Painless Loss of Vision Flashcards

1
Q

What acronym can be used to help differentiate the cause of painless loss of vision

A

5 quick questions to differentiate causes – HELLP
Headache – do an ESR and CRP in all cases urgently for GCA
Eye movement hurting – optic neuritis
Light flashing preceding visual loss – retinal detachment
Like a curtain descending – Amaurosis fugax may precede permanent visual loss – GCA or emboli
Poorly controlled DM – vitreous haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are optic neuropathies?

A

Optic Neuropathies – damage to the optic nerve that results in monocular blindness with a central scotoma, afferent pupillary defects, dyschromatopsia (colour blindness) and papillitis on fundoscopy which progresses to optic atrophy (pale disc indicates long term damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is anterior ischaemic optic neuropathy (AION)?

A

Most common cause in older patients. Posterior blood supply to the optic nerve is blocked by inflammation or atheroma. Fundoscopy – pale swollen optic disc. Two types, either arteritic AION or non-arteritic AION.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most common type of AION?

A
Giant Cell (temporal) Arteritis (GCA)
Most common type of arteritic AION. It is a medium to large vessel vasculitis in patients typically over 70 years and very rarely occurring before 50yrs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the risk factors for GCA?

A

Twice as common in women as men. Strong association with polymyalgia rheumatica, hip and shoulder girdle aching and morning stiffness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the clinical features of GCA?

A

New onset headache
Malaise
Jaw claudication (chewing pain)
Tender scalp and temporal arteries (thickened and pulseless)
Neck pain
Monocular visual loss (can be transient – amaurosis fugax)
Diplopia
Pulseless temporal artery
Skip lesions on biopsy
Features of PMR – aching, morning stiffness, lethargy, depression, low grade fever, anorexia and night sweats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How should suspected GCA be investigated?

A

ESR and CRP (before steroids)

Temporal artery biopsy within a week (but may miss affected section – skip lesions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is GCA managed?

A

Give steroids asap as other eye is at risk – prednisolone PO STAT – should see a rapid response, if not then reconsider diagnosis
Tail off steroid as ESR and symptoms settle but this may take over a year
1 in 5 left with partial or complete blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is optic neuritis?

A

Demyelinating inflammation of the optic nerve. Full recovery usually takes place over 2-6 weeks, but a very large number go on to develop multiple sclerosis in the next 15 years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Other than MS what other causes are there for optic neuropathy?

A

Syphilis
Leber’s optic atrophy
Diabetes
Vitamin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the clinical features of optic neuropathy?

A

Unilateral loss of vision occurring over hours or days
Colour vision affected first with red appearing less red (red desaturation)
Eye movements hurt
Afferent pupillary defect
Central scotoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is optic neuropahty managed?

A

High dose methylprednisolone for 72 hours
Followed by prednisolone for 11 days
On MRI if >3 white matter lesions then 5-year risk of developing MS is 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is retinal vein occlusion?

A

Incidence increases with age and is the 2nd most common cause of blindness from retinal vascular disease. If whole central retinal vein is occluded there is complete visual loss in that eye resulting in ischaemia and macular oedema. CRVO can be ischaemic or non-ischaemic. Non-ischaemic is more common and has a better prognosis and may even have normal vision but may progress to ischaemic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can cause retinal vein occlusion?

A
Arteriosclerosis 
Hypertension 
Diabetes 
Polycythaemia 
Glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the clinical features of central retinal vein occlusion?

A

Note branch retinal vein occlusion can be asymptomatic if it doesn’t affect the macula
Occurs less suddenly than central retinal artery occlusion

Non-Ischaemic
Decrease in visual acuity to >20/200, RAPD mild or absent, macular oedema, haemorrhage, cotton wool spot, venous tortuosity, and dilation

Ischaemic
Cotton wool spots, swollen optic nerve, maula oedema, severe venous tortuosity and dilation and risk of neovascularisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How should retinal vein occlusion be investigated?

A

Acuity
Retinal imaging
Fundus fluorescein angiogram – determines extend of the ischaemia

17
Q

How is retinal vein occlusion managed?

A

Refer to on call ophthalmologist
Non-Ischaemic – follow up after 3 months after exploring causes and managing this

Ischaemic – follow up monthly for 6 months
Intravitreal anti-VEGF
Dexamethasone implants or intravitreal triamcinolone
Photocoagulation if new vessels have begun to form

18
Q

What is central retinal artery occlusion?

A

A lot less common than retinal vein occlusion but considered a stroke and should be treated as such. Most commonly it is thromboembolic from AF or carotid disease. Look for heart valve disease diabetes, BP.

19
Q

How does retinal artery occlusion present?

A

Afferent pupillary defect appears within seconds and may precede retinal changes. Retina appears white with a cherry red spot at the macula.

20
Q

How should retinal artery occlusion be managed from the ophthalmic point of view?

A

Extra ophthalmic management
Attempt to increase blood flow if within 100mins
Reduce intraocular pressure with ocular massage, surgical removal of aqueous or use of intraocular hypotensive treatment.

21
Q

What is a vitreous haemorrhage?

A

This occurs after retinal revascularisation, retinal tears, retinal detachment or trauma. Small extravasation of blood results in vitreous floaters. Very common causes of painless loss of vision. After bleeding stops typically absorbed at a rate of 1% per day.

22
Q

What investigations should be done in vitreous haemorrhage?

A

Dilated fundoscopy
Slit lamp examination – red blood cells in the anterior vitreous
If retina not seen then B-scan USS – can detect retinal tear/detachment
Fluorescein angiography to identify neovascularisation
Orbital CT if globe injury

23
Q

How does a vitreous haemorrhage present and can it be treated?

A

Painless loss of vision or visual haze (more common)
Red hue in the vision
Floaters or shadows/dark spots in the vision
Visual field defect if severe haemorrhage
If bleed is large enough to obscure vision, there will be no red reflex and the retina may not be seen. In this case a B-scan US can be used to located a cause.

Usually the blood undergoes spontaneous absorption. However, in extensive and dense a vitrectomy is done to remove the blood if the retina is torn/detached.

24
Q

What is a retinal detachment?

A

Holes/tears in the retina allow fluid to separate the sensory retina from the pigment epithelium. If macula involved may not recover even after fixation.

25
Q

Describe the 3 types of retinal detachments

A

Rhegmatogenous retinal detachment – a retinal tear that allows fluid from the vitreous space into the subretinal space, typically occurring as a result of trauma.

Exudative retinal detachment – detachment without a tear due to e.g. hypertension, vasculitis, macular degenerative conditions or tumours

Tractional retinal detachments – pulling on the retina such as in proliferative retinopathy.

26
Q

What are the two important risk factors to consider for retinal detachment?

A

Myopic eyes are more prone to detachment and the greater the myopia the greater the risk. Also, cataract surgery carries an increase risk of detachment.

27
Q

How does a retinal detachment present?

A
The four f’s 
Floaters
Flashes 
Field loss opposite plane to where the detachment takes place 
Fall in acuity (painless)
28
Q

How should a suspected retinal detachment be investigated?

A
Visual acuity
Slit lamp examination 
Dilated fundoscopy - grey opalescent retina that’s ballooned forward
Pupillary examination 
Visual field testing 
IOP measurement
29
Q

How are retinal detachments managed?

A

Rest
If superior detachment lie flat
If inferior detachment, then lie at 30 degrees
Refer urgently for vitrectomy and gas tamponade
Cryotherapy or laser photocoagulation therapy is used to secure the retina.

If retinal break is detected before a detachment, then cryotherapy or retinopexy may be preventative.

30
Q

What is ischaemic optic neuropathy?

A

Ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve

31
Q

What is posterior vitreous detachment

A

Posterior vitreous detachment is the separation of the vitreous membrane from the retina, it is a common condition that does not cause any pain or loss of vision. However, rarely the separation of the vitreous membrane can lead to tears and detachment of the retina. It is important to rule out retinal tears or retinal detachment in anyone with suspected posterior vitreous detachment, as they may result in permanent loss of vision.

32
Q

What are the risk factors for posterior vitreous detachment?

A

Occur in over 75% of people over the age of 65 and is more common in females

As people age, the vitreous fluid in the eye becomes less viscous, and thus, does not hold its shape as well. Therefore, it pulls the vitreous membrane away from the retina towards the centre of the eye.
Highly myopic (near-sighted) patients are also at increased risk of developing posterior vitreous detachment earlier in life. This is because the myopic eye has a longer axial length than an emmetropic eye.
33
Q

How does posterior vitreous detachment present?

A

The sudden appearance of floaters, typically on the temporal side of central vision
Flashes of light in vision
Blurred vision and Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)
Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).

34
Q

What investigations should be done for a posterior vitreous detachment?

A

All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.

35
Q

How is a posterior vitreous detachment managed?

A

Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.

36
Q

What is non-arteritic AION?

A

Non-Arteritic AION
Typically, painless vision loss noticed upon waking affecting patients less than 50yrs old.
Associated with raised BP and lipids, DM and smoking. Treating these 4 things protects the other eye.