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The simultaneous occurrence of a central retinal vein occlusion and retinal detachment has not been previously reported. Although both are well recognized entities with characteristic appearances, their simultaneous acute onset led to a misdiagnosis in our case report. The need for a complete eye examination in the face of obvious pathology is stressed.
PURPOSE: The study was designed to quantify retinal vein width changes at the arterio-venous crossing and to evaluate the effects of hypertension on vein widths at "vein posterior to the artery" (VPA) and "vein anterior to the artery" (VAA) crossings. METHODS: The width of the retinal veins was measured at points before and after the arterio-venous crossings by a computerized image analysis system in ten normal subjects and 35 hypertensive patients. Retinal vein width changes at fixed intervals from the arterio-venous crossing points, both VAA and VPA, were measured as a function of the stage of the hypertensive retinopathy in the subjects. RESULTS: Mean retinal vein width showed significant (p < 0.05) narrowing at VPA crossings at stages 2, 3 and 4 of hypertensive retinopathy. For the VAA crossings, there was no significant decrease in the width of the vein at any stage. There was no significant narrowing of the vein at VPA crossings in normal subjects or in stage 0 and stage 1 hypertensive retinopathy patients. CONCLUSIONS: The decrease in the width of the retinal vein in stages 2, 3 and 4 hypertensive retinopathy patients at VPA crossings can cause turbulence in blood flow, leading to intimal damage and occlusion. The absence of narrowing may explain the low incidence of branch retinal vein occlusions at VAA crossings.
In a follow up of 94 patients with central retinal vein occlusion (CRVO) whose onset had taken place less than 1 year earlier, optociliary veins (OCVs) were found in 7.4% at first examination. Among the 79 eyes in which the fundus of the eye was very visible after a follow up of more than 1 year OCVs were found in 30.4%, showing a late development of OCVs in many cases of CRVO. No difference was found in the occurrence of OCVs between non-ischaemic and ischaemic forms of CRVO. The visual acuity of the eyes with CRVO that developed OCVs was not significantly different from the visual acuity of the eyes without OCVs. Thus, the presence of OCVs in CRVO does not seem to be associated with better visual prognosis.
Central retinal vein occlusion is one of the most frequently encountered vascular affections of the retina. In spite of this its management is still a matter of debate. Histopathological findings have prompted us to conduct a study in patients presenting with central retinal vein occlusion (n = 63). Exposure to plasmapheresis as treatment of the above condition (1 to 3 sessions) resulted in a significant retardation of erythrocyte aggregation, decrease in fibrinogen concentration, and in the hematocrit value, and a prolongation of activated thromboplastin time. The results obtained suggest that plasmapheresis can be recommended for use in the treatment of central retinal vein occlusion.
The author submits contemporary views on thrombosis. In all intravascular thromboses three mechanisms participate in varying extents: humoral, i.e. haemocoagulation, fibrinolytic and thrombocyte disorders, disorders of the vascular wall and rheological and haemodynamic disorders resp. Mechanisms of thrombosis are interlinked, activation of one group as a rule does not lead to the development of a thrombus unless it is particularly intense. As a rule combination with another group of factors is necessary. In case of venous thrombosis a key role is played by a combination of stasis and activation of the blood clotting system. In the aetiopathogenesis of occlusion of the retinal vein the author considers impairment of the vascular wall the key factor which leads to changes of the rheological conditions which predispose to thrombosis. The author describes the so-called critical retardation of the blood flow in the retinal vein as the critical level of changed rheological condition humoral factors begin to play a clinical role when in thrombogenesis. On this predisposed background humoral factors act and the result is occlusion of the retinal vein. The author considers occlusion proper a process which develops for a long time and the occlusion of the retinal vein is the final link of a long and very complicated process which is multifactorial and very variable.
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PURPOSE: To document a branch retinal vein obstruction secondary to a congenital arteriovenous communication. METHOD: Case report of a young patient with retinal arteriovenous communication. RESULTS: A 12-year-old girl had a grade 2 retinal arteriovenous communication in her right eye. She was asymptomatic and was subsequently followed up. Magnetic resonance imaging of the brain was normal and disclosed no signs of Wyburn-Mason syndrome. Nine years later, she developed a branch retinal vein obstruction in the area of the arteriovenous communication. Six months later, the patient was free of secondary complications of branch retinal vein obstruction; however, she is being followed up to detect any retinal or iris neovascularization. CONCLUSION: Awareness of retinal vascular obstruction associated with arteriovenous communication may help its timely recognition, as well as prompt treatment of potential complications, such as retinal and iris neovascularization.
PURPOSE: To evaluate the feasibility, safety, and efficacy of local thrombolytic agents directly injected into occluded retinal veins in an experimental animal model. DESIGN: Experimental animal study. METHODS: This experimental study was performed in two phases. In phase 1, 15 enucleated porcine eyes and 8 in vivo canine eyes were used for the development of the instrumentation and surgical technique required for retinal vein cannulation with prolonged intravascular infusion. In phase 2 of this study, experimental branch retinal vein occlusion was photo-chemically created using an intravenous injection of rose bengal followed by diode laser photocoagulation in eight eyes of eight dogs. Four eyes were treated by retinal vein cannulation and an injection of tissue plasminogen activator (t-PA) using a specifically designed microcatheter, while the remaining four eyes were untreated (control group). The total amount of t-PA injected intravenously ranged from 400 to 1000 mug, infused over a period ranging from 25 to 45 minutes with a mean pressure of 40 psi, resulting in a mean injection flow rate of 0.05 ml/min. The dogs underwent clinical examination, fluorescein angiography, and histologic examination. Main outcome measures were: Achievement of prolonged intravascular infusion of t-PA, changes in fundus appearance, fluorescein angiography, and histology. RESULTS: A microcatheter instrument and a surgical technique for retinal vein cannulation with prolonged intravascular infusion were developed. Cannulation and t-PA infusion for a period of at least 30 minutes was achieved in all four treated eyes with experimental branch retinal vein occlusion. No complications were recorded in all treated eyes. One week and 1 month postoperatively, treated eyes exhibited marked decreases in retinal hemorrhages, retinal vein dilation, and tortuosity, whereas nontreated eyes exhibited persistence of these findings. Fluorescein angiography demonstrated improved circulatory flow in treated relative to nontreated eyes. Histologic analysis confirmed the presence of thrombi in nontreated eyes only. CONCLUSIONS: Retinal vein cannulation with prolonged intravascular injection of t-PA is feasible and safe, and this may offer a new treatment option for retinal vein occlusion.
The authors report the results of laser treatment in 11 patients with chronic oedema of the macula and 6 patients with neovascularizations of the retina and disk of the optic nerve in occlusion of a branch of the retinal vein. In the treatment of chronic oedema of the macula they used their own modification of quadrant barrage suggested by L'Esperance and grid photocoagulation. After a mean follow up period of 3.2 years they achieved a resulting vision of 6/12 or better in 9 of 11 patients, i.e. in 82%, the poorest results were 6/18 in two patients of 11, i.e. in 18%. In the treatment of neovascularizations they used the method of sector photocoagulation. In all six patients, i.e. in 100% they observed regression of neovascularizations. During 2.5-3 years after photocoagulation they did not observe a relapse of neovascularization or haemorrhage into the vitreous body. The results of photocoagulation treatment in chronic oedema of the macula and treatment of neovascularization are of a long-term character.
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Retinal vein occlusion (RVO) is a relatively common disease that is often associated with a variety of systemic disorders including arterial hypertension, diabetes mellitus, dyslipidemia, and systemic vasculitis. There are various types of RVO, categorized on the basis of the site of occlusion and on the type of consequent vascular damage. Central retinal vein occlusion (CRVO) is the most frequently occurring and clinically relevant type of RVO. In addition to the well-known classical risk factors, new hemostasis-related ones have been investigated in patients affected by CRVO. The data concerning a number of parameters remain contradictory; yet, high levels of type 1 plasminogen activator inhibitor (PAI-1) and hyperhomocysteinemia appear to play a significant role in the pathogenesis of this disease. Although based on a limited number of studies, this new knowledge could eventually provide important indications regarding prognosis and therapeutic strategies.
PURPOSE/BACKGROUND: Retinal arteriovenous malformations can be seen in a variety of ways and have multiple, associated, ocular changes that can affect vision. The authors report two cases of retinal arteriovenous malformation. In each case, a central retinal vein occlusion developed. METHODS: Each patient underwent clinical examination and fluorescein angiography. One patient was followed over a long period of time. CONCLUSION: The authors propose that a turbulent flow, high intravascular volume, and arteriolar pressure in the venous side of the retinal arteriovenous malformation may lead to vessel wall damage, thrombosis, and occlusion. They also suggest that compression of the central retinal vein by the mass effect of the arteriovenous malformation on the optic nerve further leads to turbulence and thrombosis.
BACKGROUND: Laser or surgical chorioretinal venous anastomosis has not become widespread as suitable treatment for central retinal vein occlusion (CRVO). We report here the effectiveness of cutting off a retinal vein with vitrectomy in making a chorioretinal venous anastomosis in CRVO. METHODS: We performed a vitrectomy accompanied by a chorioretinal venous anastomosis procedure for seven consecutive patients with CRVO. These patients had shown no improvement in their visual acuity in the month following their first visit to our hospital and had a visual acuity of less than 20/200. Their preoperative visual acuity ranged from counting fingers to 20/300. The procedure included the complete cutting of the affected retinal vein, and the making of a small incision at both sides of the vein interruption through the full thickness of the retina, the retinal pigment epithelium and Bruch's membrane. RESULTS: In five of the seven patients, successful chorioretinal venous anastomosis was observed. All five patients showed an improvement of two or more lines in visual acuity 6 months postoperatively. In three of the five, visual acuity was 20/100 or better. A postoperative complication of recurrent vitreous hemorrhage and fibrous proliferation was observed in one patient, and a second operation was necessary. CONCLUSIONS: Surgical interruption of an affected vein was a feasible procedure and could raise the rate of successful chorioretinal venous anastomosis in CRVO.
It has been shown that dual trunk central retinal vein (CRV) occurs in 20.3 per cent of a normal population. Confirmatory evidence has been produced by the results of anatomical, histological and micro-dissection studies. Occlusion of the single trunk of such a vein in its retrolaminar, or intraneural part, would result in a venous occlusion affecting one-half of the retina similar to that of branch retinal vein occlusion (BRVO). Yet this should be regarded as a variation of CRVO. Visual prognosis seems to be better in hemi-central retinal venous occlusion than in total CRVO. The site of development of collateral gives a clue to the site of the occlusion. Therefore, it is suggested that hemi-CRVO is a distinct entity and should not be confused with so-called hemi-spherical vein occlusion which is a variation of BRVO.
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Hemispheric retinal vein occlusions involve the venous return from approximately one-half of the retina and have characteristics of both central retinal vein occlusions and branch retinal vein occlusions. One hundred six such occlusions were studied in 104 patients whose average age was 66 years. The site of the hemispheric vein occlusion was located in a branch retinal vein in 90% of the eyes, and in 10% of the eyes it was located in one of the dual intraneural trunks of the central retinal vein. Of these eyes, 11% developed neovascularization of the disc, 9% developed neovascularization of the retina elsewhere, 9% developed neovascularization of the iris, and 3% developed neovascular glaucoma. Neovascularization was positively correlated with an increasing percentage of capillary nonperfusion (ischemic index) within the area of occlusion. Prophylactic argon laser treatment was effective in reducing the incidence of neovascularization in eyes with significant capillary nonperfusion.
PURPOSE: To report the clinical outcomes in patients undergoing pars plana vitrectomy with and without vein decompression for treatment of branch retinal vein occlusion (BRVO). METHODS: Thirty-five eyes with macular edema and visual acuity worse than 20/100 secondary to BRVO were prospectively evaluated. Vitrectomy with posterior hyaloid removal and vein decompression at the arteriovenous crossing was performed on 15 eyes (Group 1); consecutively, the same technique without vein decompression was performed on 20 eyes (Group 2). Primary outcome was visual acuity and secondary outcomes were resolution of macular edema and development of neovascularization. RESULTS: No differences were found between groups in either patient age (p = 0.566) or preoperative visual acuity (p = 0.505). No differences were found in visual acuity at 3 (p = 0.651), 6 (p = 0.697), 9 (p = 0.763), 12 (p = 0.881), or 18 (p = 0.748) months. Mean time for macular edema resolution and visual acuity improvement was 9 months in both groups, with a mean improvement of 3.5 +/- 2.35 lines in Group 1 and 3.2 +/- 2.97 lines in Group 2. No eyes in either group developed new vessels. CONCLUSIONS: Results suggest that vitrectomy with posterior hyaloid removal without vein decompression can resolve macular edema, improve vision, and prevent development of new vessels in BRVO.
Central retinal vein occlusion is one of the most common retinal vascular disorders. Few and contrasting data are available on the prevalence of hemostatic risk factors in patients with central retinal vein occlusion. The aim of this study was to investigate the most common hemostasis-related inherited risk factors for venous thrombosis in a group of 53 central retinal vein occlusion patients (median age 59 years, range 18-77 years) and in 53 comparable control subjects (median age 57 years, range 22-84 years). No difference was found in antithrombin III, protein C and protein S plasma levels between patients and controls. At univariate analysis, activated protein C resistance (odds ratio 5.8) and factor V Leiden (odds ratio 4.4) were significantly associated with central retinal vein occlusion whereas G20210A polymorphism of the prothrombin gene was not. After adjustment for sex, age, and the other classic vascular risk factors (hypertension, diabetes, hypercholesterolemia, smoking) activated protein C resistance remained the only independent risk factor for central retinal vein occlusion (odds ratio 11.5). These data indicate that activated protein C resistance may play a role in the pathophysiology of central retinal vein occlusion.