Novel imaging techniques for diabetic macular edema

Retinal edema should be defined as any increase of water of the retinal tissue resulting in an increase in its volume. It may be of cytotoxic or vasogenic origin. Development of vasogenic macular edema is dependent on a series of factors such as blood pressure, blood-retinal barrier permeability, retinal cell damage, retinal tissue osmotic pressure and retinal tissue compliance. Objective measurements of retinal thickness are now possible using the Retinal Thickness Analyser. Localised measurements of blood-retinal barrier permeability may also be obtained using the Retinal Leakage Analyser, a modified confocal scanning laser fluorometer, while obtaining simultaneously angiographic images of the choroid and retina. These new imaging techniques show that cytotoxic and vasogenic retinal edema may occur independently in the early stages of diabetic retinopathy. These findings offer new perpectives for designing novel therapeutic strategies. This revised version was published online in July 2006 with corrections to the Cover Date.     

Vitrectomy for macular pucker and vitreomacular traction syndrome

During the course of a so-called posterior vitreous detachment, a thin layer of the posterior vitreous cortex often remains adherent to the underlying retina. Tangential stretch of this vitreous pseudomembrane may cause vitreomacular traction syndrome, edema, and macular hole formation. The same process appears to underlie the development of true epimacular membranes (idiopathic macular pucker). Vitrectomy is generally agreed to be the most appropriate treatment for these clinical situations. We evaluated the incidence of vitreomacular adhesion and of visual improvement after vitrectomy of eyes with macular pucker (group 1; n=60) and vitreomacular traction syndrome (group 2; n=50). Vitreomacular attachment was assessed during vitrectomy under the condition of continuous air infusion. In the two groups, complete or partial vitreous attachment to the macula was observed in 57.4% and 74%, respectively. We conclude that vitreomacular adhesion is a common feature of the two clinical situations. Visual improvement was achieved in 73% of both groups. High rates of postoperative visual acuities of 20/50 or better (60.6% in group-1; 65.7% in group-2 cases) occurred only in eyes with preoperative values of 20/100 or better. It is reported that the visual outcome of vitreoretinal surgery for the two clinical conditions deteriorates with increasing duration after initial manifestation. Vitrectomy should not be postponed in patients who complain of disturbing visual symptoms such as reduced visual acuity, metamorphopsia and disturbance of binocular reading. This revised version was published online in July 2006 with corrections to the Cover Date.     

Macular edema induced by phacoemulsification

Purpose: To characterise the association between lens phacoemulsification and the development of macular edema. Methods: We studied 15 patients who underwent lens phacoemulsification in our clinic between January and April 1998 performed by the same surgeon. Ultrasound power and cumulative time was noted. Follow-up was performed at 1 day, 1 week, 1, 3 and 6 months after operation. On each visit corneal thickness, best corrected visual acuity, biomicroscopy and fluorescein angiography were performed. Patients with systemic diseases and/or retinal diseases were not included. Results: Visual acuity was inversely related to the amount of energy delivered during phacoemulsification. In patients who had received more than 1 Joule of energy, fluorescein angiography revealed a higher incidence of blood retinal barrier breakdown. Corneal thickness was not correlated with the ultrasound energy used. Conclusions: Excessive use of power during phacoemulsification may hamper the postoperative evolution of cataract surgery. This revised version was published online in July 2006 with corrections to the Cover Date.     

Bilateral cystoid macular edema following successful treatment of AIDS-associated CMV retinitis

Background: Cystoid macular edema (CME) in AIDS patients with inactive cytomegalovirus (CMV) retinitis is an uncommon but potentially sight-threatening complication. The pathogenesis of CME in these patients is unclear. This study tries to identify possible risk factors by analyzing the charts of five patients. Methods: Ten eyes of 5 patients that finally developed CME were followed for an average of 18 months. The initial retinal lesions, their response to antiviral treatment, the development of CME, and the patients' immune status were prospectively monitored. Results: CMV retinitis was diagnosed at a median CD4+ count of 3 cells/mm³ (range 0–11). All eyes responded to the initial systemic anti-viral treatment. At the onset of CME, CMV retinitis was controlled by antiviral maintenance therapy in all patients [ganciclovir (n = 2), cidofovir (n = 2), foscarnet (n = 1)]. The median time between diagnosis of CMV retinitis and onset of CME was 11.5 months (range 5–24). Development of CME was associated with significant visual loss: acuity ranged from 0.05 to 0.7 when CME was first noticed, compared to 0.8–1.25 at diagnosis of CMV retinitis. Duration of inflammation, size or zone of retinal necrosis did not favor the development of CME, neither did the antiviral therapy. A weak correlation of CME development and immune status (expressed as increase of CD4+ cells) was found. Due to systemic corticosteroids CME resolved. Conclusions: CME is a new visual threat to AIDS-patients with CMV retinitis whose immune status improved under the latest combined antiretroviral therapy. Therapy with oral corticosteroids may positively influence this condition.      

An international registry for toxic inhalation and pulmonary edema: notes from work in progress

Acute toxic inhalation by irritant, and particularly oxidant, gases has until recently been considered to be no more complicated conceptually than a chemical burn of the epithelial surface. More recently, however, toxic inhalation has been appreciated to be a complex process involving biochemical, morphological and functional changes which are quantitatively similar, although inducible by different agents. Recent advances in pulmonary pathophysiology, inhalation toxicology, and particularly endothelial biology have clarified the events occurring at the moment of, and immediately following, exposure to oxidant gases. Studies of the pathophysiologic mechanisms associated with toxic inhalation by oxidant gases have been relatively static, however. Implications of recent findings in related fields illuminate the pathophysiology of toxic inhalation. Several principal speakers in this workshop are collaborating in an effort to develop a research facility for the study of toxic inhalation injury. This would be an international registry to serve as a teaching and research facility for documentation of cases of occupational and environmental toxic inhalation, considered as lung injury resulting from the inhalation of a toxic substance in a workplace setting or an uncontrolled release affecting residents of a community. The registry, as proposed, would encourage submissions by clinicians and institutions of a data set on each patient and on each incident; the registry would further encourage long-term follow-up of subjects and documentation of residual effects.Work presented at the 23rd Congress on Occupational and Environmental Health in the Chemical Industry (Medichem 1995) The Chemical Industry as a Global Citizen - Balancing Risks and Benefits, 19–22 September 1995, Massachusetts Institute of Technology, Cambridge, Massachusetts     

The role of the coagulation cascade in brain edema formation after intracerebral hemorrhage

Summary The coagulation cascade has a potential role in brain edema formation due to intracerebral hemorrhage. In this study blood and other solutions were injected stereotactically into the right basal ganglia in rats. Twenty-four hours following injection, brain water and ion contents were measured to determine the amount of brain edema. Intracerebral blood resulted in an increase in brain water content. The amount of brain edema surrounding the intracerebral hematoma was reduced by a thrombin inhibitor Na-(2-Naphthalenesulfonylglycyl)-4-amidino-DL-phenylalaninepiperidide, (-NAPAP) infused into the hematoma after the clot had been allowed to solidify. The inhibitor did not alter the actual size of the clot mass. An artificial clot composed of fibrinogen, thrombin, and styrene microspheres also produced brain edema. A fibrin clot led to edema formation even in the absence of mass effect provided by the microspheres. The single component responsible for production of brain edema in all these models was thrombin. The edema was formed in response to a fibrinogen-independent pathway. These results indicate that the coagulation cascade is involved in brain edema that develops adjacent to an intracerebral hematoma.     

Neuropathological and neurophysiological effects of interstitial white matter autologous and non-autologous protein containing solutions: Further evidence for a glioma derived permeability factor

Summary The feline infusion model of brain edema was used to evaluate the pathophysiological effects of 0.6ml infusions of autologous serum protein (66%), human serum protein (66%), human glioma cyst fluid and a tissue culture medium (TCM) on the structure and function of the forebrain white matter. These infusions increased local white matter water content by between 10.8 and 12.5 ml/100 g brain and were associated with moderate increases in ICP and CSF outflow resistance and a significant decrease in lumped craniospinal compliance. Cortical somatosensory potentials, motor evoked potentials, EEG and local cerebral blood flow (rCBF) at normocapnia were generally unchanged by the various infusions. All infusates except the 66% autologous serum protein infusion impaired rCBF CO₂ reactivity. Histologically all infusates caused marked extracellular edema. The autologous serum protein infusion caused no additional histological changes whereas the glioma cyst infusates caused profound endothelial and astrocytic swelling, focal endothelial necrosis, basement membrane disruption, perivascular microglial reaction and pavementation and perivascular migration of polymor-phonuclear leukocytes. Similar but less marked changes were seen after infusion of human serum protein whilst the TCM produced only minimal changes. The intensity and extent of Evans Blue extravasation into the forebrain white matter was greatest with glioma cyst infusates and with all infusions reflected the extent to microvascular changes.These studies show that products derived from gliomas cause additional damage to the blood-brain-barrier than that caused by non-autologous serum proteins. These results add further support for the existence of glioma derived permeability factors (GDPF), but suggest neither serum proteins nor glioma derived compounds in the white matter interstitium significantly influence local electrophysiological function. Some limitations of the infusion edema model when using non-autologous infusions and difficulties quantitating brain dysfunction are emphasised.Preliminary results had been presented at the symposium on Brain Edema VIII, which took place at Bern, Switzerland, in June 1990 and have been published in: Reulenet al (eds) 1990. Brain Edema VIII, Acta Neurochirurgica (Wien) [Suppl] 51: 71–73     

Cystoid macular edema in anterior chamber lens implantation following posterior capsule rupture

By comparing the incidence of cystoid macular edema (CME) in three groups of patients having different surgical procedures, we attempted to assess the role of vitreous loss as a risk factor for CME development. In the first group (n = 470), the surgical procedure was extracapsular cataract extraction followed by implantation of posterior chamber lens (EC-CE + PC-IOL). The second group (n = 42) had extracapsular cataract extraction which was complicated by posterior capsule rupture, and therefore anterior vitrectomy followed by implantation of anterior chamber lens had to be performed (ECCE + anterior vitrectomy + AC-IOL). In the third group (n = 22) the surgery was intracapsular cataract extraction followed by anterior chamber lens implantation (ICCE + AC-IOL). The third group was included in this follow up study to assess the role of AC-IOL as a possible causative factor for development of CME in uncomplicated cases of ICCE and AC-IOL. The difference of incidences of CME in the second and third group would therefore depend mostly on the vitreous loss. The incidence of CME diagnosed by fluorescein angiography in the first, second and third group was 1.5% (7/470), 35.7% (15/42) and 9.0% (2/22), respectively. All patients who developed CME were treated with combination of corticosteroid-antibiotic drops, dexamethasone retrobulbarly (40 mg/day) and peroral indomethacine (25 mg/day/6 weeks). This therapeutic regime resulted in only moderate improvement of visual acuity.Abbreviations AC-IOL anterior chamber intraocular lens - CME cystoid macular edema - ECCE extracapsular cataract extraction - ICCE intracapsular cataract extraction - IOL intraocular lens - PC-IOL posterior chamber intraocular lens     

单侧渗出型老年性黄斑变性对侧眼的吲哚青绿血管造影特征

目的 探讨单侧渗出型老年性黄斑变性(AMD)对侧眼吲哚青绿血管造影(ICGA)特征。方法 分析34例经ICGA确诊的单眼渗出型AMD患者对侧34只眼的荧光素眼底血管造影(FFA)及ICGA图像资料。结果 单眼AMD患者对侧眼分别有中晚期后极部簇状强荧光点、强荧光斑、斑片状强弱相间的荧光图像，以及脉络膜灌注不良等几种异常荧光形态。玻璃膜疣在ICGA和FFA上显示强荧光、弱荧少．和正常荧光3种表现；玻璃膜疣在FFA呈强荧光，ICGA一直为弱荧光有18只眼。ICGA中晚期后极部见簇状分布的强荧光点5只眼；中晚期出现1个或多个强荧光斑6只眼；脉络膜灌注不良7只眼。结论 一眼发生渗出型AMD，ICGA检查有助于发现对侧眼是否有病变、病变程度，以及判断预后。     

高度近视黄斑出血相关因素分析

目的对高度近视黄斑出血的相关因素进行分析。方法对55例(69眼)高度近视黄斑出血的患者进行视力、屈光度、A/B超、眼底彩色照相及荧光素眼底血管造影(fundusfluoresceinangiography,FFA)检查。结果43例(78.2%)近视病程超过20年,54眼(78.3%)眼轴超过29mm,44眼(63.8%)出现后巩膜葡萄肿,所有患者屈光度均超过-10D,黄斑出血时8眼(11.6%)可见漆样裂纹,6眼(8.7%)显示视网膜下新生血管(subretinalneovaseularization,SRNV)。出血吸收后19眼(27.5%)可见漆样裂纹,9眼(13.0%)出现SRNV。结论近视病程超过20年、眼轴超过29mm、屈光度超过-10D、有后巩膜葡萄肿的患者容易发生黄斑出血,漆样裂纹与高度近视黄斑出血有密切的关系。高度近视黄斑出血分为两种类型:一种是不伴SRNV的单纯型出血,另一种是伴有SRNV的出血。单纯型黄斑出血预后较好,伴有SRNV的黄斑出血预后差,定期检查眼底及FFA,有助于早期发现SRNV。