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We describe a bimanual technique of subfoveal neovascular membrane removal in a patient with presumed ocular histoplasmosis syndrome. His postoperative vision has improved from 20/400 to 20/100 at 3 months follow-up. No recurrence of the membrane was noted.
BACKGROUND: A pigment epithelial detachment (PED) is an exudative manifestation of late age-related macular degeneration (AMD). Its long-term unfavourable prognosis is influenced by the association of a neovascular membrane. Seemingly identical PEDs in ophthalmoscopy can be further differentiated by fluorescein and indocyanine green angiography. The purpose of this prospective follow-up study was to determine the most reliable angiographic classification to distinguish PEDs in AMD and to evaluate their outcome. MATERIAL AND METHODS: 73 eyes of 68 patients with a PED in AMD were examined with simultaneous angiography with fluorescein and indocyanine green. 34 eyes were additionally scanned by retinatomography. Fluorescein angiographic classification comprises 4 types: 1. early hyperfluorescent type, 2. late hyperfluorescent type, 3. drusen type, 4. irregular fluorescent type. Indocyanine green angiographic classification consists of the following three groups: 1. angiographically no vascularisation, 2. associated choroidal neovascularisation, 3. associated polypoidal choroidal vasculopathy. RESULTS: Both classifications show statistically significant correlation with visual acuity (fluorescein classification: P = 0.0112, ICG-classification: P = 0.0004) and area of the PEDs (fluorescein classification: P = 0.0002, ICG-classification: P < 0.0001). ICG-classification additionally is significantly associated with the volume (P = 0.0008). Both classifications correlate (P = 0.0001). Factors influencing visual acuity are: age (P = 0.0044), associated neovascular membrane (P = 0.0004), area (P < 0.0001), volume (P = 0.0077) and height (P < 0.0001). CONCLUSIONS: PEDs in AMD can best be classified by indocyanine green angiography on the basis of an associated prognostically important neovascular membrane, which can only be further distinguished into choroidal neovascularisation or polypoidal choroidal vasculopathy by indocyanine green angiography. Statistical analysis shows qualitatively and quantitatively more significant results for the indocyanine green angiographic classification.
PURPOSE: To test the hypothesis that the vitreous protein content is altered prior to the development of neovascularization in an experimental model of retinopathy of prematurity (ROP). METHODS: Newborn rats underwent either a variable oxygen exposure or room air exposure following birth. On day 13 or 14, two days prior to neovascularization, the steady state vitreous and plasma total protein levels in room-air controls or variable-oxygen-exposed newborn rats were determined; similar measurements were also made for control adult rats. RESULTS: There was a significant difference (P < 0.05, 2-tailed t-test) in the vitreous protein concentration between the age-matched control and experimental newborn rats. The protein level in the ROP rat plasma was not significantly (P > 0.05) different from that in the age-matched control animals. The vitreous-to-plasma-protein ratios of both the control and ROP newborn animals were significantly greater (P < 0.05) than that in the adults. CONCLUSIONS: The results of this study demonstrate, for the first time, increased vitreous protein levels prior to the development of neovascularization in the newborn rat model of ROP. In addition, developmental changes in vitreous protein levels were identified. The role of developmental and pathologic alterations in the blood-ocular barriers in this study is discussed.
Radiotherapy remains a controversial type of therapy for subfoveal neovascularization. Recently a peculiar pattern of neovascular growth of the irradiated choroidal neovascular membrane has been described. This evolution may be associated with extensive exudative reaction. In one of our patients with this complication, the disease progressed to a total exudative retinal detachment and neovascular glaucoma.
Diabetic retinopathy (DR) still remains the leading cause of blindness in the working population of Japan and western world, though therapies such as retinal photocoagulation and vitrectomy can be remarkably effective when administered at an appropriate stage in the disease process. Consequently, there is a need for further investigation of the pathogenesis of DR to develop better therapy. DR is characterized by gradually progressive alterations in the retinal microvasculature, leading to three fundamental morbidities: (1) vascular hyperpermeability, (2) vascular occlusion, and (3) neovascularization. Recent studies have revealed that hyperglycemia causes several metabolic disorders which cause DR directly or indirectly through the abnormal expression of cytokines including vascular endothelial growth factor (VEGF). In this study, we performed precise tests of the correlation between intraocular VEGF and the three fundamental changes in the diabetic retina mentioned above.Ultrastructural study of the human retina revealed that two major pathways are responsible for hyperpermeability of diabetic retinal vessels, ie intercellular or paracellular transport (opening of the tight junctions) and intracellular or transcellular transport (caveolae, intracytoplasmic vesicles, and fenestration). All these pathways were induced by intravitreal injection of VEGF. The major trigger of VEGF overexpression is tissue ischemia caused by vascular occlusion. However, the retinas from the eyes with background DR revealed increased expression of VEGF without apparent incidence of vascular occlusion. We have identified accumulation of advanced glycation end products (AGEs) in these retinas, and found that AGEs are a major stimulus for VEGF overexpression in background DR. Retinal vascular occlusion was caused by thrombus formation primarily in the capillary vessels. Thrombi mainly consisted of fibrin, platelets, and leucocytes in the early stage of their formation, and glial cells and macrophages were also involved in the later stage. The blood coagulation process plays an important role in fibrin formation in thrombi. The expression of tissue factor (TF), an initiator of extrinsic blood coagulation, was upregulated by VEGF in retinal vascular endothelial cells (REC). In addition, AGEs were also thrombogenic through the induction of TF expression and suppression of the expression of prostacyclin stimulating factor (PSF), which stimulate prostacyclin synthesis in vascular endothelial cells. These findings suggest that AGEs, VEGF, and TF could interact in a vicious circle because AGEs and VEGF could induce retinal vascular occlusion which results in further increase in VEGF expression.Intravitreal injection of VEGF could induce retinal neovascularization, VEGF stimulates vascular endothelial cell proliferation by binding to a specific receptor named kinase insert domain-containing receptor/fetal liver kinase (KDR/Flk-1, KDR). AGEs and basic fibroblast growth factor (bFGF) induced expression of KDR in REC, and a transcription factor Sp 1 was involved in this process. Since the expression of KDR as well as VEGF was already upregulated in the retinas with background DR, VEGF appeared to start to induce the proliferative changes long before the actual onset of proliferative DR. These findings indicated that VEGF and its receptor system plays a pivotal role all through the disease process of DR.We considered that amelioration of the activated VEGF and its receptor system could lead to the development of new therapy for DR. We have developed two novel methods to prevent retinal neovascularization by inhibiting VEGF and its receptor system. (1) An insulin sensitizing agent (troglitazone) inhibited proliferation, migration, and in vitro tube formation by REC as well as oxygen-induced retinal neovascularization in a mouse model. Thus, glycemic control by troglitazone could reduce the incidence of neovascularization in diabetic eyes. (ABSTRACT TRUNCATED)
A clinical randomized study using argon-green (532 nm) and diode (810 nm) lasers was carried out on 44 eyes (34 patients) affected by proliferative diabetic retinopathy (PDR), with the aim of evaluating the long-term effects of diode panretinal photocoagulation. Of the total 44 eyes, 22 were randomized to argon laser treatment (ALT) and 22 to diode laser treatment (DLT). The mean follow-up time was 25 +/- 5 months in the ALT group versus 24 +/- 4 months in the DLT group. In the ALT group 20 eyes (91%) showed regression of PDR whereas 2 eyes (9%) deteriorated. In the DLT group regression of neovascularization was observed in 22 eyes (100%). These results show that the long-term efficacy of diode laser PRP in the treatment of PDR is similar to that of argon-green laser PRP.
PURPOSE: To assess the role of astrocytes in controlling the growth of developing retinal vessels. METHODS: Growth of retinal vessels in the neonatal rat retina was examined in three conditions: normal development, cyclic hyperoxia, and normoxia (1 day 70% to 75% oxygen, 1 day room air for up to seven cycles from birth, and room air for up to 16 days), and direct hypoxia (10% oxygen from postnatal day 3 [P3]). Retinas were examined as wholemounts labeled for astrocytes, microglia, and blood vessels and in some experiments for the fragmentation of DNA characteristic of apoptosis. RESULTS: In normoxia, superficial retinal vessels formed to the processes of astrocytes. In cyclic hyperoxia, the depletion of superficial retinal vessels and subsequent neovascularization described by others were confirmed. The neovascularization was preceded by the depletion by apoptotic death of the astrocyte population, first between vessels but eventually breaching the glia limitans along vessels. The earliest forms of neovascularization resembled microaneurysms, each protruding through a defect in the glia limitans of a capillary. Neurons of the ganglion cell layer survived. Direct hypoxia from P3 caused hypertrophy of superficial vessels. Between P3 and P6, some vessels accelerated past the still-spreading astrocytes, often growing out of the retina into the vitreous humor. Direct hypoxia also caused astrocyte degeneration, but capillaries retained astrocyte investment and were not the site of vascular damage. By P8, breaches in the astrocytic glia limitans became prominent but were restricted to large veins. At such breaches, bleeding into the vitreous humor was common. CONCLUSIONS: Retinal vessels normally develop in close association with astrocytes. Where that association is broken, preretinal vessels may grow or bleed into the vitreous humor. Astrocytes play important roles in constraining retinal vessels to the retina and in maintaining their integrity.
Long-term observations of 4 patients with serpiginous choroidopathy indicates that it is a chronic disease with characteristic recurrences. The most severe complication is subretinal neovascularization which can develop after many years since the onset of the disease and cause significant deterioration of vision. Therefore patients with serpiginous choroidopathy ought to be followed-up for a long time and informed about the possibility of complications which can appear even after a long period.
Case records of patients who had macular detachment following argon laser photocoagulation for proliferative diabetic retinopathy were reviewed. Thirteen eyes of 11 patients out of a total of 480 patients treated had this complication, and in 12 eyes of 10 patients the short latency suggested a true precipitating effect. This represents 2.1% of patients receiving panretinal photocoagulation. Patients with detachment were younger and developed diabetes earlier than the controls (P less than 0.025), and the detached eyes had received more numerous laser burns on average per session than the controls (P less than 0.001). In 5 eyes the last photocoagulation dose exceeded 1000 burns delivered in the presence of traction membranes in an attempt to arrest continuing neovascular proliferation not responding to earlier more moderate treatment. Only 1 eye had received early, extensive and repeated photocoagulation. Vigorous treatment at an early stage of the proliferation may prevent this complication, although the advantages or disadvantages of fractionation of photocoagulation will only be shown by a prospective trial.
We have conducted a retrospective study about 25 patients who have presented subretinal neovascularization and idiopathic recurrent multifocal choroiditis. Final visual acuity level (mean 20/30) was almost the same as the pre laser treatment visual acuity level (mean 20/25) for a follow up of 12 months. We have also studied the main clinical, angiographic and serologic features of these cases of multifocal choroiditis.
PURPOSE: To report the results of surgical removal of extrafoveal peripapillary subretinal neovascular membranes (PSRNVMs) for elderly patients in whom visual acuity was threatened or affected by subretinal fluid, subretinal hemorrhage, subretinal exudate, or PSRNVM growth toward the fovea. METHODS: Retrospective review of six eyes of six patients undergoing subretinal surgical removal of PSRNVMs via pars plana vitrectomy. RESULTS: PSRNVMs were successfully removed in six eyes of six patients with initial preservation of foveal function. The preoperative Snellen visual acuity ranged from 20/40 to counting fingers, and the best postoperative visual acuity ranged from 20/25 to 20/40. The final visual acuity with a mean follow-up of 3 years (range, 6-63 months) was stable or improved in 83% (5 eyes) of cases, ranging from 20/25 to 20/80. Early recurrence of PSRNVM was noted only in 1 eye (17%) at 1 month after surgery and was successfully treated with laser photocoagulation. Late recurrence of choroidal neovascularization developed after 3 years in two eyes. Cataract developed in three of four phakic eyes. CONCLUSION: PSRNVMs sparing the central fovea in elderly patients can be successfully removed surgically with initial preservation of foveal function and with a low rate of early recurrence.
A 31-year-old woman complained of a sudden, painless decrease in vision of the right eye. Ophthalmic examination demonstrated a vitreous hemorrhage in the right eye secondary to peripheral neovascularization. The left eye demonstrated findings consistent with pars planitis. Before this episode, vision was good in both eyes. Although rare, vitreous hemorrhage can occur in the setting of pars planitis and may be a presenting symptom. Pars planitis should be considered in the differential diagnosis of young patients with vitreous hemorrhage.
This study was performed to explore the interaction between chronic neural degeneration and the subsequent vascular remodeling. Weekly urethan administration in rats from birth produces a retinopathy model characterized by photoreceptor degeneration, retinal vascular regression, and retinal pigment epithelium (RPE) neovascularization. We investigated the hypothesis that altered oxygen distribution across the retina and choroid could be involved in the vascular changes seen in this retinopathy. We compared measurements of vitreal, intraretinal, and choroidal oxygen tension (PO2) distribution in anesthetized and ventilated control and urethan-treated rats at 8 and 16 wk of age with the use of oxygen-sensitive microelectrodes. Striking differences were observed in both choroidal and intraretinal PO2 distribution in urethan-treated rats compared with controls. At both ages, intrachoroidal PO2 was much lower in the urethan-treated rats. In addition, the intraretinal PO2 distribution across the inner retinal layers was more uniform than normal. A small elevation in PO2 was present at 8 wk in the inner nuclear layer where subsequent vascular regression occurred, and a small reduction in PO2 was present at the RPE, which recovered to normal values by 16 wk in regions where RPE vessel networks were first evident. Although the retinal arteries were considerably thinner at both ages in the urethan-treated rats, the vitreal PO2 profiles and superficial retinal PO2 remained normal. The unexpected and large reduction in the oxygen delivery from the choroid found in the urethan-treated rats may account for the lack of major hyperoxia within the pathological retina and the lower oxygen tension in the RPE before the vascular proliferation in this region. We propose that tissue PO2 is an important determinant of the vascular remodeling, which is seen in this model of neural degeneration and that the PO2 distribution changes described in this study help provide a new view of the pathogenesis of this model.
Newborn mice exposed to high (greater than 98%) ambient oxygen during the newborn period and subsequently removed to room air will develop a proliferative retinopathy which mimics the neovascular component of acute retinopathy of prematurity. In this paper, we report preliminary ultrastructural findings on the vitreous new vessels in the mouse model of oxygen-induced retinopathy, and argue that the model is appropriate for research on non surgical treatments for ROP in particular and angiogenesis in general.
The eyes of 47 subjects with exudative age-related macular degeneration in the fellow eye were tested with a battery of visual function tests at baseline and followed for at least 18 mo. Fundus photographs also were obtained at baseline. These photographs were used to verify the absence of exudative lesions in the 47 eyes tested. Functional and funduscopic baseline data each were compared against outcome data obtained typically at 18 mo. The baseline data were analyzed for their ability to distinguish eyes that had developed detectable exudative age-related macular degeneration from eyes that had not. Eyes with relatively slow foveal dark adaptation rates despite low foveal quantum absorption capabilities (as inferred from the effects of test area on the Rayleigh color match) were especially likely to develop subretinal neovascularization. The resulting sensitivity/specificity and odds ratios were comparable to those of the most effective funduscopic risk indicators. Low S (blue) cone-mediated sensitivity also was associated with an exudative outcome.
PURPOSE: Atrial natriuretic peptide (ANP) has been recently described as an endogenous inhibitor of the synthesis and angiogenic action of vascular endothelial growth factor (VEGF). Given VEGF's key role in promoting neovascularization in proliferative diabetic retinopathy (PDR), this study was designed to evaluate the possibility that ANP could be involved in the neovascular and fibrotic complications of PDR. METHODS: We determined ANP by radioimmunoassay in plasma and vitreous humor samples collected from diabetic patients with and without PDR and from non-diabetic subjects. ANP was also immunohistochemically localized in the epiretinal membranes of patients with PDR. RESULTS: Vitreous ANP concentrations were significantly higher in patients with active PDR compared to patients with quiescent PDR, diabetes without PDR or controls <0.05. Significant differences were also observed between vitreous ANP levels in diabetic patients without PDR and control subjects. There was no significant correlation between serum and vitreous ANP levels in any of the patient groups. ANP was detected in the fibrovascular epiretinal tissue of patients with PDR. CONCLUSIONS: Diabetic patients with active neovascularization have significantly higher levels of ANP in the vitreous humor than those without active PDR. Diabetic patients without PDR were also found to have significantly higher vitreous ANP levels than non-diabetic patients. Since plasma and vitreous ANP concentrations were found to be unrelated, we suggest intraocular ANP synthesis and/or an increase in the release of ANP into the vitreous, as opposed to diffusion from the blood, as the main factors contributing to the high vitreous ANP levels observed in diabetic patients. In the fibrovascular epiretinal tissue of these patients, ANP was found to be localized in vascular, glial, fibroblast-like and retinal pigment epithelium cells. Our findings suggest a role for ANP in PDR.
We reviewed 287 cases of pars plana vitrectomy performed between January 1985 and June 1990 in which retinotomies were created for drainage of subretinal fluid or blood. We found subretinal neovascularization associated with the retinotomy site in two cases (1%) and focal proliferative vitreoretinopathy associated with the retinotomy site in seven cases (2%). These complications were more likely to occur with retinotomies made within the superior macular region (p = 0.002).
A 42-year-old man with idiopathic intracranial hypertension and chronic papilledema had severe visual loss in his left eye caused by subretinal bleeding from a peripapillary choroidal neovascular membrane (CNVM). After optic nerve sheath fenestration in his left eye, the papilledema improved, allowing improved visualization of the CNVM. Visual function did not improve after the surgery. CNVM can complicate chronic papilledema and account for sudden worsening of vision. The appropriate management of this type of CNVM is unresolved.