Ophthalmology: acute loss of vision Flashcards

1
Q

DDx for acute loss of vision Unilaterally

A
Amaurosis fugax
Central retinal artery occlusion
Central retinal vein occlusion
Vitreous haemorrhage
Retinal detachment
GCA
Optic neuritis
Non-arteritic ischaemic optic neuropathy
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2
Q

DDx for acute bilateral loss of vision

A

severe bilateral papilloedema (malignant HTP and highr ICP)
rapid progression of lesion compressing optic chiasm
bilateral infarcts in occipital lobes
Bilateral optic nerve damage: methanol
bilateral optic neuritis - rare

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3
Q

NON-ARTERITIC ANTERIOR ISCHAEMIC OPTIC NEUROPATHY is caused by?..

A

is caused by occlusion of the short posterior ciliary arteries. This results in infarction of the optic nerve head.

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4
Q

risk factors for nAION

A
  • Male
  • Systemic arteriopathy
  • 40-60 years of age
  • Small hypermetropic optic discs
  • Hypertension
  • Diabetes
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5
Q

Hx Ex for nAION

A
  1. Establish when vision loss occurred and in which eye
  2. Assess cardiovascular risk factors
  3. Exclude features of giant cell arteritis
  4. Palpate the temporal artery (unlike GCA expect them to be palpable and non tender)
  5. Measure visual acuity
  6. Examine the pupil reactions for an RAPD
  7. Test visual fields (typically unilateral altitudinal hemianopia)
  8. Examine the optic discs with an ophthalmoscope, ideally dilated.
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6
Q

Features of nAION

A
  • Painless, monocular, sudden loss of vision
  • Sometimes asymptomatic if good vision in fellow eye (as can still see)
  • Moderate to severely ↓ visual acuity in affected eye (typically 6/12 to 6/60)
  • A sector or all of the optic nerve may be swollen with splinter or flame shaped haemorrhages
  • Relative afferent pupillary defect
  • Visual field defect corresponding to the area of optic disc swelling. The most common is an inferior altitudinal defect
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7
Q

Mx of nAION

A

Refer to Ophthalmology urgently, to exclude giant cell arteritis with examination /ESR/CRP
Review and treat all cardiovascular risk factors
Consider aspirin

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8
Q

Prognosis of nAION

A

30% make substantial improvement (gain of 3 lines on a Snellen vision chart)
15-50% risk to fellow eye
The optic disc swelling gradually resolves, leaving optic disc pallor (due to loss of neural tissue)

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9
Q

what is GCA

A

It usually effects >50 y/o females
GCA is a vasculitis of the medium and large arteries. It often affects arteries around the temple, scalp, head and neck. The optic nerve head blood supply is compromised, producing anterior ischaemia optic neuropathy. Therefore it has a similar presentation to non-arteritic anterior ischemic optic neuropathy, but is more likely to have pain and raised ESR/CRP

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10
Q

Sx of GCA

A
  • Sudden painful severe monocular loss of vision, possibly preceded by transient episodes of vision loss
  • Headache
  • Scalp tenderness
  • Jaw claudication
  • Loss of appetite
  • Weight loss
  • Visual acuity often severely reduced e.g. count fingers
  • Usually non-pulsatile tender temporal arteries
  • Swollen optic disc & RAPD
  • May have flame shaped haemorrhages & cotton wool spots indicating retinal nerve fibre layer infarction
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11
Q

Mx of GCA

A
  • Emergency referral to ophthalmology
  • Inflammatory markers (ESR/CRP)
  • High-dose systemic steroids
  • Temporal artery biopsy, usually within no more than a few days of starting steroids
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12
Q

Aqueous humor physiology

A

Aqueous production and drainage is balanced to maintain an appropriate intraocular pressure. Aqueous humor is produced by the ciliary body in the posterior chamber. It circulates to the anterior chamber, through the pupil, and leaves the eye through the trabecular meshwork.

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13
Q

mechanism of AACG

A

Usually caused by failure of aqueous humor to pass through the pupil and drain out through the trabecular meshwork.
This can be caused by:
The iris being pushed forward against the trabecular meshwork
A pupil-block, whereby the aqueous fails to pass through the pupil
The result is often markedly raised intraocular pressure.
A glaucomatous optic neuropathy can follow→severe & permanent vision loss.
Usually presents with acute, painful loss of vision.
Caused by an acute rise in IOP

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14
Q

risk factors for acute angle closure glaucoma

A
  • Hypermetropia
  • Family history
  • Narrow anterior chamber angles
  • Age >30 years of age
  • Race
  • Women
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15
Q

Sx of acute angle closeure glaucoma

A
Sx
•	Unilateral loss of vision (can be 6/36 or worse)
•	Halos around lights
•	Unilateral red eye
•	Painful eye
•	Nausea and vomiting
•	Can be asymptomatic
•	+/-  previous intermittent symptoms
	Reduced visual acuity
	Corneal oedema
	↑ IOP (eye may feel ‘rock hard’ to palpation through lids)
	Oval unreactive pupil
	Hypermetropia (the anterior chamber is shallower and hence greater susceptibility to AACG)
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16
Q

MX of AACG

A
Refer urgently as an ophthalmic emergency 
Treatment
Lower the IOP:
Systemic:
acetazolamide 500mg IV stat
Eye drops:
timolol 0.5%
apraclonidine 1%
Laser:
YAG peripheral iridotomy (to create an alternative aqueous outflow passageway that circumvents the pupil block)
17
Q

rETINAL DETACHMENT pathology

A

The retina is made up of two main layers:
The neurosensory retina
The retinal pigment epithelium (RPE)
Posterior vitreous detachment (PVD) occurs when the vitreous separates from the retina, as part of the normal ageing process. Normally PVD does not cause a problem, but if there is an abnormal adhesion to the retina it can tear (rhegma) the retina. A rhegmatogenous retinal detachment occurs if vitreous fluid passes through the tear, separating the neurosensory retina from the retinal pigment epithelium.

18
Q

risk factors for retinal detachment

A
  • Myopia
  • Retinal detachment in the fellow eye
  • Trauma

Poorly controlled diabetics and those with some inflammatory eye problems can get tractional retinal detachment and serous retinal detachments respectively, but these are not common, and are not part of the syllabus.

19
Q

tractional retinal detachment occurs when

A

occurs when retinal scar tissue contracts, pulling the retina off the underlying retinal pigment epithelium, without formation of a retinal tear.

20
Q

serous retinal detachment occurs wje

A

occurs when exudative fluid collects between the neurosensory retina and retinal pigment epithelium, without formation of a retinal tear.

21
Q

Mx of retinal detachment

A

If the patient reports flashes, field defects and floaters refer to an ophthalmologist urgently. Retinal detachment is an emergency.
The aim is to treat before the macula detaches. Surgery involves cryobuckle surgery or pars plana vitrectomy

22
Q

Uni/bi-lateral gradual blindess: DDX

A
Cataracts
Glaucoma
Macular degeneration
Diabetic retinopathy
Otpic nerve/chiasmal compression
23
Q

retinal detachment presentation

A

• Sudden (sometimes gradual) painless loss of vision.
• Usually preceded by symptoms of flashing lights (photopsia)
and/or floaters and/or visual field defects.
• When the macula is not involved the visual loss involves the peripheral
field and visual acuity may be normal.
• Once the macula is involved the central vision is lost

24
Q

Vitreous haemorrhage presentation

A

sudden PAINLESS LOV: partial or total depending on the size of haemorrhage

25
Q

aetiology of vitreous haemorrhage

A

• Proliferative retinopathy—spontaneous rupture of abnormal
fragile new vessels that grow on the retinal surface cause bleeding into the vitreous cavity

Retinal detachment—a small retinal blood vessel may rupture when the retinal break occurs, bleeding into the vitreous cavity.

  • Trauma.
  • Posterior vitreous detachment (see Chapter 39 for details) can result in vitreous haemorrhage if, as the vitreous separates from the retina, it pulls and ruptures a small blood vessel.
  • Age-related macula degeneration (AMD)—haemorrhage may occur into the vitreous from the abnormally weak vessels forming a subretinal neovascular membrane