retinovascular document part 2

risk factors of central and branch retinal artery occlusions

• advancing age

• diabetes

• smoking

• high cholesterol levels

• cardiac disease

pathophysiology of central and branch retinal artery occlusions

sudden and often total obstructions to the retinal blood flow

the main cause is atheroma( build up of fatty deposits

what is this caused by

transient(short lasting) obstruction of retinal artery e.g embolus position may change and vary with blood flow

or

degree of inflammation may vary so diameter of artery varies

what does this cause

transient retinal ischemia which then leads to amourosis fugax

is amourosis fugax severe

yes it usually affects the whole visual field and lasts at least 7 minutes, usually resolves within the hour

if symptoms last more than an hour it means permanent vision loss

what may the patient describe

vision going back, grey or dim

depending on artery affected patient may describe the darkness spreading across the visual field at once

what is the main cause of amarosis fugax

acute retinal ischemia induced by carotid artery disease with secondary emboli causing blockage

are there any other causes

• papillodema

• migraine

what should we ask if we suspect amaurosis fugax symptoms

common symptoms of stroke/TIA: - down need to memorise just general awareness

• HA- sudden , severe, unusal, associated with stiff neck

• confusion

• weakness

• sensory loss

• speech problems

• dizziness

• nausea

• specific cranial nerve deficits(ptosis,miosis,facial anhidrosis

• difficulty with fine motor coordination

• neck or facial pain

we must check for FAST (what is this)

danger signs

f- Face, can the person smile/ has face fallen to one side

A- arms - can they raise both and keep them there

S- speech problems-

T- time- if you see any of these signs - call 999

what else should we check for 

double vision

homonymous Vf defects(suggest post chiasmal damage)

clinical signs of arterial occlusion

• poor VA

• pupil defect - +ve RAPD

• CRAO produce striking whitened opaque and cloudy appearance in fundus

• narrowing of blood vessels

• cherry red spot at central macula( CRAO characteristic sign)

cilioretinal artery

15%- 50% of population have this additional blood supply

if they get cRAO the central retinal artery maintains normal colour due to this.

may maintain VA reaso

what this and how do you know

CRAO- generalised arteriole narrowing and pale fundus

cherry red spot at macula

what this and how do you know

BRAO- only superior branch has become occluded

area of pallor is confined to this hemisphere

no cherry red spot at macula( however it is possible )

what this and how do you know

CRAO - blood flow within the retinal area between optic disc and macula is preserved

differential diagnosis

small percentage of CRAO can be attritable to Giant cell arteritis

what are distinguishing features of GCA

pain

diploipia

jaw claudication

fever

management of CRAO and BRAO

prolonged ischemia leads to infarction( irreversible cell death)

so retina cannot withstand without oxygen for very long so unless obstruction is removed within 4 hrs and under 24 hr period vision restoration is limited

management techniques

• ocular massage on closed lid- 15 minutes- help blood flow

• px breath into paper bag- elevates blood CO2 which increases vasodilation

• refer immediately for any symptoms of severe vision loss

what should you do if amaurosis fugax symptoms identified but no abnormalities idenitified

refer to GP instead of ophthalmologist because otherwise it will delay stroke investigation- should see within 24 hrs

what does the ophthalmologist do

monitor for neovascularisation - so it can remove the stimulus to new vessel growth by destroying the damaged retinal tissue

risk factors Central and Branch Vein occlusions

• age

• cardiovascular risk factors (hypertension, obesity, hyperlipidemia, diabetes, glaucoma)

pathophysiology of CRVO 

• arteriosclerosis- thickening of wall leads to vein compression- forms thrombus then occlusion

pathophysiology of BRVO

always occur at A/V crossings

60% along the superotemproal retina

what this and how do you know

BRVO- haemorrhaging confined to superotemporal arcade

yellow deposits originating in macular are hard exudates in fan pattern- indicates fluid leaked from occluded vein has been reabsorbed

this means occlusion has started some time ago

why is it mostly in the superotemporal region

highest concentration of A/V Crossings are here

what does the A/V crossing look like

In BRVO most;y arteries crossing over vein- which means the vein is getting compressed

why might retinal haemorrhaging or oedema occur

venous occlusion disrupts drainage of blood and increases the pressure, pressure is passed backwards from retinal vein via venues to capillaries which may rupture 

what does the occlusion also cause

chronic ischemia- if prolonged it leads to permanent vision loss

what’s the difference with ischemia in artery and vein occlusions

in artery occlusions retinal schema arises as a direct result of the occlusion but in vein occlusion it arises secondary to issues that occur due to the occlusion and and the impeded retinal drainage

what its the structure of arteriolar and venue capillaries 

arteries narrow progressively before becoming wider and turning into veins

what does this mean for ischemia 

drainage failure in wider diameter veins leads to increased intraluminal pressure(build up of pressure upstream from site of occlusion)

this pressure causes blood products(haemorrhaging,lipids,proteinplasma) transfer through vessel wall

this then impedes the outflow of blood which is oxygenated from arteriolar walls=ischemia

how long does this take

it takes time to develop days/weeks/months

that’s why vein occlusion is not classed as ischemic

is artery occlusion classed as ischemic

yes , acute severe ischemia leading to rapid infarction

CVRO symptoms

sudden, painless, monocular vision loss

BRVO symtoms

altitudinal or sectoral VF loss

if they have peripheral BRVO may be asymptomatic

Non ischemic CRVO signs

• dot/blot/flame haemorrhaging all over

• dilated and tortuous veins

• VA varies 6/30 to 6/60

• pupil reactions normal - may have mild RAPD

• cotton wool spots not common

management of vein occlusions

both central and branch require opthalmolagist HES referral sooner than routine

what time line of referrals 

BRVO- good vision= 4-6 weeks

BRVO - poor vision(6/12 or worse)- 2-3 weeks

all CRVO- less than 2 weeks

why do we not do routine referrals for vein occlusions

in all cases via the GP is too slow

national guidance sta