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Editor,—Central retinal vein occlusion (CRVO) is a condition which often has profound effects on vision. At present there is little to offer patients in the form of treatment to preserve vision. The visual outcome is largely determined by the severity and duration of the vein occlusion. Management is currently aimed at preventing the complications secondary to retinal ischaemia. The incidence of fellow eye involvement with CRVO is believed to be in the order of 1%. We present a patient with “second eye” CRVO, who presented with acute reduction in vision and who responded dramatically to intravenous streptokinase.
CASE REPORT
A 75 year old white man noticed a sudden reduction in vision in his right eye while walking up a hill. He already had poor vision in his left eye from a CRVO 6 years earlier. He went immediately to eye casualty and was seen within 2 hours from the onset of symptoms. His only risk factor for vein occlusion was ocular hypertension treated with timoptol 0.25% twice daily to both eyes.
On examination, visual acuities were 6/36 right eye and counting fingers left eye, there was no relative afferent pupillary defect and intraocular pressures were 21 mm Hg in both eyes. Examination of the right fundus revealed scattered tiny blot haemorrhages and tortuous veins.
A fundus fluorescein angiogram showed pulsatile arterial filling with venous filling delayed until 34.6 seconds (Fig 1). A diagnosis of acute central retinal vein occlusion was made. Because of the previous left CRVO and the short history of symptoms in his right eye, the option of thrombolysis was carefully discussed with the patient, including the small risk of cerebral haemorrhage. Streptokinase, 1.5 ×106 units, was infused 7 hours after the onset of symptoms. Within 30 minutes, his visual acuity had improved to 6/9. The patient was empirically anticoagulated with heparin and warfarin, keeping the international normalised ratio between 2 and 3. Repeat fluorescein angiogram showed marked improvement in venous filling and loss of pulsatile arterial filling. In addition, several post thrombolysis haemorrhages were evident (Fig 2). The patient took warfarin for 9 months in total and now remains on aspirin alone. His vision in the right eye remains at 6/9.
Fundus fluorescein angiogram of the right eye demonstrating early venous filling 34.6 seconds after injection.
Within 24 hours after receiving intravenous streptokinase, venous filling was evident by 23.3 seconds (note preretinal haemorrhages post thrombolysis). Images digitally processed using IMAGEnet for Windows.
COMMENT
Central retinal vein occlusion can profoundly affect vision and lead to neovascular complications. Current therapeutic options are limited mainly to the prevention or treatment of secondary complications.
Evidence for thrombus formation in CRVO has been reported by Greenet al in a prospective histopathological study of patients with CRVO. They demonstrated recanalised thrombus in 89.7% of eyes and fresh thrombus formation in the remaining 10.3%.1
Animal studies have shown encouraging responses to thrombolysis in experimental CRVO. Fibrinolysin given within 2 days of experimental vein occlusion in rabbits was shown to result in resolution of retinal haemorrhages and return of normal retinal circulation within 48 hours.2 Similar animal studies using recombinant tissue plasminogen activator shortly after experimentally induced vein occlusion resulted in significant retinal vein patency in treated eyes.3 In one randomised controlled clinical trial, patients with CRVO who received streptokinase followed by full anticoagulation within 7 days of onset of visual symptoms, showed a statistically significant improvement in visual acuity. Late presentation was identified as a possible cause of limited improvement in some cases.4 Reports of vitreous haemorrhage occurring during treatment (3/20 cases4) together with the reported incidence of cerebral haemorrhage with streptokinase (57/13607 cases5) account for the absence of a defined role of this drug in the treatment of vein occlusions.
Selective cannulation of a branch retinal vein and infusion of tissue plasminogen activator in a patient with a non-acute CRVO in the second eye has been described. Several other treatment modalities had already been tried unsuccessfully. While avoiding systemic complications, the treatment failed to show any objective improvement in visual acuity and the patient subsequently went on to develop angle neovascularisation.6
Clearly many vein occlusions present late, where irreversible retinal damage has occurred. We propose that only in those circumstances where the presentation is acute should the use of intravenous thrombolysis be considered.