Visual Loss Flashcards
1
Q
Describe the normal anatomy of the optic disc
A
- The areas of the optic disc and optic cup are correlated to each other (i.e. the larger the disc, the larger the cup)1
- The size of the optic cup may vary tremendously1
- In most normal eyes the rim tissue area is constant1
2
Q
Patient history for glaucoma
A
- History of presenting complaint
- Including incidence, duration, severity and triggers of visual symptoms of glaucoma
- Ophthalmic history
- Trauma, previous eye surgery or laser, previous ophthalmic medications
- Medication history
- Social history
- Family history
- Risk factors in family
- Blindness or eye disease in the family
3
Q
All patients with suspected glaucoma should undergo a physical eye examination that includes the following investigations:
A
- Slit-lamp examination
- Applanation tonometry
- Gonioscopy
- Optic nerve head and retinal nerve fibre layer evaluation
- Visual field examination (perimetry)
- Visual acuity
- Pachymetry
4
Q
features of POAG normal pressure glaucoma
A
- > 35 years
- Normal IOP without treatment
- Asymptomatic until field loss advanced
- ONH: typical damage
- VF: typical, paracentral defects
- Gonio: open anterior chamber angle*
- No history or signs of other eye diseases or steroid use
OAG suspect
• VF, ONH and RNFL normal or suspicious
5
Q
features of Ocular hypertension
A
- IOP > 21 mm Hg
- VF: normal
- ONH/RNFL: normal
- Gonio: open anterior angle*
- No other risk factors
6
Q
Acute angle-closure signs
A
- IOP > 21 mm Hg, often to 50 to 80 mm Hg
- Decreased visual acuity
- Corneal oedema
- Shallow or flat peripheral anterior chamber
- Peripheral iris pushed forward
- Gonio:iridotrabecularcontact360degrees
- Pupil mid dilated and reduced with no reactivity
- Gonioscopycluesfromothereye
7
Q
Signs of Intermittent angle- closure
A
- Features vary according to amount of iridotrabecular contact • Optic disc rim may show atrophy with an afferent pupil defect • Mild,intermittentsymptomsofacuteangle-closuretype
- Resolves spontaneously
8
Q
signs of Chronic angle-closure
A
- Gonio: peripheral anterior synechiae of any degree
- IOP > 21 mm Hg
- Visual acuity may be normal
- ONH damage compatible with glaucoma
- Superimposed iridotrabecular contact possible
9
Q
OVERVIEW OF PHARMACOLOGICAL treatment of glaucoma
A
• IOP reduction is the only treatment option we have
• Neuroprotection
Glaucoma & IOP reduction • 20% reduction in IOP reduces progression by 50%
- Beta blockers (1978)
- Timolol, betaxolol (betagan)
- Prostaglandin analogues (1996)
- Latanoprost (xalatan), bimatoprost (Lumigan), travoprost (Travatan) • Alpha agonists(1988)
- Brimonidine (alphagan), iopidine
- Carbonic anhydrase inhibitors (1995)
- Dorzolamide (Trusopt), brinzolamide (Azopt)
10
Q
side effects of Beta blockers for glaucoma
A
- Beta blockers (1978)
- Timolol 0.25% & 0.5%, betaxolol (betagan)
- 20-27% reduction in IOP • Twice daily regime
- Bronchospasm
- Bradycardia
- Hypotension
- One drop of 0.5% may lead to 10mg oral dose equivalent
11
Q
What drug os first line for glaucoma? list some side effects
A
Prostaglandin analogues • 20-35% reduction in IOP • Associated with decreased rate of glaucoma surgery in 1990s • First line • Once daily at night • Well tolerated • lash growth • Iris darkening • Dark circles under eyes
12
Q
Cataracts Definition
A
- An opacity that forms within the lens of the eye which can reduce the transparency of the lens
- Most common cause of blindness in the world
13
Q
Cataracts clarification
A
• Often classified according to part of lens primarily affected
• Nuclear – central part of lens, most common, change the refractive index
• Cortical – in the outer layer
• Sub-capsular – directly under lens capsule,
anterior or posterior
• Sub-classifications sometimes used by specialists, including severity, maturity and aetiology
14
Q
Risk factors for acquired cataract
A
- Ageing (most occur in >60s)
- Trauma (blunt or penetrating injury, electric shock, radiation, surgery)
- Systemic disease (diabetes mellitus, myotonic dystrophy, NF type 2, severe atopic dermatitis)
- Drugs- corticosteroids
- Family history
- Social history- Smoking/ Cumulative exposure to UV light
15
Q
Ocular conditions associated with cataract
A
- Trauma
- Uveitis
- High myopia
- Topical medication (particularly steroid drops) • Intraocular tumour
16
Q
Clinical features cataract
A
- Unilateral cataracts may often be unnoticed but loss of stereopsis may affect distance judgement
- Gradual and painless reduction in V/A (difficulty in reading, recognising faces, watching TV)
- Difficulties due to glare (problems with bright sunshine, oncoming headlights when driving at night)
- Frequent changes of spectacle prescription
- Monocular diplopia
- Opacities and reduced red reflex on ophthalmoscopy
17
Q
Differential diagnosis Other causes of painless gradual visual disturbance include
A
• Refractive error • Age-related macular degeneration • Primary open-angle glaucoma • Presbyopia • Some types of corneal disease • Chronic uveitis • Chemicals or drugs — eg methanol, chloroquine, hydroxychloroquine, isoniazid, thioridazine, isotretinoin, tetracycline, ethambutol • Pituitary tumour • Diabetic lens — undiagnosed or uncontrolled diabetes can cause vision changes • Diabetic retinopathy/maculopathy • Retinoblastoma — nearly always affects children <5 (pupil may look white (loss of red reflex),
18
Q
Management cataract
A
- If not already seen optometrist, encourage patient to see one (to assess V/A and exclude other causes of visual impairment)
- Provide advice on fitness to drive
- Consider referral for surgery
- Visual impairment which is affecting lifestyle (eg driving, reading)
- Comorbidity that may benefit from surgery (eg risk of falls)
- Surgery would facilitate treatment/monitoring of other eye conditions eg retinal screening for diabetics
- If person has capacity to cooperate with exams, surgery and post-op drops
19
Q
Post-op complications cataracts
A
- Intraoperative:
- Posterior capsule rupture and/or vitreous loss (communication between anterior and posterior chambers)
- Early complications:
- Bruising of eye or eyelids
- Infective endophthalmitis (very rare, may lead to loss of sight or eye)
- Refractive surprise (unexpectedly large need for glasses)
- Later complications
- Posterior capsule opacification (takes months to years) – treatable by laser, most common complication
- Detached retina (may occur weeks or months after surgery
- Dislocation of implant lens
20
Q
Cataracts in children
A
- Much less common than in adults
- Babies screened for congenital cataracts at birth and at 6-8 weeks of age
- Present with poor vision, a white/grey pupil, nystagmus, strabismus, light sensitivity
- Unilateral cataracts usually idiopathic and non-hereditary
- Bilateral cataracts either idiopathic in 60% cases or
- Hereditary (most often autosomal dominant)
- Intrauterine infections (rubella, varicella, CMV, HSV, toxoplasmosis) • Genetic syndromes (Down syndrome, Edward’s syndrome)
21
Q
Cataracts Prognosis
A
Adults
• Without treatment
Prognosis
• Steady decline in V/A without chance of recovery (rate of progression variable and unpredictable), leading to severe visual impairment
• With surgery
• Around 95% will have 6/12 best corrected vision on a Snellen chart
(meeting UK driving requirements)
• Generally very safe procedure but small minority develop complications which can be sight-threatening
• Children
• If congenital ones not removed within about 6 weeks of life, deprivation
amblyopia and lifelong visual impairment likely to occur
• Some visual improvement may be possible if treatment delayed or
22
Q
lid lacerations management
A
if it closes lid margin medial canthus, lacrimal apparatus, or associated iwrh globe perforations must be referred to ophthalmologist. all others repaired with 6/0 mono filament
remember tetanus
23
Q
periorbital heamatomas
A
check for other ocular damage e.g. orbital floor fracture, globe perforation hyphaema
if bone injury suspected x rY
analgesia
24
Q
Management of blow out fracture
A
x ray - tear drop sign
refer to ophthalmology or max fax
25
symptoms and signs of blow out fracture
orbital pian on occular movements, diplopia, parasthesia over maxilla
enopthalmos
bony tenderness
surgical emphysema
sensation over v2 districultuin
26
Hyphaema symptoms and signs
blurred vision, watering, photophobia
| blood in the anterior chamber
27
Hyphaema management
look for globe perforation, refer to ophthalmologist, usually admit, bed rest, topical steroids, reduce intraoccqular pressure
28
Ruptured globe management
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tetanus prophylaxis
x-ray
plastic shield
primary repair
secondary repair
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29
toxic foreign bodies in eye
Copper Thorn Twig Wood Soil Hair follicle
30
Intraocular foreign bodies management
refer and systemic antibiotics e.g. ciprofloxacin
31
chemical burns to eye management
copies irrigation urgent feral
32
Acute Closed Angle Glaucoma signs and symptoms
Blocked drainage of aqueous from anterior chamber via the canal of Schlemm.
Pupil dilatation (e.g. @ night) worsens the blockage.
Intraocular pressure rises from 15-20 >60mmHg
Symptoms
Prodrome: rainbow haloes around lights at night-time.
Severe pain ̄c n/v
acuity and blurred vision
33
Acute Closed Angle Glaucoma acute management
Pilocarpine 2-4% drops stat: miosis opens blockage
Topical -B (e.g. timolol): aqueous formation
Acetazolamide 500mg IV stat: aqueous formation
Analgesia and antiemetics
34
Sudden Loss of Vision: Key Questions
Headache associated: GCA
Eye movements hurt: optic neuritis
Lights / flashes preceding visual loss: detached retina
Like curtain descending: TIA, GCA
Poorly controlled DM: vitreous bleed from new vessels
35
Optic Neuritis signs and symptoms
Symptoms
Unilateral loss of acuity over hrs – days
colour discrimination (dyschromatopsia)
Eye movements may hurt
Signs
acuity
colour vision
Enlarged blind-spot
Optic disc may be: normal, swollen, blurred
Afferent defect
36
Optic Neuritis causes
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Multiple sclerosis (45-80% over 15yrs)
DM
Drugs: ethambutol, chloamphenicol
Vitamin deficiency
Infection: zoster, Lyme disease
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37
Retinal Detachment: presentation
Holes/tears in retina allow fluid to separate sensory retina from retinal pigmented epithelium
May be 2O to cataract surgery, trauma, DM
Presentation: 4 F’s
Floaters: numerous, acute onset, “spiders-web”
Flashes
Field loss
Fall in acuity
Painless
38
Orbital Cellulitis pathophysiology
Pathophysiology
Infection spreads locally: e.g. from paranasal sinuses, eyelid or external eye.
Staphs, pneumococcus, GAS
39
Orbital Cellulitis presentation
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Presentation
Usually a child ̄c inflammation of the orbit + lid swelling Pain and range of eye movement
Exophthalmos
Systemic signs: e.g. fever
± tenderness over the sinuses
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40
Orbital Cellulitis management
IV Abx: Cefuroxime (20mg/kg/8h IV)
41
4 areas of visual function
visual acuity
eye movements
visual fields
light reflex and pupil function
42
primary function of superior oblique muscle
incyclorotation
43
primary function of inferior oblique muscle
excyclorotation
44
Patient has complete loss of vision in one eye - where is the site of the lesion?
ipsilateral optic nerve
e.g. optic neuritis, foreign body occluding, dense cataract.
45
Patient has bitemporal hemianopia - where is the site of the lesion?
optic chiasm
bitemporal hemianopia
optic chiasm lesion e.g. pituatuary defect
46
Patient has binasal hemianopia - where is the site of the lesion?
optic chiasm
47
Patient has left homonymous hemianopia - where is the site of the lesion?
Right optic tract/radiation
48
Patient has right homonymous hemianopia - where is the site of the lesion?
Left optic tract/radiation
49
Patient has Homonymous quadrantanopia - where is the site of the lesion?
Contralateral optic tract/radiation
Top – temporal region
Bottom – parietal region
50
Patient has scotoma visual field defect - where is the site of the lesion?
Occipital region
51
What muscles contract to constrict pupil?
Circular muscles contract
radial muscles relax
52
What muscles contract to dilate pupil?
circular muscles relax
radial muscles contract
53
What do you look for on direct ophthalmoscopy of ocular media?
Red reflexes; are there any dark or light areas.
Distinguish between out-of-focus disc and light areas.
‘White eye in photos’.
54
What do you look for on direct ophthalmoscopy of optic disc/nerve head?
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Is the disc margins sharp or swollen?
Is the disc (neuro-retinal rim) pink or is there pallor?
Are the vessels normal looking?
Are there any haemorrhages.
What is the cup-to-disc ratio?
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55
What do you look for on direct ophthalmoscopy of macula?
The macula is a small darker patch compared with the of the
rest of the retina.
The bright spot is the fovea/foveola.
Are there any haemorrhages or drusen?
56
What do you look for on direct ophthalmoscopy of (Central)
| Retinal blood vessels?
Any tortuosity of the vessels?
Are there any changes in calibre. Are the reflections bright?
Are there any blockages, haemorrhages or occlusions?
57
What do you look for on direct ophthalmoscopy of peripheral retina?
Are there any haemorrhages or changes in colour?
Are there any lesions?
What is the size of the lesions c/w disc diameters?
Where is it on the retina as a polar co-ordinate?
What colour is it? Are its margins sharp? Is it raised?
