Answers
Andrew Schofield, Paul Schofield in The Complete SAQ Study Guide, 2019
Central retinal artery occlusion is one of the differential diagnoses of sudden painless loss of vision. With this particular clinical problem, a general examination should be performed as well as taking a good past medical history in order to find a root cause. The commonest cause is a thromboembolic event, hence the need for a brief cardiovascular examination. On examination of the eyes, the afferent pupillary defect will be the first noticeable sign (this is seen as an absence of pupillary constriction when a light is shone into the affected eye, whilst there will be pupillary constriction in the affected eye if light is shone into the non-affected eye). The retina will appear pale due to ischaemia, but a cherry-red spot will be evident at the macula due to blood supply coming from the underlying choroid. If central retinal vein occlusion is due to an inflammatory process, such as temporal arteritis (as in the clinical case described), then high-dose steroids are required as soon as possible, as there is only a 6-hour window in which to save the patient’s sight.
Fabry disease
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop in Atlas of Inherited Metabolic Diseases, 2020
Ocular lesions [22] regularly include dilated tortuous venules of the conjunctivae (Figure 87.5). Similar dilatation may be seen in the vessel of the retinas. Corneal opacities develop in males and in some heterozygous females. The diagnosis can be made by slit lamp examination, in which the typical cream-colored interior, whorl-like opacities are visualized. Corneal opacities have been seen as early as six months of age [23]. Cataracts of the posterior capsule of the lens are pathognomonic [22]. The ocular lesions result from the deposition of glycosphingolipid and do not usually impair vision. As the disease progresses, the retinal changes of uremia may be found. Visual loss has been observed following central retinal artery occlusion [24]. Some patients display edema of the eyelids, in the absence of renal disease [22, 23]. The ocular manifestations of disease, especially cornea verticillata correlated with severe disease in pediatric patients [25]. Neurosensory hearing loss may develop [18].
Vascular
Michael Gaunt, Tjun Tang, Stewart Walsh in General Surgery Outpatient Decisions, 2018
The classic embolic neurological event is the transient ischaemic attack (TIA). A TIA is a mini stroke (e.g. limb weakness, speech defects, facial weakness) which recovers completely within 24 hours. The symptoms affect the limbs on the opposite side to the stenosed artery. Amaurosis fugax (fleeting blindness) occurs when an embolus temporarily occludes the main stem or branch of the retinal artery causing temporary blindness. Amaurosis fugax consists of transient monocular blindness that occurs on the same side as the stenosed artery. All or part of the visual field may be lost, but usually the embolus breaks up and vision returns. Occasionally, loss of vision is permanent and complete (central retinal artery occlusion).
Diffusion-Weighted Magnetic Resonance Imaging in Acute Retinal Pathology
Published in Neuro-Ophthalmology, 2018
Omar Alsinaidi, Aasef G. Shaikh
A 57-year-old woman with history of hypertension presented with acute painless vision loss from the left eye. She reported intermittent symptoms of flashing lights and blurred vision in her left eye for 2 days prior to presentation. Subsequently, her vision acutely turned grey and then black, when she presented to the emergency room. Examination revealed light perception in the left eye, and arteriolar narrowing with boxcarring and a pale fundus. Table 1 depicts the details of pertinent ophthalmological examination. Remaining neurological examination was unremarkable. The findings were consistent with central retinal artery occlusion. DWI sequence revealed multiple areas of diffusion restriction in the left retina (Figure 1A) suggestive of multiple punctate infarcts. There were no significant vascular stenoses, as confirmed in intracranial and neck magnetic resonance angiograms (MRAs). Echocardiogram revealed a mobile mass measuring 1.28 × 0.88 cm on the posterior mitral annulus. The mass was removed surgically, and pathology showed fibrin and calcification consistent with vegetation. Microorganisms were not found, as the patient was on empiric broad-spectrum intravenous antibiotics.
Intralesional corticosteroid injections as treatment for non-infectious orbital inflammation
Published in Orbit, 2018
Sara Reggie, Michael Neimkin, John Holds
Perhaps the most feared complication is permanent vision loss from central retinal artery occlusion, which has been reported after periocular injections.29–33 For ocular embolization to occur, retrograde flow into a terminal artery must be present, as well as a sufficient volume of injected corticosteroid.31 In accordance with previous studies, triamcinolone acetonide is manufactured in a 10 or 40 mg/mL concentration; thus, about 1 mL of fluid is needed.18 Although central retinal artery occlusion has been reported with an injection amount as small as 0.5 mL, our technique ensures that very small aliquots of fluid are injected into multiple locations in order to avoid a large bolus, even if the needle is in an artery. This avoids a vision threatening rise in orbital pressure and compromise in ophthalmic blood flow.17
Neuro-Ophthalmic Literature Review
Published in Neuro-Ophthalmology, 2022
David A. Bellows, Noel C.Y. Chan, John J. Chen, Hui-Chen Cheng, Peter W. MacIntosh, Michael S. Vaphiades, Xiaojun Zhang
Chodnicki KD, Tanke LB, Pulido JS, Hodge DO, Klaas JP, Olsen TW, Bhatti MT, Chen JJ. Stroke risk before and after central retinal artery occlusion: a population-based analysis. Ophthalmology. 2022 Feb;129(2):203–208. doi:10.1016/j.ophtha.2021.07.017
Related Knowledge Centers
- Central Retinal Artery
- Edema
- Eye
- Atheroma
- Atherosclerosis
- Pallor
- Ophthalmoscopy
- Cherry-Red Spot
- Hypertensive Retinopathy
- Embolus