It is well established that retinal ischaemia stimulates the production of vascular endothelial growth factor (VEGF), a key mediator of angiogenesis. Massive expression of VEGF in the neovascular membranes in Eales’ disease has also been reported previously [6, 7]. Bevacizumab, a humanised monoclonal antibody against VEGF, is currently emerging as an effective off-label treatment for a variety of ocular disorders such as neovascular age-related macular degeneration, macular edema secondary to central retinal vein occlusion and proliferative diabetic retinopathy [8]. However, a literature search revealed only few anecdotal reports on the use of intravitreal bevacizumab in Eales’ disease [2–5]. In all the reports, bevacizumab had been used in early stages of the disease without retinal detachment. In contrast, our cases had fairly advanced Eales’ disease with tractional retinal detachment, and bevacizumab was effective in promoting regression of neovascularisation, thus facilitating membrane dissection by reducing intra-operative bleeding. Additionally, due to better visibility during surgery, the chances of causing iatrogenic retinal breaks were also reduced. Although photocoagulation is the preferred modality of treatment in the proliferative stage of Eales’ disease, it could not be performed in both our cases due to the presence of dispersed vitreous haemorrhage and tractional retinal detachment. Nevertheless, there was no recurrence of neovascularisation at 6 months follow-up in our first patient, and at the time of writing this report, the second patient had been followed up for 2 months without recurrence of neovascularisation.
In both our cases, sequential treatment with bevacizumab followed by vitrectomy was beneficial and associated with fair visual outcome, despite the presence of tractional retinal detachment. However, the appropriate time interval between bevacizumab injection and vitreoretinal surgery in the presence of tractional retinal detachment is not established. The minimum concentration (500 ng/ml) of intravitreal bevacizumab (1.25 mg) that completely inhibits VEGF-A-induced endothelial cell proliferation is reportedly maintained for 6–7 weeks, after which repeat administration of bevacizumab may be required [9]. We performed vitreoretinal surgery within 3–6 weeks after injection of bevacizumab as the anti-angiogenic effect of drug was expected to be maintained during this period while allowing reasonably sufficient time for regression of neovascularisation. Additionally, in our first case, non-recurrence of neovascularisation at 6 months follow-up suggests that intermediate-term control is achievable with intravitreal bevacizumab and vitreoretinal surgery, even with a background of ongoing ischemic disease. Although recent studies have strengthened the favourable short-term safety profile of intravitreal bevacizumab, long-term safety of intravitreal bevacizumab is still unknown [10]. Therefore, prudent clinical judgement and caution should be exercised with the off-label use of intravitreal bevacizumab, as there have been few reports of progression of tractional retinal detachment in patients with severe proliferative diabetic retinopathy [11].
To summarise, the use of intravitreal bevacizumab provided a relatively clean surgical field and facilitated membrane dissection with reduced chance of iatrogenic retinal break. Therefore, bevacizumab may have potential as an adjunctive treatment to vitreoretinal surgery for the management of Eales’ disease with tractional retinal detachment. However, well-designed randomised controlled trials are essential before such a use can be unequivocally established.