Ophthalmology - Acute visual disturbance Flashcards Preview

Year 4 - SPM > Ophthalmology - Acute visual disturbance > Flashcards

Flashcards in Ophthalmology - Acute visual disturbance Deck (44):
1

What differentials should be considered in acute painless loss of vision?

Central retinal artery occlusion
Branch retinal artery occlusion
Central retinal vein occlusion
Branch retinal vein occlusion
Anterior ischaemic optic neuropathy
Vitreous haemorrhage
Retinal detachment
ARMD (wet type)

2

What is the pathogenesis of retinal vein occlusion?

Thrombosis occurs within the lumen of the vessel. In branch occlusions, this is frequently seen at an arteriovenous crossing point. Abnormalities of blood constituents may promote thrombus formation. Clotting tendency can be increased in:
- hyperviscosity states
- smoking
- oral contraceptive pill
- pregnancy

3

What is the clinical presentation of retinal vein occlusion?

Patients are typically middle aged or elderly. Sudden painless loss of central vision occurs when the involved segment of retina includes the macula, as is the case with central and some branch occlusions. The severity of the initial fall in visual acuity varies considerably from case to case, commonly ranging from 6/9 to hand movements. There may be a relative afferent pupillary defect. On fundoscopy, flame, dot and blot haemorrhages, cotton wool spots, a swollen optic disc and macular oedema may be seen.

The condition is usually unilateral.

4

What are the important complications of retinal vein occlusion?

The two major complications are macular oedema and neovascularisation of the iris and retina. Iris neovascularisation (rubeosis) can lead to severe, painful glaucoma which is difficult to control.

5

How should a patient be assessed with retinal vein occlusion?

Common systemic associations include hypertension and diabetes. Rarely, blood dyscrasias or vasculitis may be the cause. The major ocular association is elevated intraocular pressure. The diagnosis is clinical. Investigations are directed primarily at excluding treatable associations.

6

What is the treatment of retinal vein occlusion?

Treatment is of the disease and of any systemic associations.

Macular oedema - laser treatment to reduce oedema and improve vision may be successful in branch retinal vein occlusion

Neovascularisation - as with proliferative diabetic retinopathy, laser of ischaemic areas can reverse neovascularisation. The case for prophylactic laser after vein occlusion but before the development of neovascularisation is not yet proven

Neovascular glaucoma - a variety of treatment, including laser and surgery are used, but the outcome is usually poor. A painful, blind eye may need to be removed

7

What is the pathogenesis of retinal artery occlusion?

Arterial occlusions typically lead to more severe visual loss than venous occlusions. As with venous disease, arterial occlusion can involve the central artery itself or one of its branches.

The commonest cause of aterial occlusion is embolisation, the emobolus originated most frequently from a source in a carotid artery, consisting of cholesterol, calcific plaques or fibrinoplatelet material. Emboli may pass through the retinal vascular system cause transient rather than permanent visual loss. Inflammation within the vessel wall, arteritis, may also cause occlusion.

Systemic conditions associated with retinal artery occlusion are hypertension, diabetes, IHD and CAD.

8

How does retinal artery occlusion present?

A branch retinal arteriolar occlusion may not give symptoms if the area affected is away from the macula. Central artery occlusions usually present with the sudden onset of severe monocular loss of vision, often to "counting fingers"or worse. The patient may report having experienced similar but transient episodes previously (amaurosis fugax). A marked relative afferent pupillary defect is usually present in central occlusions and frequently in branch occlusions.

9

What are the key features of retinal artery occlusion?

History of amaurosis fugax
Retinal pallor, cherry red spot (recedes after 6 weeks)
Narrow truncated arteries
Emboli visible within arterioles

Note that unlike ischaemic optic neuropathy, the optic disc is not usually pale or swollen.

10

How should patients with retinal artery occlusion be assessed?

Patients often have systemic conditions associated with microvascular disease, particularly hypertension, diabetes mellitus, IHD and peripheral vascular disease. Giant cell arteritis, although usually causing ischaemic optic neuropathy rather than embolic retinal artery occlusion, should always be considered.

Key features are pain and tenderness along the superficial temporal artery and elevated ESR and CRP. Other investigations may be performed to detect occult cardiovascular disease and potential sources of embolisation - i.e. carotid Doppler.

11

What is the treatment for retinal artery occlusion?

There is no specific treatment which reliably restores vision, but urgent referral to confirm the diagnosis is necessary, especially if a diagnosis of giant cell arteritis, which is treatable is not to be missed.

Regular prophylactic aspirin is prescribed, if not contraindicated, since it is likely to have a protective effect against arterial occlusion in the other eye and against stroke.

12

What are the clinical features of anterior ischaemic optic neuropathy (AION)?

Sudden onset sight loss, usually unilateral at first, may be preceded by transient episodes of visual loss. There is a relative afferent pupillary defect and a swollen optic disc, with haemorrhage and cotton wool spots. Field loss is usually altitudinal, in which the upper and lower half of the uniocular field is affected. In a young patient, optic neuritis is more likely, although this usually causes pain exacerbated by eye movement. Other causes of optic disc swelling are much less likely.

13

What are the different types of AION?

Two types are recognised: arteritis and nonarteritic.
The arteritic form is caused by giant cell (temporal) arteritis. Urgent diagnosis and treatment with systemic steroids is necessary to prevent bilateral blindness. Key features are scalp tenderness with inflammatory swelling of the temporal arteries, jaw claudication and an elevated ESR and CRP.

Nonarteritic ischaemic optic neuropathy has no sign of inflammation and is associated with atherosclerosis, hypertension, smoking and diabetes mellitus.

14

How many layers are there in the retina?

The retina comprises two layers:
1) the neurosensory retina, including photoreceptors and the ganglion cell layer
2) the retinal pigment epithelium

15

What are the 2 main types of retinal detachment?

Retinal detachment is a cleavage in the plane between the neurosensory retina and the retinal pigment epithelium (the subretinal space). Most cases of retinal detachment are rhegmatogenous, cause by a tear or hole in the neurosensory retina, which allows fluid from the vitreous humour to pass through into the subretinal space. Degenerative changes in the vitreous are important in the pathogenesis of rhegmatogenous retinal detachment.

Retinal detachment without a retinal break (nonrhegmatogenous) may also occur:
- tractional, when the retina is pulled off by membranes growing across its surface (e.g. advanced diabetic eye disease)
- exudative, caused by breakdown of the blood-retinal barrier allowing fluid to accumulate in the subretinal space (e.g. choroidal tumour, uveitis)

16

How does rhegmatogenous retinal detachment present?

This can present in a number of ways. Clinical features include:
- floaters/ flashing lights
- peripheral field loss
- loss of central vision
- loss of red reflex
- detached retina

Usually there is an antecedent history of vitreous detachment, but the importance of the symptom may go unnoticed, so that presentation with visual loss is usual.

Key differentiating features are:
- dense shadow that starts peripherally and progresses towards central vision
- a veil or curtain over the field of vision
- straight lines appear curved

17

How is rhegmatogenous retinal detachment detected clinically?

The peripheral field loss can be detected by simple confrontational testing. On fundal examination, detached retina is grey and the normal red reflex is lost. The grey retina seems to balloon forwards, requiring examination with "plus" lenses in the ophthalmoscope. Retinal blood vessels are seen on the surface.

18

How is rhegmatogenous retinal detachment managed?

The ONLY treatment is surgery. Patients should be referred to an ophthalmologist immediately. The principles of management are:
- relief of vitreoretinal traction
- closure of the retinal break
- drainage of subretinal fluid
- adhesion of detached retina to retinal pigment epithelium

Relief of traction can be achieved by removal of vitreous (vitrectomy) or by indenting the eye wall from the outside (placement of sutured explant).

19

What is the prognosis of retinal detachment?

Visual recovery depends on the duration of retinal detachment and whether or not foveal detachment occurred. If the detachment is a few days old only, the prognosis is good. Surgery is usually successful, but reoperation is sometimes necessary, particularly if scar-like membranes grow across the retina, pulling it off.

20

What clinical examination should be performed in cases of acute painless loss of vision?

Measure the visual acuity. Examine the pupils for RAPD. Examine the red reflex, which is reduced or absent in vitreous haemorrhage. Perform ophthalmoscopy. Look for evidence of:
- diabetic retinopathy (retinal haemorrhages, hard exudates, and cotton wool spots)
- retinal vein occlusion (retinal haemorrhages and cotton wool spots)
- retinal artery occlusion (yellow refractile plaques of bifurcation of retinal arterioles, cherry red spots on the macula, optic disc swelling)
- Wet ARMD (macular haemorrhages and hard exudates)
- Examine the cardiovascular system

21

What investigations are useful in cases of acute painless loss of vision?

In the case of ischaemic optic neuropathy or retinal artery occlusion, an ESR, plasma viscosity and/or CRP should be done to exclude giant cell arteritis. The blood sugar and lipid profile need to be measured. Do an FBC to check for thrombocytopaenia. Carotid Doppler ultrasound should be requested to determine the extent of carotid artery stenosis.

22

"I have flashing lights and floaters in one eye" What is the differential diagnosis?

Posterior vitreous detachment (PVD)
Retinal detachment
Migraine
Vitreous haemorrhage
Other visual phenomena
- retinal or cerebral underperfusion
- look for features of arteriopathy
Posterior segment inflammation (posterior uveitis)

23

What do patients mean when they talk about "spots before the eyes"?

This is a common phrase used by patients to describe two main distinct types of symptom:
1) "scintillating scotoma" - often compared to the distorting effect of water running down a window, a kaleidoscope pattern or zig zag lines

2) "floaters" - an exaggeration of the physiological phenomenon seen when staring into the distance against a pale background such as the sky

24

What is posterior vitreous detachment?

The vitreous humour is a gel consisting of water and glycosaminoglycans. Posterior vitreous detachment is the most common cause of acute onset floaters, particularly with advancing age and is one of the most common causes of acute visual disturbance.

25

What is the clinical history of vitreous detachment?

The patient presents complaining of floaters. In posterior vitreous detachment, the vitreous body collapses and detaches from the retina. If there are associated flashing lights it suggests that there may be traction on the retina, which may result in a retinal hole and a subsequent retinal detachment.

26

How is vitreous detachment managed?

Patients with an acute posterior vitreous detachment should have urgent ophthalmic referral, so that any retinal breaks or detachments can be treated at an early stage.

27

How does vitreous haemorrhage present?

Large bleeds cause sudden visual loss. Moderate bleeds may be described as numerous dark spots. Small bleeds may cause floaters. Flashing lights indicates radial traction and is a bad sign. Causes include diabetes and bleeding disorders. The red reflex may be reduced.

28

How is vitreous haemorrhage managed?

The patient should be referred to an ophthalmologist to exclude retinal detachment. Ultrasound examination of the eye may be useful, particularly if the haemorrhage occludes the view of the retina. If it fails to clear spontaneously, the patient may need the vitreous removing (vitrectomy).

29

What causes optic neuritis?

This is another cause of acute visual disturbance. Causes include:
- MS
- Syphilis
- Diabetes

30

What are the clinical features of optic neuritis?

The patient is usually female aged between 20 and 40 who presents with unilateral decrease in visual acuity over hours or days. There is poor discrimination of colours with "red desaturation" and pain is also worse on eye movement. There is also relative afferent pupillary defect.

31

How is optic neuritis managed?

The patient should be given high dose steroids.
Recovery usually takes 4-6 weeks.

A neurology referral is needed. If there are >5 white matter lesions on MRI then there is a 50% chance of developing MS within 5 years.

32

Migraine can present with acute visual disturbance. What features are usually present?

Migraine may present initially with symptoms of visual loss. The features are well known and include:
- a family history of migraine
- attacks set off by certain triggers
- fortification spectra in BOTH eyes - these include zig zag lines
- associated headache and nausea

However, if patients present for the first time after 40 years of age with migraine and associated neurological symptoms or signs, consider the need for further investigation.

33

Painful loss of vision, preceding halos around light, nausea, vomiting, red eye, cloudy cornea, non reactive mid dilated pupil

Acute angle closure glaucoma

34

Painful acute loss of vision, contact lens wearer, photophobia, fluorescein staining of corneal defect

Corneal ulcer/ keratitis

35

Painful loss of vision, painful eye movements, RAPD, red desaturation

Optic neuritis - e.g. secondary to MS

36

Painless acute loss of vision, headache, jaw claudication, scalp tenderness, malaise, weight loss

Giant cell arteritis

37

Painless acute loss of vision, sectorial fundal haemorrhage with corresponding field loss

Branch retinal vein occlusion

38

Painless acute loss of vision, stormy sunset appearance of the fundus (multiple haemorrhages)

Central retinal vein occlusion

39

Painless acute loss of vision, profound and sudden visual loss, cherry red spots at the macula, pale retina

Central retinal artery occlusion

40

Painless loss of vision with a poor fundal view

Vitreous haemorrhage

41

Painless loss of vision associated with a homonymous hemianopia (may be perceived as monocular visual loss), hemiparesis

Stroke/ TIA

42

Painless loss of vision, transient, descending curtain like loss of vision, carotid artery bruit

Amourosis fugax

43

Painless loss of vision, floaters, persistent flashing and curtain like field loss

Retinal detachment

44

Central loss or distortion of vision, sub acute onset

Wet AMD

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