Showing papers on "Retinal Vein published in 1996"

Hyperbaric oxygen treatment for macular edema in retinal vein occlusion: relation to severity of retinal leakage.

Abstract: Twelve subjects with macular edema in retinal vein occlusion received hyperbaric oxygen treatment. Median visual acuity improved from 20/100 to 20/25 (p = 0.002). Clinically significant improvement (2 lines or more) was achieved in 10 cases (83%). Evaluation of the inward permeability coefficient of the blood-retinal barrier using vitreous fluorophotometry showed no significant alteration in the permeability. Studies of larger groups of vein occlusion patients are required to better understand and characterize the visual changes after the oxygen treatment. Moreover, further follow-up is required before conclusions can be reached about the long-term effect of this treatment.

Zentralvenenthrombosen bei jüngeren Patienten

Abstract: BACKGROUND Vein thromboses are not seldom, even in young patients. The pathogenesis of such perfusion disorders is poorly understood-accordingly, it is difficult to choose therapy specific to the causality and appropriate prophylaxis against recurrence. PATIENTS AND METHODS In a retrospective study we analyzed the clinical findings of seven patients under 45 years of age who suffered a retinal vein occlusion in the past two years. RESULTS Anatomical changes of the vessels in carotis and ophthalmica regions were not found, as was the case in hemostasis and fibrinolysis, as well. However, all patients reported stress problems in family and occupation. Migraine was often mentioned in the anamnesis. Coldness of the extremities and perfusion disorders in the nailfold capillaries examined under capillary microscopy indicated increased vasospasm. CONCLUSIONS Vein thromboses are affections of both the arterial and venous circulation. We hypothesize that dysregulation of vascular tone plays an essential role in the genesis of retinal vein thromboses. Increased vasospasm and the incapacity to reactively dilate are potential mechanisms for such perfusion disorders. When counseling patients and applying medical therapy, such a possible pathogenesis should be taken into consideration.

Picture resembling hemicentral retinal vein occlusion in the acquired immunodeficiency syndrome: is it related to cytomegalovirus?

Abstract: Three HIV-seropositive subjects presented with diffuse inferior retinal hemorrhages. The first patient had an inferior hemicentral vein occlusion with subsequent development of an inferior cytomegalovirus retinitis. Two other patients had an inferior 'hemorrhagic' cytomegalovirus retinitis mimicking a venous occlusion, with the retinitis being subtle in 1 patient. We speculate that: (1) venous occlusion may predispose to cytomegalovirus infection of the retina by stasis and ischemic loss of endothelium; (2) early cytomegalovirus infection of the large retinal veins may give the picture of a hemorrhagic retinopathy in a subset of patients with cytomegalovirus retinitis. The differential diagnoses of hemorrhagic retinopathy in HIV-seropositive subjects include: cytomegalovirus retinitis, retinal vein occlusion, syphilitic retinitis and retinopathy of severe anemia.

Activated protein C and retinal vein occlusion.

Abstract: Venous thrombosis is a major medical problem which annually affects 1/1000 individuals.' Individual risk for venous thrombosis is increased in those with prothrombotic changes (thrombophilia) which can be genetic or acquired. Until recently few patients could be demonstrated to have genetic predisposition, the 'pick up rate' of patients with previous venous thrombotic events was less than 10%.2 3 The likelihood of identifying a genetic defect in patients with thrombosis changed dramatically in 1993 with the discovery of a new thrombophilic defect activated protein C (APC) resistance.4 It is a reflection ofthe current speed of scientific advance, that less than 3 years later, a large amount is known about affected individuals, the genetic defect is known, and a reliable assay is widely available. APC resistance is due to the inability of protein C, a physiological anticoagulant, to act effectively. Protein C is a plasma protein that is converted to its active form by thrombin. It functions as an anticoagulant by inactivating factors V and VIII. However, in APC resistance a point mutation in factor V (FV:Q506 also known as factor V Leiden), renders factor V resistant to inactivation.5 In cohorts of patients with previous thrombosis APC resistance is found in 20-60% of patients, differences in frequency being related to the selection criteria for the population studied and differences in population prevalence of APC resistance.6 Heterozygosity for the factor V Leiden is associated with a 5-10-fold increased lifelong risk of thrombosis compared with a normal individual, while homozygosity is associated with a 50-100-fold increased risk.7 This mutation has a prevalence of about 5% in Europeans,58 thus homozygosity is expected in 0-06-0 25% of the population. It must be stated, however, that most individuals carrying the defect will never experience a thrombotic event.9 Central retinal vein occlusion (CRVO) has been previously associated with thrombophilic abnormalities, but the prevalence of APC resistance in this condition has not been studied. In this issue of the BJO two papers from Lund (p 200) and Glasgow (p 203) demonstrate that the prevalence of APC resistance is more common than any other known thrombophilic state and was present in over one third of patients younger than 45 years. This is a similar prevalence of APC resistance to that seen in other venous thrombotic states. Thus, in an ideal world, many would argue that a full thrombophilia screening should be performed in a young patient (<50 years old) after CRVO as after any other venous thrombotic event. A more cost effective approach may be to screen initially for APC resistance. If this is negative then the residual thrombophilia screen including APC resistance, lupus anticoagulant, anticardiolipin antibodies, protein C, protein S, and antithrombin III should be performed. The test for APC resistance is relatively easy to perform, provides good discrimination between normal and APC resistant subjects, and has a specificity and sensitivity of 85-90%. It is not reliable if the patient has abnormal clotting such as lupus anticoagulant or is receiving anticoagulants.6 The gold standard is a DNA based assay for the genetic defect but this is expensive and not widely available. What effects will the discovery of APC resistance have on the future management ofthe patient with CRVO? This is not clear. The standard treatment for patients with recurrent venous thrombosis at other sites is long term warfarin. A single thrombosis is treated with a short course of anticoagulants. A single thrombosis in an individual with the antiphospholipid syndrome merits long term high dose (international normalised ratio >3) anticoagulation indefinitely.1I A single thrombosis in an individual with a genetic thrombophilic abnormality such as APC resistance is more difficult. There are not enough data, since we have not had enough time to study these individuals long term. Most haematologists would give a short course of warfarin and then follow up the individual, giving thromboprophylaxis at times of haemostatic stress such as surgery and pregnancy; some would leave patients on long term anticoagulation. Affected women should not use the combined oral contraceptive pill, for compared with women without the mutation and not using oral contraceptives, they have a 30-fold increased risk of thrombosis.11 The management of patients with CRVO and APC resistance has an added complication neovascularisation:anticoagulation and/or aspirin may contribute to the risk of intraocular haemorrhage. For the moment the risks and benefits of antithrombotic treatment in each individual must be considered carefully; a prospective study is indicated to assess the effects of long term warfarin in CRVO. Certainly the association of APC resistance with retinal vein occlusion has introduced some new management considerations in young patients with retinal vein occlusion.

[Decompression of the optic nerve sheath--results in the first 37 operated eyes].

Abstract: The authors present results of optic nerve sheath decompression in 37 eyes. The decompression surgery was performed for progressive form of anterior ischemic optic neuropathy (AION) in 11 eyes, AION combined with central retinal vein occlusion in 2 eyes, low tension glaucoma in 7 eyes (+1 reoperation), central. retinal vein occlusion in 1 eye, optic nerve head drusen in 11 eyes, chronic optic disc edema in pseudotumor cerebri in 3 eyes, amiodarone optic neuropathy in 1 eye. Postoperative findings (visual acuity and visual field) are presented for each diagnosis. After surgery a transient double vision developed in 5 patients. We have not seen any other complications. Optic nerve sheath decompression is a controversial method of treatment for optic neuropathies. We advocate this method of treatment for vision-threatening optic neuropathies after thoroughly balanced assessment of possible risks and gains.

Branch retinal vein occlusion in a patient with Waardenburg syndrome.

Abstract: A 43-year-old woman (case II-2) with dystopia canthorum, white forelock, blue iris in the left eye, hypopigmented fundi, and systemic hypertension complained of visible floaters in the left eye. Whitish branch retinal vein, preretinal hemorrhages and neovascularization were found in the left fundus. Her intraocular pressure in the left eye was sometimes elevated to 22 mm Hg. The patient's brother (case II-3) was reported to have blue irises in both eyes. We believe that these patients have Waardenburg syndrome, that branch retinal vein occlusion in case II-2 may be caused chiefly by systemic hypertension, and that elevated intraocular pressure associated with the blue iris may be partly involved in the pathogenesis of vein occlusion in the left eye.

Sulodexide treatment in retinal vein obstructions

Abstract: Retinal vein occlusion (RVO) represents one of the most frequent vascular disorders of the posterior pole. RVO treatment is disappointing because a great number of patients remains with a reduced visual acuity; the visual acuity is the functional test which shows the treatment efficacity. The study group of patients was treated with sulodexid, a therapeutic agent with thrombolytic and fibrinolytic action; sulodexid was associated with laser photocoagulation where it was required. Study's results point out efficiency only for those cases treated precociously between 48 to 72 hours from the outset.

Endoscopic Fluorescein Angiography

Abstract: . BACKGROUND AND OBJECTIVE: To assess features of various retinal and choroidal disorders by endoscopic fluorescein angiograms (EFAs) obtained intraoperatively. . PATIENTS AND METHODS: One hundred patients undergoing vitrectomy were studied intraoperatively by injecting 5 ml of 10% fluorescein intravenously. Up to 110° field of view high-resolution angiograms were obtained endoscopically. Characteristics of diabetic retinopathy, retinal vein occlusion, retinal vasculitis, exudative macular degeneration, and neovascular glaucoma were recorded. . RESULTS: Capillary nonperfusion, retinal vascular occlusion or incompetence, and neovascularization of the disc, retina, subretinal space, and posterior iris could be delineated. . CONCLUSION: EFA defines pathologic retinal/ choroidal areas intraoperatively, which may permit more selective surgical management during vitrectomy.

Control Mechanisms of Retinal Vein Pressure: Evaluation in the Cat Using an In Situ Infusion Micropipette

Abstract: Objective: Previous work in our laboratory has shown that retinal vein pressure is significantly greater than intraocular pressure in the cat. Our purpose here is to evaluate the potential of an active mechanism being responsible for the control of vein pressure in the cat retina.Methods: A double-lumen, concentric barrel micropipette assembly designed for operation within the eye of a spontaneously breathing anesthetized cat was developed. The micropipette, initially filled with hypertonic saline for use with a servonull pressure measuring system, was used to determine intravascular pressure. With the tip of the micropipette still situated in the lumen of the vessel the solution in the micropipette was exchanged for papaverine, a potent smooth muscle dilator. Following vasodilation in the distal portion of a major retinal vein, the papaverine was exchanged for hypertonic saline and intravascular pressures were measured in the dilated vessel.Results: Microinjection of papaverine caused visible dilation of...

Retinal disease-treating preparation

Abstract: (57) Abstract: To find a compound useful for the treatment of retinal vascular disorders, which occupy a particularly important position in retinal diseases. The present invention is a retinopathy therapeutic agent containing tranilast or a pharmaceutically acceptable salt thereof as an active ingredient. This compound is effective for retinal vascular obstruction such as retinal vein occlusion, retinal vasculitis, retinal vascular disorder such as diabetic retinopathy.

V ascularised vitreoretinop a thy: the role of growth factors

Abstract: Vascularised vitreoretinopathies, otherwise desig­ nated vasoproliferative retinopathies (VPRS),l are common disorders affecting the retinal circulation and constitute a major cause of visual impairment and blindness in the Western world. VPRs may be induced by a local disorder such as retinal vein occlusion, or by systemic disease which ultimately affects the ocular circulation such as proliferative diabetic retinopathy (PDR). The underlying feature of all VPRs is retinal capillary closure and non­ perfusion which results in inner retinal ischaemia and subsequent preretinal neovascularisation?·3