3. Chronic Visual Loss Flashcards
Outline ocular HTN
Intraocular pressure of greater than 21 mm Hg
Ae = steroids, trauma effecting drainage, increased prod
S+S = no signs or symptoms
Ix = gonioscopy (special contact lens to examine the drainage angles), Tonometry
Mx =
- meds: decreasing aqueous humor production and/or increasing aqueous humor outflow
- laser trabeculoplasty: increasing outflow
What is the aetiology and pathophysiology of acute closed-angle glaucoma?
Ae = narrow anatomy, traumatic haemorrhage pushing posterior chamber forward
Path = over hours, iridocorneal angle completely closed by forward displacement of the final roll and root of the iris against the cornea, inability of aqueous fluid to flow from posterior to anterior chamber and out the trabecular network, sudden rise in IOP, pain, axonal death
- PRIMARY = predisposed anatomy
- SEC = pathological process
How does acute closed-angle glaucoma present?
S+S (only late in disease process) =
- majority asymptomatic
- pupils fixed, mid-dilated
- in IOP makes eye feel hard, cornea cloudy
- headache
- PAINFUL, red eye (25%)
- blurred vision, HALOS (25%)
- part of the page missing
- loss of central fixation
Describe how acute closed-angle glaucoma should be Ix and Mx?
Ix =
- 1: visual acuity (snellen chart)
- 2: visual fields (tend to lose nasal fields first),
- 3: IOP check
- 4: gonioscopy
- 5: dilate
- 6: central corneal thickness
Mx =
- avoid eye patches/dark rooms
TRIAD =
1) B-blockers: red aqueous humour prod
2) pilocarpine: miosis opens blocked/closed angle
3) IV acetazolamide: dec aqueous formation
- Peripheral iridectomy once IOP controlled
Laser = in drainage, red prod
Surgery = destruction of ciliary body, in drainage (trabeculectomy, tube implants, minimally invasive glaucoma surgery)
What is the aetiology and pathophysiology of chronic simple (open-angle) glaucoma?
Ae = ocular HTN, east Asian (shallower anterior chamber depths), prolonged steroids, restricted blood flow to eye (severe diabetic retinopathy and central retinal vein occlusion), ocular trauma
Path = devel over time, flow is reduced through the trabecular meshwork, due to the degeneration and obstruction of the trabecular meshwork (absorbs aqueous humor), damage to optic N by raised IOP
How does chronic simple (open-angle) glaucoma present?
S+S = asymptomatic (PAINLESS) until visual fields are impaired (PERIPHERAL)
Visual field defect =
- Humphrey visual field test - arcuate scotoma
Describe how chronic simple glaucoma (open-angle) should be Ix?
Ix =
- Tonometry: IOP
- Central corneal thickness measurement
- Gonioscopy: peripheral anterior chamber configuration and depth assessment
- Visual field measurement
- Slit lamp: optic N measurement
- optic disc ratio: >0.6
How should chronic simple glaucoma (open-angle) should be Mx?
MEDS =
1) Prostaglandin analogues: in uveoscleral outflow
2) B-blockers: dec aqueous prod (? PMH asthma)
3) A-adrenergic agonist: dec aqueous prod, in uveoscleral outflow
4) Carbonic anhydrase inhib: dec aqueous prod
5) Miotics (pilocarpine): in aqueous outflow by constricting pupil that pulls on trabecular meshwork
6) Sympathomimetic: in aqueous outflow
7) Fixed-dose combination drops
SURGERY =
- Laser therapy (trabeculoplasty): in aqueous outflow
- Laser ciliary body ablation
- Surgery (trabeculectomy): establishes pressure valve at limbus so aqueous can flow into conjunctival bleb
What is the aetiology and pathophysiology of age-related macular degeneration?
RF = age, FH, race (Caucasian), smoking, obesity, CVD, light iris
Path = pigment, drusen (cellular debris from degeneration of RPE - accum between RPE + Bruch’s mem resulting in hypoxia/inflam), and bleeding at macula, progresses to retinal (photoreceptor) atrophy and central retinal degeneration
1) WET ARMD = VEGF, choroidal neovascular membranes devel under retina, can leak fluid/blood, detachment of pigment, disciform scar, gradual vision loss
- subfoveal, juxtafoveal, extrafoveal
- classic (CNV visible), occult (CNV obscured)
2) DRY ARMD = aetiology not understood, drusen and changes at macula, rapid vision loss
How does age-related macular degeneration present?
- Diff making out images due to failing contrast sensitivity
- Dec visual acuity = diff reading and making out faces
- Diff night vision, and with changing light conditions
- Visual fluctuation
- Metamorphopsia = distortion of visual images
- Central scotoma
How should suspected age-related macular degeneration be Ix and Mx?
Ix = amsler grid (distortion, vision loss), fluorescein angiogram
- Fundoscopy:
- Dry: drusen, hypo/hyperpig of RPE, atrophy of macula
- Wet: exudate, blood, elevation of retina
Mx =
- Wet: VEGF inhib: in acuity, dec cell prolif/new blood vessels/vascular leaks
- Laser photocoag
- Photodynamic therapy (PDT): IV verteporfin releases free radicals that disrupt neovascular tissue
- Intravitreal steroids
- Screening: straight line test
- Antioxidants/vits: zinc/beta-carotene/vit C+E slow progression
What is a cataract, its RF and classifications?
Cataract = any opacity in the lens (loss of red reflex)
- leading cause of blindness
- 75% of >65y
- S+S = gradual decline in visual acuity, monocular diplopia, haloes, In myopia, vision worse in bright light (constriction of pupil results in more light passing through opacity)
- RF: age, DM, smoking, alcohol, sunlight, trauma, RT, steroids
- Congenital type (maternal infection: rubella, chicken pox, CMV, herpes)
- Childhood = rubella, varicella, DM, galactosemia, trauma, radiation, inherited, trisomy 21/12
Classifications:
1) Nuclear = change in lens refractive index, dull colours, common in old age
2) Cortical = spoke-like wedge shaped opacities
3) Posterior Subcapsular = progress fast, classic glare
How should cataract be Mx?
Surgery (THRESHOLD - best corrected visual acuity of 6/12 or worse in the affected eye)
- day case, LA
- small incision 3mm, capsulorhexis, hydrodissection, phacoemulsion (US break up, aspirated out), irrigation and aspiration, intraocular lens (IOL) implant
- Abx + anti-inflam 3-6w post-op
- need to change glasses to get full benefit of surgery
Comp = posterior capsular rupture and vitreous loss, endophthalmitis, posterior capsule opacification (YAG laser Tx)
Outline the pathophysiology of diabetic retinopathy
Path (microangiopathy in capillaries) =
1) Microvascular occlusion: ischaemia, A-V shunts, angiogenesis on the iris, retinl oedema, hard exudates, vitreous haemorrhage, retraction of fibrous tissue heightens risk of retinal detachment, can block aqueous drainage (glaucoma)
2) Vascular leakage: pericytes lost, microaneurysms, rupture at N fibre level causes flame-shaped haemorrhages, when deep - blot haemorrhages form
RF for progression = DM duration, hyperglycaemia, HTN, hyperlipidaemia, nephropathy, preg
- higher risk of cataracts: lens taken up a lot of glucose converted by aldolase reductase to sorbitol
How should diabetic retinopathy be Ix and monitored?
DM type 1/2 should have eyes screened at time of Dx + annually thereafter (by dilated fundus photography)
- Dot/bold haemorrhages
- Cotton wool spots
- Hard exudates
Mx
- Target BP <140/80 (<130/80 if end-organ damage)
- Glycaemic control
- Lipid lowering
- Photocoagulation by laser to Tx maculopathy (focal or grid) and proliferative retinopathy
