Ophthalmology Flashcards
State some risk factors for age-related macular degeneration (non-modifiable and modifiable)
Non-modifiable:
- Older age
- Ethnicity
- Ocular characteristics (light coloured iris, hyperopia)
- Genetics (complement factor H)
Modifiable:
- Smoking
- Cardiovascular disease (CVS & HTN)
Outline the main causes of blindness worldwide
Most common in those ages > 50
Distance vision issues:
- Refractive errors
- Cataract
- Glaucoma
- AMD (age-related macular degeneration)
- Diabetic retinopathy
Near vision issues:
- Presbyopia
Outline the 2 muscles responsible for moving the eyelids and what nerves they are innervated by
- Levator palpebrae superioris = open eyelids
- Oculomotor nerve (CN3) - Orbicularis oculi = close eyelids
- Facial nerve (CN7)
Outline the 3 main layers of the eyeball
Outer:
- Sclera
- Cornea
Middle:
- Choroid
- Ciliary body
- Iris
Inner:
- Retina
State the 2 compartments of the eyeball and which areas they sit between
- Anterior chamber
- Between cornea and iris - Posterior chamber
- Between iris and ciliary body + lens
Age-related macular degeneration - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
Most common cause of blindness in the UK
- Progressive condition affecting the macula, with drusen deposits (proteins and lipids) between the retinal pigment epithelium and Bruch’s membrane
- 2 main types = dry (90%) and wet (10%)
Presentation:
Often unilateral, but can be bilateral
- Gradual loss of central vision
- Reduced visual acuity (variable, vision worse close up e.g. seeing faces)
- Straight lines appear wavy (metamorphopsia)
*Wet AMD presents more acutely than dry AMD, with vision loss developing within days
Investigations:
- Snellen chart (reduced visual acuity)
- Fundoscopy (drusen)
- Amsler grid test (metamorphopsia)
- Slit lamp examination
- OCT (optical coherence tomography)
- Fluorescein angiography
Management:
- NO specific treatment for dry AMD = reduce risk of progression e.g. smoking cessation, BP control. Some suggestion of Zinc and Vitamin A, C, E
- If wet AMD = Anti-VEGF as monthly injections
Outline what drusen is (in age-related macular degeneration) and the 2 main types
- Occurs due to retinal pigment epithelium degeneration
- Undigested cellular debris, deposits of proteins and lipids between the retinal pigment epithelium and Bruch’s membrane (white/yellow colour)
- Drusen may remain unchanged for years without causing vision loss (small drusen are present in up to 95% of elderly patients)
- Soft drusen - larger, soft deposits
- Hard drusen - small, hard, solid deposits
State the way in which soft drusen can contribute to age-related macular degeneration
Lift the retinal pigment epithelium away from the underlying membrane
1. Hypoxia
2. Inflammation
State the 2 main types of age-related macular degeneration and relative frequency
Dry (non-neovascular) = 90% cases
Wet (neovascular) = 10% cases
State 2 findings common to both dry and wet AMD
- Atrophy of the retinal pigment epithelium
- Degeneration of photoreceptors
Age-related macular degeneration - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Abnormal cellular deposits of proteins and fats in the layer between retinal pigment epithelium and Bruch’s membrane
- Leads to progressive central vision loss
- 2 main types of dry (non-neovascular) and wet (neovascular)
- Usually first affects people in their 50s and 60s and often unilateral but may be bilateral
Presentation:
- Gradual loss of central vision
- Reduced visual acuity e.g. difficulty in reading small text
- Crooked or wavy appearance to straight lines (metamorphopsia)
- Drusen may be seen during fundoscopy
*Wet AMD progresses presents more acutely than dry AMD (vision loss within days)
Investigations:
- Amsler grid test = assess for the distortion of straight lines
- Fundoscopy = drusen may be seen
- Slit lamp examination
- Optical coherence tomography = can help diagnose + monitor AMD
- Fluorescein angiography for suspected wet AMD
Management - depends on type:
No specific treatment for dry AMD
- Monitoring and reducing the risk of progression by avoiding smoking, controlling blood pressure
Wet AMD
- Anti-VEGF as monthly injections directly into the vitreous chamber of the eye
Outline which bones make up the superior, medial, lateral and floor of the orbital cavity
Superior = frontal bone + lesser wing of sphenoid
Medial = ethmoid bone + maxilla + lacrimal + sphenoid
Lateral = zygomatic + greater wing of sphenoid
Floor = maxilla + palatine + zygomatic
Outline what nerve and muscle causes eyelid opening and eyelid closing
Eyelid opening:
- Levator palpebrae superioris
- Oculomotor nerve (CN3)
Eyelid closing:
- Orbicularis oculi
- Facial nerve (CN7)
Outline the 3 layers of the globe of the eye
Retina (innermost)
Choroid
Sclera (outermost)
Outline the difference between rods and cones
Cones:
- Colour vision
- Active at high light levels
- High definition
- High density in fovea / macula
Rods:
- Non-colour vision
- Active at low light levels
- Low definition
- High density in peripheral retina
Outline some differentials for someone presenting with ocular discomfort (organise by structure)
Cornea:
- Trauma (corneal abrasion)
- Dry eyes
- Keratitis (viral, bacterial, parasite)
Conjunctiva:
- Conjunctivitis (viral, bacterial or allergic)
Sclera:
- Scleritis
Anterior chamber:
- Acute closed-angle glaucoma
Uvea:
- Anterior uveitis
Optic nerve:
- Optic neuritis
Other:
- Orbital cellulitis
- Cluster headaches
Outline some differentials for someone presenting with acute loss of vision
Ophthalmology:
- Vascular occlusion e.g. amaurosis fugax, central retinal artery occlusion
- Haemorrhage (diabetes or trauma)
- Retinal detachment
- Acute closed-angle glaucoma (PAIN)
- Uveitis (anterior or pan) (PAIN)
- Corneal ulcer (PAIN)
- Optic neuritis (PAIN)
Other
- Stroke / TIA
- Migraine
- Giant cell arteritis
Outline some differentials for someone presenting with gradual loss of vision
- Age-related macular degeneration
- Presbyopia
- Cataracts
- Chronic open-angle glaucoma
- Diabetic retinopathy
Concerning:
- Vitreous haemorrhage
- Giant cell arteritis
- Chronic optic nerve compression
Outline some differentials for someone presenting with transient visual loss (lasts <24hrs)
- Amaurosis fugax
- Migraine
- Papilloedema
Outline some differentials for someone presenting with sudden (painless) loss of vision
Mainly vascular:
- Vitreous haemorrhage
- Retinal detachment
- Wet age-related macular degeneration
- Retinal vein or artery occlusion
- Stroke affecting the visual pathways
- Giant cell arteritis (ischaemia)
Outline some differentials for someone presenting with gradual (painless) loss of vision
- Cataracts
- Refractive errors / presbyopia
- Cataracts
- Dry age-related macular degeneration (AMD)
- Open-angle glaucoma
- Tumours affecting visual pathway
Outline some differentials for someone presenting with painful loss of vision
- Acute closed-angle glaucoma
- Optic neuritis
- Uveitis
- Keratitis / corneal ulcer
- Endophthalmitis
- Orbital cellulitis
+ GCA (headache)
Outline some differentials for someone presenting with diplopia (double vision)
- Monocular
- Binocular
Monocular differentials - suggests distortion of light transmission through the eye:
- Cataracts
- Irregular corneal shape e.g. scarring
- Astigmatism
- Dislocated lens
Binocular differentials - suggests misalignment of the eyes:
- Cranial nerve palsy (3rd, 4th, or 6th) e.g. intracranial lesion, aneurysm
- Myasthenia gravis / MS
- Graves’ ophthalmopathy
- Trauma / damage to extraocular eye muscles
- Ocular myositis
Outline some differentials for someone presenting with red eye
Conjunctival / sclera:
- Conjunctivitis (viral, bacterial, allergic)
- Subconjunctival haemorrhage
- Episcleritis / scleritis
Cornea:
- Corneal abrasion e.g. foreign body
- Corneal ulcer
Other:
- Anterior uveitis
- Acute angle-closure glaucoma
- Herpes simplex keratitis or herpes simplex keratitis
Outline some differentials for someone presenting with ocular discharge (separate into purulent and wartery causes)
Purulent:
- Conjunctivitis (bacterial)
- Ophthalmia neonatorum (neonatal conjunctivitis)
- Blepharitis
- Corneal ulcer
- Bacterial Keratitis (infection of cornea)
Watery:
- Conjunctivitis (allergic or viral)
- Blocked tear duct / system
- Endophthalmitis
- URTI
- Dry eyes
- Trichiasis
- Dacryocystitis (infection lacrimal sac)
Outline some differentials for someone presenting with abnormal pupil shape
- Trauma (to iris sphincter muscles) e.g. cataract surgery
- Anterior uveitis can cause adhesions (scar tissue)
- Acute angle-closure glaucoma (ischaemic damage to the muscles of the iris)
- Rubeosis iridis (neovascularisation in the iris)
- Coloboma (congenital malformation)
- Tadpole pupil (muscle spasm in part of dilator muscle of the iris) = may be associated with migraines and Horner syndrome
Outline some differentials for someone presenting with mydriasis (dilated pupil)
Medications:
- Dilating drops used
- Stimulants e.g. Cocaine
- Anticholinergics e.g. oxybutynin
Cranial nerves:
- Trauma
- Raised intracranial pressure
- Third nerve palsy
Other:
- Congenital
- Acute angle-closure glaucoma
- Holmes-Adie syndrome
Outline some differentials for someone presenting with miosis (constricted pupil)
Medication:
- Opiates
- Nicotine
- Pilocarpine
Other:
- Horner syndrome
- Cluster headaches
- Advanced syphilis (Argyll-Robertson pupil)
Outline some differentials for someone presenting with loss of red reflex
- Corneal scars
- Cataracts
- Vitreous hemorrhage
- Retinal detachment
- Refractive error
- Strabismus
- Coloboma
- Retinoblastoma
Outline some differentials for someone presenting with visual hallucinations
Charles-Bonnet syndrome
Psychiatry:
- Schizophrenia
- Mood disorders / mania
- Dementia esp. Lewy Body dementia
- Delirium
- Parkinson’s disease
- PTSD
Medications:
- Substance misuse / alcohol
- Prescribed e.g. opioids, anticholinergics, anti-Parkinsonians
Outline 3 roles of the cornea
- Protection of the eye (including corneal reflex)
- Allow transmission of light (transparent)
- Refraction of light
Keratitis (infection of cornea) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Infection of cornea (non-infectious keratitis is rare)
- Causes inflammation and damage to the corneal layers
- Usually occurs secondary to damage/disruption of epithelial surface
Presentation:
Usually unilateral
- Severe pain (exposed free nerve endings from loss of epithelium)
- Red eye
- Discharge (watery or purulent)
- Reduced visual acuity
- Photophobia
- May have corneal ulcer
Investigations:
- Ophthalmoscope (may show corneal infiltrate and hypopyon)
- Corneal scraping (histology and MC&S)
Management:
- Stop contact lens use
- Analgesia
(Cycloplegic drops if photophobia e.g. Atropine)
Bacterial suspected = immediate empirical fortified eye drops e.g. Tobramycin (high risk) or Fluoroquinolone (moderate risk)
Viral suspected = antivirals
Outline some triggers/risk factors for infective keratitis (infection of cornea)
- Trauma
- Contact lenses
- Dry eyes
- Pre-existing corneal disease e.g. ulcers
Immunocompromised will make infection more likely
State what is used to measure IOP and the value at which above is considered raised IOP
Tono-meter
- Measures force needed to flatten cornea
> 21 considered to be ocular hypertension (11-21 considered normal)
Outline some classes of medications that can reduce aqueous production (and reduce IOP)
Reduce aqueous production (ABC):
Alpha agonists e.g. Apraclonidine (a receptors normally suppress)
Beta blockers e.g. Timolol (b receptors normally stimulate)
Carbonic Anhydrase inhibitor e.g. Dorzolamide
Improve outflow:
Prostaglandins e.g. Latanoprost
Parasympathomimetic e.g. Pilocarpine
Cataracts - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Cloudy lens = lens of the eye becomes progressively opaque, due to denaturation of lens proteins
- Reduces light entering the eye = reduced visual acuity
- Usually seen in the elderly (present in ~75% of individuals aged over 65), but can be congenital
Presentation:
Usually asymmetrical
- Gradual reduction in visual acuity
- Gradual blurring of the vision
- Faded colour vision
- Glare around lights (esp. driving at night)
- Loss of red reflex (grey or white)
Investigations:
- Ophthalmoscope (loss of red reflex)
- Slit lamp examination of the anterior chamber (brown/white appearance of the lens)
Management:
- May not need intervention if symptoms are manageable
- Surgery phacoemulsification (break down with ultrasound, then implant artificial lens)
List some risk factors for cataracts
- Increasing age!!
- Smoking
- Systemic steroids
- Diabetes
- Alcohol
- Hypocalcaemia
List some causes of cataracts in younger patients
- Trauma e.g. direct, electric shock
- Drugs e.g. systemic steroids, Amiodarone
- Systemic disease e.g. diabetes, neurofibromatosis type 2
List 2 main complications of cataract surgery
- 1 in 1000 risk of infection (endophthalmitis)
- 1 in 100 risk of failure to complete the procedure
+ lens capsule opacification
State the technical names for pupil dilation and contristriction and which muscles and nerves are responsible for each
Pupil dilation = mydriasis
- Dilator pupillae
- Sympathetic nerves
Pupil constriction = miosis
- Sphincter pupillae
- Parasympathetic nerves (CN3)
List the 3 structures of the uveal tract
- Iris
- Ciliary body
- Choroid
Outline the different types of uveitis
Anterior uveitis - inflammation of:
- Iris
- Ciliary body
Intermediate uveitis - inflammation of:
- Posterior ciliary body
- Peripheral retina
- Choroid
Posterior uveitis - inflammation of:
- Retina
- Choroid
Panuveitis - inflammation of:
- Whole uveal tract!
Anterior uveitis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Most common type of uveitis (75% cases)
- Inflammation of the iris and ciliary body (anterior chamber)
- Usually autoimmune cause but can be infection, trauma, ischaemia or malignancy
- Can be acute, recurrent, or chronic
- All types of uveitis are potentially blinding conditions
Presentation:
Unilateral
- Painful red eye
- Photophobia
- Reduced visual acuity
- Watery eye
- On examination: ciliary red ring, miosis, abnormally shaped pupil, hypopyon
Investigations:
Mainly clinical diagnosis
- Ophthalmoscope (keratic precipitates or synechia)
Management:
- Steroids (eye drops, oral or intravenous)
- Cycloplegics e.g. atropine eye drops
Suggest some indications for mydriatic / cyclopaedic drops
- Dilate pupil to better visualise the retina
- Children and amblyopia
- Refraction of children for prescription of glasses
Give the difference between mydriatic and cyclopaedic drops and give some examples
Mydriatic drops:
Medications that make pupils dilate
Cyclopaedic drops:
Paralysis of the muscles that are responsible for accommodation
Examples:
- Atropine (anticholinergic)
- Cyclopentolate (anticholinergic)
- Tropicamide (anticholinergic)
- Phenylephrine (sympathetic)
List contraindications for the following mydriatic and cyclopaedic drops:
- Atropine, Cyclopentolate, Tropicamide (anticholinergics)
- Phenylephrine (sympathetic)
Atropine, Cyclopentolate and Tropicamide (anticholinergics)
- Allergy
- Acute closed-angle glaucoma
- HTN for Atropine
Phenylephrine (sympathetic)
- Allergy
- Children
- Acute closed-angle glaucoma
List some side effects of mydriatic and cyclopaedic drops
- Temporary stinging (few seconds)
- Temporary blurring of vision
- Whitening of eyelids (temporary)
- Atropine = red / warm face
CAN’T DRIVE UNTIL BLURRING WORN OFF
Suggest some indications for Fluorescein eye drops
Diagnostic:
- Identify defects in corneal epithelium
- Assess tear drainage in children with congenital nasolacrimal duct obstruction
- Part of measuring intraocular pressure (tonometry)
+ combined with local anaesthetic
*Warn patients about staining (clothes and contact lenses)
Outline the general pathophysiology of glaucoma and describe the pattern of vision loss experienced initially then in later disease
Neurodegenerative condition primarily due to dysfunction in outflow of aqueous humour (produced by ciliary bodies)
- Either acute (sudden narrowing of iridocorneal angle) or chronic (wide iridocorneal angle)
- Causes build-up of intraocular pressure
- Leads to damage of optic nerve and retinal ganglion cells
Vision loss:
Early disease = peripheral vision loss
Later disease = central vision loss
Chronic (open-angle) glaucoma - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Gradual increase in resistance to flow of aqueous humour through the trabecular meshwork
- Slow increase in intraocular pressure
Presentation:
Usually asymptomatic
- Gradual peripheral vision loss (tunnel vision)
- Fluctuating pain
- Headaches
- Blurred vision
- Halos around lights (particularly at night)
Investigations:
- Slit lamp = cupping (optic cup 50% bigger than optic disc)
- Non-contact tonometry (screening)
- Contact Goldmann applanation tonometry (gold-standard)
- Visual field assessment (peripheral vision loss)
- Gonioscopy (assess angle between the iris and cornea)
- Central corneal thickness assessment
Management - when pressure > 24mmHg:
- Prostaglandin eye drops e.g. Latanoprost (improve drainage)
- Topical beta blockers e.g. Timolol
- Topical Carbonic Anhydrase inhibitor e.g. Dorzolamide
- Parasympathomimetic e.g. Pilocarpine
- Surgical: 360° selective laser trabeculoplasty
List some risk factors for chronic (open-angle) glaucoma
- Increasing age
- Family history
- Black ethnic origin
- Myopia (nearsightedness)
List some risk factors for acute (closed-angle) glaucoma
- Increasing age
- Family history
- Female (4 times more likely)
- Chinese and East Asian ethnic origin
- Shallow anterior chamber
Medications:
- Adrenergic medications e.g., noradrenaline
- Anticholinergics
- Tricyclic antidepressants (anticholinergic effects)
Acute (closed-angle) glaucoma - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
Ophthalmological emergency
- Iris bulges forward, which seals off the trabecular meshwork
- This prevents aqueous humour from draining, leading to a continual increase in intraocular pressure
- Pressure builds in the posterior chamber, pushing the iris forward and further exacerbating angle closure
Presentation:
- Severely painful red eye
- Associated headache, N&V
- Decreased visual acuity
- Fixed, mid-dilated pupil
- Hazy cornea
- Halos around lights
- Hard eyeball on gentle palpation
Management:
- Lying flat on back
- Analgesia and antiemetics
- Pilocarpine eye drops (improve drainage)
- IV Acetazolamide, Timolol, Dorzolamide or Brimonidine (reduce production of aqueous humour)
- Hyperosmotic agents e.g. IV mannitol if no improvement
- Laser iridotomy to BOTH eyes = definitive treatment
List some common eyelid disorders (differentials)
- Blepharitis
- Chalazion
- Stye
- Entropion / ectropion
- Trichiasis
- Periorbital cellulitis / orbital cellulitis
Blepharitis - state the following:
- Pathophysiology
- Presentation
- Management
Inflammation of the eyelid margins
Presentation:
Typically bilateral
- Crusting around eyelashes
- Surrounding erythema
- Gritty sensation
- Itchy eyelids
- Dry sensation
Management:
- Warm compresses
- Gentle cleaning of the eyelid margins
Chalazion (Meibomian cyst) - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Non-infectious inflammatory granuloma
- Caused by sebaceous gland blockage
Presentation:
Usually single lesions, sometimes multiple lesions
- Painless lid lump (usually upper lid)
Management:
Usually self-limiting
- Warm compress for 5–10 minutes 2–4 times daily until resolved
Stye - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Also known as a hordeolum
- Infection of either sweat or sebaceous glands at the base of upper or lower eyelid, leading to local abscess
Presentation:
Unilateral, usually solitary lesion
- Eyelid pain
- Pustule at eyelid margin
Management:
- Warm compress for 5–10 minutes 2–4 times daily until resolved
Entropion - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Inward rotation of the eyelid margin (usually lower lid)
- Causes eyelashes to come into contact with the surface of the eye
- Can result in corneal damage and ulceration
Presentation:
- Visible inturning of eyelid
- Pain
- Foreign body sensation
- Red, watery eye
- Blurring of vision
Management:
- Taping affected eyelid away from eye with supplementary lubricating eye drops
- Definitive management with surgery
Ectropion - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Outward rotation of the eyelid margin (usually lower lid)
Presentation:
Symptoms variable depending on severity
- Lower lid visibly away from eyelid
- Painful / sore
- Red
- Watery eye
Management:
Mild cases require no treatment
- Lubricating eye drops
- Definitive management with surgery
Trichiasis - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Inward growth of the eyelashes, can be secondary to a number of conditions
- Can cause corneal damage and ulceration
Presentation:
Unilateral or bilateral
- Foreign body sensation
- Red eye
- Watery eye
Management:
- Lubricating eye drops
- Epilation of eyelashes with forcep (likely to grow back)
- Definitive management with medical management e.g. electrolysis of hair follicle, cryotherapy, laser treatment
Periorbital cellulitis - state the following:
- Pathophysiology
- Presentation
- Investigation (help differentiate from orbital cellulitis)
- Management
Pathophysiology:
- Infection of tissues lying anterior to the orbital septum (orbit not involved)
- Usually mild, except in young children
Presentation:
- Acute onset of swelling, redness and tenderness of lid(s)
- Fever
- Malaise / irritability in children
Investigation (help differentiate from orbital cellulitis):
- CT scan (orbits and sinuses)
Management:
- Systemic antibiotics (oral or IV)
Orbital cellulitis - state the following:
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology:
- Infection of tissues lying posterior to the orbital septum (orbit involved)
- Severe sight and life-threatening emergency
Presentation:
- Unilateral swelling of conjunctiva and lids +/- pain
- Pain on ocular movement / restricted eye movements
- Blurred vision
- Diplopia
- Proptosis
- Fever
- Severe malaise
Investigation:
- CT scan (orbits and sinuses)
- Blood tests (CRP, ESR)
Management:
- IV antibiotics
- Possible drainage of orbital abscess + culture
Central retinal artery occlusion - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
Ophthalmic emergency
- Obstruction to blood flow through the central retinal artery (branch of ophthalmic artery)
- Most common cause is atherosclerosis, but can be caused by GCA
Presentation:
- Sudden painless loss of vision = ‘curtain coming down’
- Relative afferent pupillary defect (RAPD)
Investigations:
- Fundoscopy (pale retina with a cherry red spot)
- Try to rule out GCA as a cause (ESR blood test and temporal artery biopsy)
Management:
Aim to resolve blockage (no consensus on treatment)
- Massage eye
- Anterior chamber paracentesis (removing fluid from the anterior chamber to reduce the intraocular pressure)
- Methods to dilate artery e.g. inhaled high % oxygen, sublingual isosorbide dinitrate, oral pentoxifylline
- Methods to reduce intraocular pressure e.g. IV Mannitol or Acetazolamide, topical Timolol
(immediate systemic steroids if GCA suspected cause)
Importance on secondary prevention!
Conjunctivitis - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
- Inflammation of conjunctiva
- Bacterial, viral or allergic
= Highly contagious
Presentation:
Unilateral or bilateral
- Red eye
- Itchy or gritty sensation
- Discharge (watery or purulent)
Bacterial = purulent discharge, starting in one eye and spreading to other
Viral = watery discharge, associated with UTRI symptoms e.g. cough, runny nose
Management:
Conjunctivitis usually resolves in 1-2 weeks without needing treatment (even bacterial cases)
- Hygiene measures and clean eye to remove discharge
- If bacterial, can use: topical Chloramphenicol drops or fusidic acid eye drops
- If allergic, antihistamines (oral or topical)
**Neonates under one month with conjunctivitis need urgent ophthalmology assessment = can cause permanent vision loss
Diabetic retinopathy - outline the pathophysiology and the 3 main stages
Caused by chronic hyperglycaemia
Damages endothelium of retinal capillaries, leading to:
- Microaneurysms
- Haemorrhage
- Mini-infarctions
Risk of oxidative stress and increased VEGF production
3 main stages:
1. Background
2. Preproliferative
3. Proliferative
Outline some investigations to consider for suspected diabetic retinopathy
Investigations:
- OCT
- Fundus Fluorescein angiography
Outline some features seen on:
- Background diabetic retinopathy
- Pre-proliferative diabetic retinopathy
- Proliferative diabetic retinopathy
Background diabetic retinopathy:
- Haemorrhages
- Microaneurysms
- Cotton wool spots
- Hard exudates
Pre-proliferative diabetic retinopathy:
- Larger haemorrhages
- Venous beading / loops
- Microvascular abnormalities
Proliferative diabetic retinopathy:
- New vessel formation (disc, iris or everywhere)
Outline how the following stages of diabetic retinopathy are managed:
- Background diabetic retinopathy
- Pre-proliferative diabetic retinopathy
- Proliferative diabetic retinopathy
At every stage - improve diabetes control
Background diabetic retinopathy:
- No action required
- Annual monitoring
Pre-proliferative diabetic retinopathy:
- Closer follow up (4-6 monthly)
- Consider retinal laser treatment
Proliferative diabetic retinopathy:
- Photocoagulation of all layers of retina within 2 weeks of diagnosis
Outline how diabetic maculopathy is different from diabetic retinopathy and how it is generally managed
Diabetic maculopathy is a type of diabetic retinopathy
- Blood vessels to the macula can become blocked
- Other blood vessels enlarge to compensate but are leaky and bleed into macular
- Causes loss of central vision (peripheral vision usually okay)
Management:
- Anti-VEGFs e.g. Bevacizumab
- Intravitreal Dexamethasone implant
- Intravitreal Flucinolone implant
List some complications of diabetic retinopathy
- Retinal detachment / vitreous haemorrhage
- Cataracts
- Secondary glaucoma
- Retinal vein occlusion
- Optic neuropathy
Optic neuritis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Inflammation of the optic nerve
- Primary demyelinating disease occurring in isolation (idiopathic) or as part of MS
Presentation:
Usually unilateral
- Eye pain (worse with eye movements)
- Loss of colour vision
- Loss of vision (central)
- Relative afferent pupillary defect (RAPD)
Investigations:
Generally clinical diagnosis
- Fundoscopy (swollen optic disc)
- Testing of visual acuity, contrast and colour vision, visual field testing
- MRI optic nerve if suspecting MS
Management:
- Consider Methylprednisolone for acute symptoms (doesn’t impact level of final vision)
Retinal detachment - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Seperation of the neurosensory layer (rods and cones) of the retina from the retinal pigment epithelium (RPE)
- Usually secondary to a retinal tear, allowing vitreous fluid to get under the neurosensory retina and fill the space between the layers
- Neurosensory layer relies on the choroid for blood supply therefore detachment can disrupt blood supply = permanent damage to the photoreceptors, making it sight-threatening
Presentation:
**painless
- Peripheral vision loss (often sudden and described as a shadow coming across the vision)
- Blurred vision
- Flashes and floaters
Investigations:
- Red reflex (may be absent)
- Dilated fundal examination / slit lamp examination (visualise tears)
- Ultrasound or OCT (optical coherence tomography)
Management:
- Vitrectomy (keyhole eye surgery to remove vitreous fluid and repair tear)
- Scleral buckle (silicone “buckle” to squish retina to choroid layer again)
- Pneumatic retinopexy (inject gas bubble to squish retina to choroid layer again)
List some risk factors for retinal detachment
- Trauma
- Thinning of the retina
- Posterior vitreous detachment
- Diabetic retinopathy
- Family history
- Retinal malignancy
State 2 methods that can be used to manage retinal tears (to reduce likelihood of retinal detachment occuring)
- Laser therapy
- Cryotherapy
Creates adhesions between retina and choroid layers
Outline the key differences between episcleritis and scleritis including:
- Anatomical structures involved
- Pain
- Associated ocular symptoms
- Blood vessels
Episcleritis = inflammation of the superficial, episcleral layer of the eye
- Relatively common
- Benign and self-limiting
**Episcleritis does not progress to scleritis
Scleritis = inflammation involving the sclera
- Severe inflammation
- Often causes complications, nearly always requires systemic treatment
Pain: mild (episcleritis) severe (scleritis)
Associated ocular symptoms: none (episcleritis) diplopia, vision loss (scleritis)
Blood vessels: superficially inflamed and mobile (episcleritis) severely inflamed and immobile (scleritis)
Scleritis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Inflammation of full thickness of the sclera (outer layer of connective tissue surrounding most of the eye)
- Most cases are idiopathic or associated with inflammatory conditions (although can be associated with infection)
- Severe type of scleritis = necrotising scleritis
Presentation:
Usually unilateral, more common in women 40-60 years
- Red, inflamed sclera (localised or diffuse)
- Severe pain (typically a boring pain), worse on eye movement
- Photophobia
- Watery eyes
- Reduced visual acuity
- Tenderness to palpation of the eye
Investigations:
- Slit-lamp examination (detect intraocular inflammation)
Management:
- NSAIDs (oral)
- Steroids (topical or systemic)
- Immunosuppression of underlying systemic condition if present
Assessment for underlying inflammatory conditions if not already diagnosed
List some inflammatory conditions associated with anterior uveitis and scleritis (seperate)
Anterior uveitis:
Seronegative spondyloarthropathies e.g.
- Ankylosing spondylitis
- Psoriatic arthritis
- Reactive arthritis
IBD
Sarcoidosis
Behçet’s disease
Scleritis:
- Rheumatoid arthritis
- Vasculitis (esp. granulomatosis with polyangiitis)
Thyroid eye disease (Graves’ ophthalmology) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Most common extra-thyroidal manifestation of Graves’ (90% patients with TED have Graves)
- Autoimmune reaction to TSH causes infiltration of T lymphocytes into orbital tissue stimulates the release of cytokines
- Leads to oedema of extraocular muscles and orbital fat
- Usually develops within 2 years of hyperthyroidism
- Initial inflammatory phase lasting 6-24 months
- Followed by inactive fibrotic phase, where further changes are unlikely
Presentation:
Mostly bilateral, females 30-50 years
- Proptosis +/- lid lag (together = exophthalmos)
- Aching eyes (worse in the mornings, worse on movement)
- Diplopia
- Puffy eyelids
- Red eyes
- Discomfort / pressure
- Gritty / watery eyes
+ concurrent symptoms of hyperthyroidism
Investigations:
ADVISE ABOUT DRIVING
- Thyroid function tests and thyroid autoantibodies
- Exophthalmometry (quantify eye protrusion)
- MRI (or CT) of orbits
Management:
Generally should resolve after inflammatory phase (6-12 months)
Optimise thyroid levels + smoking cessation
- Mild = lubricating eye drops + Selenium
- Moderate = steroids (oral or IV)
If left with residual issues - surgical interventions e.g. decompression surgery or radiotherapy
Name some conditions that Graves’ disease is associated with
- T1DM
- Vitiligo
- Myasthenia gravis
- Sjogren’s syndrome
- RA
- SLE
List some complications from thyroid eye disease
- Corneal ulceration
- Superficial keratitis (inflammation of cornea)
- Diplopia/ strabismus = eye misalignment
- Optic nerve compression
- Glaucoma (increased intraocular pressure)
State some signs of optic neuropathy in thyroid eye disease
Mourits score of 4 or more (benefit from immunosuppression)
- Decreased vision
- Decreased colour vision
- RAPD
- Visual field defects
- Optic nerve compression / swelling on MRI scan
Retinitis Pigmentosa - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Genetic condition causing degeneration of the photoreceptors in the retina, particularly the rods
- Many different genetic causes, some associated with systemic conditions
Presentation:
Mostly symptoms start in childhood
- Night blindness (often the first symptom)
- Peripheral vision loss (before the central vision)
Investigations:
- Fundoscopy (pigmentations in spiky appearance, nearer edges of periphery)
- Narrowing of the arterioles
- Pale appearance of optic disc
Management:
Difficult to slow disease progression
- Vision aids
- Sunglasses (protect the retina)
- Driving limitations and informing the DVLA
- Genetic counselling
Retinoblastoma - state the following:
- Pathophysiology
- Most common age affected
- Presentation
- Investigations
- Management
Pathophysiology:
- Cancer of the retina
- Intraocular (within eyeball) or extraocular (spread outside eyeball)
- Best outcome for childhood cancer 99% survival rate
Most common age affected:
- Children under 5
Presentation:
- White reflex (leukocoria), instead of red
- Squint
- Poor visual acuity
- Erythema eye
- Nystagmus
Investigations:
- Ophthalmoscopy
- Ultrasound
- MRI scan
- Genetic testing
Management:
- Cryotherapy or laser therapy
- Chemotherapy / radiotherapy
- Surgery
Amaurosis fugax - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Retinal TIA (transient ischaemic attack) caused by an emboli
- Leads to temporary blockage of either internal carotid artery or central retinal artery
- Other causes include giant cell arteritis or optic neuritis
Presentation:
- Sudden unilateral painless vision loss ‘curtain coming across eye’
Typically self-resolving after a few minutes
Investigations:
- Angiography
- Doppler ultrasound neck (carotid atherosclerosis)
Management:
Aimed at treating the underlying vascular risk factors e.g. hypercholesterolaemia, HTN
- Anticoagulants e.g. Aspirin or Clopidogrel
Squint (strabismus) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Misalignment of the eyes
- Poor direction of light onto retina, therefore experience double vision
- In childhood, brain ‘tunes out’ weaker eye and can lead to amblyopia (‘lazy eye’)
Presentation:
- Misalignment of eye at rest (esotropia, exotropia, hypertropia, hypotropia)
- Double vision
Investigations:
- Cover test
- Hirschberg’s test (shine light directly at both corneas)
Management:
Treatment needs to begin before 8 years old (whilst still developing)
- Patch covering good eye
- Atropine drops in good eye (makes good eye blurry)
Amblyopia (‘lazy eye’) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Poor vision from one eye (can be bilateral)
- Caused by the brain ‘tuning out’ weaker eye
- May be caused by refractive errors, strabismus or cataract
Presentation:
Often picked up on routine eyesight tests aged 3-5
- Poor depth perception
- Squinting
- Shutting 1 eye
- Tilting their head
Investigations:
- Routine eyesight test at 3-5 years
Management:
Treatment needs to begin before 8 years old (whilst still developing)
- Patch covering good eye
- Atropine drops in good eye (makes good eye blurry)
Other than being idiopathic (most common), list some other acquired causes of a squint
- Cranial nerve palsy
- Trauma
- Raised ICP e.g. space occupying lesions or hydrocephalus
- Cerebral palsy
List some risk factors for development of amblyopia (‘lazy eye’)
- Family history of amblyopia or other eye conditions
- Premature / low birth weight
- Developmental disabilities
Suggest how you could differentiate between episcleritis and scleritis with medication
Use topical adrenaline drops
Episcleritis = blanching of blood vessels
Scleritis = no blanching of blood vessels (as the vessels are too deep)
List some differentials for ptosis
- Oculomotor CN3 palsy
- Horners syndrome
- Myasthenia gravis / Lambert-Eaton syndrome
- Age
List some complications of herpes zoster ophthalmicus
- Cranial nerve 3, 5, 6 palsy
- Keratitis
- Uveitis
- Conjunctivitis
List some causes of optic disc swelling
- Raised intracranial pressure (papilloedema)
- Severely raised blood pressure
- Optic neuritis e.g. in MS
- Anterior ischaemic optic neuropathy
