Unit 6 ocular disease Flashcards
DR risk factors
Type 1 more common (40%), Type 2 (20%)
Duration of Disease
Before 30yrs – 50% risk after 10 years
After 30yrs – 90% risk after 10 years
Poor Metabolic Control
Pregnancy
Hypertension (most will have both conditions)
Obesity
what is hypertension
Hypertension is a medical condition where the pressure inside the arteries is persistently elevated
The initial response of retinal arterioles to systemic hypertension is vasoconstriction
Prolonged HBP can lead to hardening of vessel walls, AV nipping and eventually increased vascular permeability
hypertensive retinopathy grading
Grade 1 – arteriolar narrowing – 2:1 - GP
Grade 2 – arteriolar narrowing / nipping – 1:3 - GP
Grade 3 – narrowing, nipping, haemorrhages, exudates and Cotton wool spots – HES
Grade 4 – narrowing, haems, exudates, Cotton wool spots, disc swelling, macular star - HES
in severe cases swollen disc, macular oedema as well
CRAO
Sudden painless monocular loss in vision
VA < CF, complete loss – generally all areas of the VF (Unless a cilioretinal artery supplying a critical macular area preserves vision)
RAPD
White, oedematous retina; cherry ret spot at fovea; Attenuation of arteries and vein
Referral emergency same day if <24hrs
Urgent if >24hrs
BRAO
Sudden painless altitudinal or sectoral visual field loss; vision may be unaffected
Signs confined to the region of the retina supplied by the affected branch
VA is variable; RAPD often present
Fundus signs may be subtle; whiteish, oedematous SECTOR of the retina (area of ischaemia)
Altitudinal or sectoral VF defect – which may become permanent if left untreated
ischaemic CRVO
- VA poor
- RAPD
- Dilation/tortuosity, flame shaped & dot-blot haem, cotton wool spots
Rubeosis develops in 50% of eyes – 100 day glaucoma, new vessels at disc and elsewhere - poss vitreous haem as complication
Macula may develop atrophic retinal and RPE changes, ERM and chronic CMO
Urgent referral to HES (same day referral to GP for blood workup)
Emergency referral if IOPs > 40mmHg
ACE inhibitors - Lisinopril & ramipril side effect
may cause ciliary body oedema which leads to reduced accommodation and angle closure
hyperthyroidism
Thyroid eye disease / Graves
WET phase (myogenic) - EOMs (recti; IR affected first) swell up to 8-10x normal size (2-3 years)
DRY phase (mechanical) - Fibrosis & secondary muscle contracture
Connective tissue inflammation; redness, discomfort, peri-orbital swelling
Corneal exposure; gritty/redness
Diplopia and proptosis
May cause visual loss due to ONH compression
Marfans syndrome
Autosomal dominant connective tissue disorder
Tall, thin stature with long limbs
Myopia, corneal abnormalities, ectopia lentis – dislocation of lens, retinal detachment
rheumatoid arthritis
Dry eye disease / Sjogrens syndrome
Iritis – 2nd episode; refer for systemic work up
Episcleritis / scleritis – refer for systemic work up at 3rd episode
multiple sclerosis
Demyelinating disease affecting CNS
Optic neuritis; mostly commonly retrobulbar
ocular manifestations of high cholesterol
o Arcus
o Xanthalesma
o Retinal emboli – Hollenhorst plaque
o CRAO
o CRVO
what is the primary response of the retinal arterioles to systemic HBP?
HBP is vasoconstriction
* Arteriolosclerosis refers to hardening and loss of elasticity of small vessel walls
o Manifested most obviously by AV nipping at crossing points
o Mild AV changes may be seen in the absence of HBP
* In sustained HBP the inner blood-retinal barrier is disrupted, increased vascular permeability leading to flame-shaped haemorrhages and oedema
* Increased venular tortuosity can be associated with chronic hypertension and pre-hypertension, though evidence on tortuosity is conflicting
* CRVO
Ankylosing Spondylitis
ocular manifestations
o Acute anterior uveitis, occurs in about 25% of pxs
o Episcleritis
o Scleritis
o Keratitis
o Mechanical ptosis
o Cataract
asthma ocular manifestations
o Dry eye
o Cataract
o Glaucoma
o CSR – due to steroid inhalers
RVO risk factors
o Increasing age (>65)
o HBP
o Hyperlipidaemia
o Diabetes
o Glaucoma
o Oral contraceptive pill
o Smoking
CRAO cause
Central retinal artery occlusion (CRAO) is caused by a blockage in the central retinal artery, usually by a blood clot or cholesterol deposit
what is non ischaemic CRVO
Where the outer retinal layers are still perfused as choroidal circulation remains
intact
* 30% will progress onto ischaemic
Sudden onset, unilateral blurred vision (6/36-6/60). Main concern: conversion to ischaemic
Signs
* Tortuous dilated veins in all 4 quadrants of the retina
* Round/Blot and flame haemorrhages
* Occasional CWS
* Mild Possible macula and disc oedema
* Mild/absent RAPD
residual signs of cRVO
- Disc collaterals
- Epiretinal Gliosis
- Pigmentary changes at the macula
Tx CRVO
Treatment – Laser PRP for neovascularisation, Intravitreal Anti-VEGF and steroids for
neovascularisation and macula oedema
Investigation – Investigate underlying cause and blood work up. Assess whether
ischaemic or non-ischaemic.
risk factors CRAO
Aged 70-80yrs
* Carotid artery occlusive disease
* systemic hypertension
* high cholesterol
* smoking
* diabetes
* history of stroke or TIA
* Amaurosis Fugax attack (sudden blanking of vision lasting a few seconds)
sudden painless loss of vision
later developments of CRAO
- Atrophy of inner retinal layers and optic nerve
- Neovascularisation at the disc and iris
- Vessels remain attenuated and cherry red spot reduces over weeks
management CRAO
- Massage the globe with px laying down
- REBREATHE CO2.
- Nd-YAG laser of embolus if visible
- Acetazolamide (Carbonic Anhydrase inhibitors): Decreases IOP by decreasing
Aqueous Humour production - Sublingual Isosorbide dinitrate: Causes vasodilation, can help move a clot
- Anti-coagulants (e.g. Warfarin) as risk of stroke/ischaemic heart disease is high.
symptoms of TIA
- Weakness
- Numbness down one side of body
- Vertigo
- Diplopia
- Slurred speech and loss of balance/co-ordination
- Transient vision loss (amaurosis fugax):
o Curtain coming down on vision, can be total or sectorial, resolves
completely (centrally first)
o Most common cause: embolism
o High risk of impending CRAO or vision loss through AION.
Urgent referral to GP and Ophthalmology for MRI and bloods.
AAION symptoms
- Sudden unilateral vision loss
- Preceeding amaurosis fugax
- Possible periocular pain
- Headache, neck or temple pain
- Scalp tenderness
- Jaw claudication
- Weight loss
- Fatigue
- Muscle pain/stiffness
- Protruding temporal artery – pulseless, tender, doesn’t compress
signs AAION
Signs
* VA <6/60
* RAPD
* Swollen optic disc
* Possible CWS
* Possible flame haemorrhages
* Arcuate VF defect
AAION can also lead to:
* CRAO
* 3rd and 4th nerve palsy
what is NAION
Infarction of the optic nerve head due to PCA occlusion as a result of atherosclerosis. No
preceding amaurosis fugax.
Can be due to:
* hypertension
* diabetes
* heart disease
* carotid artery disease
signs of NAION
Signs:
* Normal – severe reduction in VA
* RAPD
* Dyschromatopsia
* Altitudinal VF defect
* ONH signs:
o Diffuse or sectorial oedema
o Pale or mild hyperaemia
o Possible flame haemorrhages
Emergency referral
Cataract cause
Cataract – Caused by denaturation of protein fibrils within the lens due to oxidative
stress, increasing age and metabolic disturbance
causes of posterior subcapuslar
Diabetes
* High Myopia
* Steroids
* Age
* Male
* Thyroid Hormone Use
OCT scan layers
ERM cause and tx
causes:
pvd, surgery, retinal conditions like DR, RD, inflammation
tx - vitrectomy
An epiretinal membrane is a thin sheet of fibrous tissue that develops on the surface of the macula and can cause problems with central vision.
anatomy of aqueous humour
IOP is the fluid pressure inside the eye which gives structural integrity & support to refractive structures and intraocular contents
IOP is determined by the balance of secretion and drainage of aqueous humour
Aqueous humour is produced in the ciliary body (2-3 microlitres per minute) and secreted into the posterior chamber
Posterior chamber is between the anterior lens surface and posterior iris surface
The aqueous humour travels between the iris and lens into the anterior chamber via the pupil
It then drains from the AC via the trabecular meshwork into Schlemm’s canal situated in the anterior chamber angle
Schlemm’ s canal situated in the anterior chamber angle and drains into the episcleral circulation
peripheral iridotomy
A hole created to allow drainage of aqueous humour through a different channel,
allowing for the push back of the iris that may lead to iris bombe/anterior synechiae
and ultimately pupil block in ACG. Normally used for ACG or those with narrow
angles.
selective Laser trabeculoplasty (SLT)
Laser triggers the regeneration of cells in the trabecular meshwork to increase and
improve the outflow of aqueous humour in patients with OAG. Lowers IOP by
approx. 30%. Procedure can be repeated as it wears off over time.
Trabeculectomy
A bleb is created, usually at the superior part of the sclera to allow fluid to drain out
into the sub-conjunctival space. After reaching this part, it either filters into the
tearfilm, get absorbed by vascular or perivascular conjunctival tissue or through
lymphatic vessels to be drained through aqueous veins
Filtration tubes/aqueous shunt
In cases where other treatment methods have not worked. The tube creates a new
channel for aqueous humour to drain out underneath the conjunctiva. A bleb is also
created
pathogenesis of DR
- Damage to the endothelium
- Loss of pericytes)
- Breakdown of blood-retinal barrier
- Thickening of capillary basement membrane
- VEGF release
what are Flame Haemorrhages:
Flame Haemorrhages: originate from pre-capillary arterioles in the nerve fibre layer.
what are dot blot haemorrhages
: arise from the venous end of capillaries (aka. Intra-retinal haemorrhage) in the Inner Plexiform and Inner nuclear layer.
what are exudates
: Lipid laden neuronal breakdown products that have left leaky vessels with the
blood plasma and accumulate in the outer plexiform layer
what are cotton wool spots
accumulations of neuronal debris within the nerve fibre layer as a
result of interruption of normal axoplasmic flow. This debris accumulates in the ganglion
cell nerve axons.
what are microaneurysms
Weakening of the capillary walls due to a loss of pericytes resulting in
an outpouching (typically in the INL)
why doess venous beading happen
assoicated with ischaemia
why do drusen happen
Abnormal deposits of lipid material generated by the photoreceptors that
accumulate between the RPE and Bruch’s.
risk factors DR
- Longer Duration of Diabetes
- Poor glycaemic control
- Pregnancy
- Smoking
- High Blood Pressure
- High Blood Sugar
- High Cholesterol
- Black, Native American or Hispanic Ancestry
treatments - steroid injection
Dexamethasone or iLuven (Fluocinolone) (steroid) injections for Diabetic Macula Oedema: Steroids reduce the inflammation of vessels which causes the
breakdown of capillaries and pericyte loss
types of secondary glaucoma
Pseudoexfoliation (open angle)
o PXF = grey-white fibrillary amyloid-material
o Symptoms worsen following exercise
Pigment dispersion (open angle)
o Young, white, myopic males
o Pigment is deposited on corneal endothelium Krukenberg spindle
Hyphaemia (open angle)
o Blood in AC caused by trauma
Phacomorphic (closed angle)
o Lens size increases and blocks drainage
Rubeosis iridis may lead to neovascular glaucoma
o Pxs with ischaemic CRVO / DR are at risk of developing this
o Iris forms membrane onto TM and new vessels grow within the angle
sign guidelines referral
Glaucoma (SIGN GUIDELINES) for routine referral
Optic disc signs consistent with glaucoma
Reproduceable VF defect in either eye
Risk of angle closure (VG G1 / gonio > 270deg TM not visible)
OHT IOP >25mmHg, irrespective of CCT
OHT - IOP <26mmHg and CCT <555
o OHT meaning IOP >21mmHg
Emergency / same day for IOP >40mmHg / red eye / angle closure
DR grading
R0 – no retinopathy
R1 – mild background retinopathy
At least one of the following features anywhere: dot haemorrhage, cotton wool spot, blot haemorrhage, flame shaped haemorrhage
Rescreen in 12 months for DRS
R2 – moderate background
4 or more haemorrhages in one hemi-field only
Rescreen in 6 months
R3 – severe background / pre-proliferative
4 or more haems
Venous beading / IRMA routine referral
R4 – proliferative
Active new vessels
Pre-retinal haemorrhage
Retinal neovasc NVD, NVE
urgent referral
M0 – no maculopathy
M1 – early
Exudates >1 but <2DD from fovea
M2 – advanced
Haemorrhages or exudates within 1DD from fovea
urgent referral
Emergency referral
- Pre-retinal haemorrhage
- Traction retinal detachment
- Rubeosis
risks for different races
Caucasian = ARMD
Afro – Caribbean = Glaucoma (POAG)
South East Asian (Chinese) = Glaucoma (PCAG)*
Japanese = Normal Tension Glaucoma (NTG)
Asian = Diabetes/HBP
what type of glaucoma are myopes at a greater risk of
what type of glaucoma are hyperopes at a greater risk of
High Myopia = POAG and RDs
High Hyperopia = PCAG
hydroxycholoquine ocular risks
Hydroxychloroquine
Decreases pain/swelling of arthritis and prevention of joint damage
Used for RA, Lupus, other autoimmune diseases
Risks:
Usually pxs on long term treatment
Drug is slowly secreted and becomes concentrated in melanin structures (choroid/RPE)
Bulls Eye Maculopathy and central scotomas (detected best with Red Amsler)
ocular ADRs for
- amitrptyline
- steroids
- warfarin
- chlorpromazine
- amiodarone
Amitrptyline :
Antidepressants
Reduced Accommodation
Steroids :
Anti-inflammatory & Immunosuppressive
PSCC
Glaucoma
Increased IOPs
Warfarin :
Anti- Coagulant
Subconj Haemorrhage
Chlorpromazine :
Sedative for psychotic illness
Yellow/brown deposits on endothelium and anterior lens
Pigmentary changes and clumping at Retinal Layers
Amiodarone :
Anti-Arrhythemia Drug
Vortex Keratopathy
Optic Neuropathy
Subcapsular deposits
