant difference of perfusion was found between the two groups any longer. CONCLUSION: The current study suggests that EECP could be a clinically useful and safe procedure in patients with CRAO or BRAO to accelerate recovery of perfusion in ischemic retinal areas.
BACKGROUND: Retinal artery occlusions typically result in sudden, unilateral painless loss of vision and may have varying presentations. They are associated with systemic diseases such as atherosclerosis, hypertension, and valvular heart disease. Additional risk factors include diabetes mellitus, cigarette smoking, giant-cell arteritis, and hyperlipidemia. They most often occur in persons 60 to 80 years of age. METHODS: Four patients have come to our clinics with varying degrees of visual loss as a result of retinal artery occlusions. The types of arteriolar occlusions presented include: precapillary arteriole occlusion, cilioretinal artery occlusion, branch retinal artery occlusion, and central retinal artery occlusion. RESULTS: Patients were followed for their ocular involvement, but also included was medical management of the underlying systemic disease condition. Workup of retinal artery occlusion included laboratory testing, carotid duplex scans, and echocardiograms to uncover the possible systemic etiologies of the artery occlusion. CONCLUSION: Optometrists should recognize the signs and symptoms of the various arterial obstructions and refer patients for systemic treatment as indicated. Patients who manifest retinal or pre-retinal artery occlusions should undergo thorough systemic evaluations for vascular disease, including: atherosclerotic disease, hypertension, and valvular heart disease.
Central retinal artery occlusion usually results in blindness. The association between central retinal artery occlusion and extracranial carotid disease has not been clearly delineated. We reviewed the case reports of 62 patients with central retinal artery occlusion, 25 of whom underwent carotid angiography as part of the diagnostic evaluation. Fourteen of the 25 (56 percent) were found to have ipsilateral extracranial carotid disease. These patients did not generally have carotid bruits and had normal noninvasive carotid tests. Ten patients underwent ipsilateral carotid endarterectomy; these patients had either embologenic ulcerated plaque or tight stenosis of the carotid artery. There were 11 patients who showed no abnormalities on angiography. Thirteen patients who did not undergo angiography showed clinical evidence of etiologic factors, including vasculitis, an embolism of cardiac origin, and trauma. The remaining 24 patients had no diagnostic workup. Follow-up data were available in six of those patients who underwent carotid endarterectomy for a mean of 34 months; no strokes were reported. In conclusion, over half of patients with central retinal artery occlusion who undergo carotid angiography will have a carotid lesion on the ipsilateral side. This suggests that central retinal artery occlusion is a significant marker for extracranial carotid disease and should be an indication for complete carotid evaluation.
PURPOSE: Retinal artery occlusion is a common vision-threatening disease. Among other risk factors, coagulopathies leading to a hypercoagulable state have been associated with retinal artery occlusion. Numerous studies have shown that two genetic variants, factor V Leiden and prothrombin 20210A, cause a procoagulant state. However, their role in the pathogenesis of retinal artery occlusion is still unclear. The purpose of the present study was therefore to investigate a possible association between factor V Leiden, prothrombin 20210A, and retinal artery occlusion. METHODS: In the present retrospective case-control study, we studied 136 patients with retinal artery occlusion and 136 age- and gender-matched control subjects. The presence of factor V Leiden and prothrombin 20210A alleles was determined by polymerase chain reaction. RESULTS: The prevalence of heterozygosity for the prothrombin G20210A variant did not significantly differ between patients and controls (three patients vs two controls, P=0.65). Distribution of factor V Leiden genotypes revealed no significant difference among the two groups (heterozygosity: eight patients vs 11 controls, P=0.47). As for other risk factors, arterial hypertension, a history of stroke and myocardial infarction were significantly more frequent in patients than in controls. CONCLUSION: Our data suggest that factor V Leiden and prothrombin 20210A do not play a major role in patients with retinal artery occlusion.
Acute retinal arterial occlusion is an ophthalmic condition that is associated with a high prevalence of systemic disease. Recent studies have demonstrated that significant numbers of patients with acute retinal arterial occlusion have both hemodynamically significant carotid artery stenosis and cardiac pathology that necessitates systemic therapy. Furthermore, emerging evidence show that coagulopathies and hyperhomo-cysteinemia may be responsible for acute retinal arterial occlusion. In this paper, we review recent scientific evidence that supports that adoption of specific guidelines for the systemic evaluation of acute retinal arterial occlusion.
Transient central retinal artery occlusion (CRAO) was produced in 63 eyes of rhesus monkeys by lateral orbitotomy and temporary clamping of the central retinal artery (CRA) for between 15 and 270 minutes. Thirty-three eyes were examined at regular intervals for 12 to 22 weeks. Color fundus photography, fluorescein fundus angiography, electroretinography (ERG) and visual evoked response (VER) were performed before and during clamping of the CRA as well as periodically after unclamping. All the eyes were examined by light and/or electron microscopy. This study revealed that the retina suffered irreparable damage after ischemia of 105 minutes, but recovered well after ischemia of 97 minutes. As a general rule, the monkey retina can tolerate up to 100 minutes of ischemia but not more.
UNLABELLED: Retinal artery occlusion (RAO) is an ophthalmological emergency that causes a major decrease of visual parameters in most of the cases. Purpose of this pilot study was to evaluate the effect of adjunctive hyperbaric oxygen therapy (HBO) on visual acuity (VA). PATIENTS AND METHODS: Patients with acute central or branch artery occlusion (CRAO/BRAO) consecutively admitted to our hospital were offered adjunctive HBO. Standard therapy consisted of ocular massage for 3 minutes, paracentesis and intravenous acetazolamide. HBO (3 x 30 minutes at 240 kPa) was applied t.i.d. on the first day, b.i.d. on day 2 and 3 and o.d. for at least another 4 days. Patients who refused HBO or had contraindications served as controls. VA was measured according to the guidelines of ETDRS. The follow up was 3 months. RESULTS: HBO: 8 patients with CRAO showed a mean increase in VA of 1 line, 4 of 8 patients had an increase of 2 lines and more, in 3 of 8 patients VA was unchanged and one patient suffered a decrease of 6 lines. 10 patients with BRAO showed a mean increase in VA of 8 lines, 8 of 10 patients showed an mean increase of 2 and more lines, in 2 of 10 patients VA was unchanged. CONTROLS: 8 Patients with CRAO had a mean increase of 2 lines during follow up, 3 of 8 patients showed an increase of 2 lines and more, in 5 of 8 patients VA was unchanged. 6 patients with BRAO had a mean increase of VA of 4 lines, 3 of 6 patients had an increase of 2 lines and more, one patient lost 3 lines and in 2 patients VA was unchanged. The results are compared to the literature. CONCLUSIONS: HBO seems to be beneficial for VA in eyes with BRAO. Further investigations are necessary to prove this observation.
Central retinal artery occlusion very often leads to irreversible visual loss and seldom responds to treatment. Retrograde cannulation of the supraorbital artery followed by irrigation with anticoagulants and vasodilators may be of value in the early management of this problem. A case in point is described.
Central retinal artery occlusion is characterized by sudden, painless visual loss due to blockage of retinal blood flow. It has been reported in all age groups including children but is most frequent in the sixth decade. Both thrombosis and embolism have been suggested as possible mechanisms. The emergency treatment includes intravenous acetazolamide, digital ocular massage, and inhalation of 5% carbon dioxide -- 95% oxygen for ten minutes. Following emergency treatment, immediate ophthalmologic referral and consultation is required. Comprehensive medical evaluation should be initiated to exclude systemic vascular disease.
BACKGROUND: The influence of retinal artery circulation on central retinal vein occlusion (CRVO) is not well known. CASE: A 73-year-old man with hypertension complained of transient visual loss in his left eye. At initial examination, ophthalmoscopy of his left eye showed mild dilatation and tortuosity of the retinal vein and a few dot hemorrhages. Fluorescein angiography disclosed normal arm-to-retina circulation time and no leakage of dye, but delayed retinal circulation time. These findings indicated venous stasis retinopathy of CRVO. In spite of intravenous infusion of prostaglandin E1 and vasodilative treatment, four days after initial examination, the patient's left eyeground showed complication of branch retinal artery occlusion (BRAO). A fibrinolytic agent was given intravenously, but four weeks later, his left eyeground developed typical hemorrhagic retinopathy. The hemodynamics of retrobulbar arterial circulation were investigated by color Doppler imaging. CONCLUSION: We report a case of venous stasis retinopathy of CRVO associated with BRAO, that developed hemorrhagic retinopathy despite treatment with prostaglandin E1 and other vasodilative agents. We think that arterial insufficiency might be responsible for the conversion from venous stasis retinopathy to hemorrhagic retinopathy of CRVO.
PURPOSE: Retinal artery occlusion (RAO) is caused by arterio-arterial or cardiovascular emboli in about 50% of all cases, but the role of non-embolic causes remains unclear. SUBJECTS AND METHODS: We studied 27 patients with amaurosis fugax (AFX), branch retinal artery occlusion (BRAO), central retinal artery occlusion (CRAO) and anterior ischaemic optic neuropathy (AION). Patients underwent an evaluation of cerebrovascular and cardiovascular risk factors, measurement of haemorheological parameters, and Doppler/duplex sonography including ultrasound detection of cerebral microembolic signals and echocardiography. RESULTS: Forty-one per cent of the patients had internal carotid atherosclerosis but only one patient had microembolic signals, probably due to a cardiac thrombus. Vascular risk factors, especially hypertension, were present in 82% of the patients correlating with abnormal haemorheological parameters such as increased thrombocyte reactivity. CONCLUSIONS: Our results indicate that altered haemorheological parameters, especially increased thrombocyte reactivity and vascular risk factors such as arterial hypertension, are non-embolic causes of vascular disease in a significant number of patients with RAO. This should guide diagnostic and therapeutic considerations concerning RAO in cases without proven embolic sources.
OBJECTIVE: To determine the natural history and visual prognosis of patients with branch retinal arterial occlusions secondary to multifocal retinitis. METHODS: Cases were reviewed for seven patients who exhibited multifocal retinitis and branch retinal arterial occlusion. The average age of the patients was 27 years (age range, 14 to 19 years). RESULTS: Six patients had systemic illnesses associated with their ocular findings. Four patients were scratched by a cat or exposed to a cat with fleas within 1 month of symptoms. Three of these patients were tested and had positive cat-scratch disease titers. At presentation, five patients complained of a scotoma, and two noted blurred vision. On examination, visual acuity was 20/25 or better in all but one eye. Five patients had vitritis, which was bilateral in three. Four patients exhibited optic nerve edema, which was bilateral in two. White intraretinal infiltrates were present in all patients, and were bilateral in five. The six patients who were examined within 1 week of symptoms had a white retinal infiltrate at the site of vascular occlusion. The retinal findings resolved in 2 to 6 weeks and did not recur. The final visual acuity was 20/20 OU in all patients. CONCLUSIONS: Branch retinal arterial occlusions represent a complication of multifocal retinitis and idiopathic optic nerve edema. The arterial occlusions are probably caused by a focus of retinitis. This self-limited disorder has an excellent visual prognosis and may be related to cat-scratch disease.
Four patients with systemic lupus erythematosus (SLE) developed an unusual form of occlusive retinal arterial disease. The most prominent clinical features of this disorder were deposition of yellow-white material in retinal arterial walls and evidence of multifocal retinal arterial occlusion. Fluorescein angiographic findings included nonperfusion of the obstructed arteries and the retinal capillary beds fed by them, and fluorescein leakage at the sites of involvement of the retinal arteries. This ocular complication of SLE is presumably a manifestation of the widespread systemic vascular problems seen in this disorder. It may be more common in patients with lupus involving the CNS.
A 81-year-old woman developed central retinal vein occlusion (CRVO) in her left eye subsequent to central retinal artery occlusion (CRAO). She noticed sudden visual loss in the left eye. At initial examination, her left visual acuity was 0.03, and only a small visual field was preserved at temporal area. The left fundus showed findings of mild non-ischemic CRVO. In addition white clouded retina was recognized at the left posterior pole which indicated CRAO. FAG showed remarkably prolonged arterial circulation, but no retinal capillary obliteration. Then retinal hemorrhage increased rapidly and her left eye developed hemorrhagic retinopathy. Two weeks after initial examination, FAG showed extensive retinal capillary obliteration. In this case it was supposed that central retinal artery occlusion due to arteriosclerosis produced ischemic capillaropathy and venous thrombosis, after which restoration of arterial circulation caused hemorrhagic retinopathy.
PURPOSE: To report on a case of Crohn's disease and unilateral retinal vasculitis, branch retinal artery occlusion and subsequent retinal neovascularization. METHODS: We examined a 38-year-old woman with severe left visual loss and biopsy-proven Crohn's disease diagnosed four years prior to the ocular involvement. A Heidelberg scanning laser ophthalmoscope was used for fundus fluorescein angiography and indocyanine green angiography. Retinal neovascularization was detected during the follow-up. RESULTS: Successful regression of retinal neovascularization was achieved after argon green laser panretinal photocoagulation in addition to oral steroid and salazopyrine. CONCLUSION: Retinal vascular involvement is a rare ocular feature of Crohn's disease and may result in retinal neovascularization that may necessitate prompt laser photocoagulation.