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
Describe the aetiology of entropion and ectropion
Entropion – age-related degenerative changes to lower eyelid, eyelid irritation or scarring, trachoma (bacterial eye infection caused by chlamydia trachomatis)
Ectropion – age-related degenerative changes, facial nerve palsy (Bell’s palsy)
How are ectropion and entropion managed?
Examination for corneal abrasions/ulcers
Lubricating drops/gel
Eyelid taping
Surgical correction
What is trichiasis? How does it present?
Inward growth of the eyelashes due to damaged eyelash follicles
Irritate cornea causing pain, corneal ulceration, and risking sight loss
Mostly caused by chronic blepharitis
How is trichiasis managed?
Assess for corneal damage
Epilate eyelashes – recurrent as they grow back
Electrolysis or laser ablation can destroy lash follicle for more permanent solution
Describe the differential diagnosis for eyelid lumps
Infectious/inflammatory
Blepharitis
Hordeolum
Chalazion
Neoplastic
Seborrhoeic keratosis – benign tumour, darkly pigmented, raised, well-defined with scaly texture
Actinic keratosis – pre-malignant for SCC, clusters of pink scaly lesions in sun-exposed areas
Basal cell carcinoma – most common, usually on lower eyelid, mostly nodular presenting as painless nodules, pearly raised edges, telangiectasic vessels, central ulcerations
Squamous cell carcinoma – painless, small raised keratin patch, transforms to papillomatous lesion and then larger ulcerated lesion
Malignant melanoma - rare
Describe the differential diagnosis of an acute painful red eye
Corneal abrasions and superficial foreign bodies
Microbial keratitis (corneal ulcer)
Chemical injury
Acute anterior uveitis
Anterior scleritis
Acute angle-closure glaucoma
Endophthalmitis
Describe the differential diagnosis of an acute painless red eye
Dry eye
Blepharitis
Conjunctivitis – viral, bacterial, allergic
Episcleritis
Subconjunctival haemorrhage
List causes of superficial corneal injuries
Mechanical trauma e.g. twig, fingernail, mascara brush
Foreign bodies e.g. dust, glass, rust
Chemical, radiation or flash burns
Contact lenses – during insertion or removal
Recurrent erosions if structural defects of corneal epithelium
Describe the clinical presentation of superficial corneal abrasions/foreign bodies
Sudden onset eye pain on blinking
Discomfort or foreign body sensation described as gritty or scratching
Tearing
Decreased or blurred vision
Conjunctival redness
Usually history of precipitating event e.g. object striking eye, foreign body entering eye
Visible foreign body on ocular surface
Scratches on cornea – glow green with fluorescein 2%
Linear vertical abrasions – foreign body under upper eyelid
How are corneal abrasions and foreign bodies managed?
Remove foreign body to prevent secondary microbial keratitis, use topical anaesthetic drops, irrigation with saline, cotton bud or hypodermic needle
Topical antibiotic ointment e.g. chloramphenicol after removal to prevent infection
Simple abrasions heal within 48-72 hours, prescribe prophylactic antibiotic ointment and oral analgesics
Describe the aetiology of microbial keratitis
Bacterial, viral, fungal, protozoan
Bacterial – most common is staphylococcus, can also be strep, pseudomonas, neisseria gonorrhoeae
Viral – herpes simplex (HSV-1), herpes zoster ophthalmicus
Fungal – aspergillus, fusarium, candida
Protozoan – acanthamoeba
Describe the risk factors for microbial keratitis
Contact lens wear – most common risk factor, especially prolonged use and poor lens hygiene
Corneal trauma – ocular surgery, foreign body, chemical injury
Ocular surface disease – dry eye, chronic blepharitis
Immunosuppression – drugs, immunodeficiency syndromes, diabetes
Contact with infected individuals – direct contact with infected secretions or lesions
Describe the clinical presentation of microbial keratitis
General features – gradual onset pain, redness, reduced visual acuity, photophobia, watering/discharge, lid oedema/erythema
Bacterial – usually unilateral, purulent discharge, hypopyon, posterior synechiae
Herpes simplex - watering, dendritic ulcer
Herpes zoster ophthalmicus – punctate keratitis (small dots on examination under fluorescein on cornea)
Fungal – grey-white stromal infiltrate with fluffy margins, satellite lesions, cells/hypopyon in anterior chamber
Acanthamoeba – severe pain, ring shaped infiltrate with radial perineural infiltrates, pseudodendrites
How is microbial keratitis diagnosed?
Clinical diagnosed – history and features on examination
Corneal scrapes and conjunctival swabs – send for culture and sensitivity, viral PCR, gram staining, for severe or treatment-resistant cases
Send contact lenses, cases, and solutions for C&S
How is microbial keratitis managed?
Discontinue contact lens use immediately
Bacterial – topical (broad-spectrum until culture results available), oral antibiotics if severe
Herpes simplex – topical antivirals (e.g. aciclovir 3% ointment), epithelial debridement, sometimes steroids (contraindicated in active epithelial disease)
Herpes zoster ophthalmicus – oral antiviral therapy (severe may need IV), may use concurrent oral steroids
Fungal – topical antifungals, systemic antifungals if severe
Acanthamoeba – topical anti-amoebic (e.g. chlorhexidine), hourly initially then tapered according to response, debridement of corneal epithelium, topical steroids
If severe corneal scarring or extensive necrosis may require penetrating keratoplasty (full-thickness corneal transplant)
What are the potential complications of microbial keratitis?
Spread of infection
Corneal perforation
Corneal scarring
Cataract formation
Describe the aetiology of herpes zoster ophthalmicus
Shingles (varicella zoster virus reactivation) affecting the ophthalmic branch of the trigeminal nerve
Risk factors:
Advancing age
Immunosuppressed e.g. HIV, chemotherapy
Pregnant
Neonates
Describe the clinical presentation of herpes zoster ophthalmicus
Viral prodromal phase – fever, malaise, headache
Pre-herpetic neuralgia – paraesthesia, pain in V1 dermatome
Rash – characteristic unilateral rash (macules -> papules -> vesicles -> pustules -> crusted lesions) in V1 distribution
Conjunctivitis, reduced visual acuity, red eye, sharp pain, foreign body sensation, watering
Punctate keratitis
What are the potential complications of herpes zoster ophthalmicus?
Post-herpetic neuralgia
Repeat corneal ulcers resulting in corneal thinning and perforation
Vision-threatening involvement of the posterior eye – acute retinal necrosis, optic neuritis
Cranial nerve palsy – extraocular muscle involvement
Systemic complications – pneumonitis, encephalitis, vasculitis, stroke, Guillain-Barre
Describe the aetiology of chemical injuries to the eye and their clinical implications
Alkali – more severe, penetrates more deeply into ocular tissues, ammonia and sodium hydroxide injuries tend to be very severe
Acid – coagulate proteins, form a protective barrier which prevents further penetration
Describe the clinical presentation of chemical injuries to the eye
Eye pain
Reduced visual acuity
Photophobia
Watering
Conjunctival hyperaemia
Corneal haze
Blanched blood vessels
Fluorescein 2% - corneal or conjunctival defect will glow green
How should chemical injuries to the eye be managed?
Immediate – irrigation until pH neutralises
Supportive measures – control pain and nausea
If corneal epithelial injury, haze, or blanched blood vessels – need specialist management, topical/oral therapy aimed at reducing inflammation, prevent infection, promote re-epithelialisation
Describe the aetiology of conjunctivitis
Infectious
Viral – adenovirus (most common), measles, mumps, rubella
Acute haemorrhagic viral conjunctivitis - enterovirus, coxsackievirus
Bacterial – staphylococcus, streptococcus, haemophilus, chlamydia trachomatis, neisseria gonorrhoea
Reactive – after bacterial infection usually
Non-infectious
Allergic
Chemical and irritant
Describe the clinical presentation of conjunctivitis according to aetiology
General – red-eye, chemosis, epiphora, discharge
Viral – bilateral, profuse watery discharge, may have tender preauricular lymphadenopathy, concurrent URTI, papillae
Bacterial – unilateral, rapid onset, inflamed conjunctiva and sticky purulent discharge, follicles
(Gonococcal – very profuse discharge, papillae
Chlamydial – follicles, pre-auricular lymphadenopathy)
Allergic – bilateral, itching, papillae, watery discharge, triggers e.g. pollen, dust, history of atopy
How is conjunctivitis managed?
Viral – self-limiting, hygiene measures
Bacterial – supportive, antibiotic drops rarely (chloramphenicol)
Gonococcus – topical antibiotics, systemic treatment (ceftriaxone, azithromycin)
Chlamydial – topical antibiotics, systemic treatment (doxycycline, azithromycin)
Allergic – allergen avoidance, topical and oral antihistamine, topical mast-cell stabilisers, occasionally mild steroids
List the potential complications of conjunctivitis
Viral – usually self-limiting and uncomplicated
Bacterial – higher risk of complications, neisseria can be invasive and cause keratitis/endophthalmitis, leading to blindness if untreated
Repeated infection with chlamydia can cause trachoma -> blindness (entropion, trichiasis)
Describe the presentation of episcleritis
Usually asymptomatic, may be mild pain, grittiness, foreign body sensation
Segmental redness (rather than diffuse), usually patch of redness in lateral sclera
Dilated episcleral vessels
Watery eye
No discharge
30% associated with systemic conditions e.g. rheumatoid arthritis, inflammatory bowel disease
How is episcleritis managed?
Self-limiting, recovery in 1-4 weeks
Simple analgesia
Cold compresses
More severe – systemic NSAIDs or topical steroid drops
Define scleritis and episcleritis
Scleritis – inflammation of the full thickness of the sclera
Episcleritis – inflammation of episcleral, outermost layer of sclera (just under conjunctiva)
What are the conditions associated with scleritis?
Systemic conditions in 50%
Rheumatoid arthritis
SLE
IBD
Sarcoidosis
Granulomatosis with polyangiitis
Describe the clinical presentation of scleritis
Acute onset
50% bilateral
Severe pain
Pain with eye movement
Photophobia
Eye watering
Reduced visual acuity
Abnormal pupil reaction to light
Tenderness to palpation of eye
How is scleritis managed?
NSAIDs
Steroids – topical/systemic
Immunosuppression appropriate to underlying condition e.g. methotrexate in rheumatoid arthritis
Describe the aetiology of subconjunctival haemorrhage
Small blood vessel within conjunctiva ruptures and release blood into space between sclera and conjunctiva
Often after episodes of strenuous activity e.g. heavy coughing, weight lifting, straining when constipated
Predisposing conditions – hypertension, bleeding disorders (e.g. thrombocytopaenia), whooping cough, medications (warfarin, NOACs, antiplatelets), NAI
Describe the presentation of subconjunctival haemorrhages
Patch of bright red blood under conjunctiva and in front of sclera covering white of eye, painless and does not affect vision
History of precipitating event e.g. coughing, heavy lifting
How are subconjunctival haemorrhages managed?
Harmless, resolve spontaneously in around 2 weeks
Think about causes e.g. hypertension, bleeding disorders
What is anterior uveitis? Describe its aetiology? What conditions is it associated with?
Inflammation in the anterior part of the uvea – involves iris, ciliary body and choroid
Infiltration by neutrophils, lymphocytes and macrophages
Usually autoimmune, can be infectious, traumatic, ischaemic, malignant
Acute anterior uveitis associated with HLA-B27 related conditions:
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis
Chronic anterior uveitis associated with:
Sarcoidosis
Syphilis
Lyme disease
Tuberculosis
Herpes virus
Describe the clinical presentation of anterior uveitis
Unilateral
Red (ciliary flush), watery, photophobic, dull ache
Hypopyon
Miosis – sphincter muscle contraction, posterior synechiae contraction causing irregular pupil
Visual acuity mildly reduced
Slit lamp examination – keratic precipitates, cells, flare
How is anterior uveitis managed?
Steroids – topical, oral, IV
Cycloplegic-mydriatic medications – cyclopentolate, atropine eye drops (paralyse ciliary muscles, dilate pupils, prevent pain due to ciliary spasm)
Immunosuppressants – DMARDs, TNF inhibitors
Severe – laser therapy, cryotherapy, surgery (vitrectomy)
List the differential diagnosis of acute painless vision loss
Anterior ischaemic optic neuropathy – non-arteritic is painless, arteritic associated with headache, scalp tenderness
Retinal artery occlusion – central retinal artery or branch retinal artery
Retinal vein occlusion – central retinal vein or branch retinal vein
Retinal detachment
Vitreous haemorrhage – mostly due to diabetic retinopathy
List the differential diagnosis of acute painful loss of vision
Acute angle-closure glaucoma
Endophalmitis
Anterior uveitis
Keratoconus
Traumatic causes – corneal abrasion/laceration, ruptured globe, intra-ocular foreign body, CNS injury
Optic neuritis
What is the differential diagnosis for chronic vision loss?
Refractive error
Chronic open angle glaucoma
Cataract
Age-related macular degeneration
Diabetic retinopathy
Drug toxicity e.g. hydroxychloroquine
Corneal scarring
Intracranial mass, optic nerve/tract compression e.g., pituitary tumour
Describe the pathological effects of hypertension on the eyes
Pathological changes due to increased pressure and resulting damage to retinal vessels:
Silver/copper wiring – walls of arterioles become thickened and sclerosed causing increased reflection of light
Arteriovenous nipping – arterioles cause compression veins where they cross, due to sclerosis and hardening of arterioles
Cotton wool spots – ischaemia and infarction in retina causing nerve fibre damage
Hard exudates – damaged vessels leak lipids into retina
Retinal haemorrhages – damages vessels rupture
Papilloedema – ischaemia to optic nerve, oedema and blurring of disc margins
How does hypertensive retinopathy present?
Usually asymptomatic if due to chronic hypertension
If malignant/accelerated hypertension usually symptomatic – blurring of vision, visual field defects, headache, flushed/red face, nausea and vomiting, sudden painless loss of vision due to vessel occlusion
Signs of end-organ damage – heart failure, kidney disease, chest pain
Describe the classification of hypertensive retinopathy
Keith-Wagener-Barker classification
Grade 1 – mild, generalised constriction of retinal arterioles
Grade 2 – definite focal narrowing of retinal arterioles and AV nicking
Grade 3 – grade 2 with flame-shaped haemorrhages, cotton-wool spots, hard exudates
Grade 4 – severe grade three retinopathy with papilloedema or signs of retinal oedema
How is hypertensive retinopathy managed?
Primarily reducing blood pressure – lifestyle changes, oral antihypertensives
Describe the ocular manifestations of HIV infection
Adnexa:
Herpes zoster ophthalmicus
Kaposi sarcoma
Molluscum contagiosum
Conjunctival microvasculopathy
Anterior segment:
Keratoconjunctivitis sicca (dry eyes)
Keratitis – most commonly herpes simplex and varicella zoster
Iridocyclitis – VZV, CMV, toxoplasmosis, syphilis, tuberculosis
Posterior segment:
Retinal microangiopathy
CMV retinitis
VZV retinitis
Toxoplasma retinchoroiditis
Bacterial/fungal retinitis
Neuro-ophthalmic
Papilloedema
Cranial nerve palsies
Cryptococcal meningitis, CNS lymphoma, neurosyphilis, toxoplasmosis
Describe the common ocular manifestations of multiple sclerosis
Optic neuritis – 20% of initial MS presentations, occurs in 75% throughout course of disease
Internuclear opthalmoplegia – diplopia, nystagmus, loss of depth perception secondary to adduction deficit or adduction lag on conjugate gaze
Uveitis more common in patients with MS
Describe the common ocular manifestations of sarcoidosis
Uveitis most common – usually anterior
Can be posterior e.g. choroidal granulomas, can lead to visual impairment and retinal detachment
Complications of chronic uveitis – cataract formation, glaucoma and cystoid macular oedema, can lead to vision loss
Conjunctival nodules, acute follicular conjunctivitis
Neurosarcoidosis – cranial nerve palsy, including optic or facial nerves
Describe the ocular manifestations of tuberculosis
Ocular TB uncommon
Can involve any part of the eye
Anterior uveitis – granulomatous
Posterior uveitis – most common ocular presentation
Endophthalmitis
Retinal TB – vasculitis leading to neovascularisation and retinal haemorrhage
Cranial nerve palsies
Scleritis
Interstitial keratitis
Describe the ocular manifestations of rheumatological disease
Dry eye (keratoconjunctivitis sicca) – RA, SLE, scleroderma, Sjogren’s
Episcleritis/scleritis – RA, IBD, vasculitis, psoriatic arthritis, Behcet’s disease, Wegner’s granulomatosis
Keratitis – Sjogren’s, RA, vasculitis, SLA, Behcet’s, IBD, psoriatic arthritis, sarcoidosis
Uveitis – HLA-B27 associated, Behcet’s, sarcoidosis, SLE, IBD, RA, reactive arthritis
Retinal vasculitis – SLE, vasculitis, RA, Crohn’s, polymyositis
Optic neuropathy – giant cell arteritis, SLE, antiphospholipid syndrome
Describe the features of Behcet’s syndrome
Associated with HLA-B51 gene – indicator of severe disease
Oral ulcers
Genital ulcers
Anterior uveitis
Others – thrombophlebitis, DVT, arthritis, GI symptoms, erythema nodosum
Describe the clinical features of thyroid eye disease
Commonly in Grave’s but can be hypothyroid or euthyroid
Smoking and radioiodine therapy are major risk factors
Exophthalmos
Conjunctival oedema
Eyelid retraction
Lid lag
Diplopia due to restriction of extraocular muscles (most commonly on looking down)
Incomplete eyelid closure – dry eyes, excessive watering, gritty sensation
Eye pain
Optic disc swelling
Rarely - compressive optic neuropathy (sight-threatening)
How is thyroid eye disease managed?
Correct thyroid hormone levels to achieve euthyroidism
Smoking cessation
Taping of eye to prevent ulceration
Steroids in severe cases – IV methylprednisolone in compressive optic neuropathy
Surgery – orbital decompression, lid surgery
Describe the ocular manifestations of strokes
Retinal ischaemia – central/branch retinal artery occlusion
Bitemporal hemianopia – chiasmal ischaemia
Homonymous hemianopias, quadrantopias– post-chiasmal ischaemia
Cortical blindness – bilateral occipital lobe ischaemia (normal pupillary light reflexes)
Ptosis – midbrain
Ocular dysmotility – CN palsy
Describe the aetiology of giant cell arteritis
Systemic vasculitis of large and medium-sized vessels
Usually affects ophthalmic artery and carotid artery, can also affect aorta
List the risk factors for giant cell arteritis
Age >50
Female sex
Polymyalgia rheumatica
Describe the clinical presentation of giant cell arteritis
Subacute onset unilateral temporal headache
Tongue and jaw claudication
Scalp tenderness
Painless complete or partial vision loss in one or both eyes
Diplopia
Systemic symptoms – malaise, fatigue, weight loss, fever
Reduced/absent temporal artery pulse
Oedema and pallor of optic disc
How is giant cell arteritis diagnosed?
FBC – normochromic normocytic anaemia, increased platelets
CRP/ESR increased
Temporal artery US – thickening of wall of affected vessel (halo sign)
Temporal artery biopsy – mononuclear cell infiltration or granulomatous inflammation with multinucleated giant cells
How is giant cell arteritis managed?
Initial management – if visual symptoms give one off 60-100mg prednisolone, if visual loss give 500mg-1g of IV methylprednisolone once daily for 3 days
No visual symptoms – 40-60mg prednisolone per day
Ongoing management – gradually taper dose of prednisolone, give PPI and osteoporosis prevention
What are the potential complications of giant cell arteritis?
Irreversible vision loss – visual symptoms are an ophthalmic emergency
Aortic dissections, aortic aneurysms, large artery stenosis
Cardiovascular events – stroke, MI
Complications of steroids
How should eyelid lacerations be assessed/managed?
Carefully explore wound and underlying eye structures
Document location, orientation, dimensions, and depth of lacerations
Complex if: full-thickness, extensive tissue loss, involving eyelid margin, foreign body, injury to underlying ocular structure, injury to lacrimal system, injury to levator palpebrae superioris, orbital fat prolapse
If suspicion of foreign body – X-ray or CT
Management:
Irrigation
Tetanus – confirm tetanus status and follow guidelines
Antibiotics
Horizontal and small, simple lacerations away from lid – leave to heal or close with glue
Complex – refer for specialist repair
Describe the mechanism of orbital floor fractures and associated injuries
Usually blunt force trauma to globe or periocular area, especially cheek
Increase in intraorbital pressure causes thin bones of orbital floor, sometimes medial wall
Orbital tissue herniates into sinus through defect in orbital floor
May be associated injury to globe – ruptured globe, retinal detachment, intraocular bleed
Can have impingement of nerves, extraocular muscles
Describe the presentation of orbital floor fractures
Recent trauma to eye or midface
Orbital pain
Enophthalmos – eyes displaced posteriorly into socket
Vertical diplopia
Orbital and lid subcutaneous emphysema – when blowing nose or sneezing
Limitation of eye movements
Bruising
Loss of sensation in V2 distribution
Nausea/bradycardia – oculocardiac reflex
How should suspected orbital floor fracture be investigated?
CT – visualise bony fractures, prolapse of soft tissues, extraocular muscle entrapment
How are orbital floor fractures managed?
Conservative/medical management – ice packs, nasal decongestants, don’t blow nose for 4-6 weeks, may need prophylactic antibiotics, steroids for swelling
Surgical repair if non-resolving diplopia or cosmetically unacceptable enophthalmos
Describe the mechanism of hyphaema and potential complications
Shearing of blood vessels due to blunt trauma that compresses the globe – haemorrhage in anterior chamber
Results in fluid level visible in anterior chamber
Can cause uncontrolled increase in intraocular pressure leading to ischaemic optic neuropathy and vision loss
Should evaluate for other ocular trauma e.g. globe rupture
Non-traumatic causes – neovascular diabetes, sickle cell disease, ocular neoplasms, uveitis
How is hyphaema managed?
Stay upright – allows blood to settle with gravity
Rigid eye shield
Avoid strenuous activity until resolved
Conservative management – oral analgesics, antiemetics, topical cycloplegics
Specialist management to control inflammation/intraocular pressure – anterior chamber washout
How should penetrating eye injuries be assessed?
Carefully open eyelids without applying pressure to globe – risk of intraocular pressure prolapse
Examine eye, signs of open globe injury:
Shallow anterior chamber, peaked or misshapen pupil
Embedded foreign body
Red reflex diminished secondary to traumatic cataract, vitreous haemorrhage or retinal detachment
CT – don’t use MRI if metal foreign body suspected
How are penetrating eye injuries managed?
Treat associated life-threatening injuries first
Rigid eye shield to prevent further injury until definitive management can be undertaken
Manage pain and nausea
Systemic prophylactic antibiotics
Assess tetanus status and manage
Surgical repair – severe injuries with no visual potential are treated with enucleation
Describe the clinical presentation of retrobulbar haemorrhage/orbital compartment syndrome
Proptosis
Resistance to retropulsion
Tense, difficult to open eyelids
Restriction in extraocular muscle movement
Reduced visual acuity
RAPD
Impaired colour vision
How is retrobulbar haemorrhage and ocular compartment syndrome managed?
Immediate decompression with lateral canthotomy and cantholysis – any delay may cause irreversible sight loss
If vision not immediately threatened need frequent monitoring of visual acuity, pupils, intraocular pressure
What is the difference between periorbital and orbital cellulitis?
Periorbital – infection anterior to orbital septum
Orbital – infection posterior to orbital septum
Describe the anatomy of the orbital septum
Membraneous sheet that forms the anterior boundary of the orbit, separates the pre-septal and post-septal spaces
Acts as a barrier to infection
Originates superiorly and inferiorly from the orbital periosteum
Superiorly continuous with levator palpebrae superioris, inferior continuous with inferior tarsal plate
Medially attached to lacrimal bone
Describe the aetiology of orbital cellulitis
Organisms – usually bacterial e.g. strep pyogenes, strep pneumoniae, staph aureus, haemophilus influenzae type B, more rarely pseudomonas spp
Often local spread from sinuses/dental infections
Can also be due to blunt or penetrating trauma, insect bites
Describe the presentation of orbital and periorbital cellulitis and potential complications
Symptoms of both – lid erythema, oedema, tenderness, fever, malaise
Orbital – chemosis, conjunctival hyperaemia, proptosis, reduced ocular motility, diplopia, blurry vision, reduced visual acuity, colour desaturation, RAPD
Orbital cellulitis –> intraorbital/subperiosteal abscess – marked vision loss, ophthalmoplegia, proptosis
Other complications – cavernous sinus thrombosis, meningitis, cerebral abscess
How should suspected periorbital and orbital cellulitis be assessed/investigated?
Visual acuity, colour vision, visual fields, eye movements, pupillary reflexes
Blood cultures
CT with contrast of orbits and sinuses (MRI may be more sensitive)
How are orbital and periorbital cellulitis managed?
Periorbital with orbital excluded – empirical oral antibiotics
Orbital cellulitis – hospital admission for IV antibiotics, initially empirical but can be switched if organisms/sensitivities identified
Surgical interventions – drainage of abscess, collect samples for culture and sensitivities, intracranial complications
List the common dyes used for examination of the eyes and describe their uses
Fluorescein - adheres to basement membrane so can highlight areas of epithelial breakdown (green) e.g. dry eyes, corneal ulcers/abrasions
Rose bengal - stains dead/devitalises cells, used in diagnosis of dry eyes, conjunctival squamous neoplasms, herpetic dendrites, superficial punctate keratitis
Describe the mechanism of action, uses and examples of mydriatric eye drops
Either inhibit parasympathetic pathway to iris sphincter or promote sympathetic pathway to iris dilator
Muscarinic antagonists block parasympathetic - atropine, cyclopentolate, tropicamide
Alpha-1 adenergic receptors promote sympathetic - phenylephrine
Uses:
Diagnostic for fundoscopy
For procedures e.g. cataract surgery
Anterior uveitis - decrease posterior synechiae and pain
List the common imaging techniques used in ophthalmology and describe their uses
Ocular ultrasound - measure globe length to calculate lens power, measurement of tumours, visualisation of lens dislocation and retinal detachment, especially when fundus obscured by dense cataracts or vitreal haemorrhage
Optical coherence tomography (OCT) - gives cross sectional view of retina via inferometry, can detect macular oedema and exudates, retinal detachment, glaucoma, optic neuritis
Describe the potential complications of cataract surgery
Immediate, mild - discomfort, bruising and swelling of eyelid, increased intra-ocular pressure
Early, more serious - posterior capsule rupture/vitreous loss, cystoid macular oedema (most common complication), endophthalmitis, vitreous haemorrhage, retinal tears/detachment, lens dislocation
Long-term - posterior capsular opacification
What are the potential complications of retinal laser treatment?
Mild pain during/after treatment
Permanent decrease in peripheral, colour and night vision
Choroidal effusion - temporary worsening of vision
Describe the visual requirements for driving?
Visual acuity must be at least Snellen 6/12 with both eyes or in only eye if monocular
Visual field must be at least 120 degrees horizontal, 50 left and right and no significant defect in the binocular field that encroaches within 20 degrees of the fixation above or below the horizontal meridian
How do people register as visually impaired? What are the implications?
Severely sight impaired (blind) - visual acuity less than 3/60 with full visual field, between 3/60 and 6/60 with severe reduction of field of vision, above 6/60 with very reduced field of vision
Sight impaired (partially sighted) - 3/60 to 6/60 with full field of vision, up to 6/24 with moderate reduction of field of vision or central vision loss, 6/18 or better if large visual field defect
Registration after ophthalmologist assessment, they complete Certificate of Vision Impairment and register with local services
Advantages of registering:
Welfare benefits - reduced taxes, free public transport, blue badge for parking etc.
List types of low-visual aid
Magnifiers - handheld, binoculars and monoculars etc.
Typoscopes - card with holes to act as guide when reading/writing
Specialist electronic low vision devices - use camera to magnify and show on viewing screen
Large print products
Reading stands
Task lights
Describe the aetiology of/risk factors for Charles-Bonnet syndrome
Visual impairment
Older age
Social isolation
Early cognitive impairment
Most common causes of visual impairment - age-related macular degeneration, glaucoma, cataract
Describe the clinical features of Charles-Bonnet syndrome
Visual hallucinations
Simple - flashes of light, patterns
Complex - images of people, objects, life-like scenes
Insight preserved
No other significant neuropsychiatric disturbance
Define papilloedema
Optic disc swelling secondary to raised intracranial pressure
List causes of raised intracranial pressure
Skull too small for brain e.g. craniosynostosis
Brain volume too large for skull e.g. space-occupying lesion (tumour, haemorrhage), brain oedema (trauma)
Obstruction of CSF flow e.g. colloid cyst obstructing foramen of Monroe
Increased production of CSF e.g. choroid plexus papilloma
Reduced absorption of CSF e.g. meningitis, cerebral venous thrombosis
Idiopathic intracranial hypertension - young, overweight (or recent weight gain), women, PCOS, thyroid disease, obstructive sleep apnoea
Describe the appearance of papilloedema on fundoscopy
Blurred margins of optic disc
Small haemorrhages
How should papilloedema be managed?
Full visual assessment - visual fields, visual acuity (important for baseline)
Urgent referral to ophthalmology to confirm and to neurology
Neuroimaging - CT/MR venogram and CT/MRI
LP with opening pressure if no cause found on neuroimaging
Describe the diagnostic criteria for idiopathic intracranial hypertension
Require all:
Papilloedema (not mandatory if imaging suggestive)
Normal neurological exam (VI nerve palsy allowed)
Normal neuroimaging and sinus thrombosis excluded
CSF constituents normal
Elevated CSF opening pressure
Describe the presentation of idiopathic intracranial hypertension
Severe headache - worse in morning, generalised, throbbing worse with coughing/sneezing
Associated nausea/vomiting
Pulsatile tinnitus
May have VI nerve palsy
Papilloedema
How is idiopathic intracranial hypertension managed?
Weight reduction
Medical management - acetazolamide
Surgical management - shunts, CSF diversion
List the contents of the cavernous sinus and the clinical implications of this
Travels through:
Abducens nerve
Carotid plexus - post-ganglionic sympathetic nerve fibres
Internal carotid artery
In lateral wall:
Oculomotor nerve
Trochlear nerve
Ophthalmic and maxillary branches of trigeminal nerve
Cavernous sinus thrombosis - usually due to infection, most commonly affects abducens nerve
Internal carotid aneurysm - oculomotor palsy
Describe the ophthalmological implications of pituitary tumours
Compression of optic chiasm - slow decrease in visual function, bitemporal hemianopia (peripheral visual fields)
Can also cause loss of depth perception
Describe the aetiology of cavernous sinus thrombosis
Usually septic due to spread of infections (particularly within danger triangle of face e.g. sinusitis, dental infections)
Aseptic - trauma, surgery, pregnancy
How is cavernous sinus thrombosis managed?
Antibiotics
Anticoagulation
Steroids
Surgical management of abscesses etc.
Describe the aetiology of optic neuritis
Primary cause - multiple sclerosis, 70% of patients with MS will have at least one episode, presenting feature in 20%
Other less common causes:
Antibody-mediated
Non-infectious - neurosarcoidosis, systemic autoimmune conditions e.g. SLE
Infectious - syphilis, Lyme disease, cat-scratch disease, herpes zoster, sinus disease
Post-infectious - following acute infection or immunisation
Describe the clinical presentation of optic neuritis
Acute to subacute unilateral loss of vision - can be normal to no perception of light
Retrobulbar and peri-ocular pain, worse with eye movements
Photopsias (flashes) exacerbated by eye movements
Visual field loss
Reduced contrast sensitivity and colour vision
Relative afferent pupillary defect
Fundoscopy - may have optic nerve swelling, pallor
How should optic neuritis be assessed?
Visual acuity testing with Snellen chart
Colour vision assessment with Ishihara test
Fundoscopy
MRI of the brain and orbits with contrast - enhancement of optic nerve, other white matter lesions suggestive of MS
LP may be used if MRI normal - oligoclonal bands
How is optic neuritis managed?
Typical - high-dose steroids, usually IV methylprednisolone then oral prednisolone taper
Increases rate of vision recovery but does not change final visual outcome
Describe the potential complications and prognosis of optic neuritis
> 90% recover vision to 6/12 or better within a year, may have persistent RAPD, colour vision abnormalities
Overall 15-year risk of developing MS is 50%, 25% with normal MRI and 70% with one or more lesions on MRI
Describe the pathophysiology of complications in retrobulbar haemorrhage
Surrounded by bone medially, laterally and posteriorly, increase in volume causes increase in pressure which results in forwards shift
Forward displacement can compensate to some extent, increasing pressure eventually causes orbital compartment syndrome leading to compression/ischaemia of optic nerve, blockage of optic nerve venous drainage or central retinal arterial occlusion –> vision loss
Describe the aetiology of exposure keratopathy
Anything which causes incomplete eyelid closure, abnormal blink reflex/blink rate, decreased protective lubrication of cornea
Facial nerve palsy - trauma, CVA, Bell’s palsy etc.
Proptosis
Neurologic disease e.g. Parkinson’s, neuromuscular disease
Ectropion
Sedation e.g. ICU
How is exposure keratopathy managed?
Frequent use of artificial tears
Lubricating ointment for night
Eyelid closure - taping, patching
Punctal plugs
What are the potential complications of exposure keratopathy?
Corneal abrasion/ulcer
Microbial keratitis
Corneal scarring
Vision loss
List common causes of post-operative infectious endophthalmitis
Staph aureus
Strep spp
Coagulase negative staph
Describe the clinical presentation of post-operative infectious endophthalmitis
Reduced vision
Pain
Hypopyon
Intraocular inflammation
How is post-operative infectious endophthalmitis managed?
Intra-vitreal antibiotics
Describe the aetiology of endogenous endophthalmitis
Haematogenous spread of infection to eye
50% bacterial - staph aureus, strep pneumonia
50% fungal - candida albicans, aspergillus
Describe the presentation of endogenous endophthalmitis
Ranges from asymptomatic to severe uveitis with red, painful eye, photophobia, floaters, reduced vision
On examination - reduced visual acuity, conjunctival injection, cornea oedema, hypopyon, anterior chamber cells
Key finding - white infiltrate originating in choroid, can spread into vitreous cavity, can obscure fundus
How is endogenous endophthalmitis managed?
Vitreous fluid biopsy - culture, PCR
Intravitreal antibiotics, IV antibiotics
