To date, only three previous cases of retinitis pigmentosa (RP) with ischemic central retinal vein occlusion (CRVO) have been reported [5,6,7];that we summarize in (Table 1).

Previous studies have indicated that RP is associated with a decline in retinal and choroidal blood flow [8,9]. In a study by Yang et al., they investigated the blood characteristics in nonsyndromic RP and observed that RP induces Red Blood Cell (RBC) aggregation and platelet activation, resulting in blood stasis, that further triggers apoptosis [10]. Additionally, certain mutations associated with thromboembolic disorders have been reported in RP patients [11,12]. Bushehri et al. identified homozygous mutations in the Protein S (PS) gene, responsible for vitamin K-dependent anticoagulant plasma PS synthesis. It is described as a potential candidate gene for juvenile RP [11,13,14]. However, Ghribeh et al. reported no significant difference in the presence of thrombophilic mutations between RP patients and controls [15]. Another probable explanation for CRVO in RP could be the migration of retinal pigment epithelium cells into the inner retina, forming a continuous monolayer around thin-walled venules or capillaries. This leads to the deposition of extracellular matrix between the retinal pigment epithelium and vascular endothelial cells, resulting in vascular wall thickening and subsequent vessel occlusion [16]. This mechanism could potentially explain the occurrence of CRVO and subsequent CME in RP. Macular Edema (ME) is a significant complication of retinal vein occlusion, greatly impacting patients' vision [17]. Cystoid Macular Edema (CME) is observed in 10-50% of RP patients when assessed using optical coherence tomography (OCT) [18,19]. Currently, there is no definitive treatment to halt or reverse photoreceptor degeneration. However, complications such as CME have been managed using various approaches. Treatment options for CME secondary to retinitis pigmentosa include oral and topical carbonic anhydrase inhibitors, intravitreal steroids, oral corticosteroids, grid laser photocoagulation, pars plana vitrectomy, ketorolac, and intravitreal anti-Vascular Endothelial Growth Factor (anti-VEGF) agents such as ranibizumab and bevacizumab [20]. In recent years, inhibition of Vascular Endothelial Growth Factor (VEGF) has garnered attention [21]. Artunay et al. conducted a study assessing the anatomical, clinical, and visual acuity response following intravitreal ranibizumab injection in patients with CME due to RP. Their findings suggested that intravitreal ranibizumab may offer a novel therapeutic approach for treating CME secondary to RP, with no associated adverse events reported. Further experience with intravitreal ranibizumab in this population will help establish its long-term efficacy [22]. Another study by Yuzbasioglu et al. evaluated the effectiveness and outcomes of intravitreal bevacizumab injections in RP patients. They demonstrated that intravitreal bevacizumab administration effectively reduced CME in RP, as evidenced by a decrease in central macular thickness following treatment [23].

In the presented case, Cystoid Macular Edema (CME) secondary to Central Retinal Vein Occlusion (CRVO) was successfully treated with monthly intravitreal injections of bevacizumab for three times. There were no signs of relapse or anterior segment neovascularization during the two-year follow-up period. further, in a previous case report where macular edema in CRVO patients was treated with a single dose of aflibercept. However, in that specific case, the macular edema relapsed after three months following the treatment [5]. It's remarkable that in all cases of CRVO in patients with Retinitis Pigmentosa (RP) neovascularization was not observed during follow-up. also, there was an improvement in Best-Corrected Visual Acuity (BCVA) observed in all cases after the administration of anti-VEGF (vascular endothelial growth factor) injections.