Central Retinal Artery Occlusion; Central retinal vein occlusion Flashcards
(81 cards)
What is the most common cause of CRAO? [1]
Atherosclerotic disease is the most common cause of CRAO
- CRAO occurs due to occlusion of the retinal artery, usually due to an embolic event secondary to atherosclerotic disease.
- The central retinal artery supplies the surface of the optic nerve and inner retina.
Describe the arterial anatomy that is linked to CRAO [1]
The first branch of the internal carotid artery is the ophthalmic artery, which supplies the eye. The retina is supplied by two main arterial systems that arise from the ophthalmic artery:
* Retinal arteries
* Ciliary arteries
The retinal artery divides into the superior and inferior branches, which further divides into nasal and temporal terminal branches.
These arteries supplies the inner retina.
Describe the typical presentation of CRAO [+]
Patients with central retinal artery occlusion (CRAO) present with visual loss which is:
* Sudden onset (within seconds)
* Monocular
* Painless
* Severely reduced visual acuity
* Central visual sparing (15-30%): May suggest patent cilioretinal artery.
Describe the signs of CRAO [+]
Relative afferent pupillary defect (RAPD):
- Asymmetrical pupillary reaction to light due to optic nerve disease.
Pale retina
‘Cherry red spot’: Suggestive macular sparing due to patent blood supply via the cilioretinal artery.
Retinal emboli: May be seen in up to 40%.
If needed, the diagnosis of CRAO can be confirmed using []
Describe this investigation and what would present like in CRAO [1]
If needed, the diagnosis can be confirmed using fluorescein angiography
- During this procedure fluorescent dye is inserted intravenously. This allows assessment of the retinal vessels using imaging. In **CRAO there is usually evidence of slowed flow or a filling defect. **
In the work-up of CRAO, it is critical to exclude [].
In the work-up of CRAO, it is critical to exclude GCA.
Long term Mx of CRAO? [+]
CRAO is a form of ischaemic end-organ damage. Hence patients who have experienced CRAO are at increased risk of future ischaemic events such as myocardial infractions and ischaemic cerebral strokes
Long term management depends on the underlying cause of CRAO:
* Carotid source of emboli: carotid endarterectomy to correct stenosis of the carotid arteries. Stenosis of greater than 50% is classed as moderate to severe and requires surgery.
* Cardiac source of emboli: long term anticoagulation is usually recommended
* Uncertain aetiology: anti-platelet therapy and atherosclerosis risk factor modification (e.g. statins, smoking cessation and diet changes)
Describe the acute Mx of CRAO [5]
Ideally, treatment should be administered within 6 hours of onset to be effective.
- Intra-arterial thrombolysis: typically urokinase is administered via direct ophthalamic artery catheterisation
- In patients who are not candidates for thrombolysis but still present within a reasonable timeframe from onset, anterior chamber paracentesis can be completed. This aims to reduce intra-ocular pressure with the hope that it dislodges the embolus.
NB: The evidence supporting acute treatment of CRAO is limited. Treatment is usually attempted within 24 hours of presentation, but should be completed within 6 hours to improve efficacy.
Lecture
Describe the difference in presentation between central and branch RAO [2]
Visual loss in CRVO is secondary to the development of [] This develops following the venous occlusion.
Visual loss in CRVO is secondary to the development of macular oedema. This develops following the venous occlusion.
Describe the pathophysiology of central retinal vein occlusion [+]
Thrombosis in the retinal vein causes increased pressure in the vessels draining from the eye
This causes transudation of blood products into the retina from the venous capillary beds, leading to increased interstitial oncotic pressure that results in macular oedema and capillary ischaemia.
GeekyMedics:
- Pathophysiology: atherosclerotic thickening of retinal arteries compresses retinal veins, leading to endothelial damage, turbulent blood flow, thrombus formation, ischaemia, infarction, vessel leakage, and neovascularisation.
Describe the presentation of CRVO [+]
The main symptom is sudden, painless unilateral visual loss. The onset of visual loss is more gradual than with a retinal artery occlusion.
BRVO typically presents with partial visual field defect and metamorphopsia. BRVO can also be asymptomatic if the macula is spared.
90% of patients with ischaemic CRVO have visual acuity of 6/60 or worse
Relative afferent pupillary defect
Describe the fundoscopy findings of CRVO [+]
General:
- dot/blot haemorrhages, vascular dilatation and tortuosity of retinal veins (distribution of these dictates BRVO or CRVO with one, or four vein territories respectively involved)
Macular oedema
- hard exudate
Evidence of ischaemia:
- haemorrhages, cotton wool spots, optic disc swelling
Neovascular complications:
- neovascularisation and iris rubeosis, vitreous haemorrhage
Describe the fundoscopy of this CRVO [3]
Fundus photograph showing widespread haemorrhages and axonal congestion (cotton wool spots; white circles) upstream of the venous occlusion.4
Figure 3. Ischaemic central retinal vein occlusion.6
A key differential to CRVO is branch retinal vein occlusion (BRVO).
Describe the difference in pathophysiology and how it would present / be found differently [2]
A key differential is branch retinal vein occlusion (BRVO) - this occurs when a vein in the distal retinal venous system is occluded and is thought to occur due to blockage of retinal veins at arteriovenous crossings. It results in a more limited area of the fundus being affected.
- macular oedema is infrequently seen on fundoscopy
Non-ischaemic CRVO: Treatment strategy depends on the severity of presenting visual deficits.
Describe the management plan for visual acuity of:
- 6/12 or better
- 6/96 or better
- less than 6/96
6/12 or better
- Can observe with regular follow up as may spontaneously resolve. However, 30% may convert to an ischaemic CRVO over three years due to an increase in the area of non-perfusion
6/96 or better:
- Intravitreal anti-VEGF therapy indicated. Ranibizumab and aflibercept are two anti-VEGF agents recommended by NICE. Monthly intravitreal injections until stable visual acuity achieved.
Less than 6/96
- High risk of ocular neovascularisation (e.g. progression to ischaemic CRVO), and improvement with anti-VEGF therapy alone unlikely to produce improvement in visual acuity. Therefore patients should be closely observed for progression to ischaemic CRVO.
Describe the mx of ischaemic CRVO [2]
Urgent pan-retinal photocoagulation (PRP) where neovascularisation is seen, with repeat at 2 weeks if required.
In the absence of neovascularization, monthly follow-up to monitor. Where this is impractical, prophylactic PRP may be considered.
Macular oedema managed with anti-VEGF therapy.
Describe the three classifications of diabetic retinopathy? [2]
non-proliferative diabetic retinopathy (NPDR) marked by:
- microaneurysms
- retinal haemorrhages (dot haemorrhages)
- hard exudates (yellowish deposits of lipid due to vessel leakage)
proliferative diabetic retinopathy (PDR) (more advanced and severe stage), is characterized by:
- the proliferation of new, fragile blood vessels that can bleed into the vitreous, leading to vision loss due to VEGF upregulation
- can be new vessels on disc (NVD) OR new vessels everywhere (NVE)
Diabetic maculopathy:
- Presence of any retinopathy within 1 disc diameter around macula:
Can be:
- Focal
- Diffuse
- Ischaemic
What are the different types of classification of hard exudates in non-proliferatve retinopathy? [3]
Mild
Moderate
Severe: Cotton wool spots (arrow): areas of retinal ischaemia
What does this yellow arrow depict in non-proliferative diabetic retinopathy? [1]
Hard exudates
What does the yellow arrow on the image of non-proliferative retinopathy depict? [1]
Lipid exudates
Describe what the arrows & circle depict on this image of non proliferative diabetic retinopathy [3]
intraretinal microvascular abnormality (IRMA; green arrow)
venous beading and segmentation (blue arrow)
cluster haemorrhage (red circle)
featureless retina suggestive of capillary non-perfusion (white ellipse)