Ophthalmology Flashcards
normal eye pressure
11-21mmHg
what happens in posterior vitreous detachment
caused by natural changes to the vitreous gel with age - it shrinks and develops pockets of liquefaction (think gelatin dessert)
at some stage it may peel away from retina
symptoms of posterior vitreous detachment
photopsia (flashes of light) in the peripheral field of vision
sudden dramatic increase in floaters - often on the temporal side of the central vision
what is PVD more common in
myopia - eye is too long
retinal tear
retinal develops small gaps - can cause retinal detachment in rare cases. caused by ageing or injury
symptoms are mild - may see black spots or floaters and cause distorted vision
retinal detachment symptoms
floaters, flashes of light
loss of central vision - dense shadow that starts peripherally progresses towards the central vision
straight lines appear curved
painless
treatment of retinal detachment
not always required unless there is tears – symptoms gradually improve over 6 months
cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall of the areas of detachment so that it does not spread
or scleral buckle surgery or pneumatic retinoplexy or vitrectomy
85 percent of cases will be successfully treated with one operation with the remaining 15 percent requiring 2 or more operations. After treatment patients gradually regain their vision over a period of a few weeks
vitreous haemorrhage
o Leakage of blood into the areas in and around the vitreous humor
Large bleeds cause sudden visual loss
Moderate bleeds may be described as numerous dark spots
Small bleeds may cause floaters
o Causes include diabetic retinopathy, trauma, retinal tear or detachment, posterior vitreous detachment
o Treatment – advised to rest with head elevated, can put patch over eye to limit movement, stop blood thinners, retinal tears should be closed by laser treatment or cryotherapy and detached retinas should be reattached
causes of transient visual loss
unilateral
- amourosis fugax (can be one or both). embolic, haeodynamic, ocular, neurologic, idiopathic
- giant cell arteritis can cause double vision or partial loss of vision (treat with high dose prednisolone)
bilateral
- TIAs
- migraine
causes of double vision
binocular - strabismus, nerves (MS, GB, diabetes), stoke, muscle (MG, Grave’s)
monocular - cataract
primary angle closure suspect (PACS)
here goinoscopy shows some closure but the person has normal IOP and no signs of glaucoma
pressure in acute angle closure glaucoma
ophthalmic emergency
sudden risk of pressure to >50mmHg
risk factors for acute angle closure glaucoma
female asian hyermetropia because of shallower anterior chambers (smaller eye) FHx age
the attack is more likely to occur under reduced light conditions when the pupil is dilated
acute angle closure glaucoma presentation
sudden onset of a red painful eye and blurred vision
and patients become unwell with N+V
the cornea is hazy and the pupil is semi-dilated
gets halos around lights (rainbow-coloured)
investigations for acute angle closure glaucoma
goinoscopy -definitive test - trabecular meshwork won’t be visible
slit lamp exam - will see shallow anterior chamber and large optic cup (NB goinoscopy is usually performed at the slit lamp)
automatic static perimetry using Humphrey’s visual field test to check for the amount of glaucomatous visual field loss during initial diagnosis
treatment of acute angle closure glaucoma
URGENT
lie flat with their face up and head not supported by pillows
IV acetazolamide 500mg to reduce IOP (CA inhibitor) and pilocarpine 4% drops to constrict the pupil and to prevent iris adhesion to trabecular meshwork
other topical drops like beta blockers (timolol) and prostaglandin analogues can also be instilled if available
DEFINITIVE TREATMENT = laser iridotomy after initial corneal oedema resolves
the unaffected eye is also usually treated
most common type of glaucoma
primary open angle glaucoma
risk factors for primary open angle glaucoma
FHx high myopia (short-sightedness) DM age (subtle changes in structure of trab mw occur) 2x more common in black steroids HTN CV disease
reduced drainage of aqueous humour from the anterior chamber
vision loss in primary open angle glaucoma
peripheral occurs first
presentation of primary open angle glaucoma
usually asymptomatic and insidious in onset - e.g. picked up by routine eye exam
usually affects both eyes
visual loss only noticed when advanced - peripheral
investigations for primary open angle glaucoma
tonometry - Goldmann tonometry to determine IOP
direct ophthalmoscopy to view cup to disc ratio
indirect opthalmoscopy can also show cup to disc ratio
slip lamp exam is most frequent method used - IOP can be measured and drainage angle assessed
visual field testing should be done on all - scotoma with either an elevated IOP or enlarged cup to disc ratio have high sensitivity and specificity
primary open angle glaucoma treatment
topical prostaglandin analogues e.g. latanoprost or topical beta blocker like timolol
2nd line treatments include CA inhibitors, alpha 2 adrenergic agonsits or a combination
if eye drops fail, surgery can be done like laser trabeculoplastyto improve drainage
PAOG blindess
deveops in 5-10%
pathophysiology of diabetic retinopathy
hyperglycaemia damages retinal pericytes which results in weakening of cap walls and increased blood flow leading to microaneurysms at areas of weakness
it also means vessels are more leaky to proteins and lipids leak out forming hard exudates
= pre-proliferative stage (typically 15 years after diagnosis and can last a few years before becoming proliferative)
at proliferative stage, there is vascular prolideration and most patients will have at least blurry vision or floaters
