Ocular vascular occlusive disorders collectively represent one of the leading causes of visual disability among middle-aged and older populations, with significant visual morbidity and systemic associations (1). In recent years, retinal vascular occlusions affecting both the arterial and venous systems have been reported, usually presenting with sudden, painless diminution of vision (2–8). In particular, the combination of branch retinal artery occlusion (BRAO) and branch retinal vein occlusion (BRVO) is an exceedingly rare event.

Although BRVO can lead to widespread capillary non-perfusion (CNP), combined BRAO and BRVO should not be mistaken for ischemic BRVO, as well-demarcated, wedge-shaped areas of complete capillary dropout are not a feature of ischemic BRVO (8). In addition, macular edema (ME) is the leading cause of vision impairment in patients with RVO (1, 9, 10). At present, anti-vascular endothelial growth factor (anti-VEGF) agents have become the first-line therapy for ME secondary to RVO (10). Therefore, in this case, angiography-guided sectoral laser photocoagulation and intravitreal injections of anti-VEGF agents were used to treat retinal ischemia and ME secondary to combined BRAO and BRVO.

Simultaneous retinal vascular occlusion affecting both the vein and artery is a rare occurrence and can present in various permutations, such as the combination of central retinal vein occlusion (CRVO) and central retinal artery occlusion (CRAO), CRVO and BRAO, BRVO and CRAO, BRVO and BRAO, and cilioretinal artery occlusion (CLRAO) and CRVO (2–8, 11–31). Among them, the combination of CRVO and CRAO is relatively more common (12–25). This report describes a rare case of combined BRVO and BRAO. Although ischemic BRVO can also cause extensive areas of CNP, fluorescein angiography and OCT examinations are valuable for establishing the correct diagnosis of combined BRVO and BRAO at an early stage.

Many systemic comorbidities, including hypertension, diabetes, hyperlipidemia, hyperhomocysteinemia, atherosclerosis, hyperviscosity syndromes, blood disorders, infections, tumors, pulmonary arterial hypertension, systemic vasculitis, and autoimmune diseases, can cause combined vascular occlusion (1–8, 11–13, 16–27, 29–31). The most commonly reported systemic associations are diabetes, hypertension, and dyslipidemia (1–8, 11, 12, 23, 31). In our case, these factors contributed to the occurrence of combined BRVO and BRAO.

The pathogenic mechanism underlying the occurrence of combined BRVO and BRAO remains unclear. Sengupta et al. (8) postulated that BRVO might be the initial event, resulting from compression of the vein by an atherosclerotic artery at an arteriovenous crossing site, leading to turbulent blood flow, dynamic obstruction, and even thrombus formation or mechanical blockage. If this situation is severe, a sudden increase in intravenous pressure exceeding the systolic BP may lead to the transmission of “back-pressure” to the arterial circulation, resulting in impaired arterial perfusion and the development of BRAO (8). In our case, the fundus images also appear to support this mechanism.

Lee et al. (32) reported that the incidence of neovascularization elsewhere (NVE) and/or neovascularization of the disc (NVD) was 21.4% in patients with BRVO combined with major arterial insufficiency. Sengupta et al. reported a case series of NVE, NVD, and neovascular glaucoma (NVG) secondary to combined BRVO and BRAO (8, 30). In addition, foveal neovascularization associated with combined BRVO and BRAO has also been reported (7). Management strategies for combined BRVO and BRAO are aimed at reducing posterior segment ischemia, improving vision, and decreasing the neovascular drive. Among the cases reported in the literature, Christodoulou et al. (31) described a patient with NVD, NVE, and ME secondary to combined BRAO and BRVO in the right eye, who was treated with angiography-guided sectoral laser photocoagulation and intravitreal therapy, achieving a good visual outcome. In general, the prognosis of combined BRAO and BRVO depends on the ischemic index and macular perfusion status, and earlier identification and appropriate treatment may result in better visual outcomes (8, 31).

In this case, we administered intravitreal injections of anti-VEGF agents and performed retinal laser photocoagulation to treat retinal ischemia and ME and to prevent the development of NVE, NVD, rubeosis iridis, and NVG. Three months later, visual acuity and ME in the left eye improved. Unfortunately, after that, the patient refused to return to the clinic for further examinations. Long-term monitoring would have added greater value to this case. Therefore, further studies are needed to investigate the management of recurrent ME secondary to combined BRAO and BRVO. In addition, systemic evaluation and close monitoring of cardiovascular risk factors are essential (2, 11, 12, 23, 31).

Combined BRVO and BRAO is an uncommon and extremely rare retinopathy. Multimodal imaging, such as fluorescein angiography and OCT, is valuable for establishing the correct diagnosis, as well as for monitoring disease progression and treatment response. Combined BRVO and BRAO can be effectively managed with retinal laser photocoagulation and anti-VEGF agents. In addition, systemic evaluation and close monitoring of cardiovascular risk factors should not be overlooked.