Optical coherence tomography as a means of evaluating acute ischaemic retinopathy in branch retinal artery occlusion

Abstract

A 57-year-old man with hypertension and diabetes presented with loss of vision in the right eye of 3 days' duration. Best corrected visual acuity (VA) was 20/40 in the right eye and 20/20 in the left. Intraocular pressure (IOP) was 14 mmHg in both eyes. The patient was using timolol maleate 0.5% b.i.d. Fundus examination revealed a localized, whitish area characteristic of retinal oedema along the inferior temporal artery branch (Fig. 1A). Computerized perimetry showed a superior altitudinal defect. Fluorescein angiography (FA) showed asymmetry in the retinal arterial filling between the superior and inferior temporal branches and retrograde filling of the inferior temporal artery branch (Fig. 1B, C). Optical coherence tomography (OCT) showed an increase in retinal thickness caused by intracellular oedema, characterized by optical hyperreflectivity of the inner retinal layers (inner plexiform and inner nuclear layers) and attenuation in the reflectivity of the retinal pigment epithelium (RPE)−choriocapillaris complex and choroid located beneath the thickened region of the retina. Moreover, it was possible to observe a deformation in the foveal contour (Fig. 1D). Approximately 3 months after the branch retinal artery occlusion (BRAO), the patient suffered a myocardial infarction and ophthalmic follow-up was no longer possible. (A) Occlusion of the inferior temporal artery in the right eye, showing a whitish area along the inferior temporal branch and a partially compromised fovea. (B, C) Fluorescein angiography shows asymmetry in vascular filling in the early phase of the examination and retrograde filling of the inferior temporal branch in the transit phase. (D) Optical coherence tomography shows an increase in retinal thickness in the inferior macula as a result of oedema in the inner layers of the retina (arrow). Attenuation of the optical reflectivity of the subjacent retinal pigment epithelium?choriocapillaris complex and choroid is also observed. Note distortion of the foveal anatomy secondary to the thickened inferior juxtafoveal retina. An 82-year-old hypertensive woman complained of a sudden decrease in vision in her left eye of 12 hours' duration. Best corrected VA was 20/25 in the right eye and 20/30 in the left. Her IOP was 13 mmHg in the right eye and 12 mmHg in the left, with topical use of latanoprost once a day. Fundus examination revealed a discrete paleness and a localized retinal oedema in the upper region of the macula in the left eye, as well as the presence of a possible embolus at the emergence of the superior temporal artery branch (Fig. 2A). Computerized perimetry showed a new scotoma in the lower paracentral region. Fluorescein angiography showed asymmetrical retinal vascular filling between the superior and inferior temporal branches (Fig. 2B). Examination by OCT showed an increase in the optical reflectivity of the inner retinal layers, as well as a mild attenuation of the optical reflectivity of the subjacent RPE−choriocapillaris complex and choroid (Fig. 2C). Over 6 months' follow-up, vision in the left eye improved to 20/25, the inferior paracentral scotoma was unchanged and OCT showed local thinning of the retinal layers (Fig. 2D). (A) Occlusion of the superior temporal artery branch in the left eye, with a retinal paleness in the upper region of the macula and the presence of an embolus at the emergence of the superior temporal artery branch. (B) Fluorescein angiography shows asymmetrical vascular filling between the superior and inferior temporal branches during the early phase. (C) Optical coherence tomography (OCT) shows superior juxtafoveal thickness resulting from intracellular oedema in the inner layers, causing optical hyperreflectivity in this region (arrow), and mild attenuation of the optical reflectivity of the subjacent retinal pigment epithelium?choriocapillaris complex and choroid. (D) Six-month follow-up with OCT shows a decrease in retinal thickness in the superior juxtafoveal area (arrow) secondary to local retinal atrophy. The outer layers have normal optical reflectivity. Retinal artery occlusions are caused by embolization, thrombosis or vasospasm, and affect mainly elderly patients with associated systemic diseases, of which hypertension is the most frequently seen (Brown & Magargal 1982). Branch retinal artery occlusions represent approximately 38% of all retinal artery obstructions (Brown & Shields 1979) and are clinically characterized by a whitish, thickened area located along the compromised vessel in the acute phase. These anatomical changes are the result of the denaturation of intracellular proteins, with accumulation of intracellular fluid and consequent cellular necrosis (Dahrling 1965). Gass (1997) proposed that the name ‘retinal oedema’ should not be used for this clinical condition, as the extravascular fluid is found in the intracellular space, and suggested that the term ‘acute ischaemic retinopathy’ would be more appropriate. In a clinicopathological study, Dahrling (1965) observed that the increase in retinal thickness was related to intracellular oedema in the inner nuclear and inner plexiform layers, with no evidence of fluid in the extracellular space derived from retinal capillaries. In vivo, the microscopic anatomy of the retina can be evaluated by OCT, but very few reports of OCT features in early BRAO are available in the literature. Using OCT, Cruz-Villegas et al. (2004) described increased thickness and hyperreflectivity of the inner retinal layers with secondary shadowing and attenuation of subjacent structures due to intracellular oedema. Chronic cases are characterized by localized retinal atrophy (Cruz-Villegas et al. 2004). In our experience, the increase in retinal thickness was caused by intracellular oedema of the inner nuclear and inner plexiform layers, characterized by the optical hyper reflectivity of that region. The intracellular oedema is responsible for shadowing and attenuation of optical reflectivity of the subjacent structures. In agreement with previous histopathological research (Dahrling 1965), extracellular fluid was not observed, mainly characterized by cystic spaces within the retina. In addition, deformation of the foveal contour due to asymmetry between the superior and inferior juxtafoveal areas caused by localized intracellular oedema was observed. In these reports, OCT enabled a more thorough assessment of the retinal anatomy in early BRAO. Examinations by OCT can be repeated every 6 months for the first 12 months, allowing for closer clinical and imaging control of the disease evolution process.