Acute Posterior Eye Presentations Flashcards
What is the Edinburgh Visual Loss Diagnostic Algorithm?
- Designed to improve accuracy of non-expert clinicians
- Has improved accuracy of optometric referrals
- Not diagnostic, used to triage referral of sudden visual loss effectively
Can be used when px presents with reduction/loss of vision
Useful in determining if pre- or post-chiasmal or if anterior or posterior within eye
What are the causes of visual loss (& what is the mnemonic)?
- V - Vascular – e.g. CRAO or CRVO
- I – Inflammatory – e.g. posterior uveitis and panuveitis
- T - Trauma – e.g. blunt, penetrating or perforating trauma that results in commmotio retinae, choroidal rupture or retinal detachment
- A - Autoimmune – e.g. Behcet’s Autoimmune disease which causes posterior uveitis/pan uveitis resulting in vitritis & choroiditis
- M – Metabolic – e.g. diabetes which causes ocular complications including diabetic maculopathy and vitreous haemorrhage
- I – Infection – e.g. microbial keratitis
- N - Neoplastic – e.g. tumour can compress structures at some points along visual pathway
- C - Congenital – e.g. Leber’s hereditary optic neuropathy
What are the most important tests to investigate sudden visual loss (depending on px and clinical judgement)?
- Tailored History
o How sudden is sudden? Find out exactly when it happened, is it truly an acute presentation?
o Did they notice their vision has very suddenly deteriorated over a few minutes? Or has it been days (indicating more sub-acute presentation)? - Slit Lamp Assessment – will help exclude any anterior causes and will help look for signs indicative of pathology within structures of eye
- Visual Acuity – will help isolate where in the visual pathway is affected
o Use pinhole acuity if px not have glasses with them or if you suspect their refraction may have changed since the last time - Visual Fields – much better idea of location of the abnormality
o Is it monocular or binocular?
Monocular indicates pre-chiasmal – affecting retina or optic nerve
Binocular indicates chiasmal or post-chiasmal - Pupils
o RAPD indicates an intraocular asymmetry in visual input – caused by abnormality affecting optic nerve or RNFL
o Would not expect to get RAPD in a post-chiasmal defect as this would affect both eyes and not result in asymmetrical visual input - Eye movements
o Pain on eye movements can be indicative of optic neuritis - Dilated Fundoscopy
o One of most important tests to carry out – give careful attention to structures in retina and optic nerve to solidify diagnosis
o Also do Fundus photography & OCT – allows direct comparison between clinical appearance that day and appearance on previous visits & also help to document findings
What are the symptoms and signs of CRAO?
- Symptoms
o Sudden painless monocular loss in vision – affects all areas of visual field if CRAO - Signs
o Profound RAPD present (amaurotic pupil – pupil completely unresponsive to light entering that eye)
o Emboli? – look for Hollenhurst plaque – yellow plaque – look for it as central retinal artery leaves the disc – can be difficult to see these at the disc as they are similar colour to disc
May see these plaques in BRAO at the bifurnication of the arteries
Can get other plaques too – fibrinoplatelet ones (more whitish/greyish in colour)
o Whitish, oedematous retina – varies depending on how long the CRAO has been present and may not see a v obvious white retina in a new CRAO
o Cherry red spot (if established) – in contrast to white, oedematous retina – not that there is much change to colour of fovea itself
o Disc pallor
o Retinal vasculature narrowing
Check if they have has recent signs of TIA/Stroke – explore symptoms of stroke with the patient
Ask about arterial fibrillation – px more at risk of developing an emboli – most common place these emboli are derived from is carotid artery, sclerotic plaque – a bit breaks off and this emboli moves along. Central retinal artery is the first artery from the carotid artery so CRAO common.
Ask about other risk factors e.g. smoking
Red free image can show cherry red spot
What is the management of CRAO?
Management:
* College CMG - CRAO if less than 12 hours old same day referral to ophthalmology. Greater Glasgow - CRAO if less than 24 hours old same day referral to ophthalmology
* Initiate Ocular Massage whilst patient lies supine in new cases – this should allow blood supply to reoccur through central retinal artery
EMERGENCY SAME DAY REFERAL – these pxs are at high risk of stroke
Management by ophthalmology:
* Systemic Acetazolamide – to reduce IOP
* Intra-arterial fibrinolytic therapy
* Aspirin – antiplatelet properties
* Follow up to detect neovascular changes
* Dietary advice, smoking cessation, managing blood pressure
Ask about sxs of TIAs to see if they’ve had one in the days leading up to this
* Ocular Massage dilates the ophthalmic and retinal arteries, can cause a thrombus to disintegrate and may cause an impacted emboli to move to a more peripheral part of retinal circulation, and reduces the IOP
* CRVO if elevated IOPS refer within a week, if IOPS over 40 refer same day
* Patients will be referred by ophthalmology for a stroke work up
What are the symptoms and signs of BRAO?
- Symptoms
o Sudden painless monocular drop in vision…. However vision is often unaffected
o Depends which artery has been affected to whether there will be any vision loss – if it is a branch that supports the macula then will have a drop in vision - Signs
o RAPD often present – depends on severity and how much of retina affected
o Emboli at bifurnication points
o Whitish, oedematous sector of retina
o Retinal vasculature narrowing in area supplied by the affected branch
o Altitudinal or sectoral visual field defect – if left untreated then can become permanent
Embolic BRVO - symptoms and signs often more subtle than CRAO
Neovascular glaucoma can also occur as a result of CRAO
What is the management of BRAO?
Management:
* College CMG - CRAO if less than 12 hours old same day referral to ophthalmology. Greater Glasgow - CRAO if less than 24 hours old same day referral to ophthalmology
* Initiate Ocular Massage whilst patient lies supine in new cases
Consult with local health board to see if the px needs a same day referral or not
Management by ophthalmology:
* Acetazolamide
* Intra-arterial fibrinolytic therapy
* Aspirin - antiplatelet properties
* Follow up to detect neovascular changes
* Dietary advice, smoking cessation, managing blood pressure
* Referred by ophthalmology for stroke work up
These pxs must have the necessary systemic follow ups – so phone ophthalmology to determine how to refer
What are the symptoms and signs of RVO?
- V variable presentation – depends on where the thrombus has occurred
- Thrombus in the CRV or a branch of the CRV – blood clot blocking
- Atherosclerotic aetiology
- Common associations – hypertension, older age, hyperlipidaemia, diabetes, glaucoma, contraceptive pill, smoking
Relatively common
Can result in neovascular glaucoma due to ischaemia – most common in CRAO or CRVO
Signs: - Variable presentation – blurred vision, metamorphopsia, visual loss
o If thrombus has occurred right at beginning of Central Retinal Vein and thus affecting all of the venous system then will get much more significant visual loss
o Poorer prognosis is vision worse on presentation and neovascularisation more likely as a late stage consequence
Also risk of neovascular glaucoma
o If branch retinal vein occlusion – severity depends on where it has lodged
If lodged at junction between artery & vein in far periphery then may not be any visual symptoms
If lodged at more central junction then may have blurred vision and metamorphopsia - Dilation and tortuosity of retinal veins
- Blot and flame haemorrhages
o In affected area if branch – or all over if central retinal vein occlusion - Cotton wool spots and retina oedema
- CMO – these pxs would benefit from tx
- Retinal whitening – laterally as time goes on – with ischaemic changes especially in CRVO
- Disc oedema – more severe cases
- RAPD only in ischaemic CRVO
- Secondary changes e.g. neovascularisation
What is the optometric management and optometrist referral for RVO?
Optometric Management:
* BRVO 5-6 x more common than CRVO
o Needs seen at ophthalmology & tends to be followed up due to risk of secondary complications
* Referral urgency depends on presentation
* If CMO present secondary to BRVO/CRVO then intravitreal anti-vegf will generally be given so referral urgency is usually within 1-2 weeks
* Not as worried about stroke in this case – more so in artery occlusion
o But linkages between all the risk factors – so these pxs should have a blood work up – to look for the risk factors
* Lothian guidelines - (only ones could find)
o Any Branch retinal vein occlusion (BRVO) with a reduction in vision (i.e. cystoid macular oedema present) should be referred to PAEP ARC clinic for review in 1-2 weeks and possible listing for treatment with intra-vitreal anti-VEGF (lucentis)
o Any BRVO with no reduction in vision (i.e. no CMO) should be referred routinely to PAEP outpatients and should be advised to attend their GP within 1-2 weeks for BP check and routine blood tests.
o Routine investigations include: FBC, Electrolytes, Cholesterol/Lipids, Glucose and LFTs.
Optometrist Referral:
* Patients should be referred urgently to a TIA clinic for review within 48hrs if they present with the following symptoms
o Amaurosis Fugax of sudden onset within 2 weeks, with no headache or associated pain and no ocular pathology/abnormality present
o Sudden onset previously undiagnosed visual field total scotoma of less than 2 weeks with no ocular pathology (i.e. homonymous hemianopia or quadrantopia)
* To refer to a TIA clinic there is a direct phone number available 24 hours a day 7 days a week
What are the differential diagnosis for Retinal Detachment?
- Differential Diagnosis
o Posterior Vitreous Detachment
o Retinoschisis Choroidal Mass
MUST LOOK FOR SHAFFERS SIGN - PVD - look for a weiss ring, carefully examine all peripheral retina to exclude a retinal tear occurring as a result of a PVD
- Retinoschisis - no symptoms common in hyperopia, benign splitting of neurosensory retina at the level of the outer plexiform layer - OCT can be handy here to determine where the splitting of the retina has occurred
o No retinal break generally
o Tends to occur inferior-temporal peripheral area
o Usually bilateral
o Quite common
o Leads to loss of visual function in this area but as peripheral rarely noticed. Inferior-temporal generally bilateral dome shaped elevation 5% of the population
o Not an eye emergency if found – not usually sight-threatening observe the px and make sure doesn’t change over time
o More longstanding retinoschisis – dome shaped elevation in periphery – more longstanding, some changes in the colour of the vasculature – no retinal tears or breaks within it - Choroidal masses can be distinguished from retinal detachment by observing the characteristics of imaging with ultrasound.
o Urgent referral if thought it was choroidal melanoma – that was causing the retinal detachment
What signs can help you differentiate between retinal detachment and other conditions?
Look to see if bilateral more likely retinoschisis – especially if dome shaped and cannot find a break
Look for Schaffers Signs if see this then v indicative of retinal detachment – will not see Schaffers Sign in retinoschisis – pigmented particles in anterior vitreous is very subtle – check once dilated px – even if still cannot find retinal break/detachment but see Schaffers Sign then refer urgently anyway
Shaffers Sign – not seen in PVD but is seen in retinal detachment
Shifting fluid – ask px to move their eyes – if see fluid moving within retina then more likely retinal detachment
What is the management of retinal detachment?
- Emergency referral – same day
o Retinal detachment
o Pigment in the anterior vitreous (tobacco dust)
o Vitreous, retinal or pre-retinal haemorrhage, or
o Lattice degeneration or retinal break, with symptoms
The majority of patients presenting with flashes and/or floaters will not have a retinal detachment. If you do not feel competent to manage a patient presenting with flashes and/or floaters you should refer them to an appropriate colleague.
What should be emergency referred (relating to retinal detachment)?
- retinal detachment
- pigment in the anterior vitreous (tobacco dust)
- vitreous, retinal or pre-retinal haemorrhage, or
- lattice degeneration or retinal break, with symptoms.
It should be noted that a retinal hole or tear does not always lead to retinal detachment. You should refer the patient, however, if the patient is having relevant symptoms and any of the signs in para above are present.
Describe vitreous haemorrhage: symptoms and signs and types?
- A sign of another pathology – is not in itself a diagnosis
- Symptoms:
o Painless, unilateral floaters and variable vision loss - Signs:
o Depend on aetiology: Dilated fundus exam important, including of the other eye, gonioscopy, visual fields
May not be able to view retinal structures – then very important to look at other eye as may give a clue as to what has caused the vitreous haemorrhage – e.g. is there proliferative/diabetic changes in other eye. If retinal detachment then may not see signs in other eye but hx v important e.g. high myopia? Trauma? Diabetic?
Gonioscopy – especially if vitreous haemorrhage is not new then px at risk of developing rubeotic glaucoma – do gonio to exclude that
VFs – will mirror what see – may have mild superior VF defect is sub-hyaloid haemorrhage as all blood has settled in inferior sub-hyaloid cavity - If dispersed vitreous haemorrhage then may have extensive VF loss
o Appearance is very variable
o Should be able to see red blood cells in anterior vitreous
o May have:
Sub-hyaloid pre-retinal vitreous haemorrhage – where blood has settled in sub-hyaloid space – boat-shaped haemorrhage – settles inferiorly in posterior chamber
Dispersed vitreous haemorrhage – dispersed throughout vitreous
What are the mechanisms of vitreous haemorrhage?
- Abnormal Vessels:
o Diabetic retinopathy (specifically proliferative with neovasc) (31–54%) of vitreous haemorrhages are caused by diabetes
o Neovascularization from branch or central retinal vein occlusion (4–16%)
o Sickle cell retinopathy (0.2–6%) - Rupture of Normal Vessels:
o Retinal tear (11–44%)
o Trauma (12–19%)
o Posterior vitreous detachment with retinal vascular tear (4–12%)
o Retinal detachment (7–10%)
o Terson’s syndrome (0.5–1%) - Blood From Adjacent Source
o Macroaneurysm (0.6–7%)
o Age-related macular degeneration (0.6–4%) - All of these conditions need seen on emergency/urgent basis – to have full investigations and rule out rubeotic glaucoma
