⭕️ OPEN ANGLE GLAUCOMA

Treatment
first line: prostaglandin analogue (PGA) eyedrop
second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop

⭕️
if more advanced: surgery or laser treatment can be tried
DRUGS
Increases uveoscleral outflow
Prostaglandin analogues (e.g. latanoprost)
Miotics (e.g. pilocarpine, a muscarinic receptor agonist)
Decrease aqueous production
Beta-blockers (e.g. timolol, betaxolol)
Carbonic anhydrase inhibitors (e.g. Dorzolamide)
Reduces aqueous production and increases outflow
Sympathomimetics (e.g. brimonidine, an alpha2-adrenoceptor agonist)

AGE RELATED MACULAR DEGENERATION

Overview
Most common cause of blindness in the UK.
Degeneration of central retina (macula) is the key feature with changes usually bilateral.
Characterised by degeneration of retinal photoreceptors that results in formation of drusen which can be
seen on fundoscopy and retinal photography.
More common with advancing age and is more common in females.
Risk factors
advancing age : greatest risk factor
smoking
family history
Increased risk of ischaemic cardiovascular disease, such as HTN,DM, dyslipidaemia
Types
dry macular degeneration (90% of cases) / early age-related macular degeneration
also known as atrophic
characterised by drusen - yellow round spots in Bruch's membrane
wet macular degeneration (10% of cases) / Late age related(neovascularisation, exudative)
also known as exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries the worst prognosis

Clinical features
typically present with a subacute onset of visual loss with:
Reduction in visual acuity, particularly for near field objects
gradual in dry ARMD
subacute in wet ARMD
difficulties in dark adaptation with an overall deterioration in vision at night
fluctuations in visual disturbance which may vary significantly from day to day
Photopsia, (a perception of flickering or flashing lights), and glare around objects
visual hallucinations may also occur resulting in Charles-Bonnet syndrome
Signs
distortion of line perception may be noted on Amsler grid testing
fundoscopy : Presence of drusen, yellow areas of pigment deposition in macular area, which may become
confluent in late disease to form a macular scar.
wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid
leakage or haemorrhage.

Investigations:
Slit-lamp microscopy is the initial investigation of choice
Fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide
intervention with anti-VEGF therapy. This may be complemented with indocyanine green
angiography to visualise any changes in the choroidal circulation.
ocular coherence tomography is used to visualise the retina in three dimensions because it can
reveal areas of disease which aren't visible using microscopy alone.

Treatment
● Combination of vitamins A,C and E reduced progression of disease
● VEGR is a potent mitogen & drives increased vascular permeability in patients with wet
ARMD
○ Anti-VEGF agents : ranibizumab, bevacizumab and pegaptanib
○ Complication : Bacterial endophthalmitis

OPTIC NEURITIS

Causes :
multiple sclerosis: commonest associated disease
diabetes,syphilis
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
Investigation : MRI of brain and orbits with gadolinium contrast is diagnostic in most cases
Management
high-dose steroids
recovery usually takes 4-6 weeks
Prognosis
MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%

RED EYE

Causes
● Acute angle closure glaucoma
● Anterior uveitis
● Scleritis
● Episcleritis
● Keratitis
● Conjunctivitis
● Subconjunctival haemorrhage
 ● Endophthalmitis

ACUTE ANGLE CLOSURE GLAUCOMA (AACG)

● Rise in IOP secondary to an impairment of aqueous outflow.

Factors predisposing to AACG include:

● Hypermetropia (long-sightedness)
● Pupillary dilatation
● Lens growth associated with age
● TCA / Amitriptyline, Topiramate

Features
● 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
● Semi-dilated non-reacting pupil
● Halos around lights
● Corneal oedema results in dull or hazy cornea
● Systemic upset may be seen, such as nausea, vomiting and even abdominal pain

Investigations
● Tonometry to assess for elevated IOP
● Gonioscopy (literally looking, oscopy, at the angle, gonio): a special lens for the slit lamp
that allows visualisation of the angle

Management
● Urgent referral to an ophthalmologist
● IV analgesia and antiemetics, lie patient supine.
● 1st line : IV acetazolamide
● Combination of eye drops, for example : IV acetazolamide + Topical Pilocarpine
○ After initial treatment, pilocarpine will induce meiosis and open the angle. This is
initially ineffective due to pressure induced ischaemic paralysis of the iris
● Topical beta blockers and steroids.
● Definitive management : laser peripheral iridotomy 24-48 hours after intraocular pressure is
controlled to prevent recurrence > Creates a tiny hole in the peripheral iris → aqueous
humour flowing to the angle
● Direct parasympathomimetic (e.g. pilocarpine > contraction of ciliary muscle → opening the
trabecular meshwork → increased outflow of the aqueous humour)

Acute angle closure glaucoma

● Severe pain + decreased visual acuity + Halo + Semi dilated pupil + Hazy cornea
● Symptoms worse in dark

Anterior uveitis
 ● Acute painful
● Small, fixed oval pupil, Ciliary flush ,inflammatory cells in the anterior chamber
● Treatment : Topical steroids + Cycloplegic / Mydriatic

Episcleritis
● Majority of cases are idiopathic, associated conditions include:
○ Inflammatory bowel disease
○ Rheumatoid arthritis
● Features
○ Red eye
○ Classically not painful (in comparison to scleritis), but mild pain/irritation is common
○ Watering and mild photophobia may be present
○ Approximately 50% of cases are bilateral
● Management
○ Conservative
○ Artificial tears may sometimes be used

SCLERITIS

● Scleritis describes full-thickness inflammation of the sclera

Risk factors
● Rheumatoid arthritis: Most commonly associated condition
● Systemic lupus erythematosus
● Sarcoidosis
● Granulomatosis with polyangiitis

Features
● Red eye
● Classically painful (in comparison to episcleritis), but sometimes only mild pain/discomfort is
present
● Watering and photophobia are common
● Gradual decrease in vision

Management
● Same-day assessment by an ophthalmologist
● Oral NSAIDs are typically used first-line
● Oral glucocorticoids may be used for more severe presentations
● Immunosuppressive drugs for resistant cases (and also to treat any underlying associated
diseases)

Differentiating episcleritis vs scleritis

● Episcleritis
 ○ Mild pain / irritation
○ Injected vessels are mobile when gentle pressure is applied on sclera
○ Phenylephrine drops blanches conjunctival & episcleral vessels
● Scleritis
○ Severe pain
○ In scleritis, vessels are deeper, hence do not move
○ Phenylephrine drops doesn't blanch scleral vessels

Conjunctivitis
● Mucoid / purulent discharge if bacterial, clear discharge if viral
● More likely to be bilateral

Keratitis

Subconjunctival haemorrhage
● History of trauma or coughing bouts

Endophthalmitis
● Typically red eye, pain and visual loss following intraocular surgery

SUDDEN PAINLESS LOSS OF VISION

Most common causes of a sudden painless loss of vision are as follows:

● Ischaemic/vascular
● Occlusion of central retinal vein & central retinal artery
● Vitreous haemorrhage
● Retinal detachment
● Retinal migraine

ISCHAEMIC / VASCULAR

● Often referred to as 'amaurosis fugax'

● Differential including
○ large artery disease (atherothrombosis, embolus, dissection)
○ Small artery occlusive disease (anterior ischemic optic neuropathy
○ Venous disease and hypoperfusion
○ Vasculitis e.g. temporal arteritis
● May represent a form of TIA. It should therefore be treated in a similar fashion, with aspirin
300mg being given
● Altitudinal field defects are often seen : 'curtain coming down'
● Ischaemic optic neuropathy is due to occlusion of short posterior ciliary arteries, causing
damage to optic nerve
Central ● Incidence increases with age, more common than arterial occlusion
retinal vein Causes:
occlusion ● Glaucoma, polycythaemia
● Hypertension, hypertriglyceridemia, Diabetes
Findings:
● Severe retinal flame shaped &/or dot & blot haemorrhage in all 4 retinal
quadrants
● Cotton wool spots characterized by yellow-white deposits on retina
● Severe macular edema & papilledema
● Afferent pupillary defect
Investigation of choice : Fluorescein angiography

Central Causes
retinal artery ● Thromboembolism (from atherosclerosis) or
occlusion ● Arteritis (e.g. temporal arteritis)
Findings
● Sudden, painless unilateral visual loss
● Cherry red spot on a pale retina
● Afferent pupillary defect
Management
● Management is difficult & the prognosis is poor
● Any underlying conditions should be identified & treated
● IV acetazolamide & ocular massage
● If a patient presents acutely : Intra Arterial thrombolysis may be attempted

Branch ● Sudden onset of visual field defects (scotomas) in the affected eye
retinal artery ● No afferent pupillary defect
occlusion ● Fundoscopy : Grayish-white discoloration of retinal quadrant supplied by
affected vessel

Vitreous Common causes (collectively account for 90% of cases):

haemorrhag ● Proliferative diabetic retinopathy (over 50%)
e ● Posterior vitreous detachment
● Ocular trauma : Most common cause in children and young adults
● Bleeding disorders, anticoagulants

Features
● Patients typically present with an acute or subacute onset of:
○ Painless visual loss or haze (commonest)
○ Red hue in the vision
○ Floaters or shadows/dark spots in the vision
● Large bleeds : Sudden visual loss
● Moderate bleeds : Numerous dark spots
● Small bleeds : May cause floaters

Investigations:
● Dilated fundoscopy: may show haemorrhage in vitreous cavity
 ● Slit-lamp examination: red blood cells in anterior vitreous
● Ultrasound : Useful to rule out retinal tear/detachment & if haemorrhage
obscures the retina
● Fluorescein angiography : to identify neovascularization
● Orbital CT : used if open globe injury

Retinal ● Dense shadow that starts peripherally progresses towards central vision
detachment ● A veil or curtain over the field of vision
● Straight lines appear curved
● Central visual loss
Fundoscopy
● A freshly detached retina has a grey colour instead of normal pink colour
& may appear crinkled.A retinal tear may be visible

POSTERIOR VITREOUS DETACHMENT

● Flashes of light (photopsia) - in the peripheral field of vision

● Floaters, often on the temporal side of central vision
● Normal visual acuity

🔴 Retinitis pigmentosa
Association :
Alports syndrome
Abetalipoprotinemia
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Features
Night blindness is often the initial sign
Tunnel vision / Loss of peripheral vision due to loss of peripheral retina (occasionally referred to as funnel
vision)
Family H/0
Fundoscopy :
Black bone spicule shaped pigmentation at the periphery of retina
Mottling of retinal pigment epithelium

⭕️ ANGIOID RETINAL STREAK

Caused by degeneration, calcification and breaks in Bruch's membrane .
Causes
Pseudoxanthoma elasticum
Ehler-Danlos syndrome
Paget's disease
sickle-cell anaemia
acromegaly
fundoscopy : irregular dark red streaks radiating from the optic nerve head
SYSTEMIC DISEASE

⭕️ HYPERTENSIVE RETINOPATHY
Stage 1
Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring
Stage 2 : Arteriovenous nipping
Stage 3
Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a 'macular star'
Stage 4 : Papilloedema

⭕️ DIABETIC RETINOPATHY
Earliest lesion : Capillary microaneurys
Background
Microaneurysm
Blot haemorrhage < 3
Hard exudate
Pre proliferate
Venous beading/looping
Blot haemorrhage > 3 / Deep or dark cluster haemorrhage
Soft exudate / Cotton wool spot
Proliferative
Retinal neovascularisation
Maculopathy
Based on location rather than severity, anything is potentially serious
Hard exudates and other 'background' changes on macula
check visual acuity
more common in Type II DM
Management
● All patients
● optimise glycaemic control, blood pressure and hyperlipidemia
● regular review by ophthalmology
● Non-proliferative retinopathy
● regular observation
● if severe/very severe consider panretinal laser photocoagulation
● Proliferative 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
○ Intravitreal VEGF inhibitors : Ranibizumab
○ often now used in combination with panretinal laser photocoagulation
○ Both slow progression of proliferative diabetic retinopathy and improve visual acuity
○ if severe or vitreous haemorrhage: vitreoretinal surgery
● Maculopathy
○ Focal laser therapy
 ○ if there is a change in visual acuity : intravitreal VEGF inhibitors

⭕️ HORNER'S SYNDROME
Central lesions
Features : Anhidrosis of the face, arm and trunk
Causes
Stroke, Syringomyelia, Multiple sclerosis, Tumour, Encephalitis
Pre ganglionic
Anhidrosis of face
Causes : Pancoast's tumour, Thyroidectomy, Trauma, Cervical rib
Post ganglionic
Features : No anhidrosis
Causes : Carotid artery dissection, Carotid aneurysm, Cavernous sinus thrombosis,Cluster headache

⭕️ RHEUMATOID ARTHRITIS
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration

🔴
keratitis
ALPORTS SYNDROME
Anterior lenticonus : Pathognomonic
Dot & fleck retinopathy : Most common
Retinitis pigmentosa
Subscapular cataracts

INFECTION

⭕️ ORBITAL CELLULITIS
Risk factors
Childhood
Previous sinus infection
Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
Ear or facial infection
Lack of Haemophilus influenzae type b (Hib) vaccination
Presentation
Severe ocular pain
Visual disturbance
Redness and swelling around the eye
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema and ptosis
Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
Treatment : IV antibiotics

🔴 Herpes simplex
Herpes simplex keratitis
Acute, painful red eye with photophobia & epiphora
Fluorescein stain : Ragged area of cornea
Herpes simplex ophthalmicus
Painful, vesicular rash
Fluorescein stain : Multiple small defects on cornea

Herpes zoster ophthalmicus • 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. Features • 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 Management • Oralantiviral treatment for 7-10 days, ideally started
within 72 hours. Topical antiviral treatment is not given in HZO • oral corticosteroids may reduce the
duration of pain but do not reduce the incidence of postherpetic neuralgia • ocular involvement requires
urgent ophthalmology review Complications • ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis •
ptosis • post-herpetic neuralgia

Fundoscopic featuresin eye infections • Cytomegalovirus(CMV) retinitis secondary to human

immunodeficiency virus (HIV) Fundoscopy of the left eye revealed an extensive 'brushfire-like' lesionin the
major superior temporal arcade with a large patch of white fluffy lesion mixed with extensive retinal
haemorrhages. • Ocular histoplasmosis and syphilitic choroiditiswould give a fundus picture of multiple
whitish lesions. • Syphilitic neuroretinitiswould normally give a picture of a macular star exudation. •
Tuberculous periphlebitisgives a picture ofperivenous sheathing and minimal retinal haemorrhages.

Blindness
● Trachoma : Middle east
● Onchocerciasis : Africa