Gradual Loss Of Vision Flashcards
Cataract
Loss of transparency in the lens - most common disorder of the lens and of treatable blindness in the world
Usually due to age and common in the over 70s
Presents with gradual blurring of vision, increasing myopia and glare
Lens anatomy
Behind the iris, in front of the vitreous humour
Suspended on spoke-like zonules
Composed of a capsule - thin, elastic, outer basement membrane
Cortex - outer layer of lens epithelial cells
Nucleus - central lens fibres
Assessment of cataracts
Measure acuity
On ophthalmoscopy - diminished red reflex and difficult view of the fundus
Causes of cataracts
Age-related - most common, degeneration of the lens due to age, UV and smoking
Congenital - rare, 1/3 inherited autosomal dominant, 1/3 due to birth trauma/rubella/toxoplasmosis infection from mother, detected as loss of red reflex in newborns
Early onset - due to systemic disease (diabetes), trauma, steroids or ocular disorders (uveitis)
Presentation of age-related cataracts
Can be:
nuclear - central
Posterior sub-capsular - small at the back of the lens
Cortical - wedge shaped segments coming in from the outside
My present as a combination of types
Cataract surgery
Benefits of surgery - low risk, quick, cost effective
Risks - rarely complications such as rupture of posterior lens capsule
1/500 may suffer - suprachoroidal (intraocular) haemorrhage or endophalmitis
Procedure of cataract surgery
LA - self-sealing corneal incision into anterior chamber
Circular opening in the anterior lens capsule (capsulorhexus)
Break-up (phakoemulsification) and aspiration of lens material
Insertion of intraocular lens with correct power
Outcomes of cataract surgery
90% achieve visual acuity of 6/12 or better
May develop posterior capsular opacification where lens cells proliferate and opacify the capsule - this can be treated with lasers (YAG laser capsulotomy)
Age related macula degeneration (AMD)
Leading cause of blindness in the western world
Associated with increasing age
Affects central vision - peripheral vision unaffected, so pts often live independently
Can be wet or dry AMD
Anatomy of the macula
Located at the posterior pole of the eye and includes the fovea
Cones are concentrated in the macula which is responsible for colour and acuity of vision
Rods are distributed throughout the retina and are responsible for low light vision and movement detection
Symptoms of AMD
Dry - gradual loss of central vision
Wet - acute or semi-acute loss of central vision
Distorted central vision
Both will have reduced acuity and require dilated fundoscopy
Signs of dry AMD
Drusen - tiny yellow accumulations of extra cellular waste from photoreceptors. They accumulate under the neuro-retina
Mottled appearing macula - patches of hyper- and hypo- pigmentation
In advanced disease there is marked central atrophy
Signs of wet AMD
Choroidal neovacularization - grey/green lesions of new vessels
Yellow exudates
Retinal haemorrhage
Fluorescein angiography
a technique to identify areas of micro- vascular leakage
Can identify the extent of the lesion
Required for wet AMD but not AMD
Optical coherence tomography
Laser scanner used to capture a detailed cross-sectional image of the macula
Shows intra-retinal fluid in wet AMD
Amsler chart
Essentially graph paper which displays any central vision distortion in wet AMD
Management of AMD
In unilateral disease use ambler chart to monitor the other eye
dietary supplements may reduce the risk of other eye involvement
Counselling/low vision aids/registration as sight impaired
No treatment for dry AMD but wet AMD can be treated with intravitreal injections of anti-VEGF drugs
Stop smoking
Prognosis of AMD
Dry AMD - a slow deterioration in vision but may progress to wet AMD
Wet AMD - without treatment 75% have marked vision loss over 3 years, 60% have fellow eye involvement within 5 years
With anti-VEGF treatment most maintain vision with slight reductions over time
Primary open angle glaucoma
A progressive optic neuropathy associated with optic head damage and visual field loss, typically with raised intraocular pressure (IOP)
Most common type - incidence 2% >40yro and 10% >80yro
A progressive disease if untreated
Types of glaucoma
Primary open angle (POAG)
Closed/narrow angle -usually presents acutely with a red painful eye
Congential glaucoma (rare)
Presentation of primary open angle glaucoma
Optic nerve head damage (cupping,or increased cup to disc ratio)
Loss of peripheral visual field
Usually raised IOP (above 21mmHg is abnormal)
Usually bilateral but often asymmetric
Pathogenesis of primary open angle glaucoma
With age or idiopathically the trabecular meshwork may not drain as effectively causing IOP to rise
This can damage the nerve fibres in the optic disc producing a field defect, or may be asymptomatic (ocular hypertension)
Normal pressure glaucoma
Some people have disc cupping and field loss with normal IOP
Risk factors for glaucoma
IOP - most important and modifiable
Family history of glaucoma - also being black
Age / Diabetes / Myopia
Early disease is often asymptomatic, picked up in routine eye screens - by the symptomatic late stage vision can’t be restored
Signs of POAG
Raised IOP
Cupped optic nerve head - cup-to-disc ratio should be 0.2/3, greater than 0.6 is suspicious
Progressive peripheral visual field defects
Non contact tonometry
Also known as air-puff tonometry
A rapid air pulse is used to flatten (applanate) the cornea, detected by an electro-optical system
The IOP is estimated by the force of air at the time of applanation
This has historically been considered only and estimate and is useful for children/non-complient patients
Goldman tonometry
Most widely accepted and gold standard of IOP measurement
A disinfected prism is placed on the cornea and a colbalt blue filter is used to view 2 green semi-circles
Force is applied until they meet and when 3.06mm of cornea is flattened corneal rigidity and tear film cancel out and IOP is determined from the force applied
Visual field testing
Confrontation testing is not sensitive enough
Humphrey visual field testing is used
Classical field defect is ‘arcuate scotoma’ which extends from the enlarged blind spot around the macula
Treatment of POAG
1st - suppress aqueous humor production using beta-blockers, carbonic anhydrase inhibitors or alpha-agonists
2nd - increase aqueous outflow using prostaglandin analogues
If unresponsive - surgery - trabecular meshwork can be layered to open drainage, or trabeculectomy to open alternative drainage
Trachoma
A bilateral follicular, non-purulent conjunctivitis due to chlamydia trachomatis infection
Progression of trachoma infection
Follicles on superior tarsal conjunctiva and superior limbus leading to conjunctival cicatrisation (scarring) - this can cause Entropian (inversion of the eyelid)
Trachomatis (eyelashes growing towards the cornea)
Dry eyes - this all leads to scarring, opacification and blindness
Diagnosis of trachoma
Conjunctival scrappings
Treatment of trachoma
Oral antibiotics (azithromycin)
The WHO SAFE strategy
Surgery to treat trichiasis
Antibiotics to treat infection
Facial cleanliness
Environmental improvement
Onchocerciasis
‘River blindness’ due to infection by onchocerca volvulus
It is transmitted by black fly and has an incubation of 1year
Endemic to equatorial Africa and central/south America
Progression of onchocerca infection
Black fly bites form subcutaneous nodules
Adult female worm sheds microfilariae which migrate through the skin
Eye symptoms occur when chronic infection reaches the conjunctiva
Ocular signs/complications of onchocerciasis
Lid nodules/depigmentation
Chronic conjunctivitis with punctuate keratitis
Corneal opacification, iritis and cataract
Glaucoma and optic neuritis
Treatment of onchocerciasis
Ivermectin
Xerophthalmia
Gradual blindness due to vitamin A deficiency
Vit A is required for synthesis of rhodopsin
Major cause of blindness in children in developing countries
Complications of vitamin A deficiency
Initially Night blindness
Corneal/conjunctival dryness and keratinisation
Corneal ulcers which can lead to perforation - advanced disease can show progressive corneal necrosis
Treatment of Xerophthalmia
Oral vitamin A
Ocular lubrication
Infective keratitis can be treated with antibiotics
Prevention of Xerophthalmia
Diet with enough vitamin A - fat soluble form (dairy, eggs, fish liver oil) or pro-vitamin form (fruit and veg)
Supplementation may be needed for vulnerable populations
