CM- Causes of Acute Vision Loss Flashcards
Where is the likely lesion if a patient has unilateral vision loss?
Bilateral vision loss?
Unilateral = disease of the eye itself, or optic nerve Bilateral = lesion of the chiasm, or posterior to the chiasm [unless both optic nerves are blown]
If vision loss is improved by viewing through a pinhole, what is the vision loss due to?
What if vision is NOT improved?
- uncorrected refractive error
- media disturbance- tear film abnormality, cataract, vitreous opacity]
If vision is not improved, the problem is structural or has some other physiologic etiology
A patient experiences transient loss of vision and “sparkles” in both eyes lasting 15-20 minutes. What is this highly suggestive of?
Migraines [bilateral nature suggests occipital cortex involvement]
What is transient painless monocular loss of vision due to?
emboli from the carotid arteries [Hollenhorst plaques] or from the heart
What is the DDx for sudden unilateral visual loss?
- retinal vascular occlusion
- optic neuritis
- ischemic optic neuropathy
- embolic phenomenon
What is the DDx for progressive visual loss with insidious onset?
compression of the optic pathway by:
- tumor
- aneurysm
The visual phenomenon of _______ always recovers fully after 20 minutes. __________ is significantly resolved after 6-8 weeks. ____________ typically does not improve.
Migraines- recover in 20 min
Optic neuritis= 6 to 8 weeks
Ischemic optic neuropathy = no improvement
What can color vision defects imply?
- optic nerve disease
- central macular disease
- congenital
What 3 main things cause media opacity and acute vision loss?
How are they differentiated?
irregularity/opacity of the clear refractive media can cause blurred/decreased vision with NO pupillary changes
- acute-angle glaucoma causes corneal edema. it is a RAPID process with increased ICP
- cataracts opacify the lens. Usually it develops slowly& with age, but it cn arise quicker with trauma or inflammation. PUPIL WILL BE WHITE/CLOUDY, decreased red reflex
- vitreous hemorrhage- secondary to trauma or neovascularization [diabetes or retinal vein occlusion]
A patient says that in his left eye he saw flashing lights and small black dots that drifted about. After that he experienced a shade of darkness over the vision in one eye that started peripherally and worked toward central vision. What is the most likely problem?
What will you notice when assessing his pupils?
Retinal detachment He will have developed an afferent pupillary defect in the affected eye [left] So when you do the flashlight test: 1. light in right eye = both constrict 2. light in left eye = both dilate
What is the pathological cause of retinal detachment?
How is it treated?
a hole in the retina allows fluid to flow under the sensory retina and detach it from the back of the eye.
It needs to be surgically treated prompty to close the hole and reattach the retina
How do you differentiate retinal detachment from migraine in terms of presentation?
Migraine- bilateral “sparkles’ and vision loss that lasts 15-20 minutes then is fixed
Retinal detachment- unilateral flashing lights and floaters followed by peripheral to central curtain of darkness with pupillary defect. Does not improve spontaneously and requires prompt surgery
What are the similarities and differences between central retinal artery occlusion [CRAO] and central retinal vein occlusion [CRVO] ?
Similarities:
- sudden, painless vision loss
- both present with afferent pupil defect
Differences
- CRAO - white,opaque retina with thin cherry red fovea; attenuated arterioles
- CRVO - retinal hemorrhages, venous engorgement, cotton-wool spots [white patches of retina that are microinfarcts]
- CRVO seen in hypertension, atherosclerotic vascular disease
Why is CRAO a true ophthalmic emergency?
What is treatment?
It is a true emergency because permanent retinal damage can occur in 2hrs.
Treatment:
1. lowering intraocular pressure
2. attempting to induce arterial dilation to move the clot downstream
[treatment is of questionable efficacy]
A 50 year old patient experiences painless transient vision loss in one eye. He says he has “attacks” where it looks as if a curtain were coming down over his vision. He said they develop in 30 seconds and usually last about 10minutes.
What is the Dx?
What is the pathological cause?
What is further treatment/assessment for the patient?
What is a person with this Dx at increased risk for?
Amaurosis fugax
It is caused by embolization from atherosclerotic plaques in the ipsilateral carotid [Hollenhorst plaque] or calcified heart valves
On fundic exam you may or may not see plaques lodged at the bifurcation of retinal arteries.
Requires complete neurological and medical assessment to determine the source of the embolus because these patients are at 4% increased risk of stroke w/in 5 years
A 25 year old presents with sudden vision loss that is unilateral and painful on eye movement. She says it got progressively worse over about a week, but now it has stabilized.
Upon examination, you note an afferent pupillary defect. The optic disk shows swelling.
What is the most likely Dx? What is the usual pathologic cause? When should the patients vision improve? What are possible lingering effects? What are next steps for assessment/treatment?
Optic neuritis
- usually caused by MS causing inflammation of the optic nerve due to demyelination
- vision typically improves in 6-8 weeks
- some lingering effects will be color vision and contrast sensitivity changes
- MRI to look for evidence of MS, IV steroids/IFNb1a to delay onset of other symptoms of MS
