Viscosity and retinal vein thrombosis.

Ring, Christoffer; Pearson, Thomas C.; Sanders, M. D.; Wetherley‐Mein, G.

doi:10.1136/bjo.60.6.397

Cited by 121 publications

(55 citation statements)

References 27 publications

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“…Arterial hypertension, diabetes and glau coma may be associated with CRVO [Ring et al, 1976] but these diseases did not occur in our patient. Factors other than arterial disease may be operative in causing a stag nation thrombosis, such as failure of the cir culation in cardiac insufficiency, emphysema, or when the viscosity of the blood is in creased as in polycythaemia [Duke-Elder and Dohree, 1967], In our patient, pulmo nary fibrosis was followed by pulmonary dys function, cor pulmonale, cardiac decompen sation and secondary polycythaemia.…”

Section: Discussionmentioning

confidence: 62%

Bilateral Central Retinal Vein Occlusion in a Patient with Scleroderma

Saari¹,

Rudenberg²,

Laitinen³

1981

Ophthalmologica

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A 53-year-old man with scleroderma, pulmonary fibrosis, cardiac decompensation and secondary polycythaemia, but no arterial hypertension, developed central retinal vein occlusion (CRVO) in the left eye. 1.5 years later, during the treatment with systemic steroids and anticoagulants, he developed CRVO in the right eye, and a further half year later, secondary glaucoma in the left eye and loss of the visual acuity to counting fingers at 2.5 m in the right eye and at 0.5 m in the left. Retinal vascular changes, pulmonary and cardiac insufficiency and secondary polycythhaemia, symptoms of scleroderma, most probably contributed to the development of bilateral CRVO.

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Section: Discussionmentioning

confidence: 62%

Bilateral Central Retinal Vein Occlusion in a Patient with Scleroderma

Saari¹,

Rudenberg²,

Laitinen³

1981

Ophthalmologica

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“…Lowering the PCV effectively decreases whole blood viscosity whether systemic rhe ological abnormalities are present [12][13][14]31] or not [15]. Thus the question is raised, wheth er a higher blood fluidity can overcome or at least partly reduce local retinal microcirculatory disturbances.…”

Section: Discussionmentioning

confidence: 99%

“…data], we were able to show that the visual outcome of pa tients with CRVO can be improved by isovolacmic haemodilution (1HD). This kind of treatment had been prompted by findings of increased whole blood and plasma viscosity in patients with CRVO [12][13][14], Our results on rheological changes in patients with CRVO be fore and after I HD have been published else where [15]. This paper presents results of a prospective study on IHD with special regard to the type of disease (ischaemic vs. non-ischaemic) and the clinical applicability of IHD.…”

Section: Introductionmentioning

confidence: 98%

Effect and Compatibility of Isovolaemic Haemodilution in the Treatment of Ischaemic and Non-ischaemic Central Retinal Vein Occlusion

Hansen¹,

Wiek²,

Schade³

et al. 1989

Ophthalmologica

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In a prospective study, 48 eyes with non-ischaemic and 35 with ischaemic central retinal vein occlusion (CRVO) were treated by isovolaemic haemodilution (IHD). Two or more cardiovascular risk factors were present in 42% of patients with non-ischaemic and in 69% of patients with ischaemic CRVO (p < 0.025). Nevertheless, IHD in no case caused serious cardiovascular complications. Minor problems were short fainting spells in 5% and a general weakness in 16% of the haemodiluted patients. The effect of IHD was measured by determining the time of maximal venous filling (t_mvf) in fluorescein angiographies. Lowering the packed cell volume to 32–35% accelerated the t_mvf from 18.4+1.61 to 13.1 ± 1.0 s (p < 0.001) in eyes with non-ischaemic CRVO and from 24.5 ± 1.2 to 14.8 ± 1.3 s (p < 0.001) in eyes with ischaemic CRVO. After 3 months, an increase in visual acuity had occurred in 27% of eyes with non-ischaemic CRVO and in 48.5% with ischaemic CRVO. These improvement rates could nearly be maintained after 1 year. 59% of eyes with non-ischaemic and 25% with ischaemic CRVO were able to read (visual acuity ≥6/15) after 1 year.

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“…Nearly all previous studies referred to coagulative changes in unselected patients with acute or recent RVO [2,4,6,8,[14][15][16], In our patients affected by long-standing branch RVO, the presence of a statistically significant fibrinogen increase, even at dis tance from the appearance of the thrombo sis, was confirmed [15,16], However, no dif ference was seen between patients with or without new vessel formation [16]. More over a significant shortening of PTT was found in our patients.…”

Section: Discussionmentioning

confidence: 99%

“…At the level of arteriovenous crossing, endothelial swelling and proliferation alone, not neces sarily with thrombosis, seem to be capable of producing the RVO syndrome [12], Ana tomic and hemodynamic changes in the re tinal circulation and a defective control of intraocular pressure are thought to play an important role in the pathogenesis of RVO [14,17]. There is, however, some evidence suggesting that generalized hemostatic alter ations are also involved [8], Some authors have shown changes of the coagulation, platelet and fibrinolytic systems in most pa tients with occlusion of retinal vessels [2,4,8,15,16].…”

Section: Introductionmentioning

confidence: 99%

Fibrinolytic Behavior in Long-Standing Branch Retinal Vein Occlusion

Patrassi

M²,

Piermarocchi³

et al. 1987

Ophthalmic Res

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The aim of our study was to evaluate the fibrinolytic system in patients with retinal branch vein occlusion (RVO). The following tests were carried out: prothrombin time, partial thromboplastin time (PTT), fibrinogen degradation products, euglobulin lysis time, fibrinogen, pasminogen, antithrombin III, α₂-antiplasmin and α₂-macroglobulin. Comparing the results of patients with those of normal controls, only the fibrinogen increase and PTT shortening were significantly different. All other tests taken into account were within normal limits. Only the patients without other associated diseases (diabetes or hypertension) showed a significant activation of fibrinolysis (either with respect to normal or to other RVO patient groups). In conclusion, no important fibrinolytic impairment was seen in our longstanding RVO patients. Fibrinolytic activation seen in patients without verified associated diseases may be related to the presence of a sound endothelium, still able to release plasminogen activators in response to RVO. The fibrinogen and PTT changes in RVO were probably due to other associated diseases.

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Viscosity and retinal vein thrombosis.

Cited by 121 publications

References 27 publications

Bilateral Central Retinal Vein Occlusion in a Patient with Scleroderma

Bilateral Central Retinal Vein Occlusion in a Patient with Scleroderma

Effect and Compatibility of Isovolaemic Haemodilution in the Treatment of Ischaemic and Non-ischaemic Central Retinal Vein Occlusion

Fibrinolytic Behavior in Long-Standing Branch Retinal Vein Occlusion

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