Ophthalmology Flashcards
Borders of the orbit
Floor - maxilla, zygoma, palatine
Roof - frontal bone, lesser wing of sphenoid
Medial border - maxilla, lacrimal, ethmoid, sphenoid
Lateral border - zygomata and greater wing of sphenoid
Apex - optic foramen
Base - eyelid margins
Innervation of the extraocular muscles
CNIII: levator palpebrae superioris, superior rectus, inferior rectus, medial rectus, inferior oblique
CNIV: superior oblique
CNVI: lateral rectus
Components of the retina
Two cellular layers:
- Neural layer: innermost layer, consisting of photoceptors, located posteriorly and laterally
- Pigmented layer: outer layer, attached to the choroid and supports the neural layer, continues around the whole inner surface of the eye
Macula: centre of the retina. Yellow. Highly pigmented.
Contains a depression (fovea) which has a high conc of light detecting cells.
Optic disc: where the optic nerve enters the retina. Contains no light detecting cells. Blind spot.
Anterior chamber and posterior chamber
Anterior chamber is located between the cornea and iris, filled with aqueous humor
Posterior chamber is located between the iris and ciliary processes, filled with aqueous humor
Aqueous humor production and drainage
Clear plasma-like fluid that nourishes and protects the eye.
Produced constantly by the ciliary body in the posterior chamber, and diffuses into the anterior chamber and drains via the trabecular meshwork at the base of the cornea into the Schlemm canals and then in to the vascular system
Vasculature of the eye ball
Eyeball receives arterial blood from ophthalmic artery (branch of ICA)
Central artery of the retina is a branch of the ophthalmic artery, supplying the internal surface of the retina
Venous drainage via superior and inferior ophthalmic veins -> drains into cavernous sinus
Layers of the eyelid
Skin and subcut tissue
Orbicular oculi muscle (CNVII, closes the eyelid)
Tarsal plates (contains meibomian glands)
Levator apparatus: levator palpebrae superioris (CNIII, opens the eye lid), and superior tarsal muscle (Muller muscle, opens eyelid, innervated by sympathetic fibres)
Conjunctiva (palpebral part on the eyelid and bulbar part reflects onto the sclera)
Sensory innervation of the eyelid
Motor innervation of the eyelid
Upper eyelid - ophthlamic branch of trigeminal (CNV1)
Lower eyelid - maxillary branch of trigeminal (CNV2)
Motor:
CNIII opens the eyelid (levator palpebrae superioris)
CNVII closes the eyelid (orbicularis oculi)
Sympathetic fibres opens the eyelid (superior tarsal muscle)
Lacrimal apparatus: production and drainage
Lacrimal fluid is produced in the lacrimal gland (sits at the upper lateral corner of the eye)
Spreads over cornea
Accumulates in the lacrimal lace (medial canthus of the eye)
Then drains into lacrimal sac via a series of canals
Then down the nasolacrimal duct
Then empties into the inferior meatus of the nasal cavity
Innervation of the lacrimal system
Sensory: lacrimal nerve (branch of ophthalmic, CNV1)
Parasympathetic fibres stimulate lacrimal fluid secretion (preganglionic greater petrosal branch of CNVII, postganglionic maxillary nerve CNV2 and zygomatic nerve CNVII)
Sympathetic fibres inhibit lacrimal fluid secretion (originate from superior cervical ganglion)
Normal pupil size in light and in dark
Light: 2-4mm diameter
Dark: 4-8mm diameter
Accommodation reflex
Automatic constriction of pupil and convergence of eyes when suddenly moving gaze from a far object to a near object
Afferent= CNII Efferent= CNIII
Contraction of ciliary muscles loosens suspensory ligaments causing lens to become rounder and focuses on the near object
Presbyopia
Ageing causes lens to become denser and less elastic -> reduced accommodation capacity
Corrected with glasses or bifocals
Near light dissociation
- how to test
- what is it
- 2 conditions
Patient looks at distant target, shine light in both eyes and observe pupil constriction
Patient then looks at near object and observe constriction (without shining the light)
Near-light dissociation = patient has a better pupillary near reflex (accommodation) than a pupillary light reflex
Argyll-Robertson pupil (neurosyphilis) causes a pupillary response to accommodation but not to light
Holmes-Adie pupil slowly reacts to accommodation and poorly responds to light/if at all
Direct pupillary light reflex
Shine light into pupil 1 and observe constriction of pupil 1
Lack of constriction = CNII damage (afferent) or CNIII damage (efferent)
Consensual pupillary light reflex
Shine light into pupil 1 and observe constriction of pupil 2
Lack of pupil 2 constriction = CNII damage in pupil 1, CNIII damage in pupil 2, or damage in Edinger-Westphal nucleus in pupil 2
Swinging light test and relative afferent pupillary defect
- what does the swinging light test assess?
- what is the test?
- what happens in the test with RAPD?
Compares direct and consensual pupillary constriction of each eye to look for a difference in afferent conduction between them
Test: shine light into pupil 1, both eyes constrict -> shine the same light into pupil 2 and the degree of constriction should remain the same because the intensity of light is the same
RAPD= CNII damage or severe retinal disease.
RAPD in pupil 1: shine light into pupil 1, both pupils constrict because although there is optic nerve damage the light is still brighter than the surrounding environment. Move light to pupil 2 and both pupils remain constricted. When light moves back to pupil 1 both pupils will dilate because the light is perceived to be darker compared to when the light was in pupil 2.
RAPD in pupil 2: shine light into pupil 1, both pupils constrict. Then shine the same intensity light into pupil 2 -> the optic nerve won’t recognise that light as being as intense so the pupils will dilate in response to a perceived ‘darker’ environment.
Visual pathway
Light enters the left side of each eye -> light hits the retina on the right side of each eye. The left nasal optic nerve fibres cross at the optic chiasm to the join the right temporal optic nerve fibres, forming the right optic tract. They reach the right lateral geniculate nucleus where they separate into superior (parietal) and inferior (temporal) radiations. The radiations then reach the right side of the occipital lobe where the image is processed.
Light enters the right side of each eye and hits the retina on the left side of each eye (left temporal retina and right nasal retina). The right nasal optic fibres cross at the chiasm to meet the left temporal fibres, forming the left optic tract. The left optic tract travels to the left lateral geniculate nucleus. They then separate into superior and inferior radiations and terminate at the left occipital lobe.
What information does the superior optic radiation carry to the primary visual cortex?
What visual defect occurs when there is damage to the superior optic radiation?
Superior optic radiation travels through the parietal lobe and carries the information from the superior portion of the retina, which represents the inferior part of the visual field.
Damage to the left superior optic radiation causes a right inferior quadrantanopia
What information does the inferior optic radiation carry to the primary visual cortex?
What visual defect occurs when there is damage to the inferior optic radiation?
The inferior optic radiation travels through the temporal lobe (meyers loop) and carries information from the inferior portion of the retina which represents the superior visual field.
Damage to the left inferior optic radiation causes a right superior quadrantanopia
Causes of painless sudden visual loss
Vitreous haemorrhage CRVO CRAO WARMD Diabetic maculopathy Stroke Retinal detachment
Causes of painful sudden visual loss
Iritis Scleritis Keratitis AACG Optic neuritis Migraine Benign Intracranial HTN
Myopia vs. Hypermetropia vs. Astigmatism
Myopia: light from a distant object focuses in front of retina (long axial length with average cornea, or average axial length with high power cornea). Correct with biconcave lens.
Hypermetropia: light from distant object focuses beyond the retina (short axial length with average cornea, or lower power cornea with average axial length). Correct with biconvex lens.
Astigmatism: anatomical variation
Blepharitis
- what is it
- two types
Chronic, intermittent inflammation of the eyelid margins
Anterior blepharitis: inflamm of the base of the eyelashes. Caused by Staphylococci, may be associated with seborrhoeic dermatitis
Posterior blepharitis: inflamm of the meibomian glands. Associated with meibomian gland dysfunction and rosacea
Blepharitis features
Bilateral symptoms
Grittiness, discomfort, particularly around eyelid margins
Eyes may be stuck together in the morning
Eyelid margins may be red
Swollen eyelidds may be seen in Staphylococcal blepharitis
Styes and chalazions more common with blepharitis
Secodary conjunctivitis may occur
Function of the meibomian gland and consequences of meibomian gland dysfunction
Meibomian gland secretes oil on to the eye surface to prevent rapid evaporation of the tear film -> any problems with the gland causes drying of the eye, leading to irritation
Management of blepharitis
Softening and cleaning the lid margin using hot compresses twice a day
Mechanical removal of debris from lid margins
Artificial tears for symptomatic relief
If ineffective ->
Anterior = topical abx (chloramphenicol)
Posterior = oral abx (doxycycline)
Chalazion/ meibomian cyst
- what is it
- features
- management
- most common type of benign eyelid lump, due to an obstructed meibomian gland, leading to a granuloma within the tarsal plate
- Features: painless swelling in the posterior lamella, may discharge anteriorly or posteriorly, more common in patients with chronic blepharitis, seborrhoeic dermatitis, rosacea
Stye
- what is it
- different types
- features
- management
-Acute abscess within a lash follicle and its associated glands
- External stye: staph infection of the glands of Zeis (sebum) or glands of Moll (sweat)
- Internal stye: infection of the meibomian glands, may leave residual chalazion
-Features: tender lump with associated inflammation
-Management: hot compress, analgesia
Only consider topical abx if there is associated conjunctivitis
Entropion vs ectropion
Entropion: in-turning of the eyelid (usually lower eyelid)
Ectropion: out-turning of the eyelid (usually lower eyelid)
Causes of ptosis
Lid pulled down due to gravitational effect of mass/ scar
Defect in levator aponeurosis
Myopathy of levator muscle or NMJ (MG, myotonic dystrophy)
Innervational defect (Horners, CNIII palsy)
Blow out fracture pathophysiology (including trapdoor fracture in children)
Blunt trauma to the orbit -> the force of the blow is dissipated by a fracture of the orbital floor (maxillary bone) and/or medial wall (ethmoidal bone)
Maxillary bone fracture opens up into the maxillary sinus, causing blood to leak into the maxillary sinus
In children, the flexibility of the orbital floor causes the fracture maxillary bone to snap back, causing a trapdoor fracture. It traps the inferior rectus, leaving the eye stuck in a down and out position. Requires surgery.
Features of a blow out fracture
Periorbital bruising Periorbital oedema Subconjunctival haemorrhage Surgical emphysema Vertical diplopia due to mechanical restriction of upgaze Pain Enophthalmos Infraorbital anaesthesia due to nerve damage in the infraorbital canal
Investigations and management of blow out fracture
CT head is first line
If X-ray is done, a teardrop sign is seen (polypoid mass hanging from the floor into the maxillary sinus)
Air-fluid level in the maxillary sinus due to blood
Mx:
- Avoid blowing nose in case of orbital emphysema
- Nasal decongestants
- Prophylactic co-amoxiclab
- Surgery required if: enophthlamos, diplopia, inferior rectus entrapment, large fracture
LOOK OUT FOR RETROBULBAR HAEMORRHAGE (emergency)
Retrobulbar haemorrhage
- what is it
- when do you get it
- features
- management
Ophthalmic emergency
Risk with any direct trauma to the orbit, including surgery
It is effectively a compartment syndrome of the eye socket with risk of complete loss of vision within hours
Features: Tight swollen eyelid Unilateral fixed dilated pupil Reduced eye movements Profound vision loss
Must force eyelids open to check pupil reaction (optic nerve in check)
Management: urgent canthotomy and cantholysis
Orbital cellulitis features
Ophthalmic and medical emergency Fever, malaise, periocular pain Inflamed lids May have chemosis and proptosis Painful restricted eye movements Diplopia Lagophthalmos Optic nerve dysfunction (reduced VA, reduced colour vision, RAPD)
What is the orbital septum and what is its function
Thick piece of connective tissue, between the lids and the orbit, acting as a barrier to the spread of infection
Orbital cellulitis causative organisms
Streptococcus pneumoniae
Staphylococcus aureus
Streptococcus pyogenes
Haemophilus influenzae (commoner in children but reducing because of HiB vaccine)
Orbital cellulitis risk factors and complications
Risk factors: sinus disease (ethmoidal sinusitis), trauma (sepal perforation, retained FB), recent orbital surgery, immunocompromised
Ocular complications:
Exposure keratopathy, raised intraocular pressure, CRAO, CRVO, optic neuritis
Systemic complications:
Orbital and periorbital abscess, cavernous sinus thrombosis, meningitis, cerebral abscess
Orbital cellulitis investigations
Temperature
FBC
Blood culture
CT orbit/sinus/brain
Management of orbital cellulitis
Admit for IV cefuroxime
Monitor extent of skin inflam
Regular review of orbital and visual functions
ENT input to assess sinus drainage
Repeat CT if there is deterioration to exclude abscess formation
Preseptal cellulitis
- causative organisms
- at risk population
- risk factors
Causative organisms: Staphylococci and Streptococci
Common in children
Risk factors:
Infection of adjacent structures (dacrocystitis, styes)
Systemic infection (URTI)
Trauma (lacterations)
Preseptal cellulitis features
Fever, malaise
Painful, swollen lid/periorbital
Inflamed lids but with no proptosis (bulging of eye)
Normal eye movements, white conjunctiva, normal optic nerve function
Preseptal cellulitis investigations and management
Ix: clinical diagnosis. investigations are not usually necessary unless there is doubt about orbital or sinus involvement
Mx: daily review until resolution, oral antibiotics (flucloxacillin or co-amoxiclav)
Dacrocystitis
- what is it
- common organisms
- in what patients is it more common in
Infection of the lacrimal drainage sac
Usually due to Staph or Strep
Common in patients with partial or complete nasolacrimal duct obstruction
Features of dacrocystitis
-Red, very tender swelling at the medial canthus
-Worsening epiphoria (excessive lacrimation)
-May express pus from puncta on palpation
+/- Localised cellulitis
Investigations and management of dacrocystitis
Ix: clinical diagnosis, can send discharge to microbiology
Mx: urgent management to prevent spreading cellulitis
- High dose oral co-amoxiclav
- Analgesia
- Warm compress
- Gentle massaging
- Consider incision and drainage
- Surgical correction of nasolacrimal duct obstruction
- Referral to lacrimal clinic
Complications of dacrocystitis
Rarely becomes a severe cellulitis
Spontaneous or surgical drainage through the skin risks the formation of a fistula
Risk factors for cataracts
Smoking, alcohol, trauma, DM, long term corticosteroids, radiation, myotonic dystrophy, hypocalcaemia
Features of cataracts
Gradual onset monocular diplopia Gradual onset reduced vision Faded colour vision Glare (lights appear brighter than usual) Halos around lights
Investigations for cataracts
Defect in red reflex (cataracts prevents light from getting to the retina)
Ophthalmoscopy following pupil dilation (normal)
Slit lamp examination shows visible cataract
Types of cataract
Nuclear: most common, old age. Clouding of central lens.
Polar: localised, commonly inherited. Lies in visual axis
Subcapsular: common in steroid use. Opacity often focal of the posterior lens
Dot opacities: common in normal lenses, also seen in DM and myotonic dystrophy
Management of cataract
First line: stronger glasses/contact lenses, brighter lighting
Surgery is the only effective treatment - remove cloudy cataract and replace with artificial one
Complications of cataract surgery
Posterior capsule opacification
Retinal detachment
Posterior capsule rupture
Endophthalmitis
Allergic conjunctivitis features and management
Features:
Bilateral
Very itchy, conjunctival erythema, swelling, watery discharge
History of atopy (seasonal variation)
Mx:
avoid allergen
Topical or systemic antihistamines or mast cell stabilisers
Bacterial conjunctivitis features, causative organisms and management
Features:
Usually unilateral
Acute, red, gritty eyes with purulent discharge
Common organisms:
Staphylococcus epidermidis, Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae
Management:
Topical chloramphenicol abx or fusidic acid if pregnant
Viral conjunctivitis features, causative organisms, investigations, management, complications
Features:
Bilateral, acute watery discharge, periauricular lymph nodes, lid oedema
History of recent URTI
Highly infectious but usually self limiting
Common causes: adenovirus, molluscum contagiosum, HSV1
Ix: conjunctival swabs for PCR
Mx: cool compress, artificial tears, follow-up if condition worsens
If molluscum, remove the lesion
If Herpes give aciclovir
Complications: may develop secondary corneal involvement with blurring of vision -> rapid access eye clinic -> give topical steroids to treat it and prevent corneal scarring
Chlamydial conjunctivitis
- features
- systemic features
- ix
- mx
2-3weeks after infection
Usually unilateral, mucopurulent discharge, lid oedema, ptosis, follicles, non-tender lymphadenopathy, keratitis
May also have cervicitis and urethritis
Ix: conjunctival swabs for PCR, refer to GUM clinic
Mx: topical chloramphenicol, systemic treatment (azithromycin)
Alkali corneal burn
- why is alkali worse than acid burn?
- management
Emergency- rapid absorption and intraocular penetration of alkali, leading to both superficial and intraocular complications
More serious than acid burns as it continues to denature surface proteins and penetrate eyeball for hours
Mx: copious irrigation for prolonged period until pH normalises, if severe then on call team should be called and fornices should be swept with a glass rod following irrigation. Analgesia, topical abx, topical steroids, bandage contact lens
White eye in a history of severe burn is worse than red eye (white = ischaemia)
Risk factors for infective keratitis
Contact lenses Corneal trauma Corneal abrasions/ erosions Poor immune function history of autoimmune disease
Common causative bacteria and viruses for infection keratitis
Bacteria: pseudomonas aeruginosa, Stap aureus, Staph epidermidis, Strep pneumoniae, Haem influenzae, Moraxella catarrhalis
Viruses: Herpes simplex, Herpes zoster
Features of infective keratitis
Redness, severe pain, increased lacrimation, lid oedema, discharge, reduced visual acuity, photophobia, raised intraocular pressure
Dendritic ulcer = herpes simplex
Infective keratitis investigations and diagnosis
Corneal scraping for a microscope slide
Corneal scraping for cultures and sensitivity
FBC
HIV test
Diagnosis =
Presence of risk factors
Corneal infiltrate (oedema and opacification)
Corneal ulcer
Dendritis or geographical epithelial lesion (herpes)
Management of bacterial keratitis
- Topical quinolone
- Cytoplegics (atropine, cyclopentolate): paralyse the ciliary muscles, thus dilating the eye and preventing ciliary spasm (prevents pain and photophobia), and prevents posterior synechiae
- Simple analgesia
Management of herpetic keratitis
Topical aciclovir or trifluridine
Cycloplegics (relieves pain/photophobia, and prevents synechiae formation)
Simple analgesia
May require topical corticosteroids
Herpes zoster ophthalmicus
- where does the virus lie dormant?
- features
- Hutchinsons sign
Herpes zoster (DNA virus) lies dormant in the ophthalmic division of the trigeminal ganglion (varicella zoster lies dormant in the dorsal root ganglion)
Features:
Tingling over scalp and forehead
Vesicular rash around the eye and forehead that doesnt cross the midline
Hutchinson’s sign - rash/vesicles on the tip or side of the nose indicates nasociliary involvement and is a strong risk factor for ocular involvement
Herpes zoster ophthalmicus
- diagnosis
- management
- consequences
Clinical diagnosis
Management:
Oral antiviral treatment 7-10days
IV antivirals if severe or immunocomp
Topical corticosteroids for secondary inflam of the eye
Ocular involvement requires ophthalmology review
Consequences:
Conjunctivitis, keratitis, episcleritis, anterior uveitis
Ptosis
Post-herpetic neuralgia
Corneal abrasion
- what is it
- features
- investigations
- management
Defect of the corneal epithelium, usually due to local trauma causing a superficial corneal wound
Features: Eye pain (FB grittiness), lacrimation, photophobia, reduced visual acuity, ciliary flush (red ring around cornea), conjunctival injection
Investigations:
Visual acuity
Fluorescein examination (fluorescein drops + cobalt blue slit lamp = corneal abrasions stain yellow)
Management:
Topical chloramphenicol
Topical NSAIDs or oral paracetamol
Cycloplegics (cyclopentolate)
Management of corneal foreign body
Only remove corneal foreign body under slit-lamp visualisation, and with topical anaesthesia
Topical chloramphenicol
Topical NSAIDs
Cycloplegics
Causes of anterior uveitis
Idiopathic HLA-B27 positive Post-op Ankylosing spondylitis Autoimmune (RA, SLE, IBD, etc) Reiters syndrome
HLA-B27 conditions
Anterior uveitis Ankylosing spondylitis Inflammatory bowel disease Reiters syndrome Psoriasis Sarcoidosis
Causes of posterior uveitis
Sarcoidosis, Behcets, MS, TB, syphilis, post-op, trauma, immunocomp, POHS
What is anterior uveitis?
Inflammation of the anterior uveal tract: iritis, anterior cyclitis (ciliary body), iridocyclitis
Iritis is the most common form of uveitis
Features of anterior uveitis / iritis
Including systemic features
Acute onset painful red eye with photophobia
- Ocular discomfort (pain increases with movement)
- Miosis (sphincter muscle contraction -> constriction)
- Irregular shaped pupil due to posterior synechiae (adhesions) pulling the iris into an oval shape
- Blurred vision
- Lacrimation
- Ciliary flush (ring of red spreading form cornea)
- Floaters and flashes
- Hypopyon (pus and inflamm cells in the anterior chamber causing a visible fluid level)
-Visual acuity is initially normal and then may become impaired
May have systemic features
- rash
- cough
- dyspnoea
- arthritis
- urethritis
- mouth/ genital ulcers
Examination findings with anterior uveitis
- Flare in the anterior chamber (inflam and leukocytes floating in the aqueous humor): hallmark feature of anterior uveitis
- Sedimentation of the lueokcytes may form a hypopyon (fluid level of pus in the pupil)
- Mutton fat (granulomatous inflam)
- Synechiae: anterior if iris adheres to cornea, posterior if iris adheres to lens. Seen on slit-lamp examination.
- Acute angle closure glaucoma
Investigations for anterior uveitis
Ocular tests: slit lamp examination with dilated pupils, fundoscopy, fluoroscein angiogram, ocular coherence tomography, check IOP
Bloods: FBC, U+E, LFT, ESR, CRP, serum ACE, calcium, autoantibodies, HLA, syphilis, HIV, toxoplasmosis, lyme
Imaging: CXR (sarcoidosis, TB), X-ray lumbosacral spine (ankylosing spondylosis), MRI brain and optic nerve (MS)
Skin tests: Mantoux (TB)
Lumbar puncture
Management of anterior uveitis/ iritis
Urgent ophthalmology review
Cycloplegics
Topical corticosteroid drops
Control any rise in IOP (avoid prostaglandin analogues)
Treat underlying cause (immunosuppression)
Laser therapy, cryotherapy, surgery (vitrectomy) in severe cases
Complications of anterior uveitis/ iritis
Cataract
Glaucoma
Retinal detachment
Causes of scleritis
Idiopathic
Post-op
Systemic vasculitis (RA, polyarteritis nodosa, Wegeners granulomatosis)
Invections (herpes zoster, syphilis, TB)
Types of scleritis
Anterior (most common) - associated with autoimmune disease. Diffuse anterior scleritis, nodular anterior scleritis, necrotising anterior scleritis.
Posterior (rare): not related to autoimmune
Features of scleritis
Severe boring pain with global tenderness Pain worse on eye movement and palpation Pain radiated to jaw, neck and head Blue hue to sclera (=sclera thinning) Deep-red conjunctival injection Blurred vision Lacrimation Photophobia Gradual decrease in vision No response to phenylephrine drops
Management of scleritis
Refer to eye emergency department
IV systemic corticosteroids
NSAIDs
Systemic immunosuppression if due to autoimmune
Episcleritis features
Red eye Mild pain (not painful in comparison to scleritis) Lacrimation Mild photophobia May be recurrent 50% of cases are bilateral
Redness improves with phenylephrine drops
Diagnosis of episcleritis
Clinical diagnosis but can do phenylephrine test if there is doubt about scleritis
Phenylephrine drops (topical vasoconstrictors) cause blanching of conjunctival and episcleral vessels but not scleral vessels -> episcleritis if redness improves, scleritis if redness does not improve
Management of episcleritis
Self-limiting
Symptomatic relief:
Cold compresses
Topical lubricants/ artificial tears
NSAIDs
Refer to rapid access clinic if persisting
Primary open angle glaucoma
- what is it
- risk factors
- features
Chronic onset optic neuropathy due to gradual increase in resistance through the trabecular meshwork (rise in IOP)
Risk factors: age, family history, black patients, myopia, HTN, DM, steroids
Features: asymptomatic rise in IOP over a long period of time, often diagnosed at routine eye check. Affects peripheral vision first, gradually causing tunnel vision.
Gradual onset of fluctuating pain, headaches, blurred vision and halos around lights
Primary open angle glaucoma
- fundoscopy findings
- investigations
Fundoscopy:
- Optic disc cupping (cup to disc ration >0.7)
- Optic disc pallor (optic atrophy)
- Bayonetting of vessels (vessels break as they disappear into the deep cup and reappear at the base)
- Cup notching
- Disc haemorrhage
Investigations
- Automated perimetry (peripheral visual field loss)
- Slit lamp exam with pupil dilation (optic nerve head damage)
- Tonometry (raised IOP >24)
- Gonioscopy to assess peripheral anterior chamber configuration and depth
Management of primary open angle glaucoma
First line: prostaglandin analogue eyedrops (latanoprost)
Second line: beta blockers, carbonic anhydrase inhibitors, sympathomimetics
Trabeculectomy surgery if eyedrops are ineffective (flap of sclera lifted beneath the conjunctiva and a hold made into the anterior chamber to improve drainage)
Prostaglandin analogues
Example
MoA
Side effects
Latanoprost
Increases uveoscleral outflow
SE: brown pigmentation of iris, increased eyelash length
Beta blocker eye drops
Example
MoA
Side effects
Timolol
Reduces aqueous production
SE: hypotension, bradycardia, fatigue, SOB
Avoid in asthmatics and heart block
Carbonic anhydrase inhibitors
Example
MoA
Side effects
Dorzolamide
Reduces aqueous production
SE: stinging, burning, eye discomfort
Sympathomimetics
Example
MoA
Side effects
Brimonidine
Alpha agonist, reduces aqueous production and increases uveosclral outflow
SE: hyperaemia, burning/stinging, fatigue, headache, drowsiness
Avoid if taking MAOI or TCAs
Miotics
Example
MoA
Side effects
Pilocarpine
Muscarinic receptor agonist, increases uveoscleral outflow
SE: constricted pupil, headache, blurred vision
Pathophysiology and classification of angle closure glaucoma
Pathophysiology: iris blocks trabecular meshwork, preventing the aqueous humor from being drained into the trabecular meshwork and schlemm canals -> build up of aqueous humor -> rise in IOP
Classification:
- Acute
- Subacute
- Chronic
Acute angle closure glaucoma risk factors
Ophthalmic emergency
Risk factors: female, asian, FHx, age >60, shallow anterior chamber, hypermetropia (smaller anterior chamber), medications that induce angle narrowing (cycloplegics, sulphonamides, topiramate)
Acute angle closure glaucoma features
Ophthalmic emergency Halos around lights Severe aching pain around eye or brow pain Severe periocular headache N+V Reduced visual acuity Eye redness Raised IOP Corneal oedema Fixed mid-dilated pupil due to iris ischaemia
Normal IOP and acute angle closure glaucoma IOP
Normal IOP = 10-21
AACG IOP = >21, rapidly rising to >40
Acute angle closure glaucoma examination and investigations
- Palpation (rock hard eyeball)
- Pen torch (red, fixed mid-dilated pupil, corneal oedema/cloudy)
- Reduced visual acuity
- Slit lamp examination and fundoscopy (large optic cup and nerve fibre loss)
- Gonioscopy (unable to visualise trabecular meshwork because the peripheral iris is in contact with it)
- Tonometry
- OCT
Management of acute angle closure glaucoma
First line: acetazolamide
Second line: mannitol
Adjunct:
Topical pilocarpine causes pupil constriction thus opening the angle
Beta blockers
Alpha-2 agonists
Laser peripheral iridotomy once the acute attack has resolves (allows aqueous humor to bypass pupil, preventing recurrence)
Complications of acute angle closure glaucoma
Retinal vein occlusion
Loss of vision
High risk for developing glaucoma in the other eye (prophylactic laser iridotomy)
Permanent reduction in visual acuity
Congenital glaucoma
- why does it happen
- primary vs secondary
Occurs when there is incorrect or incomplete development of the eye’s drainage canals during the prenatal period
Primary: predisposition to optic nerve damage, causing optic nerve cupping and optic nerve pallor
Secondary: trabecular dysfunction, lens dislocation, increased uveoscleral resistance causing increased resistance to aqueous humor outflow -> raised IOP and optic nerve damage)
Features and management of congenital glaucoma
Features: enlarged eyes, cloudiness of cornea, photosensitivity, lacrimation
Management:
First line = surgery (goniotomy and trabeculotomy)
Medical management may help as a temporary treatment to reduce IOP
Diabetic retinopathy pathophysiology
Hyperglycaemia -> damaged retinal small vessels and endothelial cells -> microaneurysms (small bulges) and venous beading (veins are no longer straight, and look like strings of beads)
Increased vascular permeability leads to leakage of blood vessels -> blot haemorrahges and formation of hard exudates (yellow lipid deposits in retina)
Damage to nerve fibres causes cotton wool spots
Intraretinal microvascular abnormalities: dilated and torturous capillaries in the retina
Risk factors for diabetic maculopathy
Type 2 > type 1
HTN
Renal disease
Hypercholesterolaemia
Features of diabetic retinopathy
- May be asymptomatic or present with gradual deterioration of vision over months
- Microaneurysms
- Leakage (retinal thickening/oedema, hard exudates) with or without macular ischaemia (seen on fluorescein angiogram)
Fundoscopy findings of non-proliferative diabetic retinopathy (different severities)
Mild: microaneurysms
Mod: microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous beading
Severe: blot haemorrhages and microaneurysms in 4 quadrants, venous beading 2 quadrants, intraretinal microvascular abnormalities in any quadrant
Proliferative diabetic retinopathy
Neovascularisation
Vitreous haemorrhage
More common in type 1 diabetes
50% become blind in 5 years
Diabetic maculopathy features
Based on location rather than severity
Macular oedema
Ischaemic maculopathy
More common in type 2
Complications of diabetic retinopathy
Retinal detachment Vitreous haemorrhage Rebeosis iridis (new blood vessel formation in the iris) Optic neuropathy Cataracts
Management of diabetic retinopathy
Laser photocoagulation
Anti-VEGF medications (ranibizumab)
Vitreoretinal surgery
Keep BP <140/80 (or <130/80 if end-organ damage)
Hypertensive retinopathy features
- Retinal arteriolar narrowing
- Copper/silver wiring due to sclerosis and thickening of arteriolar walls causing increased reflection of light
- Arteriovenous nipping (sclerosed arterioles compress veins at crosspoints)
- Artery/vein occlusion
- Cotton wool spots
- Hard exudates
- Retinal flame-shaped haemorrhage
- Microaneurysms
- Macular oedema
- Papilloedema (optic nerve ischaemia)
Hypertensive retinopathy investigations
Blood pressure Blood glucose FBC and U+E Fluoroscein angiogram Fundoscopy
Classification for hypertensive retinopathy
Keith-Wagener classification
1- arteriolar narrowing and tortuosity, silver wiring
2- arteriovenous nipping
3- cotton wool spots, flame and blot haemorrhages
4- papilloedema
Management of hypertensive retinopathy
Treat BP
Monitor eyes
Target BP <140/90 for most patients
<130/80 for diabetics
<125/75 for diabetics with proteinuria
Amaurosis fugax
- what is it
- causes
Painless temporary loss of vision in one/both eyes, like a black curtain coming down
Usually lasts seconds, but may be hours
Causes:
- Idiopathic
- Embolus/haemodynamic: TIA, cardiac emboli, GCA, vasospasm, SLE, hyperviscosity
- Ocular: iritis, keratitis, blepharitis, increased IOP, glaucoma
- Neuro: optic neuritis/ MS, compressive optic neuropathies, papilloedema, migraine
Central retinal vein occlusion risk factors and features (inc fundoscopy findings)
Risk factors: HTN, high cholesterol, diabetes, smoking, glaucoma, SLE
Features: sudden painless loss of vision
Fundoscopy: flame haemorrhages, blot haemorrhages, optic disc oedema, macular oedema, neovascularisation
Central retinal vein occlusion investigations and management
Ix: FBC (leukaemia), ESR (inflam disorders, GCA), BP, serum glucose
Management: Ophthalmology review Aim to treat macular oedema and prevent neovascularisation Laser photocoagulation Intravitreal dexamethasone Anti-VEGF (ranibizumab)
Central retinal artery occlusion
- risk factors
- features
- fundoscopy findings
Risk factors: age, FHx, smoking, alcohol, HTN, DM, poor diet, inactivity, obesity
Features: sudden painless loss of vision, RAPD (due to ischaemic retina)
Fundoscopy: pale retina with a cherry red spot (red spot = macula)
Central retinal artery occlusion management
Immediate referral to ophthalmology
Test and treat giant cell arteritis (ESR and temporal artery biopsy -> treat with high dose prednisolone)
Acute Mx:
Ocular massage
Remove fluid form anterior chamber to reduce IOP
Inhaling carbogen to dilate artery
Sublingual isosorbide dinitrate to dilate artery
Long term management of risk factors
What are drusen?
Yellow deposits of protein and lipids between the retinal pigment epithelium and Brush’s membrane
Small numbers may be normal
Large numbers may be suggestive of early macular degeneration
Dry age related macular degeneration vs wet age related macular degeneration
DARMD: 90% of cases, drusen more commonly seen
WARMD: 10% of cases, choroidal neovascularisation seen (leak of serous fluid and blood result in rapid vision loss), carries a worse prognosis
Risk factors for age related macular degeneration
Advancing age, smoking, family history, white or chinese, HTN, high lipids, DM
Clinical features of age related macular degeneration
Subacute central vision loss (straight lines appear curved)
Reduced visual acuity (esp near field objects)
Deterioration in night vision due to degeneration of photoceptors
Photopsia (flickering/flashing)
Glare around objects
Atrophy or retial pigment epithelium
Wet ARMD: presents more acutely, sometimes visual loss over a few days, full blindness in 2-3 years, often progresses to bilateral
Investigations and examination findings with age related macular degeneration
Fundoscopy:
Drusen
Intra-retinal and sub-retinal fluid leaks and haemorrhages in WARMD due to neovascularisation
Examination:
Reduced acuity on snellen chart
scotoma
amsler grid test shows distortion of straight lines
Investigations: Slit lamp OCT (diagnoses WARMD) Fluoroscein angiogram used if OCT does not exclude WARMD Colour fundus photography
Management of age related macular degeneration
Dry: zinc with anti-oxidant vitamins A/ C/ E reduce progression of disease by around one third
Wet: Anti-VEGF (ranibizumab) prevent neovascularisation. Injected into vitreous chamber one a month
Laser photocoagulation is an alternative
Posterior vitreous detachment
- what is it
- features
- management
Detachment of vitreous humor from retina, often caused by trauma
Features: painless, spots of vision loss, floaters, photopsia (flashing lights) in the peripheral visual field
Management: no treatment needed usually, improves over time
Retinal detachment
- what is it
- risk factors
- features
Emergency
Retina separates from choroid. usually due to a retinal tear that allows vitreous fluid to get under retina. Outer retina relies on blood vessels from the choroid for its blood supply therefore is a sight threatening emergency
Risk factors: posterior vitreous detachment, diabetic retinopathy, trauma, retinal malignancy, increasing age, family history
Features: sudden peripheral vision loss which progresses towards central vision loss, blurred or distorted vision, amaurosis fugax, flashes (photopsia) and floaters
Retinal detachment investigations and management
Ix: always exclude retinal detachment in all presentations of flashes and floaters. must look at the back of the eye (fundoscopy, OCT)
Management of retinal tear:
-Laser therapy or cryotherapy to create an adhesion between retina and choroid
Management of retinal detachment:
- Vitrectomy (remove relevant parts of vitreous body and replace it with oil or gas)
- Scleral buckling (force pressure from outside the eye so the choroid indents and makes contact with the retina)
- Pneumatic retinopexy (inject gas bubble into vitreous body to create pressure that forces retina onto choroid
Rheumatoid arthritis ocular manifestations
Scleritis and episcleritis
Keratoconjunctivitis sicca (dry eye syndrome) - most common
Peripheral ulcerative keratitis (corneal thinning and ulceration)
Treat with topical lubricants, analgesia, steroids, systemic immunosuppression +/- surgery
Keratoconjunctivitis sicca features, investigations and management
Features: FB sensation, burning, reduced visual acuity, photophobia, pruritus
Ix: clinical diagnosis.
- Slit lamp with fluorescein staining shows corneal filaments
- Tear film meniscus height (reduced)
- Schirmers test (reduced secretion)
Management: topical lubricants, immunosuppression/RA treatment, topical corticosteroids, lid hygiene
2 stages of thyroid eye disease
Acute inflammatory (risk of sight loss) - lasts 12-18 months, causes proptosis and may cause compressive optic neuropathy
Chronic fibrotic - restrictive myopathy and diplopia
Classification of thyroid eye disease
(NO SPECS)
0- no signs or symptoms
1- ocular irritation (dryness, FB sensation)
2- soft tissue (conjunctival chemosis, oedema)
3- proptosis
4- extraocular muscle fibrosis
5- corneal exposure and ulceration
6- sight loss (due to corneal ulceration, compressive optic neuropathy or raised IOP)
Management of thyroid eye disease
Manage systemic thyroid disease Ocular lubricants Glaucoma topical medications Acute optic nerve compression treatment Systemic corticosteroids Orbital radiotherapy Surgical orbital decompression
Treat diplopia with squint surgery, prisms, botox
Retinitis pigmentosa
- what is it
- associated condition
- features
Congenital inherited condition causing progressive dysfunction, cell loss and atrophy of retinal tissue (rods affected initially)
Associated with alport’s syndrome
Features:
Night blindness is an initial sign (loss of rod cells)
Tunnel vision due to loss of peripheral retina
Peripheral vision lost before central vision
Ocular associations - cataract, myopia, primary open angle glaucoma
Retinitis pigmentosa fundoscopy findings, investigations and management
Fundoscopy: mid peripheral bone spicule pigmentation, may have narrowing of arterioles, waxy/pale optic disc
Ix: visual acuity, full field perimetry (mid peripheral visual field defect), full field electroretinogram (abnormal ERG is an essential feature of RP)
Mx:
- Referral to ophthalmologist, genetic counselling, vision aids, sunglasses, inform DVLA, regular follow up
- Gene therapy
- May slow disease progression: vitamins and antioxidants, oral acetazolamide, topical dorzolamide, steroid injections, anti-VEGF injections
Retinoblastoma features and pathophysiology
Patho: 10% are hereditary. Autosomal dominant. Loss of function of tumour suppressor gene on chromosome 13.
Average age of onset 18 months
Features: absence of red reflex, white pupil (leukocira), strabismus, visual problems
Retinoblastoma investigations, management and prognosis
Ix: fundoscopy and examination under anaesthesia, optical coherence tomography, ultrasound
Management: enucleuation (removal of eye)
Depending on how advanced the tumour is -> external beam radiotherapy, chemo, photocoagulation
Prognosis: >90% survive into adulthood
Risk factors and classification of strabismus (squint)
Abnormal alignment of the visual axes of the eye
Risk factors: family history, prematurity, refractive error
Classifications:
Manifest squint - the squint is present and cannot be controlled (esotropia= inward deviation, exotropia= outward deviation, hypertropia=upwards, hypotropia=downswards)
Latent squint - deviation that can be controlled so you cant see it (esophoria, exophoria, hyperphoria, hypophoria)
Features of strabismus
Latent squint may be asymptomatic or present with intermittent diplopia, headache and eye strain
May present in adults as diplopia (may be suppressed as a child)
Eye misalignment
Abnormal eye movements
Amblyopia common in children - active process of the CNS to ignore visual input from the eye that has squint so child sees a clear image. If not corrected in time it results in irreversible visual loss in that eye. Develops <7yrs
Cover-uncover test
Detects a manifest squint
Process:
- shine light into both eyes at same time, look for reflection in pupil centre (misalignment indicates squint)
- Focus on a detailed near object, and cover and uncover one eye repeatedly (slow) whilst observing the other eye
- Repeat with other eye
- Focus on an object at 6m
- Repeat with other eye
Results:
eg. squint in eye 2:
Both eyes focus on a near object. Eye 1 gets covered, eye 2 moves to fixate on object. Eye 1 cover is removed, eye 2 moves back into squint position.
If the squint is a exotropia, when the cover is applied to eye 1, eye 2 will move inwards to pick up fixation.
Alternate cover test
Detects a latent squint
Process:
- Focus on an object at 30cm
- Briskly move the cover between both eyes
- Brain is unable to keep up so can’t control the squint anymore -> squint becomes apparent
- Repeat at 6m
Tests and investigations for strabismus
Cover-uncover test
Alternate cover test
Full ophthalmology examination
MRI brain or CT/MRI orbit
Management of strabismus
First line: correct any refractive errors, and treat amblyopia/ diplopia
Second line: extra-ocular muscle surgery
Third line: chemodenervation (botulinum toxin A)
Risk factors for amblyopia
Age<9yrs
Presence of strabismus
Refractive errors
Family history
Congenital cataracts or other opacities in the visual axis
Prematurity
Prolonged occlusion of 1 or both eyes (eg. severe ptosis)
What is amblyopia and what’s the difference between primary and secondary amblyopia?
Amblyopia is CNS suppression of vision from an anatomically normal eye
Primary amblyopia: develops in a while with an otherwise normal ocular examination, due to a central developmental anomaly, and there may be a positive family history
Secondary amblyopia: (secondary to ocular disease)
- Refractive difference between the two eyes results in a blurred image -> CNS suppresses one eye so theres no longer a difference in refraction and no longer blurry
- Media opacity (corneal opacity, cataract, vitreous haemorrhage)
Which refractive error should be corrected in order to treat a converging squint? (eg. esotropia, esophoria)
Which refractive error should be corrected in order to improve a divergent squint? (exotropia, exophoria)
Correcting hypermetropia should correct a convergent squint
Correct a myopia to improve a divergent squint
Features and management of amblyopia
Features:
- asymptomatic
- subnormal visual acuity for age in 1 or both eyes
- asymmetrical corneal light reflex
- unequal behaviour response to alternate eye occlusion
- abnormal cover-uncover test
- blurred vision
- eye strain
Management:
- optical correction of refractive error
- patch the normal eye to force CNS to use the abnormal eye
- Atropine drops (dilates the pupil) in the normal eye, in order to utilise the abnormal eye
Features of congenital cataracts
Causes of congenital cataracts
Screening for congenital cataracts
Bilateral and symmetrical
Causes: FHx (autosomal dominant), Down’s, hypoparathyroidism, ToRCH
Screened for using red reflex test during neonatal examination
Retinopathy of prematurity
- at what point do retinal vessels develop
- when is the retina at particular risk of damage?
- screening
- management
Retinal vessels develop at 4m gestation, they reach the nasal periphery at 8m gestation and the temporal periphery by 1m after birth
Therefore premature babies don’t have completely vascularised retinas
In preterm infants the incomplete vascularised retina is susceptible to damage, esp from high conc oxygen
Screening: babies born less than 32 weeks, babies weighing less than 1500g
Management:
Laser treatment to ablate ischaemic retina
Neonatal conjunctivitis
- what age group
- gonococcal features
- chamydial features and management
Under 1 month
Notifiable disease
Gonococcal: 2-4 days post birth, can cause corneal ulceration and perforation
Chlamydial: 5-14 days post birth, most common, requires topical tetracycline or oral erythromycin
Horner’s syndrome triad and pathophysiology behind the triad
Sympathetic nerve lesion
- Partial ptosis: mullers muscle (superior tarsal muscle) innervated by sympathetic fibres and acts to open the lid
- Miosis: pupillary dilator muscle innervated by sympathetic fibres, works by dilating the pupil
- Anhydrosis: sweat glands of the face innervated by sympathetic fibres
Causes of Horner’s syndrome
4S’s 4T’s 4C’s
Stroke, MS, swelling (tumour), syringomyelia
Tumour (pancoast), trauma, thyroidectomy, top rib (cervical rib)
Carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache
Argyll-Robertson pupil
- features
- causes
Prostitutes pupil. Very specific sign of neurosyphilis.
Features:
Usually bilateral
Anisocoria (unequal size of pupil)
Small pupils that constrict to near objects but not to light (near-light dissociation)
The pupils are difficult to pharmacologically dilate
Believed to be due to bilateral damage to midbrain nuclei
Causes: Neurosyphilis Diabetic neuropathy Alcoholic midbrain degeneration Encephalitis Amyloidosis MS Midbrain tumours
Adie’s tonic pupil (Holmes-Adie syndrome)
- what is it
- cause
- features
Neuro disorder causing one or both eyes to be abnormally dilated with delayed constriction in response to light
Due to a disorder in the parasympathetic nervous system (responsible for constriction)
Features:
Most common in women
Absent knee/ankle reflexes
Dilated pupil
Once pupil has constricted it remains small for a long time (sluggish response)
Constricts on accommodation but doesnt constrict to light (near-light dissociation)
CNIII palsy
- features
- causes
- management
Worry about aneurysm
Features:
- Ptosis
- Dilated non-reactive pupil (due to CNIII carrying parasympathetic fibres)
- Down and out position
Causes:
- POSTERIOR COMMUNICATING ARTERY ANEURYSM (URGENT MRI)
- Idiopathic
- Tumour
- Trauma
- Cavernous sinus thrombosis
- raised ICP
- If pupil is spared: DM, HTN, ischaemia
Management: urgent MRI to exclude aneurysm
Usually resolves in 4-6m although may require surgery
CNIV palsy
- features
- causes
Worry about canial trauma
Features
- characteristic head tilt
- subtle diplopia, especially on down gaze (downstairs) due to SO paralysis
Causes
- Head trauma (because CNIV is longest cranial nerve in the brain so more sensitive to trauma)
- Congenital
- DM, HTN
- Demyelination
- Tumour
- GCA
- Aneurysm
CNVI palsy
- features
- what to exclude
Features: horizontal diplopia, lateral rectus paralysis causes adducted resting eye
Must exclude raised ICP, perform a dilated fundoscopy (papilloedema)
Nystagmus causes
- physiological
- congenital
- acquired
Physiological causes:
- Caloric testing (warm/cold water put into ear induces nystagmus)
- Gaze evoked (extreme left or right gaze evokes nystagmus)
Congenital:
- usually X-linked recessive (ocular albinism, retinal dystrophies, optical nerve hypoplasia)
Acquired causes:
- Recent visual los
- Toxicity
- Cerebral disease (Stroke, MS, tumour)
What is pendular nystagmus?
Nystagmus where there is no fast or slow phase
Features of congenital nystagmus
Initially horizontal pendular nystagmus, later developing a jerk stage
seen in children up to 1 year of age
Indicator of poor vision in child -> ophthalmology referral needed
Types of nystagmus associated with neurological diseases:
- Dorsal midbrain disease
- Foramen magnum lesions
- Cerebellar lesions
- Chiasmal lesions
- Dorsal midbrain disease: convergence retraction (eyes converge on upgaze)
- Foramen magnum lesions: downbeat nystagmus (nystagmus when looking down)
- Cerebellar lesions: upbeat nystagmus
- Chiasmal lesions: see-saw nystagmus
Optic neuritis
- features
- causes
- investigations
- management
- prognosis
Features:
- Unilateral reduction in visual acuity over hours/days
- Poor discrimination of colours (red desaturation)
- Pain worse on movement
- RAPD
- Central scotoma
- Fundoscopy (optic disc swelling)
Causes:
- MS
- DM
- Syphilis
- Glaucoma
Ix:
- MRI of optic nerve
- FBC, CRP
- ESR (exclude GCA)
- ANA (exclude SLE)
- Blood glucose
Mx:
- High dose steroids
- Recovers usually in 4-6 wks
> 3 white-matter lesions on MRI = 50% risk of MS in 5yrs
Papilloedema
- what is it
- features
- fundoscopy
- causes
- ix
-Bilateral disc swelling due to raised ICP
Features:
- Asymptomatic
- Transient loss of vision when standing up
- Headache with N+V
- Low acuity and colour vision
Fundoscopy:
- Bilateral swollen hyperaemic discs
- Disc haemorrhages
- Absent venous pulsations at disc
- Optic atrophy
- Champagne cork if chronic
Causes:
- Intracranial tumour
- Benign idiopathic HTN
- Meningitis
- Brain abscess
- Ocular causes (CRVO, uveitis, etc)
Ix:
- Urgent CT head
- LP
- BP
Optic atrophy
- what is it
- acquired causes
- congenital causes
Well demarcated pale disc on fundoscopy, due to death of nerve fibres within optic nerve
Usually bilateral
Acquired causes:
- MS
- Papilloedema
- Raised ICP
- Retinal damage
- Ischaemia
- Toxins (tobacco, quinine, etc)
- Nutrition (vit deficiencies)
Congenital causes:
- Friedreich ataxia
- Mitochondrial disorders
- DIDMOAD (DI, DM, optic atrophy and deafness)
Requires neuroimaging to rule out life threatening intracranial causes
Features and causes of chiasmal disease
Features:
- Blurred vision
- Constricted visual field
- Headache
- Bitemporal hemianopia
- See-saw nystagmus
Causes:
- Pituitary tumour (compress from below -> supero-temporal vision affected first)
- Meningioma
- Craniopharyngioma (compress from above -> infero-temporal vision affected first)
Mechanism of action of cycloplegics
Examples of cycloplegics
Anticholinergics
Block response of iris sphincter muscles, and accommodative muscles of the ciliary body
Therefore dilates pupils
Relieves pain and photophobia as it prevents vasospasm in response to light
Examples of cycloplegics: atropine, cyclopentolate
Side effects of mydriatic drops and cycloplegics
Whitening of the eye lids due to vasoconstrictions
Atropine can cause redness of the face and warm sensation
Stings the eyes for a few seconds
Patients cant drive until the blurring has worn off
Fluoroscein drops
- indications
- MoA
- side effects
Indications: highlights defects in the corneal epithelium, can be used when measuring IOP, can be given with a local anaesthetic
MoA: fluoroscein is a precursor of the eosins and temporarily stains any cell it enters therefore marking any damaged area
SEs: check allergies, skin discolouration for 6-12 hours, warn patients about staining skin/clothes, may discolour contact lenses
