CRAO is a relatively common emergency in ophthalmology, and it is one of the main causes of acute vision loss in patients. The incidence is approximately 1 per 100,000 people, accounting for about 1 in 10,000 of ophthalmology outpatients.[5, 6] CRAO can be divided into 4 subtypes[1, 2]:permanent CRAO (P-CRAO), T-CRAO, CRAO with ciliary retinal artery, and arteritic CRAO. T-CRAO is one of these subtypes, with a relatively low incidence, accounting for only about 1/6 of all CRAO. Risk factors for CRAO include hypertension, obesity, previous stroke or transient ischemia, coronary heart disease, arrhythmia, valvular heart disease, smoking, hyperlipidemia, diabetes, etc., among which hypertension is considered the most common risk factor.[7, 8] Six patients in this study were accompanied by hypertension, indicating that hypertension was also the most common independent risk factor in patients with T-CRAO. The pathogenesis of T-CRAO is unclear currently, which is similar to the visual impairment caused by transient ischemic attack (TIA).[6] In a study on atherosclerotic monkeys, it found that serotonin, released by platelet aggregation on atherosclerotic plaques in the carotid artery, can cause transient, complete occlusion or impair blood flow in the central retinal artery by producing a transient spasm, resulting in transient ischemia and hypoxia of retinal tissue.[9]
FFA is the golden standard for diagnosing retinal ischemic diseases at present. All patients in this group manifested as sluggish filling of retinal arteries, with filling front, which was consistent with the diagnostic characteristics of CRAO. Although the FFA showed sluggish filling of retinal arteries, the retinal arteries filled completely in 5 to 10 seconds, which was significantly different from P-CRAO, indicating that the ischemia of T-CRAO was slighter than that of P-CRAO. Fundus examination showed multiple patchy "cotton-wool spot"-like lesions in the posterior pole observed in CFP, and no nonperfusion area in the lesions observed in FFA, indicating that the lesions were not caused by anterior retinal arteriole occlusion. Combined with OCT findings, it was considered that the patchy "cotton-wool spot"-like lesions were focal edema and thickening of the retinal nerve fiber layer caused by transient retinal ischemia.
FFA can only clearly show the large retinal vessels and some superficial capillaries, so it is difficult to detect the ischemia of middle and deep capillaries in the macular region for T-CRAO. The retinal capillaries in the macular area are divided into superficial, middle and deep layers. The superficial layer is located at the nerve fiber layer, the middle layer is located at the interface of INL and IPL, and the deep layer is located at the interface of INL, OPL and Helen fiber layers. OCTA can display the retinal capillaries in the macular area hierarchically, and provide B-scan image of SCP, DCP, outer retinal vascular plexus and choroid capillary layer. OCTA cannot distinguish the middle and deep retinal capillaries, so collectively called DCP. The essence of T-CRAO is the ischemic damage of the retina, the transient spasm of the central retinal artery leads to blood supply disorders in the superficial, middle and deep retinal capillaries. In this study, OCTA revealed that the VD of SCP and DCP were significantly decreased in lesions, and the decrease of VD of DCP was more severe than that of SCP, further confirming the pathological damage mechanism of the disease.
En-face image of OCTA showed patchy hyperreflective lesions in the SCP and DCP, which was the characteristic imaging manifestation of T-CRAO. It showed as isolated patchy hyperreflective lesions in SCP, which was completely consistent with the "cotton-wool spot"-like lesions observed in CFP and fused patchy hyperreflective lesions in DCP. The above characteristic manifestations suggested that the DCP was more sensitive to ischemia and more prone to ischemic damage.
In the eyes with T-CRAO, OCT showed intermittent thickening and enhanced reflexes in the inner layer of the retina, while the outer retina was not involved. In the eyes with paracentral acute middle maculopathy (PAMM), OCT showed the hyperreflective band at INL.[10] In the eyes with acute macular neuroretinopathy (AMN), OCT showed patchy hyperreflective lesions in the outer nuclear layer (ONL), involving the ellipsoid zone and the myoid zone.[11] Characteristic manifestations in OCT are helpful in distinguishing T-CRAO, PAMM and AMN.
Studies found that in T-CRAO with initial visual acuity of counting finger or worse, visual acuity improved, remained stable, or deteriorated in 82%, 18%, and none, respectively.[2] In this study, after active treatments in accordance with the treatment principles of acute CRAO, the visual acuity of the affected eyes was improved in varying degrees, and OCTA revealed that the VD of SCP and DCP were significantly improved compared with the initial diagnosis. It indicated that the ischemic degree of T-CRAO was relatively mild compared with P-CRAO, the ischemia could be improved after active treatment, and the prognosis was relatively good. Unfortunately, the compliance of patients in this group was poor, and we didn’t obtain long-term follow-up data, especially OCTA, so we couldn’t determine whether the VD of SCP and DCP can be fully recovered.