|Year : 2012 | Volume
| Issue : 1 | Page : 69-70
Central retinal artery occlusion
Kanchan Sawant, Ashis Ghosh, RP Gupta, S Patra
Department of Ophthalmology, Dr. D. Y. Patil Medical College, Pune, Maharashtra, India
|Date of Web Publication||20-Jun-2012|
701 Vakratunda CHS, Bhakti Mandir Road, Thane West, Mumbai
Source of Support: None, Conflict of Interest: None
A 60-year-old male patient reported to eye Outpatient Department with the complaint of sudden painless diminution of vision in right eye of 10 h duration. We found a Cherry red spot in the macula and a pale white posterior pole of the retina. Parameters of investigations showed hypertension, ischemic heart disease, and the presence of a carotid plaque in the Doppler study. Paracentesis was done with a 30-Gauge needle immediately within 15 min of the patient reporting to the Eye OPD. Any delay in reporting or institution of treatment can lead to irreversible blindness.
Keywords: Central retinal artery obstruction, outpatient department, relative afferent pupillary defect, Two-dimensional echocardiography
|How to cite this article:|
Sawant K, Ghosh A, Gupta R P, Patra S. Central retinal artery occlusion. Med J DY Patil Univ 2012;5:69-70
| Introduction|| |
Central retinal artery obstruction (CRAO) occurs when the site of blockage is at or just proximal to lamina cribrosa of the optic nerve. A majority of the retinal artery occlusion are either thrombotic or embolic in nature. CRAO is rare event and encountered 1 in 10,000 out patients. Bilateral involvement is even rarer, found in only 1-2% of total cases.  Bilateral CRAOs were reported in the setting of Wegener's granulomatosis, temporal arteritis, homocystinuria, sickle cell disease, Henoch-Schonlein purpura, mitral valve prolapse, atherosclerosis, and migraine. ,,, Atherosclerosis is implicated as the inciting event in about 80% cases. In only 20-25% cases emboli are visible in the central retinal artery or one of its branches. Inflammation, trauma, and arterial spasm are the other causes.
| Case Report|| |
A 60-year-old male retired factory worker, resident of Pune, reported to eye outpatient department (OPD) with sudden painless diminution of vision in right eye of 10 h duration.
On examination the patient was found to have DVR finger counting close to face with no improvement with glasses and DVL 6/60 improving to 6/9 with glasses. In the right eye, anterior segment examination showed relative afferent pupillary defect (RAPD) while fundus examination revealed retinal background pale white with cherry red spot in macula and thread like blood vessels and Grade II Hypertensive retinopathy.
Anterior segment examination of the left eye was normal and fundus examination revealed Grade II Hypertensive retinopathy. Applanation tonometry revealed 14 mmHg pressure in both eyes. A diagnosis of non-arteritic CRAO sparing the cilio-retinal artery was made in the right eye. Urgent paracentesis with 30-G needle was done in the right eye within 15 min of patient's arrival, which was followed by ocular massage.
We have done fundus fluorescein angiography which showed delayed arteriovenous transit time of 14 s, choroidal filling was normal and narrowed arterioles at perifoveolar regions in the right eye.
We have done routine blood investigations which revealed raised ESR 22 mm at the end of 1 h, raised blood sugar level (RBS = 190 mg%), raised serum cholesterol 205 mg%, and raised serum triglycerides 160 mg%. ECG, chest X-ray, and USG abdomen and pelvis were within normal limits. 2D-Echo was done which showed diastolic dysfunction and good systolic function. Bilateral carotid Doppler was done which showed a right-sided plaque in Carotid bulb, extending into internal carotid artery and a left-sided plaque in common carotid artery, extending into carotid bulb.
| Discussion|| |
Central retinal artery is a single source of blood supply to the entire retinal vasculature.
CRAO was first described by Von Graefe in 1859 as an embolic event in a patient of endocarditis. Retinal emboli are usually of three types: calcific, cholesterol, and platelet-fibrin.  In more than 50% of patients who experience retinal arterial occlusions, the presence of significant cardiovascular disease has been confirmed. Atherosclerosis is the causative factor in about 80% cases. In our case, the carotid Doppler revealed a right-sided plaque in carotid bulb extending to internal carotid artery and from there it might have gone to central retinal artery. There are various triggering factors for atherosclerosis; in our case, the patient was found to be hypertensive and diabetic both. Another triggering factor smoking was also found in our case.
The cattle-truck appearance of vessels, characteristic of branch retinal artery occlusion was not seen in our case. After paracentesis, there was not marked visual recovery. Vision improved from finger counting close to face to finger counting at 3 feet distance. Within 4 to 6 weeks, the retinal whitening usually resolves and optic disc pallor sets in. In our case, retinal whitening resolved in 6 weeks and optic disc pallor was noted after 12 weeks.
In central retinal artery occlusion cases, the visual prognosis is good if paracentesis and ocular massage is done within 90 min of occlusion. In our case, the gap between attack of sudden onset of blindness and reporting to OPD was more than 10 h, hence paracentesis and ocular massage was not much effective.
A patient coming with complaints of sudden diminution of vision should be immediately referred to Eye OPD. Prompt measures may be efficacious in improving vision if instituted within 90 to 120 min of arterial occlusion.
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