Glaucoma And Cataracts Flashcards
Most common glaucoma?
Primary open angle glaucoma
RFs for primary open angle glaucoma?
Increasing age FH Race-black-African-American and hispanic Myopia(short sighted) Raynauds-?vasculopathy may be cause of normal tension glaucoma where IOP is normal (AI component may also cause normal tension) Migraine thin central corneal thickness
Define glaucoma*
Progressive optic neuropathy with a particular pattern of nerve damage and corresponding characteristic visual field loss which matches the optic disc and absence of other causes of optic neuropathy.
RFs for angle closure glaucoma?
CT diseases e.g. Ehlers-Danlos syndrome, as suspensory ligaments of the lens are affected which causes the lens to move forwards into the anterior chamber, causing crowding of drainage angle
Hypermetropia- assoc. smaller anterior chamber
Iatrogenic-drugs-anticholinergics e.g. TCAs, SSRIs
sympathomimetics
idiosyncratic-antihistamines, topiramate
corticosteroids-GAG deposition in the drainage angle*-increased resistance in trabecular meshwork-open angle?
proliferative diabetic retinopathy or central retinal vein occlusion-abnormal iris blood vessels can obstruct angle and cause adhesion of iris to peripheral cornea, closing the angle (rubeosis iridis), as forward diffusion of vasoproliferative factors e.g. VEGF from ischaemic retina
uveitis-can cause adherence of iris to trabecular meshwork
cataract-can swell, pushing iris forward and closing the drainage angle
large choroidal melanoma-push iris forward against peripheral cornea, causing acute attack of angle closure glaucoma.
presenting features of acute angle closure glaucoma?
ocular pain-severe and rapidly progressive
blurring of vision
haloes around lights due to corneal oedema
headache-frontal or generalised
patient systemically unwell-nausea, vomiting, abdo pain, due to high pressure
signs: red eye, ciliary flush-deep inflammation
RAPD, pupil oval, fixed and dilated
globe is hard on palpation-notable difference on palpating both eyes
reduced visual acuity
cornea cloudy
shallow anterior chambers in both eyes, closed iridocorneal angles and corneal epithelial oedema on slit lamp examination
may be evidence of secondary causes e.g. peripheral anterior synechiae assoc. with uveitis
appearance of optic disc on fundoscopy in glaucoma?
optic disc cupping (this is a normal feature but central cup expands in chronic glaucoma)-increased optic cup to optic disc ratio-vertical ratio becomes more than 0.4 and the cup deepens
rim may also notch, implying focal axonal loss
in chronic glaucoma, axons leaving the optic nerve head die (optic disc-nerve axons, optic cup-blood vessels leaving)
classification of glaucoma?
primary open angle glaucoma-most common, and of which normal tension glaucoma is a subtype
primary closed angle glaucoma-acute and chronic angle closure glaucoma
congenital glaucoma-primary, secondary to maternal rubella infection, secondary to inherited ocular disorders e.g. aniridia-absence of iris, outflow resistance increased with abnormal iridocorneal angle. trabecular mesh work not formed properly. secondary glaucoma-other ocular disease e.g. uveitis-iris adherence to trabecular meshwork (closed angle), inflammatory cell blockage of trabecular meshwork (open angle), cataracts, choroidal melanoma, rubeosis iridis
trauma-blood (hyphaema)-blocks trabecular meshwork
ocular surgery
raised episcleral venous pressure
steroid induced-?raised resistance of trabecular meshwork due to GAG deposition
causes of aq outflow obstruction in primary open angle glaucoma (peripheral iris is clear of trabecular meshwork)?
thickening of trabecular lamellae which reduces pore size
reduction in number of lining trabecular cells
increased EC material in trabecular meshwork spaces
pathology of angle closure glaucoma?
resistance to aq outflow at the point of contact between the pupil margin and the lens is increased, and increased pressure gradient between posterior and anterior chamber bows the iris forward and closes the drainage angle.
peripheral iris contact with trabecular meshwork ultimately leads to adhesion formation=peripheral anterior synechiae (PAS), which consolidate the obstruction.
massive degree of corneal oedema and clouding occurs due to deprivation of whole cornea of nutrition and posterior cornea of O2 due to stagnant aq, which causes failure of corneal endothelial pumping function. this is amplified by raised IO pressure.
symptoms and signs of chronic open angle glaucoma?
symptomless in early stages, many pts diagnosed when signs detected by optometrist white eye and clear cornea raised IO pressure visual field defect cupped optic disc
components to examining patient to assess glaucoma?
full slit-lamp examination
ocular pressure measurement with tonometer
thickness of cornea measured with pachymeter-must adjust IOP measurement according to corneal thickness
gonioscopy to examine iridocorneal angle
exclude other ocular disease that may be cause of secondary glaucoma
optic disc examination on fundoscopy
characteristic visual field loss pattern in chronic open angle glaucoma?
upper arcuate scotoma-reflects nerve fibre damage of those entering lower pole of optic disc
tunnel vision, poss. sparing of island of vision in temporal field
loss of vision is gradual
aim of treatment in chronic open angle glaucoma?
reduce IOP to minimise further glaucomatous visual loss
medical treatment to reduce IOP in chronic open angle glaucoma?
PG analogues e.g. latanoprost, bimataprost ON-increase uveoscleral outflow of aq, often 1st line*
beta blockers e.g. timolol, carteolol OD-BD-reduce aq production
alpha agonists e.g. apraclonidine BD-reduce aq production and increase drainage through trabecular meshwork
parasympathomimetics e.g. pilocarpine QDS(when used as monotherapy)-increase drainage through trabecular meshwork by causing ciliary muscle contraction
carbonic anhydrase inhibitors e.g. dorzolamide TDS-reduce aq production.
ADRs of PG analogues used to reduce IOP in treating chronic open angle glaucoma?
eyelashes grow longer
darkening of iris colour
rarely-macular oedema, uveitis
NICE recommended treatment for advanced chronic open angle glaucoma?
offer drainage surgery-trabeculectomy, with pharmacological augementation-5-FU or mitomycin C, which are used at time of surgery to prevent subconjunctival scarring, and give interim treatment with PG analogue e.g. latanoprost whilst pt listed for surgery.
trabeculectomy-fistula created between anterior chamber and subconjunctival space, so aq can leave anterior chamber via a bleb of conjunctiva, into the space. procedure can be modified by removing sclera under scleral flap but not making a fistula into anterior chamber-LT benefit currently being assessed.
how does NICE recommend management of chronic open angle glaucoma to proceed after starting PG analogue for early or moderate disease?
if IOP not being reduced sufficiently, check adherence and eyedrop instillation technique, if these satisfactory offer alternative pharm. treatment, may need more than 1 agent concurrently, or laser trabeculoplasty, or surgery with pharm. augementation as indicated.
consider offering surgery or laser trabeculoplasty after 2 alternative pharm. treatments have been given.
how is laser trabeculoplasty used in treatment of chronic open angle glaucoma?
series of laser burns placed in trabecular meshwork to improve aq outflow
although effective initially, IOP may slowly increase
RFs for normal tension glaucoma?
old age female Raynaud's phenomenon migraines paraproteinaemia
define normal tension glaucoma
glaucomatous optic neuropathy with an open iridocorneal angle and in absence of raised mean IOP on diurnal testing.
management of normal tension glaucoma?
despite IOP normal, aim of treatment is still to reduce IOP by 30%, although some pts appear to have non-progressive visual field defects and may require no treatment
also, systemic BP should be measured over 24hrs as condition may be assoc. with nocturnal systemic hypotension, and a significant nocturnal drop needs r/v of antihypertensive med.-Ca2+ blockers preferred
glaucoma filtering surgery (trabeculectomy) best tment when medication doesn’t stabilise nerve damage.
what might an acute attack of angle closure glaucoma be preceded by?
subacute episodes of angle closure, assoc. with transient rises of IOP, headaches and experience of coloured haloes around bright lights-result of mild corneal epithelial oedema.
management of acute angle closure glaucoma?
IV acetazolamide 500mg over 10 mins, and further 250mg slow release tablet after 1hr-check for sulphonamide allergy, and sickle cell disease/trait, monitor Us and Es. reduces aq secretion and pressure gradient across iris.
give together with topical agents-pilocarpine 1-2% in those with natural lens, causes pupil constriction drawing peripheral iris out of drainage angle, may be started prophylactically in other eye, beta blockers, steroids-pred 15mg every 15 mins for 1 hr, then hrly
systemic hyperosmotics if no response e.g. oral glycerine or IV mannitol
offer systemic analgesis with or without anti-emetics
definitive tment=laser iridotomy to peripheral iris within 1 wk of acute attack once corneal oedema cleared sufficiently, treat both eyes-as pt susceptible to attack in other eye, with usually 2 holes in peripheral iris to provide alternative pathway for aq humour to flow from post to anter chamber bypassing pupil and reducing pressure gradient across iris.
if this cannot be performed, surgical iridectomy performed-more invasive
if a cataractous lens has swollen to precipitate attack, lensectomy performed urgently.
presentation of congenital glaucoma?
excessive tearing, photophobia and blepharospasm
increased corneal diameter and globe enlargement (buphthalmos) causing progressive myopia
cloudy cornea due to epithelial and stromal oedema
splits in descemet’s membrane
tment of congenital glaucoma?
usually surgical:
goniotomy-incision made into trabecular meshwork to increase aq drainage
or
trabeculotomy-direct passage created between schlemm’s canal and anterior chamber
importance of early diagnosis of glaucoma?
if late diagnosis, when already significant visual damage, eye more likely to become blind despite treatment
early diagnosis with lowering of IOP results in future age-related neuronal loss only
even if some continued glaucomatous damage, rate of visual loss slowed and pt unlikely to suffer visual loss during their lifetime
