Ophthalmology Flashcards
Describe the anatomy of the visual pathway
Optic nerve formed by convergence of axons from the retinal ganglion, temporal retina sees nasal visual field and nasal retina sees temporal visual field
Nerve leaves bony orbit via optic canal (passage through sphenoid bone), enter cranial cavity and runs along surface of middle cranial fossa (close to pituitary gland)
Optic nerves from each eye unite to form optic chiasm, nasal fibres cross and temporal fibres remain ipsilateral
Left optic tract – fibres from left temporal retina and right nasal retina
Right optic tract – fibres from right temporal retina and left nasal retina
Optic tracts travel to lateral geniculate nucleus –> optic radiation
Upper optic radiation – fibres from superior retinal quadrants, which correspond to the inferior visual field quadrants, goes through parietal lobe
Lower optic radiation – fibres from inferior retinal quadrants, which corresponds to superior visual field quadrants, goes through temporal lobe (Meyer’s loop)
Describe the pathway responsible for the pupillary light reflex
Afferent – retinal ganglion cell layer to optic nerve, optic chiasm, optic tract, brachium of superior colliculus, to pretectal area of midbrain, send fibres bilaterally to efferent Edinger-Westphal nucleus
Efferent – begins in Edinger-Westphal nucleus, efferent parasympathetic preganglionic fibres travel on outside of oculomotor nerve to synapse in ciliary ganglion which sends parasympathetic postganglionic axons in the short ciliary nerve to innervate the iris sphincter smooth muscle via M3 muscarinic receptors
Due to bilateral EW nucleus innervation, direct and consensual response produced
Describe the function and innervation of the extraocular muscles
Levator palpebrae superioris – elevates upper eyelid, oculomotor nerve
Muscles of eye movement
Superior rectus – elevation, adduction and medial rotation, oculomotor nerve
Inferior rectus – depression, adduction and lateral rotation, oculomotor nerve
Medial rectus – adduction, oculomotor nerve
Lateral rectus – abduction, abducens nerve
Superior oblique – depression, abduction and medial rotation, trochlear nerve
Inferior oblique – elevation, abduction, lateral rotation, oculomotor nerve
Describe the anatomy of the carotid arteries (particularly in relation to the eyes)
Right common carotid arises from bifurcation of brachiocephalic trunk (subclavian artery is other branch), at the level of the sternoclavicular joint
Left common carotid branches directly from the arch of the aorta
Left and right common carotids ascend up neck, lateral to tracheal and oesophagus
At the level of the superior margin of the thyroid cartilage (C4) they split into external and internal, dilations at this level = carotid sinus
External carotid supplies head and neck outside cranium, travels anterior to ear and terminates in parotid dividing into – superior thyroid, lingual, facial, ascending pharyngeal, occipital, posterior auricular, maxillary, superficial temporal arteries
Internal carotid enters cranial cavity via carotid canal in petrous part of temporal bone
Eyeball receives arterial supply via ophthalmic artery, branch of internal carotid which arises distal to cavernous sinus
Branches of ophthalmic artery supply eye, central artery of the retina is most important, occlusion causes blindness quickly
Describe the origin and path of the abducens nerve and the clinical consequences of an abducens nerve palsy
Abducens nerve nucleus is in the dorsal pontomedullary junction, nerve exits and emerges in the cerebellopontine angle on the medial aspect of the ventral pontomedullary junction
Exit brainstem, travel through middle cranial fossa, travels through Dorello’s canal in the temporal bone to the cavernous sinus, where it travels close to the internal carotid artery
Exits skull through superior orbital fissure to innervate lateral rectus
Abducens nerve palsy – horizontal diplopia, worse when trying to look towards affected side, convergent strabismus
Describe the origin and path of the trochlear nerve and the clinical consequences of a trochlear nerve palsy
Trochlear nucleus anterior to cerebral aqueduct at level of inferior colliculus
Efferent fibres decussate and exit brainstem lateral to inferior colliculi, passes within subarachnoid space of middle cranial fossa, enters cavernous sinus, passes through superior orbital fissure and innervates superior oblique muscle
Trochlear nerve palsy – vertical diplopia when looking inferiorly, may try to compensate by tilting head forwards
Also causes torsional diplopia, often tilt head to opposite side to put two images together
Describe the origin and path of the oculomotor nerve and the clinical consequences of an oculomotor nerve palsy
Oculomotor nucleus at level of superior colliculus and Edinger-Westphal nucleus (parasympathetic), both fibres travel through middle cranial fossa, enter cavernous sinus, travels through superior orbital fissure to innervate extraocular muscles and ciliary ganglion
Oculomotor nerve palsy – unopposed lateral rectus and superior oblique pull eye inferolaterally, causing ‘down and out’ appearance, can also cause ptosis (loss of innervation to levator palpebrae superioris) and mydriasis (loss of parasympathetic fibres)
‘Medical’ – pupil spared
‘Surgical’ – pupil fixed and dilated
Describe the anterior and posterior chambers of the eye, production of aqueous and normal intraocular pressure
Anterior chamber between cornea and iris and posterior chamber between iris and lens
Filled with aqueous humour which supplies nutrients to cornea
Aqueous is produced by ciliary body, flows from ciliary body around lens and under iris, into anterior chamber through trabecular meshwork and into the canal of Schlemm, then enters general circulation
Normal intraocular pressure is 10-21mmHg, created by resistance to flow through trabecular meshwork
Obstruction of drainage of aqueous causes rise in intraocular pressure
Describe the mechanism of the accommodation reflex
Coordinated change which occurs when you switch focus from far to near object
Involves three separate processes:
Accommodation reaction
When focusing on distant object, ciliary muscles relax, which creates tension in the zonule fibres and causes lens to become flat and thin
When focusing on near object, ciliary muscles contract, which allows zonule fibres to relax and lens becomes thicker and rounder
Convergence
Simultaneously inward movement of both eyes towards each other, caused by bilateral contraction of medial recti
Miosis
Decrease in diameter of pupil, contraction of iris sphincter muscles to increase depth of focus
Describe the layers of the retina
Retinal pigment epithelium – single layer of cuboidal epithelial cells, outermost layer of retina, responsible for nourishment and support of neural retina
Tight junctions between RPE cells form blood-retinal barrier
Neural retina – from outer to inner
Photoreceptor cells – rods (low-light), cones (daylight, high acuity, concentrated on fovea) and intrinsically photosensitive retinal ganglion cells
Bipolar cells
Retinal ganglion cells
Describe the structures of the retina visible on fundoscopy
Macula – pigmented area in the centre of the retina, contains fovea at centre which is a depression densely packed with cones
Optic disc – point of retinal ganglion cell axons leaving eye, cup in centre, no photoreceptor cells (blind spot)
Vasculature – veins are thicker and darker than arteries
What are the important points in a vision loss history?
Onset – sudden or gradual
Timing
Duration – transient?
Progression
Associated symptoms – pain, flashes or floaters, haloes, headache, red eye, nausea/vomiting
Uni or bilateral
Characterise vision loss – central, peripheral, quadrant, patchy
Ocular history - glasses/contact lenses
PMHx
DHx
FHx
How is visual acuity assessed?
Distance vision – Snellen chart
Wear glasses/contact lenses if have them
Stand 6m away from chart
Cover one eye and read to lowest line they are able to, record as 6/line they get to (- letters they get incorrect)
Can use pinhole to see if it improves vision (suggests refractive component)
Repeat with other eye
If poor vision even with pinhole – reduce distance to 3m, reduce distance to 1m, count fingers, hand movements, perception of light
Near vision
Wear reading glasses if have them
Cover one eye and read from small print in a book/newspaper
Repeat on other eye
How are the visual fields assessed?
Sit directly opposite patient, 1m away
Patient cover one eye, you mirror this
Focus on my nose and don’t move eyes or head
Ask if any part of face is missing or distorted – screen for central visual field loss/distortion (can check further with Amsler chart)
Position hand at equal distance between you and patient, start from peripheral and move in towards centre, ask patient when they see it, compare to your own visual field
Repeat for each visual field quadrant and repeat for other eye
If find visual field defect define its boundaries
How are the pupils examined?
Inspect for size, asymmetry (anisocoria), shape, iris colour
Pupillary reflexes – direct, consensual, swinging light test (for relative afferent pupillary defect), accommodation
How do you perform fundoscopy with an ophthalmoscope?
Dilate pupils with short-acting mydriatic eye drops (e.g. tropicamide 1%) – have to assess acuity, colour vision, visual fields, pupillary reflexes before this
Patient looking straight ahead
Assess fundal reflex
Ophthalmoscope settings – net of yours and patient’s refractive error (if not wearing glasses)
Put right eye to right eye, hold ophthalmoscope in right hand
Assess optic disc – follow blood vessel back to find disc, assess contour (should have clear borders), colour (normal is orange/pink), cup (0.3 cup-to-disc ratio is normal)
Retina – assess each quadrant (superior temporal, superior nasal, inferior nasal, inferior temporal) for vascular arcades, macula (exudates, drusen, cherry-red spot)
Repeat on other eye
How do you examine the movements of the eyes?
Hold finger (or pin) approx 30cm in front of patient’s eyes, ask them to focus on it
Observe for any deviation or abnormal movements
Keep head still and follow finger with eyes, move finger in ‘H’ pattern
Observe for restriction of eye movements, note any nystagmus
Ask about any diplopia, pain
What are cataracts? What are the causes/risk factors for cataracts?
Opacification of the lens that causes blurred distance and near vision
Causes:
Ageing – most commonly, usually >60s
Eye disease – develop as a complication of another eye disease e.g. chronic anterior uveitis, acute congestive angle-closure glaucoma, high myopia
Trauma – blunt or penetrating injury to eye, exposure to radiation, complication of eye surgeries
Systemic disease e.g. diabetes
Congenital cataracts in children – idiopathic (unilateral), bilateral (idiopathic, hereditary, intrauterine infections, genetic syndromes, metabolic conditions)
Other risk factors:
Steroids
Exposure to UVB light
Ethnicity – Asian
FH
Female
Hypertension
Smoking
Describe the clinical presentation of cataracts
Slow progressive blurring of vision
Difficulty seeing at night
Glare when looking at lights – haloes
Colours appearing dull
Reduced red reflex – leukocoria
Clouded lens
Poor visual acuity
List the types of cataracts and their features
Nuclear – sclerosis of lens nucleus, common in old age, cause myopia and dullness of colours (short-sightedness, used to need reading glasses but no longer do)
Cortical – opacification of lens cortex, looks like spokes of a wheel around the edge of the lens
Posterior subcapsular cataracts – opacification in posterior aspect of lens capsule, tends to be younger and those taking steroids, causes glare looking at lights, more rapid progression
How are cataracts managed?
If early/not causing significant visual impairment – may not need intervention
Cataract surgery if:
Patient is symptomatic and their lifestyle is affected
To treat acute angle closure glaucoma
To allow better visualisation of retina to manage co-pathology e.g. diabetic retinopathy
Cataract surgery:
Small incision made at corneal margin, phacoemulsification probe inserted, US breaks up cataract into microscopic fragments which are aspirated using probe tip, pseudophakia inserted (biometry to calculate power of implant)
What are the potential complications of cataract surgery?
Intraoperative – posterior capsular rupture
Postoperative – endophthalmitis, uveitis, cystoid macular oedema, retinal detachment, posterior capsular opacification
Endophthalmitis – infection of acqueous/vitreal humour, rare severe complication which can lead to visual loss, presents with pain, red eye, ocular discharge, blurring, treated with intravitreal antibiotics
What is glaucoma? Describe the types of glaucoma
Progressive optic neuropathy associated with raised intraocular pressure
Open angle or closed angle:
Open angle – angle between iris and cornea is normal
Angle closure – angle between iris and cornea is at least partially closed
Can be primary (more common) or secondary
Can be acute, subacute or chronic
Describe the cause of and risk factors for primary open angle glaucoma
Increasing age - >65
Myopia – short-sightedness
Family history
African-Caribbean ethnic origin
Untreated ocular hypertension – raised IOP
Cardiovascular disease and hypertension
Steroids
Type 2 diabetes
How does primary open angle glaucoma present? How is it diagnosed?
Often asymptomatic rise in intraocular pressure – may be picked up on routine screening
Affects peripheral vision first, gradual development of tunnel vision, arcuate scotoma – assess visual fields
Can present with gradual onset of fluctuating pain, headaches, blurred vision, halos around light at night (if advanced)
Intraocular pressure >21mmHg – measure using Goldmann applanation tonometry
Optic disc rim notching and cupping (cup:disc ratio enlarged/asymmetrical) - fundoscopy
How is primary open-angle glaucoma managed?
Laser trabeculoplasty – everyone with IOP >24 if at risk of visual impairment in lifetime
Medical management
1st line – generic prostaglandin analogues (e.g. latanoprost)
Others – beta-blockers (timolol), carbon anhydrase inhibitors (e.g. acetazolamide) and sympathomimetics (e.g. pilocarbine)
Surgical management
Trabeculectomy – create channel in sclera for drainage of aqueous humour, forms bleb under conjunctiva, reabsorbed to general circulation, mitomycin-C given alongside (prevents excessive postop scarring)
Can also insert plastic shunts if needed to create permanent drainage channel
What are the causes of and risk factors for acute angle-closure glaucoma?
Increasing age
Female
Family history
Chinese and East Asian ethnic origin – rare in African Caribbean people
Anatomical predisposition – hypermetropia, short eyeball length, shallow anterior chamber
Medications – adrenergic (e.g., noradrenaline), anticholinergic (e.g., oxybutynin, solifenacin), tricyclic (e.g., amitriptyline)
Describe the presentation of acute angle closure glaucoma
Acute presentation – develop over hours-days
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting
Unilateral conjunctival injection
Diffusely hazy cornea limiting view of iris and pupil
Fixed, non-reactive, mid-dilated pupil
Eye hard on palpation
Impaired visual acuity
Very high IOP - >30, can be as high as 60-80mmHg
How is acute angle-closure glaucoma diagnosed?
Gonioscopy – gold standard for investigating angle between iris and cornea, needed for diagnosis of angle closure
Goldmann applanation tonometry used to measure intraocular pressure
Describe the management of acute angle closure glaucoma
Immediate management:
Lie flat – helps to open angle
Give pilocarpine drops (2% for blue eyes, 4% for brown eyes)
Acetazolamide 500mg orally daily
Definitive management:
IV/oral acetazolamide
Drops - beta-blockers (timolol), steroids, carbonic anhydrase inhibitor (dorzolamide), sympathomimetic (brimonidine)
?pilocarpine
Laser iridotomy
Describe the effect of diabetes on the eyes
Retinopathy
Increased susceptibility to infection
Dry eyes and keratitis
Anterior uveitis
Cataract
Diabetic papillitis
Cranial nerve palsies
Describe the pathophysiology of diabetic retinopathy
Prolonged hyperglycaemia – damage to retinal small vessels and endothelial cells
Increased vascular permeability leads to leakage from blood vessels, blot haemorrhages and formation of hard exudates (lipid deposits)
Damage to blood vessel walls causes microaneurysms and venous beading (string of beads appearance)
Ischaemia of the retinal nerve fibre layer causes fluffy white patches to form – cotton wool spots
Blood flow compromised, regions of retina starved of oxygen, stimulates release of mediators e.g. VEGF, promotes neovascularisation
Neovascularisation into vitreous humour may cause widespread vitreous haemorrhage (leads to sudden and complete vision loss)
Increased retinal traction due to blood vessels growing into vitreous, can cause retinal detachment
Describe the classification of diabetic retinopathy and the implications for screening and referral
R0 – no signs of diabetic retinopathy, re-screen in 12 months
Non-proliferative – background diabetic retinopathy
R1 (mild) – at least one dot haemorrhage or microaneurysm with or without hard exudates, re-screen in 12 months
R2 (moderate) – four or more blot haemorrhages in one hemi-field only, hard exudates, cotton wool spots, venous beading, rescreen in 6 months
R3 (severe) – four or more dot haemorrhages in both inferior and superior hemi-fields, venous beading, intra-retinal vascular abnormalities, refer to ophthalmology
Proliferative
R4 (proliferative) – new vessels, vitreous haemorrhage, refer to ophthalmology
List risk factors for diabetic retinopathy
Longer duration of hyperglycaemia
Hypertension
Ethnicity
Pregnancy
Hyperlipidaemia/hypercholesterolaemia
Describe the clinical presentation of diabetic retinopathy
Often asymptomatic – only present with clinically significant macular oedema or large vitreous haemorrhage
Symptoms of diabetic retinopathy:
Floaters
Blurred vision and distortion – if macula affected
Decreased visual acuity – gradual, painless
Loss of vision – severe haemorrhage
Describe the features of diabetic maculopathy
M1 – hard exudates within 1-2 disc diameters of centre of fovea
M2 – blot haemorrhages or hard exudates within 1 disc diameter of centre of fovea
List the complications associated with diabetic retinopathy
Retinal detachment
Cataract
Optic neuropathy
Glaucoma
Retinal vein occlusion/optic disc swelling
Rubeosis iridis - growth of new vessels on iris
Vitreous haemorrhage
Blindness
How is diabetic retinopathy diagnosed?
Fundoscopy features – microaneurysms, dot and blot haemorrhages, hard exudates, cotton wool spots, venous beading, intraretinal microvascular abnormalities
HbA1c – assess glycaemic control
Optical coherence tomography – cross-sectional view of retina, used to quantify levels of macular oedema
Fluorescein angiography – gold-standard for visualising the vasculature of retina
How is diabetic retinopathy managed?
Medical management
Glycaemic control – aim for HbA1c 48-58
Blood pressure control – aim for <140/80 in all diabetics, if have severe diabetic retinopathy should aim for systolic <130
Lifestyle – diet, exercise, smoking cessation
Photocoagulation
For proliferative and sometimes severe non-proliferative diabetic retinopathy
Use laser to create burns in retina, destroying photoreceptors to reduce retinal oxygen demand and expression of VEGF, delaying progression
Focal – target specific point or general area (grid)
Pan-retinal – whole of periphery of retina targeted
Intravitreal anti-VEGF/steroid injections
Minimise neovascularisation e.g. aflibercept and ranibizumab
Vitrectomy – persistent vitreal haemorrhage or tractional retinal detachment
Describe screening for diabetic retinopathy
Annual eye screening for everyone >12 with diabetes
Screening on diagnosis of diabetes
List risk factors for age-related macular degeneration
Increasing age
Family history
Caucasian
Smoking
Hypertension, cardiovascular disease
Obesity
Diet – high fat intake
Drugs – aspirin
Describe the pathophysiology and classification of age-related macular degeneration
Drusen – yellow deposits of proteins and lipids which appear between retinal pigment epithelium and Bruch’s membrane (above choroid)
Small numbers of Drusen are normal, accumulation of more Drusen is indication of early AMD
As AMD progresses other abnormalities including pigment abnormalities and geographic atrophy develop
Wet AMD = formation of choroidal neovascular membrane made of new abnormal blood vessels beneath the retina, driven by VEGF
Dry AMD = non-exudative and non-neovascular, Drusen, pigmentary changes and geographic atrophy only
Describe the clinical presentation of age-related macular degeneration
Gradually worsening central visual field loss (if acute – wet)
Reduced visual acuity
Crooked or wavy appearance to straight lines (metamorphopsia)
Symptoms worse in low light
Can be unilateral or bilateral
How is age-related macular degeneration diagnosed?
Acuity – Snellen chart
Visual field – Goldmann perimetry
Amsler grid – assess for metamorphopsia
OCT – assess thickness of retina and presence of retinal fluid
Fluorescein angiography – detect choroidal neovascularisation
How is age-related macular degeneration diagnosed?
Acuity – Snellen chart
Visual field – Goldmann perimetry
Amsler grid – assess for metamorphopsia
Fundoscopy - features including Drusen, geographic atrophy, pigmentation abnormalities, neovascularisation
OCT – assess thickness of retina and presence of retinal fluid
Fluorescein angiography – detect choroidal neovascularisation
How is age-related macular degeneration managed?
Dry – no specific management, lifestyle factors e.g. smoking, control blood pressure, vitamin supplements (Vitamins C and E, zinc etc.)
Wet – anti-VEGF (ranibizumab, bevacizumab) intravitreal injections, given monthly for three months
List potential complications of intravitreal injections
Usually benign and transient
Chemosis – oedema of conjunctiva
Scleral injection – swelling of conjunctival vessels, bloodshot eye
Sensation of grittiness/itchiness at injection site
Infection, including endophthalmitis (<1%)
Retinal detachment (<1%)
Cataract formation (<1%)
Describe the aetiology and pathophysiology of retinal vein occlusion
Atherosclerosis leads to thrombus formation, occludes retinal veins and blocks drainage of blood flow from retina – can be obstruction of one of four retinal branch veins or central retinal vein
Pooling of blood in retina leads to macular oedema and retinal haemorrhages –> loss of vision
Also stimulates release of VEGF, leading to neovascularisation
List risk factors for retinal vein occlusion
Age
Atherosclerosis – hyperlipidaemia, hypertension, diabetes
Open-angle glaucoma
Inflammatory causes – sarcoidosis, Lyme’s disease
Hypercoagulable states – smoking, COCP, pregnancy, malignancy, sickle cell disease
Myeloproliferative disorders
Systemic vasculitis – Behcet’s disease, polyarteritis nodosa
Describe the clinical presentation of retinal vein occlusion
Sudden, painless unilateral vision loss (can be bilateral occasionally)
Branch – partial visual field defect and metamorphopsia (can be asymptomatic if macula spared)
Reduced visual acuity
Relative afferent pupillary defect – suggests ischaemia
Visual field defect
On fundoscopy – flame and dot haemorrhages, optic disc oedema, macula oedema, ischaemic changes (haemorrhages, cotton wool spots, optic disc swelling) and neovascular complications (neovascularisation, iris rubeosis, vitreous haemorrhage)
How should retinal vein occlusion be investigated?
Check for associated/predisposing conditions
FBC – leukaemia
ESR – inflammatory disorders
BP – hypertension
Glucose – diabetes
Thrombophilia screen – SLE auto-antibody, antiphospholipid antibody
Ophthalmic imaging
Fundal photography
Optic coherence tomography – macular oedema
Fundus fluorescein angiography
How is retinal vein occlusion managed?
Identify and optimise systemic risk factors to minimise risk of vein occlusion to other eye (and other systemic effects) – control blood pressure, blood glucose
Definitive ophthalmic management
No treatment to reverse pathology
Macular oedema – anti-VEGF agents (e.g. bevacizumab), intravitreal steroid implant, macular laser therapy
Neovascular complications – pan-retinal photocoagulation
Ophthalmology review and follow-up
Describe the aetiology of and risk factors for central retinal artery occlusion
Most commonly due to embolism – carotid artery disease or AF
Can also be due to in-situ thrombosis, due to atherosclerotic disease, vasculitis, inflammatory disorders, hypercoagulable states
Risk factors:
Hypertension
Smoking
Hyperlipidaemia
Diabetes
Hypercoagulable states – sickle cell anaemia, multiple myeloma, SLE, Factor V Leiden, polyarteritis nodosa, giant cell arteritis, antiphospholipid syndrome, Behcet’s disease
Male
Carotid artery stenosis
Describe the clinical presentation of central retinal artery occlusion
Sudden painless loss of vision – very rapid
Profound unilateral reduction in visual acuity
Relative afferent pupillary defect
Pale retina with central cherry-red spot
How should central retinal artery occlusion be investigated?
ESR/CRP – giant cell arteritis
FBC – myeloproliferative disorders
Coagulation screen
HbA1c, lipid profile
Vasculitic screen – ANA, ENA, ANCA, ACE
Carotid duplex US – carotid artery stenosis
ECG – AF
Echo – mural thrombus
How is central retinal artery occlusion managed?
Immediate management (little evidence) – ocular massage, dilate artery (inhaled carbogen, sublingual isosorbide dinitrate), reduce intraocular pressure (IV acetazolamide, mannitol)
If presenting within 24 hours – intra-arterial fibrinolysis (local urokinase injection) or IV thrombolysis (tPA e.g. alteplase)
Long-term management – address and modify underlying risk factors (diet, lifestyle, smoking, hypertension, hyperlipidaemia, AF, carotid artery disease)
Describe the aetiology of anterior ischaemic optic neuropathy
Ischaemia of the optic nerve which results in visible optic disc swelling (if no disc swelling it is posterior ischaemic optic neuropathy)
Broadly divided into arteritic (giant cell arteritis) and non-arteritic
Arteritic due to inflammation of the temporal arteries, thrombosis in posterior ciliary arteries which leads to ischaemia of optic disc, almost always due to giant cell arteritis
Non-arteritic due to non-inflammatory disease of short posterior ciliary arteries supplying optic disc, e.g. atherosclerosis, more common
Describe the clinical presentation of anterior ischaemic optic neuropathy
Arteritic:
Sudden loss of vision
New-onset headache (temporal)
Jaw claudication
Scalp tenderness
Diplopia
Reduced visual acuity
Pale swollen optic disc
Relative afferent pupillary defect
Non-arteritic:
Acute painless loss of vision in one eye – blurring/cloudiness
Visual loss on waking
Reduced visual acuity – less profound
Pale swollen optic disc with splinter haemorrhages
Relative afferent pupillary defect
How is anterior ischaemic optic neuropathy managed?
Temporal arteritis – high-dose systemic steroids
NAION – no proven treatment, optimise risk factors
Describe the pathophysiology of retinal detachment
Neurosensory retina separates from retinal pigment epithelium
Usually occurs secondary to full-thickness retinal tear, allows vitreous fluid to build up behind neurosensory retina (= rhegmatogenous retinal detachment)
Other causes – tractional (vitreous membranes pull on retina which separates it from epithelial layer, more common in diabetic retinopathy), exudative (build-up of exudative fluid under retina)
List risk factors for retinal detachment
Age >40
Male
Myopia
FHx
Ocular surgery
Trauma
Diabetic retinopathy
Retinal detachment in contralateral eye
Describe the clinical presentation of retinal detachment
Painless vision loss
Shadow across vision, peripheral vision affected
Blurred/distorted vision
Flashes and floaters
Poor visual acuity
Relative afferent pupillary defect
Altered fundal reflex
Slit lamp – tobacco dust (due to pigment cells migrating through tear in retina)
How is retinal detachment diagnosed?
Visual acuity
Visual field testing
Slit lamp examination
Indirect ophthalmoscopy
US – vitreal haemorrhage
How is retinal detachment managed?
Preventative – retinal tears treated with laser photocoagulation
Surgical management
Vitrectomy – vitreous removed and subretinal fluid drained, cryotherapy/laser therapy used to seal retinal tear and eye filled with absorbing gas, air or silicone bubble to hold it in place
Pneumatic retinopexy – if straightforward, expansile gas injected into the vitreous, laser or cryotherapy creates adhesive scar which holds retina in place
Scleral buckle – cryotherapy/laser photocoagulation used to create scar, silicone band sutured onto sclera to close retinal break and relieve traction
Describe the aetiology of strabismus
Primary – idiopathic, congenital
Secondary – cranial nerve palsies, intracranial infection, intracranial/intraorbital/intraocular masses, orbital fracture or other trauma, myopathies, endocrinological condtions (diabetes, Grave’s)
Heavy metals and toxins
How should strabismus be assessed/described?
Light reflex (Hirschberg test)
Cover and cover-uncover tests
Describe – direction, laterality, frequency, comitant or noncomitant
Describe the presentation of blepharitis
Inflammation of the eyelid
Usually bilateral
Gritty, itchy, dry, foreign body sensation
Redness, crusting
Watering of eyes
Describe the aetiology of blepharitis
Anterior blepharitis – staphylococcal infection or seborrhoeic dermatitis of the base of the eyelashes
Posterior blepharitis – meibomian gland dysfunction (secrete oils which contribute to tears)
How is blepharitis managed?
Self-care measures – warm compress on eyes, eyelid massage, cleaning lids with cotton wool
If anterior blepharitis – topical antibiotic (e.g. chloramphenicol)
Lubricating eye drops for symptoms e.g. polyvinyl alcohol
If chronic posterior – low-dose oral tetracycline, regular omega-3 fatty acid supplements
Describe the aetiology of styes
Hordeola – acute localised infection/inflammation of eyelid margin due to staphylococcal infection
External – infected eyelash follicle/gland
Internal – conjunctival surface of eyelid, infection of Meibomian gland
How do styes present?
External - tender, red eyelash follicle swellings, small pus-filled spot
Internal – deeper, more painful, point inwards towards eyeball under eyelid
How are styes managed?
Warm compress
Usually resolve spontaneously
Removal of associated eyelash
Incision with fine sterile needle
Topical antibiotics e.g. chloramphenicol or oral antibiotics e.g. co-amoxiclav if recurrent/severe
What is a chalazion? Describe its aetiology and presentation.
Granulomatous inflammatory lesion that forms in obstructed meibomian gland, non-infectious
Painless red eyelid cyst in internal eyelid
How is chalazion managed?
Usually spontaneously resolve
Hot compress, eyelid massage and analgesia
Consider topic antibiotics (e.g. chloramphenicol) if acutely inflamed
Rarely may need incision and drainage
Define entropion and ectropion and describe their clinical features
Entropion – inward turning of the eyelid, eyelashes can irritate cornea causing ulceration and potentially sight loss
Ectropion – eyelid turns outward with inner aspect of eyelid exposed, usually affects bottom lid, can result in exposure keratopathy, presents with sore red eye, watery
