Special Senses Flashcards
What should IOP (intraocular pressure) be?
11-21 mmHg
How is IOP measured
with a tonometer
force needed to flatten the corneal surface
What is ocular HTN
raised IOP (>21mmHg) without developing the changes of glaucoma.
define the anterior chamber of the eye
between the iris and the cornea’s innermost surface, the endothelium.
How is aqueous humour made
produced by the ciliary bodies
Describe the passage of aqueous humour through the anterior chamber
made in ciliary body passes posterior to iris, anterior to the lens, and then through pupil flows out via trabecular meshwork then canal of Schlemm then episcleral vessels then systemic venous circulation
also the uveoscleral route:
instead drains into root of iris/ciliary muscle before draining into scleral vascular system
What is acute angle closure glaucoma
there is a junction between the iris and cornea at the periphery of the anterior chamber = the anterior chamber angle.
the iris can become apposed to the trabecular meshwork and so block off the aqueous drainage.
What is the difference between primary and secondary angle closure glaucoma
primary = as a consequence of the anatomy of the eye: some people’s angles are naturally very narrow which makes the angle more vulnerable to blocking off. Severe hypermetropes, advanced age, asian
secondary = as a result of forces exerted on the iris either anteriorly or posteriorly (eg, the lens bulging forward as a result of swelling) or blockage, as a result of the trabecular meshwork being blocked by matter such as blood (from a hyphaema), blood vessels (from poorly controlled advanced diabetic eye disease) or proteins (as seen in hypertensive uveitis).
Describe the control of aqueous humour production
autonomic - adrenergic
alpha 2 - stimulation reduces aqueous production and increases uveoscleral outflow, leading to fall in IOP
beta 2 - stimulation increases aqueous producion adn therefore increases IOP
What are the symptoms of acute angle closure glaucoma
Pain - this is severe and rapidly progressive.
Blurred vision (rapidly progressing to visual loss).
Coloured haloes around lights.
N+V
What situations can precipitate acute angle closure? Why?
during a moment of stress or excitement,
whilst watching TV in dim lighting conditions
after topical mydriatics or systemic anticholinergics.
due to pupillary block. - The mid-dilated pupil snags on to the lens, so causing a build-up of aqueous beneath it which further pushes the iris forward, so eventually blocking off the trabecular meshwork.
Give some signs of acute angle closure glaucoma
generally unwell.
red eye - more marked around the periphery of the cornea.
There is a hazy cornea
non-reactive (or minimally reactive) mid-dilated pupil.
Globe hard on palpation
What is the diagnostic criteria for angle closure glaucoma
History of at least 2 of:
Ocular pain.
Nausea/vomiting.
History of intermittent blurring of vision with haloes
AND
at least three of the following signs:
IOP greater than 21 mm Hg (clinically this can mean a stony hard pupil).
Conjunctival injection.
Corneal epithelial oedema.
Mid-dilated non-reactive pupil.
Shallow chamber in the presence of occlusion.
How is angle closure glaucoma managed pharmacologically
give all topical glaucoma medications that are not contra-indicated in the patient, together with intravenous acetazolamide. Patients are lain supine.
Topical agents inlude:
Beta-blockers - eg, timolol, cautioned in asthma.
Steroids - prednisolone 15 every 15 minutes for an hour, then hourly.
Pilocarpine 1-2% (in patients with their natural lens).
Phenylephrine 2.5% (in patients who do not have their own lens).
Acetazolamide is given intravenously (500 mg over 10 minutes) and a further 250 mg slow-release tablet after one hour - check for sulfonamide allergy and sickle cell disease/trait.
Offer systemic analgesia ± antiemetics.
Describe the mechanism of action of beta blockers on the eye eg. timolol
reduce production of aqueous by ciliary body
Describe the mechanism of action of alpha agonists on the eye eg. apraclonidine
reduced production of aqueous by ciliary body
increased outflow via uveoscleral tract
Describe the mechanism of action of prostaglandin analogues on the eye eg. latanoprost
increase uveoscleral outflow
Describe the mechanism of action of carbonic anhydrase inhibitors on the eye eg. acetazolamide
decrease production aqueous
Describe the mechanism of action of parasympathomimetics on the eye eg. pilocarpine
increases outflow of aqueous by ciliary muscle contraction, opening trabecular network
How is angle closure glaucoma managed surgically
Peripheral iridotomy (PI) - this refers to (usually two) holes made in each iris with a laser, usually at around the 11 and 2 o’clock positions. This is to provide a free-flow transit passage for the aqueous. Both eyes are treated, as the fellow eye will be predisposed to an AAC attack too
Surgical iridectomy - this is carried out where PI is not possible.
Lensectomy - one of the few situations where cataract surgery is performed on an urgent basis is when the cataractous lens has swollen to precipitate an attack of AAC. The lens is extracted at the earliest opportunity.
Give some complications of angle closure glaucoma
permanent loss of vision,
repetition of the acute attack,
attack in the fellow eye
central retinal artery or vein occlusion
Give some risk factors for open angle glaucoma
age >65 Family history Race - it is three to four times more common in Afro-Caribbean people Ocular hypertension myopia (short-sightedness) retinal disease (eg, central retinal vein occlusion, retinal detachment and retinitis pigmentosa) Diabetes a systemic hypertension
Describe briefly the pathophysiology of open angle glaucoma
The primary problem in glaucoma is disease of the optic nerve.
there is a progressive loss of retinal ganglion cells and their axons. (optic neuropathy)
associated with a raised IOP
flow is reduced through the trabecular meshwork
How does open angle glaucoma present?
most people are asymptomatic, because initial visual loss is to peripheral vision and the field of vision is covered by the other eye,
patients do not notice visual loss until severe and permanent damage has occurred, often impacting on central (foveal) vision.
Open-angle glaucoma may be detected on checking the IOPs and visual fields of those with affected relatives.
Suspicion may arise if abnormal discs, IOPs or visual fields are noted.
How is the eye examined for potential open angle glaucoma
Gonioscopy - used to measure the angle between the cornea and the iris
Corneal thickness - this influences the IOP reading. If it is thicker than usual, it will take greater force to indent the cornea and an erroneously high reading will be obtained.
Tonometry
Optic disc examination - this is a direct marker of disease progression. Optic disc damage is assessed by looking at the cup:disc ratio: normal is 0.3, although it can be up to 0.7 in some normal people: Glaucoma is suggested by an increase in cupping with time, rather than by cupping alone.
Visual fields
Hoe is the cupping of the optic disc measured?
cup = bright bit in middle disc = dark bit around it
cup radius:disc radius
increased = more than 0.3
Do I need to inform the DVLA if my patient has glaucoma
The onus is on the patient to inform the DVLA (and it is important to document that you have advised them of this).
It is the DVLA (and approved opticians) who will assess the visual fields and decide whether a patient can continue to drive.
If you are concerned that the patient should not drive and has not told the DVLA (despite your clear advice to do so), it may be appropriate to inform the DVLA medical advisors
What treatments are available for open angle glaucoma
drugs to reduce IOP - beta blockers, alpha agonists, sympathomimetics, carbonic anhydrase inhibitors, miotics
laser - Argon laser trabeculoplasty (ALT) (lasering to the trabecular meshwork in the iridocorneal angle, so enhancing aqueous outflow), Selective laser trabeculoplasty (SLT)
surgery - trabeculectomy, artificial shunt, canaloplasty
What is AMD
age-related macular degeneration
changes, which occur in the central area of the retina (macula) in people aged 55 years and above.
without any other obvious precipitating cause,
What are the key findings on examination of the retina in AMD
drusen
dry - hypo/hyperpigmentation of RPE, geographic atropy
wet - neovascularisation
What are drusen
lipid and protein deposits beneath the RPE in AMD
How is the severity of AMD classified
No AMD: none or a few small drusen.
Early AMD: multiple small or a few intermediate drusen +/- abnormalities of the RPE.
Intermediate AMD: extensive intermediate or one or more large drusen +/- GA not involving the fovea.
Advanced AMD: GA involving the fovea +/- any features of wet AMD.
What are the risk factors for AMD
smoking
age
FH/genetics
cardiovascular
obesity
What are the symptoms of AMD
may be no symptoms at first if only one eye is affected! - other eye compensates
Painless deterioration or blurring of central vision, typically in a person aged 55 or more.
Metamorphopsia — distortion of vision, where straight lines (such as window blinds) appear crooked, wavy or bent.
Scotoma — the person may describe a black or grey patch affecting their central field of vision.
Light glare.
Loss of (or decreased) contrast sensitivity (the ability to discern between different shades).
Size or colour of objects appearing different with each eye.
Abnormal dark adaptation (difficulty adjusting from bright to dim lighting).
Photopsia — a perception of flickering or flashing lights.
Visual hallucinations (Charles Bonnet syndrome).
Give some differences in the presentation of dry and wet AMD
dry:
gradual visual deterioration
difficulty with reading, initially with the smallest sizes of print and then later with larger print.
wet:
visual deterioration can develop quickly.
central vision blurring and distortion
A person may suddenly become unable to read, drive, and see fine detail such as facial expressions and features.
Give some differentials for AMD
refractive error cataracts open angle glaucoma retinal detachment amaurosis fugax diabetic maculopathy
What investigations should be done in AMD
test visual acuity
Amsler grid - distortion
slit lamp
What management is needed for dry AMD
urgent referral within one week to specialist services
no specific treatment
stop smoking - reduces risk of progression
multivitamins if intermediate or advanced - reduces risk of progression
visual rehabilitation
treat other visual problems to make vision as good as possible
What management can be given for wet AMD. Why does it work and how is it given
anti-VEGF
VEGF acts as a proangiogenic growth factor and stimulates permeability of blood vessels
given by intravitreal injections one a month for 3 months. continued if beneficial
in most people it stops progression. in a few it even improves vision!
Give some examples of anti-VEGF meds
ranibizumab
aflibercept
What causes diabetic retinopathy
microvascular occlusion leads to retinal ischaemia. leads to formation of AV shunts and neovascularisation
leakage from vessels leads to intraretinal haemorrhage and oedema
What are the key features of DR on visualisation of the retina
Microaneurysms
Hard exudates - precipitates of lipoproteins
Haemorrhages
Cotton wool spots - build-up of axonal debris due to poor axonal metabolism at the margins of ischaemic infarcts.
Neovascularisation
Define the stages of diabetic retinopathy
Background (mild) non-proliferative DR: at least one microaneurysm.
Moderate non-proliferative DR: microaneurysms or intraretinal haemorrhages ± cotton wool spots, venous beading, intraretinal microvascular abnormalities (IRMAs).
Severe to very severe non-proliferative DR (sometimes referred to as pre-proliferative disease), as above: blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
Non-high-risk proliferative DR: new vessels on the disc (NVD) - or within one disc diameter of it or new vessels elsewhere (NVE).
High-risk proliferative DR: large NVD or NVE (defined by comparing to the optic disc surface area) or presence of pre-retinal haemorrhage. In advanced disease, there may also be an accompanying retinal detachment.
Define the stages of diabetic maculopathy
Focal or diffuse macular oedema: areas of leakage which may be well circumscribed or diffuse.
Ischaemic maculopathy: the clinical appearance may be relatively normal but the visual acuity has dropped and ischaemia is seen on fluorescein angiography.
Clinically significant macular oedema (CSMO): there may be thickening of the retina and hard exudates which, when found within a specific distance of the fovea or when found to be above a certain size, define CSMO.
What are the risk factors for DR
poor glycaemic control
HTN
renal disease
pregnancy - may cause fast progression
What might a patient with DR notice about their vision
asymptomatic
painless gradual deterioration of central vision
dark painless floaters - due to haemorrhages
How should a patient with DR be examined
acuity test
slit lamp
dilated fundal photographs
Describe the screening program for diabetic retinopathy
visual acuity and fundal photography at diagnosis of T1/T2DM
retested every year
starts at 12 years old
What symptoms in a patient with DR would require an emergency review?
Sudden loss of vision.
Rubeosis iridis (formation of abnormal blood vessels on the anterior iris).
Pre-retinal or vitreous haemorrhage.
Retinal detachment
State primary prevention methods for DR
glycaemic control - <7% blood pressure control <140/90 (<130 if DR established) lipid control smoking cessation balanced diet
When might treatment be offered in DR
no clear cut lines
proliferative or maculopathy can be offered treatment
What treatments are available for DR
laser treatment
intravitreal corticosteroids
anti-VEGF
surgery - vitrectomy if intravitreal bleed
What does laser treatment for DR help with
induces regression of new blood vessels
reduces central macular thickening
arrests progression, but does not restore sight
What are some causes of sudden painless loss of vision
retinal artery occlusion retinal vein occlusion retinal detachment vitreous haemorrhage ischaemic optic neuropathy
Describe how retinal vein occlusion leads to the loss of vision
vein occluded due to formation of thrombus, external compression or disease of vein wall
leads to ischaemic damage to retina
VEGF leads to neovascularisation and haemorrhages
What is the difference between branch retinal vein occlusion (BRVO) and central retinal vein occlusion
branch - more common. only part of retina affected
central - can be non-ischaemic or ischaemic. affects whole of retina
What are the symptoms of BRVO
unilateral painless loss of vision
metamorphopsia - linear objects look curvy or rounded.
visual field defects
What is found on examination in BRVO
vascular dilatation
tortuosity of vessels
haemorrhages in one area
no RAPD
What is the management of BRVO
urgent r/v with opthalmologist
panretinal photocoagulation laser treatment if macular oedema or neovascularisation
triamciolone
What are the risk factors for retinal vein occlusion
age HTN hyperlipidaemia diabetes smoking obesity raised IOP sarcoidosis hyperviscosity thrombophilia
What is the diffrence between non-ischaemic and ischaemic CRVO in terms of outcome
non-ischaemic = milder and more common. most resolve fully. ischaemic = severe. can end up with painful eye and severe visual impairment
What are the symptoms of CRVO
sudden unilateral painless loss of vusion or blurred vision
often on waking
What is found on examination of CRVO
non-ischaemic - mild or absent RAPD, dot blot and flame haemorrhages everywhere
ischaemic - severe visual impairment, marked RAPD, disc oedema, haemorrhages!
What is a RAPD and how is it seen
relative afferent pupillary defect
if left eye affected:
light shone in right eye, both pupils constrict
light shone in left eye, both pupils dilate
light shone in right eye, both pupils constrict
What can cause a retinal artery occlusion
most commonly:
embolism - from AF or carotids
vasoobliteration
vascular compression
Where is the occlusion in CRAO? What defect does this cause?
in the central retinal artery before it branches as it emerges from the optic nerve
affects whole of retina
macula can be preserved due to blood supply from choroid
What is found on examination in CRAO
unilateral acute painless loss of vision history of amaurosis fugax RAPD pale retina attenuation of vessel
What systemic examination needs to be done in CRAO
pulse - AF
BP
carotid bruits
heart murmurs
