• Transient visual loss like a 

curtain coming down (suggestive 
of amourosis fugax)
 
• Visual loss or field loss preceded

by sudden onset floaters and flashing 
light (photopsia), this is suggestive of 
retinal detachment
 
• History of poorly controlled diabetes 

mellitus and laser treatment to the 
retina (vitreous haemorrhage)
 
• Headache +/- jaw claudication (pain 

in the jaw on eating) in the elderly 
(giant cell arteritis)
 
• Pain on eye movement in young patients 

(optic neuritis)

• Visual acuity 

• Assess the visual field by confrontation, 

some patients may have homonymous 
hemianopia and yet complain of uniocular 
visual loss.
 
• Full ocular examination which should 

include:
 
• pupil reaction for afferent pupillary

defect (this occurs in optic nerve
disorder and extensive retinal
pathology.)
 
• retinal examination for any obvious 

signs

Occlusion of the retinal artery may be caused by arteriosclerotic changes, embolus 
(from heart or carotid artery) or inflammation (rare)

History:

• Sudden painless visual loss which may be complete (due to central retinal artery 

occlusion) or partial (due to branch retinal artery occlusion)
• Patient usually have a history of hypertension or heart disease

• The visual acuity is reduced in central retinal artery occlusion but may be normal 

in branch retinal artery occlusion
• Relative afferent pupillary defect is present in central retinal artery occlusion
• The retinal arteries are narrow or collapsed. 
• In central retinal artery occlusion, the fovea shows a cherry-red spot against the 

white infarcted retina. 
• In branch retinal artery occlusion, the white infarcted retina corresponds to the 

occluded retina. 
• Emboli may be seen in the arteries if the cause is emboli

• Immediate referral if the visual loss is less than 6 hours as treatment may restore 

some or most of the function. 
• Treatment involves the use of intravenous acetazolamide and globe massage to 

lower the intraocular pressure and hopefully re-establish the arterial flow.
• Further management aim to uncover any underlying diseases such as hypertension, 

cardiac or carotid thrombus. An ESR is usually performed in the absence of obvious 
embolus to exclude arteritic causes.
• Long term low dose aspirin is advised to reduce the risk of occurrence.

Figure 1 Central retinal artery occlusion showing the typical cherry-red spots again  the white infarcted retina. This appearance is not permanent and usually  disappears after about three days when the flow of the retina artery  is re-established but the retina does not regain its function.

Figure 2 Branch retinal artery occlusion due to emboli. Note their  presence in the inferior retinal artery. The infarcted  retina appears as white.

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Retinal vein occlusion is a common vascular disorder caused by impaired venous blood flow. 
It is second only to diabetes mellitus as a vascular cause of impaired vision.

Presentation:

• Sudden onset painless blurred vision
• Less commonly the patient may present with painful red eye due to neovascular glaucoma
• as a result of recent central retinal vein occlusion.

• The visual acuity is reduced in central retinal vein occlusion. However, the reduction is 
• dependent on the severity of the occlusion. In branch retinal vein occlusion, the visual 

acuity may be normal if the fovea is not involved. 
• Relative afferent pupillary defect may be present in patient with severe central retinal vein 

occlusion
• Ophthalmoscopy reveals extensive intraretinal and pre-retinal haemorrhage with distended 

retinal veins.

• Refer within 24 hours.
• Although there is no immediate treatment that can restore the vision, it is important to 

examine the patient for hypertension and glaucoma. A blood test is usually performed for 
full blood count, ESR and in young patients auto-immune screening.
• Follow-up in the clinic is arranged so that those at risk of neovascular glaucoma may be 

treated with laser pan-photocoagulation

Figure 1 A classical picture of central retinal vein occlusion showing extensive  flamed haemorrhages.

Figure 2 This hypertensive patient complains of a sudden onset drop in his left vision.  Fundal examination reveals a left superior temporal branch retinal vein  occlusion. There are multiple flammed haemorrhages and cotton wool spots along  the occluded vein.

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History:

• A recent history of floaters and flashes of light are common
• Curtain coming across the vision 

• Visual acuity variable depending if the macula is involved. If the vision is normal,

referral becomes more urgent as the macular function may be involved by the extension 
of the detachment.
• Visual field defect 
• Ophthalmic examination in a dilated pupil shows greyish retina, hole and tear may be seen. 

• Refer the patient the same day 
• Patients will require surgical management which consists of sealing the retinal breaks 

(using cryotherapy or laser) and relieving the vitreous traction (using indentation or vitrectomy)

Figure 1 This patient presented to the eye casualty with a sudden onset black shadow over his right  eye.Fundoscopy reveals a retinal detachment. Note the wrinkled retina; this is a common  sign of retinal detachment.

Figure 2 A patient with retinal detachment showing retinal tear.This patient requires treatment to seal the hole in order to prevent retinal detachment. This can either be achieved with laser or  cryotherapy. In patients who complain of sudden onset floaters, it can be difficult  to find abnormalities with a direct ophthalmoscope as the tears or holes are often in  the peripheral retina. Therefore, it is important to refer all patients with sudden onset floaters.

 
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In ischaemic optic neuropathy, there is occlusion of the small arteries around the optic disc. 
It is important to differentiate arteritic optic neuropathy from non-arteritic optic neuropathy. 
Arteritic optic neuropathy is caused by giant cell arteritis and prompt treatment with systemic 
steroid can prevent involvement of the contralateral eye. 

Presentation:

• Sudden visual loss in a patient with a history of persistent headache (which may be 

temporal or occipital) or jaw claudication (pain in the jaw on eating) suggest giant cell arteritis

• The visual loss is usually profound 6/60 or less in giant cell arteritis and less severe in 

non-arteritic ischaemic optic neuropathy.
• Afferent pupillary defect is common
• Fundal examination reveals swollen optic disc caused by occlusion of the arteries around 

the optic disc
• In giant cell arteritis there is tenderness over the affected artery (usually the temporal artery) 

and the artery is usually not palpable.

• Refer immediately any patient with sudden visual loss and swollen disc for exclusion of 

giant cell arteritis.
• ESR and the C reactive protein are usually raised in giant cell arteritis but non-specific. 

A definite diagnosis is by temporal artery biopsy for the typical granulomatous changes 
in the arterial wall. However, systemic steroid is usually given while this is arranged.
 

Figure 1 Swollen optic disc with decreased vision and headache requires the exclusion of  giant cell arteritis.

 
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This condition typically affects patients in the 20 - 45 age group.

Presentation:

• Impaired vision 
• Central field defect

• Visual acuity may be as poor as perception of light
• Central scotoma is typical
• Impaired colour discrimination (best demonstrated with red object, the affected eye 

will see the red object less bright than the unaffected eye)
• Relative afferent pupillary defect of the affected eye
• Pain on eye movement especially on adduction
• Fundal examination is normal as most cases have retrobulbar neuritis.

• Refer the patient within 24 hours for confirmation of the diagnosis
• Normal or near-normal vision usually returns within 6 weeks
• As treatment does not affect the outcome, unilateral optic neuritis is not treated by 

most ophthalmologists. However, follow-up is important as radiological investigation 
may be needed to exclude compressive lesion in cases where spontaneous recovery 
fails to recur.

 

Figure 1 Optic atrophy in a patient with a past history of optic neuritis. Optic atrophy is a late  sign. In acute optic neuritis, the optic disc is typically normal.

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This may occur spontaneously or after trauma. The main causes of spontaneous vitreous 
haemorrhage are: posterior vitreous detachment with or without retinal breaks, proliferative
diabetic retinopathy, central retinal vein occlusion and subretinal neovascular membrane in 
age-related macular degeneration with breakthrough bleeding.

Presentation:

• Sudden onset of floaters causing impaired vision

• Depending on the severity of the haemorrhage, the view may be impossible with 

a direct ophthalmoscope

• Refer within 24 hours
• In the casualty, the ophthalmologists will examine the eye for any posterior vitreous 

detachment and diabetic changes.
• An ultrasound is often performed if the view is poor to exclude a retinal detachment
• These patients require close observation until the cause has been established or treated

Figure 1 This diabetic patient complains of blurred right vision. Fundoscopy reveals a subhyaloid haemorrhage (haemorrhage between the retina and the vitreous). Note the haemorrhage has a fluid level (which is typical of subhyaloid haemorrhage) and the presence of previous laser  photocoagulation scars.This patient certainly has new vessels and  requires further laser photocoagulation.

 
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