|Year : 2022 | Volume
| Issue : 1 | Page : 48-51
Hemiretinal artery occlusion as a variant of retinal arterial occlusive disease
Anuj Sharma1, Syed Mohideen Abdul Khadar2, YC Venugopal Reddy3
1 Amritsar Eye Clinic, Dehradun, Uttarakhand, India
2 Retina Services, Aravind Eye Hospital, Tirunelveli, Tamil Nadu, India
3 Retina Services, Aravind Eye Hospital, Tirupati, Andhra Pradesh, India
|Date of Submission||04-Aug-2021|
|Date of Decision||29-Sep-2021|
|Date of Acceptance||01-Oct-2021|
|Date of Web Publication||22-Mar-2022|
Dr. Anuj Sharma
Amritsar Eye Clinic, Dehradun, Uttarakhand
Source of Support: None, Conflict of Interest: None
Central retinal artery occlusion is an established and potentially blinding ocular condition. It is the most common presentation of the spectrum comprising retinal arterial occlusive diseases. The presence of a hemicentral retinal artery is an anatomical variation and few reports on its occlusion are noted in literature. Here, we present the case of a 45-year-old male who was diagnosed with hemiretinal artery occlusion occurring secondary to an embolus from the carotid artery. He was also noted to have systemic hypertension at presentation along with dyslipidemia. The visual acuity loss improved over a follow-up period of 1 week post presentation before the patient was lost to follow-up. This case report highlights the role of a thorough systemic evaluation and prompt referral to an internist of the patient presenting with retinal arterial occlusive disease. It also showcases an uncommon presentation retinal arterial occlusion that may occur as an anatomical variant much as the case of a hemiretinal vein occlusion.
Keywords: Hemicentral retinal artery occlusion, hemiretinal artery occlusion, retinal arterial occlusive disease, retinal artery occlusion, systemic hypertension
|How to cite this article:|
Sharma A, Abdul Khadar SM, Venugopal Reddy Y C. Hemiretinal artery occlusion as a variant of retinal arterial occlusive disease. TNOA J Ophthalmic Sci Res 2022;60:48-51
|How to cite this URL:|
Sharma A, Abdul Khadar SM, Venugopal Reddy Y C. Hemiretinal artery occlusion as a variant of retinal arterial occlusive disease. TNOA J Ophthalmic Sci Res [serial online] 2022 [cited 2022 Jun 29];60:48-51. Available from: https://www.tnoajosr.com/text.asp?2022/60/1/48/340345
| Introduction|| |
Acute retinal arterial occlusion is a catastrophic event presenting most commonly as a central retinal artery occlusion (CRAO). Analogous to a stroke, retinal arterial occlusion is an ophthalmic emergency with an estimated incidence of 1 in 100,000 population. Less common presentations may include occlusion of the branches of the retinal artery or occlusion of the cilioretinal artery. Reports on hemiretinal artery occlusion are sparingly noted on a literature search.
| Case Report|| |
A 45-year-old male patient presented with complaints of sudden diminished vision in the left eye for 2 days, this decrease in vision was persistent. There was no associated history of pain or ocular trauma. There was no history of any systemic illness in the patient; however, on clinical presentation, a markedly elevated blood pressure recording of 170/100 mmHg was noted. The patient did not report any previous instances of intermittent blurring or obscurations in vision.
On systemic examination, apart from the raised blood pressure levels, the remainder of the examination was found to be normal. Ocular evaluation revealed a visual acuity of 20/20 (OD) and 20/320 (OS). Anterior segment examination of both the eyes was within normal limits. Fundus evaluation of the right eye was normal on examination. The fundus of the left eye, however, revealed a cherry-red spot with whitening of the inferior hemiretina. Arteriolar attenuation was also noted [Figure 1].
|Figure 1: The fundus photograph of the left eye shows the presence of a cherry-red spot with retinal edema of the inferior hemiretina. Closer evaluation of the optic nerve head reveals the presence of two hemiretinal arteries supplying the superior and inferior hemiretina, respectively|
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An initial diagnosis of hemiretinal arterial occlusion was made and emergency maneuvers of restoring circulation by lowering the intraocular pressure were carried out. These procedures included gonio massage, oral therapy with acetazolamide (two tablets of 250 mg stat), and anterior chamber paracentesis. However, no improvement was noted despite these procedures.
An optical coherence tomography (OCT) examination and a fluorescein angiogram (FFA) were carried out to confirm the diagnosis. The OCT revealed an increased thickening and hyper-reflectivity of the inner retinal layers in the inferior hemiretina involving the fovea [Figure 2]. A middle limiting membrane sign was seen in the scans passing through the inferior hemiretina. The scan passing through the superior retina was essentially normal, wherein the retinal architecture was well made out [Figure 3].
|Figure 2: The optical coherence tomography scan passing through the fovea shows the presence of retinal thickening with an evident middle limiting membrane which defines the retinal insult caused by the arterial occlusion. No structural alteration in the retinal layers is noted|
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|Figure 3: The horizontal optical coherence tomography scan showcases the foveal involvement and the presence of the middle limiting membrane, while the vertical optical coherence tomography scan shows a clear demarcation in the retinal thickening of the inferior hemiretina as compared to the superior retina|
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The FFA revealed an increased arm to retina time of 16 s in the left eye. The inferior hemi-trunk of the central retinal artery showed a marching of the dye as the angiogram progressed and even at 9 min post injection, the inferior trunk was not fully perfused. A retrograde filling of the arteries along the horizontal meridian was noted. No evidence of a patent cilioretinal artery was noted on the FFA [Figure 4] and [Figure 5].
|Figure 4: The fluorescein angiogram of the patient shows a delayed arm to retina time with delayed perfusion of the inferior hemiretina. Perfusion in the inferior hemiretinal artery is seen initially at 31 s and proceeds slowly. Retrograde filling of the inferior arterial branches is noted across the horizontal meridian at 5 min post dye injection|
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|Figure 5: This fundus photo montage shows the extent of diminished perfusion in the inferior hemiretina|
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On retrospective clinical evaluation, a note was made of the two separate hemiretinal arteries supplying the superior and the inferior halves of the retina. No evidence of a plaque or embolus could be seen.
Detailed systemic evaluation was carried out for the patient. Blood investigations revealed normal HbA1c and kidney function tests. The lipid profile showed elevated low-density lipoprotein levels (157.4 mg/dl) with elevated total cholesterol levels (217 mg/dl). The echocardiogram noted a normal sinus rhythm with an atrial septal infarct, while the two-dimensional echocardiogram revealed a normal wall motion. The carotid Doppler evaluation showed the presence of an increased intimal thickness (1.1 mm in the right, 1.3 mm on the left) with the reduced flow in both the right and the left internal carotid arteries. There was evidence of both calcified and noncalcified atheromatous plaques in the carotid arteries on both sides causing a 50% lumen narrowing on the left side, while the blockage was not significant on the right side. On the basis of the systemic evaluation, dyslipidemia with systemic hypertension and an embolus from the atheromatous plaque was presumed to be the cause of the hemi-arterial occlusion. At 1-week follow-up visit, the visual acuity had improved to 20/125, after which the patient was lost to follow-up.
| Discussion|| |
The central retinal artery, arising from the ophthalmic artery, supplies the surface of the optic nerve head and inner layers of the retina. Upon entering the eye, it divides into superior and inferior trunks before the nasal and temporal arteries branch out from these trunks. Apart from the aforementioned course, various anatomical variations of the central retinal artery have been noted.
Singh and Dass evaluated, via cadaveric dissection, the anatomical variations of the central retinal artery in 106 orbits and noted a duplication of the central retinal artery in one specimen. This variation may be responsible for the clinical presentation of hemiretinal arterial occlusion. In their evaluation of four patients with hemiretinal artery occlusion, Rishi et al. confirmed, via color Doppler evaluation, a bifurcation of the central retinal artery behind the lamina cribrosa. Similarly in our case upon closer examination, we noted a presence of two central retinal arteries emanating from the optic nerve head.
Loss of the superior or inferior visual hemifield is the most common presenting feature of hemiretinal artery occlusion. Some case reports have also documented a diminished central visual acuity, as in our scenario. This may be due to the dominant vascular supply of one of the trunks of the central retinal artery.
Reports on hemi-CRAO have noted a remarkable improvement in visual acuity. Rishi et al. in their case series noted an improvement in all cases to 20/60 or better. Similarly in our patient, we noted an improvement in the visual acuity from 20/320 to 20/125 within 1 week of follow-up.
In a retrospective evaluation of the risk factors for CRAO, Rudkin et al. found that hyperlipidemia was the most common newly diagnosed cardiovascular risk factor followed by hypertension and diabetes. Similar risk factors should also hold true for hemi-CRAO. In our patient, investigations revealed the presence of hyperlipidemia with increased total cholesterol and low-density lipoprotein levels.
Mathys and Garg reported a case of a 65-year-old woman with superior central hemiretinal artery occlusion and attributed the condition to her hypertension and smoking habit. Similarly in our case, the presence of an elevated blood pressure points toward this being one of the major triggering factors for the event. Although an embolic event was suspected, unlike the authors above, we were not able to note any emboli on clinical examination.
Hemiretinal artery occlusion is managed on the same lines as an acute CRAO. Mukhtar et al. in their report have shown a successful transluminal Nd: Yag laser embolysis in a 22-year-old female presenting with hemiretinal artery occlusion. Another treatment modality shown to be effective in CRAO is the administration of tissue plasminogen activator to dissolve the embolus within 6 h of the retinal insult.
The role of pars plana vitrectomy as a therapeutic maneuver to rescue patients with CRAO is being extensively studied. In their report, Tang and Topping performed pars plana vitrectomy with vessel cannulation and thrombus disruption in a 68-year-old diabetic male who presented 30 h after vessel occlusion. They noted a significant improvement in the visual acuity 4- months following the procedure. Lu et al. performed vitrectomy with direct massage of the central retinal artery with a specially designed probe in 10 consecutive patients with CRAO. They noted an improvement in circulation in four cases and concluded that the procedure was effective and relatively safe in patients with CRAO. Recently, a case study from Jordan has highlighted that early treatment for hemi-CRAO can prove to be effective. The authors performed pars plana vitrectomy with massage of the superior branch of the central retinal artery and restored circulation in a patient who had undergone cardiac catheterization 1 h before complaining of diminished vision.
Hayreh et al. in their study on rhesus monkeys noted a retinal survival time of 4 h following CRAO. In our case, the patient presented 48 h post the onset of symptoms, and hence, only noninvasive treatment modalities were employed.
| Conclusion|| |
Hemiretinal artery occlusion is a distinct morphological entity that should be distinguished from a branch retinal artery occlusion as well as a cilioretinal artery occlusion. Its management principles and pathophysiology are essentially identical to CRAO; however, a better prognosis may be expected as the retinal edema settles.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]