Opthalmology Flashcards
acute angle-closure glaucoma (AACG) there is a rise
in IOP secondary to an impairment of aqueous outflow.
Factors predisposing to AACG include:
acute angle closure glaucoma
Factors predisposing to AACG include:
hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age
Features
of acute angle closure glaucoma
severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain
ARMD
ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography. It is more common with advancing age and is more common in females.
dry macular degeneration
characterised by drusen - yellow round spots in Bruch’s membrane
wet macular degeneration
characterised by choroidal neovascularisation
a reduction in visual acuity, particularly for near field objects
timeframe in AMRDS TWO SUBTYPES
gradual in dry ARMD
subacute in wet ARMD
FUNDOSCOPY IN DRY AMRDS
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
FUNDOSCOPY IN WET AMRDS
in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
TX FOR DRY AMRDS
combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.
TX FOR WET AMRDS
vascular endothelial growth factor (VEGF)
VEGR is a potent mitogen and drives increased vascular permeability in patients with wet ARMD
within the first two months of diagnosis of wet ARMD if possible
examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.
Anterior uveitis
Features
acute onset
ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired
Tx for anterior uvetits
urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops
Argyll-Robertson pupil
small, irregular pupils
no response to light but there is a response to accommodate
A mnemonic used for the Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
Causes of
Argyll-Robertson pupil
causes
diabetes mellitus
syphilis
Blepharitis
Blepharitis is inflammation of the eyelid margins.
It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).
Blepharitis is also more common in patients with rosacea
Features OF BLEPHARITIS
symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur
Mx of Blepharitis
softening of the lid margin using hot compresses twice a day
‘lid hygiene’ - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
Central retinal artery occlusion
Central retinal artery occlusion is a relatively rare cause of sudden unilateral visual loss. It is due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
Central retinal artery occlusion
features
Features
sudden, painless unilateral visual loss
relative afferent pupillary defect
‘cherry red’ spot on a pale retina
Management is difficult and the prognosis is poor
of Central retinal artery occlusion
any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)
if a patient presents acutely then Intraarterial thrombolysis may be attempted but currently, trials show mixed results.
Central retinal vein occlusion (CRVO) is a differential for sudden painless loss of vision.
Features
loss of visual acuity, usually unilaterally
fundoscopy
widespread hyperaemia
severe retinal haemorrhages - ‘stormy sunset’
Central retinal vein occlusion
Management
the majority of patients are managed conservatively
indications for treatment in patients with CRVO include:
macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
retinal neovascularization - laser photocoagulation
Non-proliferative diabetic retinopathy
Mild
mod
severe
Mild NPDR
1 or more microaneurysm
Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots, venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
Severe NPDR
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
Proliferative diabetic retinopathy
Key features
retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years
Non-proliferative retinopathy
mx
Non-proliferative retinopathy
regular observation
if severe/very severe consider panretinal laser photocoagulation
Proliferative retinopathy
mx
oliferative retinopathy
panretinal laser photocoagulation
following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue
other complications include a decrease in night vision (rods are predominantly responsible for vision in low light conditions, the majority of rod cells are located in the peripheral retina), a generalised decrease in visual acuity and macular oedema
intravitreal VEGF inhibitors
often now used in combination with panretinal laser photocoagulation
examples include ranibizumab
strong evidence base suggests they both slow progression of proliferative diabetic retinopathy and improve visual acuity
if severe or vitreous haemorrhage: vitreoretinal surgery
Herpes simplex keratitis most commonly presents with a dendritic corneal ulcer.
features
Features
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer
Herpes simplex keratitis
Mx
Management
immediate referral to an ophthalmologist
topical aciclovir
Herpes zoster ophthalmicus (HZO) describes the reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles.
vesicular rash around the eye, which may or may not involve the actual eye itself
Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement
Mx
Management
oral antiviral treatment for 7-10 days
ideally started within 72 hours
intravenous antivirals may be given for very severe infection or if the patient is immunocompromised
topical antiviral treatment is not given in HZO
topical corticosteroids may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review
Holmes-Adie pupil is a benign condition most commonly seen in women. It is one of the differentials of a
dilated pupil.
association of Holmes-Adie pupil with absent ankle/knee reflexes
Horner’s syndrome
features
Features
miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)
Hypertensive retinopathy
stages anf features
Keith-Wagener classification of hypertensive retinopathy
Stage Features
I Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring
II Arteriovenous nipping
III Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a ‘macular star’
IV Papilloedema
Keratitis featurs
Features
red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen
amoebic keratitis
amoebic
acanthamoebic keratitis
accounts for around 5% of cases
increased incidence if eye exposure to soil or contaminated water
pain is classically out of proportion to the findings
Bacterial keratitis
bacterial
typically Staphylococcus aureus
Pseudomonas aeruginosa is seen in contact lens wearers
Management
of keratitis
stop using contact lens until the symptoms have fully resolved
topical antibiotics
typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate
Congenital lacrimal duct obstruction affects around 5-10% of newborns. It is bilateral in around 20% of cases
features
watering eye (even if not crying)
secondary infection may occur
Dacryocystitis is infection of the lacrimal sac
features
watering eye (epiphora)
swelling and erythema at the inner canthus of the eye
Drug causes of mydriasis
topical mydriatics: tropicamide, atropine
sympathomimetic drugs: amphetamines, cocaine
anticholinergic drugs: tricyclic antidepressants
Optic neuritis
features
unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma
Investiagtion of Opric neuritis
mx
MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases
management
high-dose steroids
recovery usually takes 4-6 weeks
Differentiating orbital from preseptal cellulitis
reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis
Blood culture and microbiological swab to determine the organism. Most common bacterial causes -
for orbitial cellulitis
Blood culture and microbiological swab to determine the organism. Most common bacterial causes - Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
imaging for orbital cellultis
CT with contrast - Inflammation of the orbital tissues deep to the septum, sinusitis.
Papilloedema
Papilloedema describes optic disc swelling that is caused by increased intracranial pressure. It is almost always bilateral.
Causes of papilloedema
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
Posterior vitreous detachment
Posterior vitreous detachment is the separation of the vitreous membrane from the retina. This occurs due to natural changes to the vitreous fluid of the eye with ageing. Posterior vitreous detachment is a common condition that does not cause any pain or loss of vision.
Symptoms of posterior vitrous detachment
The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)
PVD signs
Posterior vitreous detachment
Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).
Management of Posterior vitreous detachment
Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
#
If there is an associated retinal tear or detachment the patient will require surgery to fix this.
IOP of ≥ 24 mmHg NICE
tx
offer 360° selective laser trabeculoplasty (SLT) first-line to people with an IOP of ≥ 24 mmHg NICE
Prostaglandin analogues (e.g. latanoprost)
Increases uveoscleral outflow
Beta-blockers (e.g. timolol, betaxolol)
Reduces aqueous production
Should be avoided in asthmatics and patients with heart block
Sympathomimetics (e.g. brimonidine, an alpha2-adrenoceptor agonist)
Reduces aqueous production and increases outflow
Avoid if taking MAOI or tricyclic antidepressants
Carbonic anhydrase inhibitors (e.g. Dorzolamide)
Reduces aqueous production
Miotics (e.g. pilocarpine, a muscarinic receptor agonist)
Increases uveoscleral outflow
Adverse effects included a constricted pupil, headache and blurred vision
RED EYE
AAS CSE
CAASES
Acute angle closure glaucoma
severe pain (may be ocular or headache)
decreased visual acuity, patient sees haloes
semi-dilated pupil
hazy cornea
Anterior uveitis
acute onset
pain
blurred vision and photophobia
small, fixed oval pupil, ciliary flush
Scleritis
severe pain (may be worse on movement) and tenderness
may be underlying autoimmune disease e.g. rheumatoid arthritis
Conjunctivitis
purulent discharge if bacterial, clear discharge if viral
Subconjunctival haemorrhage
history of trauma or coughing bouts
Endophthalmitis
typically red eye, pain and visual loss following intraocular surgery
Relative afferent pupillary defect
FINDING IN A SWINGING LIGHT TEST
the affected and normal eye appears to dilate when light is shone on the affected
Relative afferent pupillary defect CAUSES
retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis
Retinitis pigmentosa Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision
It may be autosomal recessive, dominant, X-linked or sporadic.
FESTURES
night blindness is often the initial sign
tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Fundus examination RETINITIS PIGMITOSA
Fundus examination reveals a triad of a waxy optic disc, bone-spicule pigmentation and arteriolar attenuation.
The most common causes of a sudden painless loss of vision are as follows:
ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery
vitreous haemorrhage
retinal detachment
retinal migraine
Vitreous haemorrhage
causes: diabetes, bleeding disorders, anticoagulants
features may include sudden visual loss, dark spots
Retinal detachment
features of vitreous detachment, which may precede retinal detachment, include flashes of light or floaters (see below)
Differentiating posterior vitreous detachment, retinal detachment and vitreous haemorrhage
Posterior vitreous detachment
Retinal detachment
Vitreous haemorrhage
- Flashes of light (photopsia) - in the peripheral field of vision
Floaters, often on the temporal side of the central vision - Dense shadow that starts peripherally progresses towards the central vision
A veil or curtain over the field of vision
Straight lines appear curved
Central visual loss - Large bleeds cause sudden visual loss
Moderate bleeds may be described as numerous dark spots
Small bleeds may cause floaters
Tunnel vision
Causes
papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
