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We report one case of subretinal neovascularization developed on a chorioretinal scar after metallic intraocular foreign-body trauma. New vessels, occurred three years after the injury at the initial impact site, reached first the foveola and could not be treated by laser photocoagulation.
Background/Purpose. Recent findings suggest that an objective assessment of retinal vessel caliber from fundus photographs provide information about the association of microvascular characteristics with macrovascular disease. Current methods used to quantify retinal vessel caliber, introduced by Parr(1,2) and Hubbard,(3) are not independent of scale and are affected by the number of vessels. To improve upon these methods we introduce revised formulas for quantifying vessel caliber. Methods. Revised formulas were estimated using retinal vessel measurements from 44 young adults free of hypertension and diabetes. Comparisons between the two methods were done using digitized photographs from 4926 participants at the baseline examination of the Beaver Dam Eye Study (BDES), an ongoing population-based cohort study initiated in 1987. Individual arterioles and venules were measured using semi-automated computer software from which summary measures were calculated. Results. Correlation coefficients between the Parr-Hubbard and revised formulas were high (Pearson correlation coefficients ranging from 0.94 to 0.98). Both arteriolar and venular caliber significantly increased with an increasing number of vessels measured using the Parr-Hubbard formulas (p < 0.001), which in turn affected the relationship to mean arterial blood pressure. To the contrary, the revised formulas were not affected by the number of measured vessels (p > 0.50). Conclusions. We describe revised formulas for summarizing retinal vessel diameters measured from fundus photographs to be used in future studies and analyses. The revised formulas correlate highly with the previously used Parr-Hubbard formulas, but offer the advantages of being more robust against variability in the number of vessels observed, being independent of image scale, and being easier to implement.
OBJECTIVE: To evaluate whether the position of the central retinal vessel trunk exit on the lamina cribrosa spatially correlates with the location of parapapillary atrophy in glaucoma. DESIGN: Clinic-based, observational, cross-sectional study. PATIENTS: Color stereo optic disc photographs of 95 patients with primary or secondary open-angle glaucoma and 65 healthy persons were morphometrically evaluated. The intrapapillary and parapapillary region was divided into four quadrants. We determined the position of the central retinal vessel trunk exit on the lamina cribrosa surface and measured the area of parapapillary atrophy and neuroretinal rim in the four quadrants. MAIN OUTCOME MEASURES: The area of neuroretinal rim and parapapillary atrophy and the position of the central retinal vessel trunk exit. RESULTS: Comparing measurements between opposite disc quadrants showed that beta zone of parapapillary atrophy was significantly (P < 0.05) larger and that the neuroretinal rim was significantly smaller when beta zone and neuroretinal rim were measured in the disc quadrant most distant to the central retinal vessel trunk exit, than if the beta zone and neuroretinal rim were measured in the quadrant containing the vessel trunk exit. Comparing measurements in the disc quadrants between eyes with different positions of the central retinal vessel trunk exit revealed that, in the respective disc quadrant, the beta zone was significantly larger and the neuroretinal rim was smaller in eyes with the vessel trunk exiting in the opposite disc quadrant than in eyes with the vessel trunk exit located in the respective disc quadrant where the measurements were obtained. CONCLUSIONS: Position of the central retinal vessel trunk exit on the lamina cribrosa influences the location of parapapillary atrophy in glaucoma. The longer the distance to the central retinal vessel trunk exit, the more enlarged is parapapillary atrophy and the smaller is the neuroretinal rim. This relationship agrees with the spatial relationship between glaucomatous neuroretinal rim loss and enlarged parapapillary atrophy in glaucoma. Diagnostically, it may indicate that, in eyes with an abnormal configuration of parapapillary atrophy or with an abnormal position of the central retinal vessel trunk exit, early glaucomatous rim changes should be looked for in the disc sector that is most distant to the central retinal vessel trunk exit and where parapapillary atrophy may be relatively large.
Retinopathy of prematurity (ROP) is characterized by inhibition of the growth of the retinal vessels and subsequent neovascularization. Pharmacologic doses of glucocorticoids are known to decrease growth and to suppress inflammation. The aim of the present study was to investigate whether hyperoxia and/or glucocorticoid affect the growth of the retinal vessels and the expression of the anti-inflammatory cytokine IL-1 receptor antagonist (IL-1ra). The following treatments were given to newborn rabbits during the rapid growth of retinal vessels: 1) placebo and room air (n = 14); 2) dexamethasone (Dx) at 1 mg/kg/d during d 3 to 8 and room air (n = 14); 3) placebo and 100% oxygen (d 3 to 7) (n = 14); 4) Dx and O2 (n = 16). On d 12, the eyes were studied for retinal vessel length and vascular surface area from India ink-perfused vessels. When indicated, retinas were harvested on d 7 and studied for the expression of IL-1ra mRNA using Northern blot analysis. Hyperoxia decreased the length and area of the retinal vessel complexes (p < 0.01) and induced neovascularization in three of eight animals (38%). Dx decreased the length and area (p < 0.01) and tended to increase the tortuosity of the retinal vessels. Dx did not potentiate the hyperoxia-induced suppression of retinal vessel growth and prevented the hyperoxia-induced neovascularization (p = 0.04). Hyperoxia inhibited the expression of IL-1ra mRNA, whereas Dx ameliorated the hyperoxia-induced suppression of IL-1ra. According to present results, glucocorticoid decreases the retinal vessel growth and may decrease the hyperoxia-induced neovascularization. We propose that immature and damaged retinal vessels are affected by pharmacologic dosage of glucocorticoid.
PURPOSE: To determine retinal vessel diameter variations in response to neuronal activity induced by diffuse luminance flicker. METHODS: The diameter of retinal arteries and veins was measured in 9 normal subjects by computer analysis of fundus pictures taken in monochromatic light under normal conditions of illumination and after 1 min of sinusoidally varying diffuse luminance flicker at 10 Hz. RESULTS: The diameter immediately after flicker was significantly larger than the pre-stimulus diameter by 4.2 +/- 2.2% for the retinal arteries and 2.7 +/- 1.7% for the retinal veins (mean +/- SD). Six is after cessation of the flicker, arterial diameter was not significantly different from that of pre-flicker value. CONCLUSIONS: Diffuse luminance flicker induces an increase in retinal vessel diameter. This increase most probably reflects an increase in retinal blood flow previously evidenced in humans by the blue field simulation technique. The technique needs to be optimized in terms of flicker parameters, to determine whether flicker-evoked retinal diameter changes could represent a useful clinical measure of the capability of the retinal vascular system to vasodilate.
Retinal vessels can be observed noninvasively and provide a window to microvascular systems elsewhere in the body. Generalized retinal arteriolar narrowing can represent structural changes resulting from persistent high blood pressure. However, data from recent studies also suggest that generalized retinal arteriolar narrowing might precede hypertension and contribute to its pathogenesis. To determine whether vessel diameters in the eye are genetically determined, we conducted a genome-wide linkage scan on retinal vessel diameters (central retinal artery equivalent and central retinal vein equivalent) using data from the Beaver Dam Eye Study. There were 7 regions on 5 chromosomes (3q28, 5q35, 7q21, 7q32, 11q14, 11q24, and 17q11) showing linkage signals at the nominal multipoint significance level of 0.01 for either covariate-unadjusted or -adjusted central retinal artery equivalent; there were 7 regions on 6 chromosomes (1p36, 6p25, 6q14, 8q21, 11p15, 13q34, and 14q21) showing linkage signals at the nominal multipoint significance level of 0.01 for either covariate-unadjusted or -adjusted central retinal vein equivalent. The linkage results for retinal vessel diameters indicate genetic contributions that remain significant even after adjusting for hypertension and other covariates. In summary, we provide evidence demonstrating that genetic factors independent of hypertension affect retinal vessel diameters.
INTRODUCTION: Diffuse luminance flicker increases retinal vessel diameters in animals and humans, indicating the ability of the retina to adapt to different metabolic demands. The current study seeks to clarify whether flicker-induced vasodilatation of retinal vessels is diminished in glaucoma patients. METHODS: Thirty-one patients with early stage glaucoma (washout for antiglaucoma medication) and 31 age- and sex- matched healthy volunteers were included in the study. Retinal vessel diameters were measured continuously with a Retinal Vessel Analyzer. During these measurements three episodes of square wave flicker stimulation periods (16, 32, and 64 secs; 8 Hz) were applied through the illumination pathway of the retinal vessel analyser. RESULTS: Flicker-induced vasodilatation in retinal veins was significantly diminished in glaucoma patients as compared with healthy volunteers (ANOVA, P < 0.01). In healthy volunteers, retinal venous vessel diameters increased by 1.1 +/- 1.8% (16 seconds, P < 0.001), 2.0 +/- 2.6 (32 seconds, P < 0.001), and 2.1 +/- 2.1% (64 seconds, P < 0.001) during flicker stimulation. In glaucoma patients, venous vessel diameters increased by 0.2 +/- 1.7% (16 seconds, P < 0.6), 1.1 +/- 2.1% (32 seconds, P < 0.01), and 0.8 +/- 2.5 (64 seconds, P < 0.09). In retinal arteries, no significant difference in flicker response was noticed between the two groups (ANOVA, P < 0.6). In healthy controls, flicker stimulation increased retinal arterial vessel diameters by 1.0 +/- 2.4% (P < 0.03), 1.6 +/-3.2% (P < 0.004) and 2.4 +/- 2.6% (P < 0.001) during 16, 32, and 64 seconds of flicker, respectively. In glaucoma patients, flickering light changed arterial vessel diameters by 0.3 +/-2.6% (16 seconds, P = 0.4), 1.3 +/-3.1% (32 seconds, P = 0.03), and 1.8 +/- 3.8% (64 seconds, P = 0.005). CONCLUSION: Flicker-induced vasodilatation of retinal veins is significantly diminished in patients with glaucoma compared with healthy volunteers. This indicates that regulation of retinal vascular tone is impaired in patients with early glaucoma, independently of antiglaucoma medication.
AIMS/BACKGROUND: Retinal vessel dilatation is a well known phenomenon in diabetes. In this study, the theory of whether excessive changes in diameter and length of retinal vessels occur in the development of diabetic macular oedema was tested, supporting a hypothesis that the development of diabetic macular oedema may be linked to hydrostatic pressure changes described in Starling's law. METHODS: From fundus photographs of diabetic patients attending a regular eye screening programme, the diameter and segment length of retinal vessels were measured in three retinopathy groups (12 patients each) with diabetic macular oedema (DMO), background retinopathy and no retinopathy, over a period of approximately 4 years, ending at the time of diagnosis of diabetic macular oedema in the DMO group. RESULTS: A statistically significant dilatation and elongation of retinal arterioles, venules, and their macular branches was found before the diagnosis of macular oedema in the DMO group. No significant changes were found in the other two groups. CONCLUSION: It is suggested that Starling's law applies to the formation of oedema in the retina as in other tissues.
The Retinal Vessel Analyzer (RVA) is a measuring device for online measurement of the diameter of retinal vessels in relation to time and locations along the vessel. It is furthermore provided with several tools for analyzing the measured data. The fundamental components consist of a fundus camera with CCD measuring camera attached and an advanced image-processing unit. The measurement range is from 90 microns, temporal resolution is 40 ms and measurement resolution is less than 1 micron. Systematic error of non-linearity is S < or = 1.6%, reproducibility is given by variation coefficient: short term vcs = 1.5%, long term vcl = 2.8%.
Monosodium glutamate (MSG) administered to neonatal rats on postnatal days 1 to 10 caused a generalized degeneration of the inner retinal layers. MSG administered only on postnatal days 8, 9, 10, and/or 11 caused a retinopathy limited to more peripheral retinal areas corresponding to currently existing regions of immature retinal vessels. Ink-injected retinal vessel studies showed a delay in development of the retinal vessel network but no alterations in vessel patency. Fluorescence microscopic examination of freeze-dried tissues revealed to abnormalities of the blood-retinal barriers to sodium fluorescein. We conclude, as demonstrated by these methods, that MSG retards development of the retinal vessels but does not affect development of the blood-retinal barriers. The retinotoxic effect of MSG apparently results from a mechanism(s) other than a breakdown of the blood-retinal barrier.
The retinal vessel calibre responses to systemic sympathetic stimulation, were studied in nine patients (eight male; mean age: 31.7 years; range: 19-58 years) with unilateral disruption of their cervical sympathetic tract. All patients had ipsilateral decreased/absent facial sweating and a Horners syndrome, evidence of unilateral sympathetic denervation. Both eyes of each patient were studied and the results were analysed in two groups: the group of nine sympathectomised eyes and the control group of unaffected fellow eyes. During handgrip contraction there was a significant difference in the mean retinal arteriolar constriction (mean +/- SEM) between the group of sympathectomised eyes (4.6 +/- 0.89%) and control eyes (7.1 +/- 1.13%), p less than 0.01. Similarly, there was a significant difference in mean venule constriction during sustained handgrip contraction between the group of sympathectomised eyes (1.5 +/- 0.67%) and control eyes (4.9 +/- 0.98%), p less than 0.05. There was no significant difference in the mean rise in diastolic blood pressure between the two groups: control eyes +27.9 +/- 2.38 mmHg and sympathectomised eyes +27.8 +/- 2.25 mmHg. There was no correlation between the blood pressure and retinal vessel responses in either group. These results suggest that the sympathetic nervous system plays an integral role in retinal blood flow regulation.
PURPOSE: To determine if refractive errors influence the association of blood pressure and retinal vessel diameters. DESIGN: Population-based, cross-sectional study. METHODS: Retinal photographs from the right eyes of participants (n = 3,654, aged 49+ years) in the Blue Mountains Eye Study taken during baseline examinations (1992 to 1994) were digitized. The diameter of all retinal vessels located half to one disk diameter from the disk margin was measured using a computer-assisted imaging program. These measurements were combined to provide the average diameters of retinal arterioles and venules of that eye, and the ratio of their diameters, the arteriole-to-venule ratio (AVR). The association of blood pressure and retinal vessel diameters was analyzed before and after correction for refraction using the Bengtsson formula. RESULTS: Before correction, each 10-mm Hg increase in mean arterial blood pressure was associated with a 3.7-microm (95% confidence interval [CI], 3.2-4.3) decrease in arteriolar diameter and a 0.9-microm (95% CI, 0.3-0.9) decrease in venular diameter. After correction for refraction, each 1-mm Hg increase in mean arterial blood pressure was associated with a 3.7-microm (95% CI, 3.2-4.2) decrease in arteriolar diameter and a 0.8-microm (95% CI, 0.3-0.9) decrease in venular diameter. Refraction was not associated with the AVR and had no effect on the association of blood pressure and AVR. CONCLUSION: Refraction had no appreciable effect on the association of blood pressure and retinal vessel diameters or on the AVR. Correction for refraction is important for quantifying absolute retinal vessel caliber, but may not be particularly important in epidemiologic studies investigating the association of generalized retinal arteriolar narrowing and hypertension.
PURPOSE: To describe the cross-sectional relationships between age, blood pressure (BP), and quantitative measures of retinal vessel diameters in an older Australian population. METHODS: Retinal photographs from right eyes of participants (n = 3654, aged 49+ years) in the Blue Mountains Eye study taken during baseline examinations (1992-1994) were digitized. The width of all retinal vessels located 0.5 to 1.0 disc diameters from the disc margin was measured by a computer-assisted method. Summarized estimates for central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent (CRVE) represent average retinal vessel diameters. The arteriole-to-venule ratio (AVR) was calculated. Associations between age and BP and CRAE, CRVE, and AVR were assessed with generalized linear models. RESULTS: Retinal vessel diameters decreased with increasing age in both men and women. CRAE and CRVE decreased by 4.8 microm and 4.1 microm, respectively, per decade increase in age, after adjusting for sex and mean arterial blood pressure. Mean AVR declined by 0.01 for each increasing decade of age, until 79 years. After adjustment for age, sex, smoking, and body mass index, CRAE, CRVE and AVR were all significantly and inversely associated with BP. For every 10-mm Hg increase in mean arterial blood pressure, AVR decreased by 0.012 and CRAE and CRVE decreased by 3.5 microm and 0.96 microm, respectively. CONCLUSIONS: Retinal arteriolar and venular diameters narrow with increasing age, and these parameters are inversely related to BP, independent of age, gender, and smoking. The findings are consistent with those from the Atherosclerosis Risk in Communities Study suggesting that decreased retinal vessel diameters may reflect microvascular damage from elevated blood pressure.
Changes in retinal hemodynamics are a factor of major influence in diabetic retinopathy. With the aid of videoangiography, the changes in retinal circulation times before and after therapeutic laser coagulation were examined in a prospective study. A marked diminution of all circulation times was observed after laser coagulation procedures: the arterial circulation time decreased from 1.02 s to 0.74 s average, the early venous circulation time from 5.18 s to 3.50 s average, and the late venous circulation time from 9.07 s to 8.16 s. Laser coagulation has a more significant influence on the capillary circulation of the retina than on the venous phase. In diabetic retinopathy, the improvement in pathologic hemodynamic situations in the retina may be a very important mechanism of action in laser coagulation therapy.
Alcohol use is a recognized risk factor for stroke. We hypothesized that alcohol use may increase the risk of stroke, independent of an effect on blood pressure, by causing cerebral vasoconstriction. To examine this, we used retinal vessels as a marker for cerebral vessels and analysed the cross-sectional associations between alcohol use and total retinal vessel width in 741 Japanese and 434 American white male telephone executives. Systolic and diastolic blood pressures were negatively associated with retinal vessel width in the Japanese (p less than 0.0001, 0.0001, respectively) but this association did not achieve statistical significance in the Americans (p less than 0.1, 0.3). Japanese drinkers had a larger mean retinal vessel width than Japanese abstainers, while American drinkers had a smaller retinal vessel width than abstainers. These associations between alcohol use and retinal vessel width were not significant within nationalities but the interaction between alcohol use and nationality was significant, independent of other stroke risk factors (p less than 0.04). Although these results do not support the initial hypothesis, they are consistent with known biological differences in alcohol metabolism between Japanese and American men and support different effects of alcohol use on retinal vessel calibre in these two nationalities.
During intracapsular lens extraction the extreme retinal periphery is subjected to zonula-mediated traction and possible damage to the retinal vessels. The vascular pattern at the ora serrata was studied with special reference to the frequency and distribution of vessels positioned adjacent to the ora structures. The possible role of leakage from such vessels in vitreo-retinal pathology of the aphakic eye is discussed.
BACKGROUND: Cerebral and retinal vessels behave similarly under the influence of vascular risk factors. Several groups have shown that retinal microvascular abnormalities represent an independent risk factor with regard to strokes and heart attacks. AIM OF THE STUDY: The aim of this study was to perform a prospective screening examination with regard to retinal microvascular abnormalities as well as an extended vessel diagnosis in a subgroup of patients with lower arteriovenous risk values. METHODS: In the course of a prospective cross-sectional study ("Talking Eyes") between 1.9.2001 and 1.8.2002 a telemedical-supported screening of the retina (study I) was carried out in 7,163 subjects. The patients were selected without any inclusion or exclusion criteria. The mean age was 48.2 +/- 8 years (18 - 83 years) with a sex distribution of 39.2 % females to 60.8 % males. Digital fundus photos of the right and left eyes were taken for all patients. The pictures were taken without pupil dilation using a CANON-NM camera. The pictures and case histories were stored in a central server using web-based software (MedStage, Siemens). In a central reading centre, the arteriovenous ratio of both eyes was determined telemedically using the Parr-Hubbard formula and the retinas subjected to a standardised examination by an ophthalmologist. The retinal risk factor was calculated on the basis of the arteriovenous ration, the presence of microvascular abnormalities and the case history. The reproducibility of measurement of the arteriovenous ratio (Kronbach alpha coefficient) was evaluated by double measurements on 1,332 images. In a subgroup of study I with arteriovenous ratio values < 0.76 (N = 107), an extended vessel diagnosis with measurement of 24-h blood pressure and vessel-relevant blood values (homocysteine, cholesterol, LDL, HDL, CRP, TG, HbA1c) was carried out (study II). RESULTS: Study I: The Kronbach alpha coefficient as a measure of reproducibility amounted to 0.77. The mean arteriovenous ratio of the retinal vessels was 0.83 +/- 0.09 and showed a pronounced age dependence (R = 0.9, p < 0.0001). On multivariate testing the arteriovenous ratio correlated significantly (R = 0.33, p < 0.001) with the factors age, systolic blood pressure, diastolic blood pressure and body mass index. Diastolic blood pressure followed by age had the largest influence. The prevalence of microvascular abnormalities in the right (RE) and left (LE) eyes, respectively were: cotton wool foci RE 0.0015 %, LE 0.003 %, retinal haemorrhage RE 0.1 %, LE 0.1 %, focal stenoses RE 3.4 %, LE 3.4 %, tortuositas vasorum RE 4.1 %, LE 4.0 %, arteriovenous crossing signs RE 11.2 %, LE 11.2 %. On multivariate testing the occurrence of microvascular abnormalities correlated significantly (R = 0.38, p < 0.001) with the factors high blood pressure known from case history, body mass index, and gender. Arterial hypertension had the strongest influence followed by diastolic blood pressure. The calculated retinal risk factor correlated with the prevalence of angina pectoris. Study II: 2/3 of the subjects with arteriovenous risk factor values < 0.76 exhibited pathologically high 24-h blood pressure values. For these patients there were significant correlations between the arteriovenous ratio and the low-density lipoprotein concentration as well as the Framingham risk score. CONCLUSION: In the course of a prospective, telemedical-supported screening examination of the retinal vessels of more than 7,000 subjects the arteriovenous ratio exhibited a strong dependence on age and blood pressure. Among the subjects with lowered arteriovenous ratio values, 2/3 exhibited arterial hypertension in the 24-h blood pressure determination.
The course of 18 patients (19 eyes) with the avulsed retinal vessel syndrome and its variants was followed up for an average of 54 months. This syndrome consists of recurrent vitreous hemorrhages from an avulsed retinal vessel caused by retinal tear formation. Even after the retinal tears are closed by various techniques, vitreous hemorrhages may recur until the retinal vessel ruptures. The visual prognosis is generally good.