Ophthalmology

Question 1

Describe the borders of the orbital cavity

Answer 1

• Pyramidal structure, apex points posteriorly, base anteriorly
• Four bony walls
  
  • Medial wall- ethmoid, maxilla, lacrimal, lesser wing sphenoid (MLES)
  • Lateral wall- zygomatic bone, greater wing sphenoid (2)
  • Superior wall- frontal bone, lesser wing sphenoid (2)
  • Inferior wall- maxilla, palatine, zygomatic bone (3)
• 7 bones: Many Friendly Zebras Enjoy Lazy Summer Picnic
  
  • Maxilla, Frontal bone, Zygomatic bone, Ethmoid bone, Lacrimal bone, Sphenoid bone, Palatine bone

Question 2

There are three main pathways into the orbit at the orbital apex; what are they and what do they transmit?

Answer 2

1. Optic canal
   
   1. Optic nerve
   2. Ophthalmic artery
2. Superior orbital fissure
   
   1. Oculomotor nerve
   2. Trochlear nerve
   3. Abducens nerve
   4. Ophthalmic nerve (Va)
   5. Superior ophthalmic vein
3. Inferior orbital fissure
   
   1. Infraorbital nerve (branch of maxillary CN Vb)
   2. Inferior ophthalmic vein
   3. Sympathetic nerves

Question 3

What is the main arterial supply of the orbit?

Answer 3

• The eyeball receives arterial blood primarily from ophthalmic artery
  
  • This is a branch of the internal carotid artery, arising immediately distal to the cavernous sinus
• Branches of ophthalmic artery-
  
  • Central retinal artery supplying internal surface of retina
    
    • Occlusion à blindness
• Venous drainage
  
  • Superior ophthalmic vein
  • Inferior ophthalmic veins
  • These drain into cavernous sinus

Question 4

Describe the layers of the eyelid

Answer 4

• Skin and subcutaneous tissue (most superficial)
• Orbicularis oculi
  
  • Palpebral part- gentle closing of eyelids
  • Lacrimal part- tear drainage
  • Orbital part- tight closing of eyelids
  • Innervated by zygomatic & temporal branches of facial nerve
• Orbital septum
  
  • Tough thin sheet of fibrous tissue originating from orbital rim periosteum blends with tarsal plates
  • Acts as a barrier against superficial infection spreading from the pre-septal space (subcutaneous tissue, orbicularis oculi) and post-septal space (orbital cavity proper)
• Tarsal plates
  
  • Dense CT scaffolding
    
    • Provide stability & convexity to the lids
  • Superior tarsus = levator palpebrae superioris attachment
  • Inferior tarsus
  • Contain meibomian glands (tarsal glands)- secrete oily substance that slows evaporation of the eye’s tear film & prevents eyelids sticking together when closed
• Levator apparatus
  
  • Levator palpebrae superioris
    
    • Opens the eyelid
    • Innervation- superior branch of oculomotor nerve
  • Superior tarsal muscle
    
    • Assists LPS in opening eyelids
    • Innervation- sympathetic fibres
• Conjunctiva
  
  • Thin mucous membrane reflected on sclera of eyeball
  • Includes goblet cells that produce the mucous layer of the tear film

Question 5

Describe the difference between a stye and a chalazion?

Answer 5

• A stye is an infection of a hair follicle or Meibomian glands around the eyelash, painful and self-limiting
• A chalazion is a painless granuloma of the Meibomian glands, absence of pain

Question 6

Describe how compartment syndrome in the orbit can occur?

Answer 6

• Uncommon surgical emergency
• Acute rise in orbital pressure
• Causes- retrobulbar haemorrhage from trauma
• Haemorrhage into orbit, compression of ophthalmic artery, ischaemia of optic nerve, fixed dilated pupil, severe pain, ischaemia of ocular muscles too

Question 7

Describe the contents of the orbital cavity?

Answer 7

• Eyeball
• Fat
• Associated extra-ocular muscles
• Nerves and blood vessels
• Lacrimal apparatus

Question 8

What is the lacrimal apparatus?

Answer 8

• Lacrimal gland- anteriorly in the superolateral aspect of orbit, within the lacrimal fossa (depression in orbital plate of frontal bone). Produces watery serous liquid- lacrimal fluid
• After secretion, lacrimal fluid circulates across the eye and accumulates in the lacrimal lake
• Then drains into lacrimal sac (dilated end of the nasolacrimal duct)
• Lacrimal duct- fluid empties into the inferior meatus of the nasal cavity

Question 9

Briefly describe the action and innervation of the extraocular muscles?

Answer 9

• Levator palpebrae superioris
  
  • Elevates upper eyelid
  • Oculomotor nerve
  • Superior tarsal muscle within- sympathetic innervation
• Superior rectus
  
  • Elevates + adducts + medial rotation
  • Oculomotor nerve
• Inferior rectus
  
  • Depresses + adducts + lateral rotation
  • Oculomotor nerve
• Medial rectus
  
  • Adducts
  • Oculomotor nerve
• Lateral rectus
  
  • Abducts
  • Abducens nerve
• Superior oblique
  
  • Depresses + abducts + medial rotation
  • Trochlear nerve
• Inferior oblique
  
  • Elevates + abducts + lateral rotation
  • Oculomotor nerve

Question 10

What are the 3 layers of the eyeball?

Answer 10

1. Outer: fibrous layer-
   
   1. Sclera- attachment for extraocular muscles, optic nerve penetrates through. Visible as the white part of the eye
   2. Cornea transparent & continuous with the sclera at the front, refracts light
2. Middle: vascular layer- 3 continuous parts
   
   1. Choroid- ct and blood vessels, nourishes outer layers of retina
   2. Ciliary body- muscle and processes- control shape of lens & contributes to formation of aq. humour
      The ciliary processes project from surface of ciliary body, attach the lens to the ciliary body- controls shape of lens
   3. Iris- gives eye colour, aperture in centre called the pupil
3. Inner: retina
   
   1. Pigmented outer layer- single layer of cells, absorbs light, prevents scattering of light within the eyeball
   2. Neural inner layer- consists of photoreceptors
   3. Centre of retina = macula- highly pigmented-
   4. Fovea- highest concentration of light detecting cells, only cones, high acuity vision

Question 11

Pituitary macroadenoma- how does it present clinically, what imaging is best, and what is the treatment?

Answer 11

• Sellar mass
• Pituitary gland not seen separately
• Suprasellar extension- optic chiasm
• Rarely parasellar
• Clinically: bitemporal hemianopia
• Imaging: MRI best
• Surgery: transsphenoidal

Question 12

Mimics of a PCA infarction? Presenting complaint: homonymous hemianopia

Answer 12

• Abscess- acutely unwell
• Metastasis- hx of cancer

Question 13

Describe the visual pathway

Answer 13

• Photons of light enter the eye, stimulating the photoreceptors (rods and cones) in the retina
• The photoreceptors synapse with retinal bipolar cells which transmit these signals to retinal ganglion cells
• The retinal ganglion cells converge at the optic disc, forming the optic nerve
• The optic nerve exits the eye, travelling through a defect of the lamina cribrosa of the sclera
• The optic nerve can be considered an extension of the forebrain as it is covered by the meninges of the CNS
• The optic nerve travels through the bony orbit and enters the middle cranial fossa through the optic canal (defect in lesser wing of sphenoid)
• The optic nerve then travels along the floor of the middle cranial fossa, through the medial aspect of the cavernous sinus
• Left and right optic nerves converge at the optic chiasm, which is located directly above the sella turcica of the sphenoid bone
• Fibres from the nasal aspect of each retina decussate at the chiasm, whilst fibres from the temporal retina remain on their respective sides
• The optic tracts extend from the chiasm to the thalamus
• Afferent sensory nerves from the eye synapse with the second-order sensory neurones at the lateral geniculate nucleus in the thalamus
• The sensory nerves radiate dorsally to the calcarine sulcus of the occipital lobe
• Optic radiations loop either through the parietal lobe or through the temporal lobe (Meyer’s loop)
• The optic radiations terminate in the calcarine sulcus of the occipital lobe where the cortical visual centre is situated
• The calcarine sulcus is responsible for retinal image processing- images from both eyes are collated & a final image is formed
• The image is inverted- so the brain has to re-invert the image
• From the occipital visual centre, signals are sent to the frontal, parietal and temporal lobes to further make sense of the input information

Question 14

Where is the visual cortex?

Answer 14

• Calcarine cortex of the occipital lobe

Question 15

What imaging is best for visual pathway?

Answer 15

MRI

Question 16

How is the shape of the eyeball maintained?

Answer 16

• Aqueous humour, fluid produced by the anterior and posterior chambers of the eyeball
  
  • The anterior chamber is the space between the cornea and the iris
  • Communicates with posterior chamber through the pupil
  • The posterior chamber is the space between the iris and lens
• Aqueous humour is secreted by ciliary body and processes, fills the chambers of the eye, supports the shape of the eyeball by the pressure it exerts

Question 17

Functions of aqueous humour?

Answer 17

• Maintaining intraocular pressure and shape of globe
• Provide nutrients and oxygen for ocular tissue including posterior cornea, trabecular meshwork, lens
• Removal of metabolic by-products from intraocular cells
• Facilitating passage of light from intraocular cells

Question 18

How does aqueous humour drain?

Answer 18

• Through iridocorneal angle (between iris and cornea)
• Via trabecular meshwork (deteriorates with age- chronic open angle glaucoma)
• Into canal of Schlemm
• Blockage of this drainage à increase in intra-ocular pressure à glaucoma

Question 19

Describe the accommodation reflex?

Answer 19

1. Convergence- keeps image focused on fovea (highest visual acuity here)
2. Pupillary constriction- to ensure image isn’t blurred
3. Suspensory ligament relaxes- lens becomes fatter/ rounder (biconvex)- can focus image on fovea

Question 20

What is presbyopia & briefly why does it happen?

Answer 20

• Gradual loss of eye’s ability to focus on nearby objects
• Insufficiency of accommodation
• Age-related changes of the lens- decreased elasticity and increased hardness of the lens

Question 21

Why does every normal eye have a small blind spot in the temporal visual field?

Answer 21

• The optic nerve enters the retina at the optic disc
• Here there are no photoreceptor cells
• Hence blind spot

Question 22

Describe the function of the lens?

Answer 22

• Needed for normal vision
• Refraction- change in direction of light, helps converge light onto the retina
• Accommodation- maintaining focus on image as the distance varies, lens alters its shape through contraction or relaxation of the ciliary bodies

Question 23

Why does cataracts occur, who is affected, & how do they present?

Answer 23

• Opacification of the lens
  
  • Unilateral or bilateral
  • Lack of blood supply to lens means it is susceptible to damage from normal ageing and environmental insults eg UV light
  • Without transparency of the lens, light is unable to be refracted onto the retina to enable vision
• Common as we age
• Other causes- trauma, uveitis, scleritis, intra-ocular tumours, radiation, medications, systemic disease eg DM
• Can be congenital
• Hallmark feature: painless loss of vision
• Symptoms: visual loss, blurred vision, poor night vision, sensitivity to light & glare, seeing ‘Halos’ around lights, polyopia (multiple images seen), reduction in colour intensity (lots of blues), changes in glasses prescription
• Signs: reduced VA (snellens), loss of red reflex on ophthalmoscopy, white/ grey pupil due to opacification, nystagmus

Question 24

Risk factors for developing cataracts?

Answer 24

• Increasing age
• Smoking
• Alcohol
• Diabetes
• Steroids
• Hypocalcaemia

Question 25

How is cataracts diagnosed? Suggest some differential diagnoses

Answer 25

• Clinically with ophthalmoscope
  
  • Loss or darkening of red reflex
  • Opacification seen within red reflex
  • Obscuration of ocular detail due to opacification and crystallisation
• Slit-lamp confirms cataracts, type, and excludes other causes of visual loss such as glaucoma
• Ddx- refractive error, corneal disease presbyopia, age related macular degeneration (ARMD), retinopathy, open angle glaucoma, uveitis

Question 26

How is cataracts managed? Complications?

Answer 26

• Definitive treatment: surgical replacement of lens
  
  • Phacoemulsification- breaking up diseased lens and aspirating the leftover content, lens remains in situ and new lens is placed into the capsule
  • Extracapsular cataract extraction- removal of the diseased nucleus and aspiration of the lens cortex, capsule left in situ and new rigid lens inserted, bigger incision required
• Complications-
  
  • Immediate: endophthalmitis (bacterial or fungal infection of the intra-ocular fluid)- intravitreal abx required, can lead to loss of vision and the eye
  • Delayed- retinal detachment, macular degeneration, posterior capsule opacification

Question 27

What is glaucoma?

Answer 27

• NICE definition: glaucoma is a group of conditions with characteristic optic nerve head changes associated with corresponding visual field defects, +/- raised intraocular pressure
• Recognised types of glaucoma:
  
  • Primary open-angle glaucoma
  • Angle closure glaucoma
  • Secondary glaucoma (due to uveitis, trauma etc)
  • Congenital glaucoma

Question 28

How does glaucoma affect vision?

Answer 28

• Loss of peripheral fields- tunnel vision
• Night vision often worse
• Damage to the optic nerve affects the peripheral vision first then gradually causes total sight loss if left untreated

Question 29

What is the normal intraocular pressure? What is it created by?

Answer 29

• 10-21 mmHg
• This pressure is created by resistance to flow through the trabecular meshwork

Question 30

What happens in open angle glaucoma?

Answer 30

• Gradual increase in resistance through the trabecular meshwork
• à difficult for aqueous humour to flow through the meshwork to exit the eye, hence pressure slowly builds up within the eye
• Increased pressure in the eye causes cupping of the optic disc – normally the optic cup is less than half the size of the optic disc; in increased intraocular pressure the indent is wider- cupping of the optic disc occurs

Question 31

Risk factors for primary open angle glaucoma?

Answer 31

• Age
• FHx
• Black ethnic origin
• Diabetes
• Htn
• Myopia (near sightedness)

Question 32

Is there any screening for glaucoma?

Answer 32

• No
• However the following groups of people should have their eyes examined by an optometrist
  
  • Older age- >60 every 2 years, >70 every year (free through NHS)
  • FHx of glaucoma- people >40 with first-degree relative with open angle glaucoma have eye test annually (free through NHS)
  • People >40 of black African family origin- annual eye test (not through NHS)

Question 33

How does primary open angle glaucoma present and how is it diagnosed?

Answer 33

• Largely asymptomatic
• Visual loss may occur but central vision is preserved until later in disease
• Diagnosis via routine ophthalmic examination at optometrists
• GPs may suspect if they visualise cupped discs during ophthalmoscopy
• Diagnosis-
  
  • Ophthalmoscopy- cupped disc
  • Visual fields
  • Intraocular pressure- may or may not be elevated

Question 34

How is intra-ocular pressure measured?

Answer 34

• Goldmann Applanation Tonometry (GAT)- gold standard test
  
  • Special device mounted on slit lamp, makes contact with cornea and applies different pressures to the front of the cornea to get an accurate measurement
• Non-contact tonometry- used by opticians
  
  • Shooting a puff of air at the cornea and measuring the corneal response to the air, less accurate, but gives helpful estimate for general screening purposes

Question 35

How is open-angle glaucoma managed?

Answer 35

• Management of ocular hypertension- treatment started at pressures >24 mmHg
  
  • First-line: topical prostaglandin analogue eg Latanoprost
    
    • These reduce IOP by increased uveosacral outflow
    • C/I: pregnancy & BF
    • S/E: brown pigmentation of iris, pigmentation of peri-ocular skin, local irritation
  • Topical beta blocker eg Timolol
    
    • These reduce IOP by lowering the production of aqueous humour
    • Caution asthma, COPD
    • S/E: local irritation
  • Lifetime monitoring is routine once treatment is commenced
  • Second-line: if first-line is unsuccessful or not tolerated
    
    • Switching to a drug in the other first-line drug class
    • Combining a topical prostaglandin analogue or prostamide with topical beta blocker
      Or switching to any of the following:
    • Topical sympathomimetic eg Brimonidine tartrate
      
      • Reduce production of aqueous humour and increased uveoscleral outflow
      • S/E: local irritation, dry mouth, unpleasant taste
    • Topical carbonic anhydrase eg topical Acetazolamide, topical Brinzolamide
      
      • Reduce aqueous humour secretion
    • Topical miotic eg Pilocarpine
      
      • Induce miosis- pulls iris away from trabecular meshwork allowing for improved outflow of aqueous humour
      • S/E: local irritation, myopia, vitreous haemorrhage, retinal detachment
• Surgical options
  
  • Laser trabeculoplasty
    
    • Low-energy laser fired at trabecular meshwork
    • Increased drainage capacity of trabecular meshwork
  • Trabeculectomy
    
    • Creating a new channel from the anterior chamber through the sclera to a location under the conjunctiva
    • Causes a ‘bleb’ under the conjunctiva where the aqueous humour drains
    • The bleb is normally hidden by the upper eyelid
    • The fluid is reabsorbed from the bleb into the blood supply of the conjunctive, into the general circulation
  • Insertion of a drainage shunt
    
    • Small silicon flexible tube inserted through the sclera into the anterior chamber, allowing the aqueous humour to drain out into a tiny artificial reservoir attached to the end of the tube under the conjunctiva

Question 36

Describe how acute angle closure glaucoma occurs

Answer 36

• The iris bulges forward and seals off the trabecular meshwork from the anterior chamber
• This prevents aqueous humour from being able to drain away
• This results in continual build up of pressure in the eye, esp in the posterior chamber, which causes pressure behind the iris and worsens the closure of the angle
• OPHTHALMIC EMERGENCY! Can lead to permanent vision loss

Question 37

Describe some risk factors for developing closed angle glaucoma

Answer 37

• Increasing age
• Females > males
• FHx
• Chinese and East Asian ethnic origin- rare in black ethnicity (unlike open-angle glaucoma)
• Shallow anterior chamber
• Drugs
  
  • Adrenergic medications eg noradrenaline
  • Anticholinergic medications eg oxybutynin, solifenacin
  • Tricyclic antidepressants eg amitriptyline- anticholinergic effects

Question 38

How do patients with closed angle glaucoma present?

Answer 38

• Appear generally unwell in themselves
• Short hx of severely painful red eye, blurred vision, halos around lights, associated headache, N&V
• O/E- red eye, teary, hazy cornea, decreased VA, dilatation of affected pupil, fixed pupil size, firm eyeball on palpation

Question 39

How to manage acute primary angle closure glaucoma?

Answer 39

• Immediately admit- if there is a delay to admission do the following
  
  • Lie pt on their back w/o pillow
  • Give pilocarpine eyedrops
  • Give acetazolamide 500mg orally
  • Give analgesia and anti-emetic if required
• In secondary care, various medical options to reduce IOP-
  
  • Pilocarpine
  • Oral or IV acetazolamide
  • Hyperosmotic agents eg glycerol or mannitol to increase osmotic gradient between the blood and fluid in the eye
  • Timolol- BB- reduces production of aqueous humour
  • Dorzolamide- CA inhibitor- reduced production of aqueous humour
  • Brimonidine- sympathomimetic- reduces production of aqueous humour & increased uveoscleral outflow
• Definitive treatment-
  
  • Laser iridotomy- makes hole in iris to allow aqueous humour to flow from posterior chamber into anterior chamber, relieving pressure that was pushing the iris against the cornea, allows fluid to drain

Question 40

How does pilocarpine work in acute angle closure glaucoma?

Answer 40

• Acts on muscarinic receptors in sphincter muscles in iris and causes constriction of pupil
• Therefore it is a miotic agent
• Also causes ciliary muscle contraction
• These 2 effects cause the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork to open up

Question 41

How do pts develop diabetic retinopathy (pathophysiology)?

Answer 41

• Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells
• Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages and the formation of hard exudates (yellow/ white deposits of lipids in the retina)
• Damage to blood vessel walls à microaneurysms and venous beading (walls of veins no longer straight/ parallel, look like strings of beads or sausages)
• Damage to nerve fibres in the retina causes fluffy white patches to form on the retina- cotton wool spots
• Intraretinal microvascular abnormalities (IMRA)- dilated and tortuous capillaries in the retina, can act as a shunt between the arterial and venous vessels in the retina
• Neovascularisation- growth factors released in the retina causing new blood vessel development
  
  • May culminate in widespread vitreous haemorrhage causing sudden and complete visual loss

Question 42

Risk factors for developing diabetic retinopathy?

Answer 42

• Long period of exposure to hyperglycaemia
• Htn
• Ethnic minority background
• Renal disease- proteinuria
• Pregnancy
• Rapid improvement of blood sugar levels
• Hyperlipidaemia/ hypercholesterolaemia

Question 43

How is diabetic retinopathy classified?

Answer 43

• Non-proliferative (no new blood vessels)
  
  • Mild: microaneurysms
  • Moderate: microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous beading
  • Severe: blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrants, intraretinal microvascular abnormality in any quadrant
• Proliferative (new blood vessels)
  
  • Neovascularisation- may lead to vitreous haemorrhage
  • Fibrous tissue forming anterior to retinal disc
  • More common in T1DM
• Diabetic maculopathy
  
  • Macular oedema
  • Ischaemic maculopathy
  • Only sign may be change in VA
  • More common in T2DM

Question 44

Screening for diabetic retinopathy?

Answer 44

• All pts >age 12 with diabetes get a yearly eye test

Question 45

How to treat diabetic retinopathy?

Answer 45

• Laser photocoagulation
• Anti-VEGF medications eg ranibizumab, bevacizumab
• Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease

Question 46

Complications of diabetic retinopathy?

Answer 46

• Neovascular glaucoma (secondary glaucoma)- acutely painful red eye, vision loss
• Retinal detachment
• Vitreous haemorrhage

Question 47

What is Age-related macular degeneration?

Answer 47

• AMD is the term applied to changes, without any other obvious precipitating cause, which occur in the central area of the retina (macula) in people age >50

Question 48

Describe the changes that can occur in dry ARMD?

Answer 48

• Drusen- collections of lipid beneath the retinal pigment epithelium (RPE) and within Bruch’s membrane
  
  • Some drusen can be normal. Normal drusen are small <63 micrometres and hard
  • Large and greater numbers of drusen can be early sign of macular degeneration
• Retinal pigment epithelium (RPE) abnormalities- areas of hypo/ hyperpigmentation
• Atrophy of retinal pigment epithelium
• Degeneration of photoreceptors
• Serous pigment epithelial detachment (PED) without neovascularisation

Question 49

What are the 2 types of ARMD?

Answer 49

• Dry- 90% cases- better prognosis
• Wet- 10% cases- worse prognosis
  
  • Development of new vessels growing from the choroid layer into the retina
  • These vessels can leak fluid or blood, cause oedema, and more rapid vision loss
  • VEGF stimulates new vessel growth- target of medications to treat wet AMD

Question 50

What are the layers of the macula?

Answer 50

4 key layers of the macula-

1. Choroid layer at the bottom, contains blood vessels that provide the blood supply to the macula
2. Bruch’s membrane
3. Retinal pigment epithelium
4. Photoreceptors (at the top)

Question 51

What are some risk factors for age-related macular degeneration?

Answer 51

• Age
• Smoking
• White or Chinese ethnicity
• FHx
• CVD, htn
• Drug- aspirin
• High fat diet
• Other- sunlight exposure, blue eyes, females> males, previous cataract surgery

Question 52

How do pts with AMD present?

Answer 52

• Gradual worsening central visual field loss
• Reduced visual acuity
• Crooker or wavy appearance to straight lines
• Wet AMD more acutely- loss of vision over days, full loss of vision over 2-3 yrs, often progresses to bilateral disease

Question 53

What to expect on examination in AMD pts?

Answer 53

• Snellen chart- reduced acuity
• Scrotoma- central patch of vision loss
• Amsler grid test- distortion of straight lines
• Fundoscopy- Drusen
• Slit lamp
• Optical coherence tomography- cross-sectional views of layers of retina, to diagnose wet AMD
• Fluorescein angiography- to see neovascularisation- wet AMD diagnosis if optical coherence tomography didn’t exclude it

Question 54

How is AMD managed?

Answer 54

• Dry AMD
  
  • No specific treatment
  • Avoid smoking, control BP, vitamin supplements
• Wet AMD
  
  • Anti-VEGF medications- ranibizumab, bevacizumab, pegaptanib- injected directly into vitreous chamber once a month
    
    • See benefit after ~ 3 months

Question 55

Who typically gets central retinal vein occlusion (CRVO)? (state the risk factors)

Answer 55

• Patients > 45 secondary to retinal vein thrombosis
• Diabetes
• Hypertension
• Hyperlipidaemia
• Glaucoma
• <45: clotting disorder- thrombophilia
• Systemic inflammatory conditions eg SLE
• Smokers

Question 56

Describe the anatomy of the central retinal vein?

Answer 56

• A short vein that runs through the optic nerve
• 4 branched veins come together to form the central retinal vein
• Leaves the optic nerve 10mm from the eyeball and drains blood from the capillaries of the retina into either superior ophthalmic vein or into the cavernous sinus directly

Question 57

What happens when a retinal vein is blocked?

Answer 57

• Pooling of blood in retina
• Macular oedema & retinal haemorrhage
• Retina tissue damage & loss of vision
• Release of VEGF- neovascularisation

Question 58

Describe the classification of central retinal vein occlusion?

Answer 58

• Ischaemic- these pts are at risk of neovascular glaucoma. Some features suggesting ischaemia are:
  
  • Poor visual acuity
  • RAPD
  • Multiple dark deep intra-retinal haemorrhage
  • Multiple cotton wool spots
  • Thunder fundus
• Non-ischaemic

Question 59

How does CRVO present?

Answer 59

• Sudden painless loss of vision
• O/E- fundoscopy:
  
  • Flame and blot haemorrhages
  • Optic disc oedema
  • Macula oedema

Question 60

How to manage retinal vein occlusion?

Answer 60

• 2 main aims in the mx of retinal vein occlusion:
  
  • Identification of modifiable risk factors & their medical management eg treat glaucoma
  • Recognition & management of sight-threating conditions- treat macular oedema and prevent complications such as neovascularisation of the retina and iris and glaucoma
• Laser photocoagulation
• Intravitreal steroids
• Anti-VEGF therapies

Question 61

Describe the anatomy of the central retinal artery?

Answer 61

• Branch of the ophthalmic artery, branch of the internal carotid artery arising immediately distal to the cavernous sinus
• The ophthalmic artery gives rise to many branches which supply different components of the eye
• The central retinal artery supplies the internal surface of the retina and the optic nerve

Question 62

Causes of central retinal artery occlusion?

Answer 62

• Most common cause: atherosclerosis
• Giant cell arteritis, where vasculitis affecting the ophthalmic or central retinal artery causes reduced blood flow

Question 63

Risk factors for developing central retinal artery occlusion?

Answer 64

• Atherosclerosis- same risk factors as for cardiovascular disease- age, fhx, smoking, alcohol, htn, DM, poor diet, inactivity, obesity
• Risk factors for GCA- age> 50, females, those already affected by GCA or PMR

Question 65

How do pts with central retinal artery occlusion present?

Answer 65

• Sudden painless loss of vision
• Relative afferent pupillary defect
  
  • The pupil in the affected eye constricts more when light is shone in the other eye compared when it is shone in the affected eye
  • This occurs because the input is not being sensed by the ischaemic retina when testing the direct light reflex but is being sensed by the normal retina during the consensual light reflex
• Fundoscopy
  
  • Pale retina with a cherry-red spot- this is the macula, which has a thinner surface that shows the red-coloured choroid below and contrasts with the pale retina
  • Retina is pale due to lack of blood perfusion

Question 66

How to manage central retinal artery occlusion?

Answer 66

• Immediate referral to Ophthalmology
• Giant cell arteritis- ESR, temporal artery biopsy, high dose steroids
• If symptoms suggest occlusion within 24 hrs, attempt to dislodge the embolus by:
  
  • Firm ocular massage through closed eyelids for 15 mins
  • Stat crushed acetazolamide 500mg PO and beta blocker
  • Offer anterior chamber paracentesis
  • Inhaling carbogen to dilate the artery
  • Sublingual isosorbide dinitrate to dilate the artery
• Long term mx-
  
  • Treating reversible risk factors
  • Secondary prevention of CVD

Question 67

What is anterior ischaemic optic neuropathy?

Answer 67

• AION is caused by infarction of the optic nerve head
• It may be non-arteritic or arteritic (GCA)
• Sudden loss of vision

Question 68

Risk factors for developing AION?

Answer 68

• Male
• Systemic arteriopathy
• Age 40-60
• Disc vessel crowding (disc w/o a cup, small hypermetropic discs, disc drusen)

Question 69

How do you treat non-arteritic anterior ischaemic optic neuropathy?

Answer 69

• There is no effective treatment
• Review all vascular risk factors in casualty & exclude GCA
• Re-check clinical findings, particularly fields- expect 3 lines of VA improvement in 30% pts
• AION is unlikely to recur in the same eye after nerve fibre atrophy relieves disc vessel congestion
• Review in 6 months, discharge if stable

Question 70

What is retinal detachment?

Answer 70

• Refers to the separation of the inner neurosensory retina from the underlying retinal pigment epithelium
• This means vitreous fluid will accumulate in the subretinal space
• The outer retina relies on the blood vessels of the choroid for blood supply

Question 71

Risk factors for retinal detachment?

Answer 71

• Posterior vitreous detachment
• Diabetic retinopathy
• Eye trauma
• Retinal malignancy
• Older age
• Fhx
• Myopia
• Cataract surgery

Question 72

When to suspect retinal detachment?

Answer 72

• New onset floaters
• New onset flashes
• Sudden-onset painless & progressive visual field loss
• Reduction in visual acuity, blurred or distorted vision, causing persistent and progressive visual loss

Question 73

How to manage retinal detachment?

Answer 73

• Reattach retina and reduce traction or pressure that may cause it to detach again-
  
  • Vitrectomy- removing relevant parts of vitreous body and replacing with oil or gas
  • Scleral buckling- using a silicone buckle to put pressure on the sclera so that the outer eye indents to bring the choroid inwards and in contact with the detached retina
  • Pneumatic retinopexy- injecting a gas bubble into the vitreous body and positioning the pt so that the gas bubble creates pressure that flattens the retina against the choroid and close the detachment
• Repair retina tear-
  
  • Laser therapy
  • Cryotherapy

Question 74

What is binocular vision?

Answer 74

• The ability to use both eyes simultaneously so that each eye contributes to a common vision perception

Question 75

What is strabismus? What terminology is used to describe strabismus?

Answer 75

• AKA squint
• An ophthalmic condition where the eyes do not properly align with each other when focusing to look at an object ie poor fusion
• May be constant or intermittent and may vary with direction of gaze
• Latent deviation- controlled by subconscious effort, only appears when binocular viewing is broken and the 2 eyes are not looking at the same object- unilateral cover test
  
  • -phoria
• Manifest deviation- in certain situations such as fatigue, control is lost and the deviation becomes manifest. Present while the person views a target binocularly, with no occlusion in either eye
  
  • -tropia
• When the eyes are convergent, the deviation is eso-, when the eyes are divergent, the deviation is -exo
• Eso/exo - tropia/phoria

Question 76

List 4 things to ask in a history of strabismus?

Answer 76

• Diplopia? Is it monocular or binocular (only present with one eye open or both eyes), constant or intermittent, the position of gaze it occurs in, does it produce vertical/ horizontal/ tilted images?
• Does it stop pt from doing things?
• Is the deviation socially embarrassing?
• Birth hx
• Fhx of amblyopia, strabismus, refractive error
• Previous visual acuity or ophthalmic testing results
• PMH to include ophthalmic trauma, autoimmune or neoplastic conditions, toxin exposure, head trauma

Question 77

How is the presence of strabismus confirmed clinically?

Answer 77

• Cover test (single cover test) will detect manifest strabismus
  
  • Ask pt to focus on a target
  • Cover one eye and look at the other
  • If there is no shift in fixation of the uncovered eye, the patient has normal alignment = orthotropic
  • If there is a shift in fixation in the uncovered eye, then the patient has heterotropia
    
    • Exotropia: the eye is outwards at rest, and moves nasally when the opposite eye is covered
    • Esotropia: the eye is inwards at rest (nasal direction), and moves temporally when the opposite eye is covered
    • Hypertropia: the eye is upwards at rest and moves inferiorly when the opposite eye is covered
    • Hypotropia: the eye is downwards at rest and moves superiorly when the opposite eye is covered
• Cover-uncover test (alternating cover test) will detect if a latent strabismus
  
  • If the above single cover test demonstrates no tropia
  • Cover one eye for 1-2 seconds, then quickly remove the occlude to restore binocular vision
  • The eye that was covered is observed (rather than the uncovered eye as in single cover test) for refixation movement
  • If a phoria is present, this eye will shift back to being orthotropia to re-establish sensory fusion with the other eye
    
    • Exophoria: the covered eye moves nasally when uncovered
    • Esophoria: the covered eye moves temporally when uncovered
    • Hyperphoria: moves inferiorly
    • Hypophoria: moves superiorly

Question 78

Difference between concomitant and incomitant strabismus?

Answer 78

• Concomitant
  
  • Angle of deviation is the same in all positions of gaze
  • Extraocular movements are full
  • Usually occurs in childhood
• Incomitant
  
  • Angle of deviation is different in different positions of gaze
  • Extraocular movements are not full
  • Often compensated by involuntary adoption of a compensatory abnormal head posture – in this position, the angle of deviation is least & binocular vision may be achieved
  • It is mostly associated with defective eye movements eg third nerve palsy, thyroid eye disease
  • May be caused by restriction or paralysis of the extraocular muscles
    
    • Restriction: trapping or shortening of the muscle- due to orbital trauma, inflammation, tumour
    • Paralysis: loss of innervation to muscle- due to cranial nerve palsy(s)
  • Usually occurs in adults

Question 79

Common causes of concomitant strabismus (squints) in children?

Answer 79

• Refractive error
• FHx
• Prematurity
• Developmental delay
• Idiopathic

Question 80

Risk factors for developing strabismus?

Answer 80

• FHx of strabismus
• Low birth weight
• Premature birth
• Maternal smoking
• Vision problems such as farsightedness or cataract
• Illness that affects muscles or nerves
• Down syndrome
• Head injury

Question 81

Risk factors for developing strabismus in adulthood?

Answer 81

• Eye or blood vessel damage
• Loss of vision
• Eye tumour or brain tumour
• Graves’ disease
• Stroke
• Various muscle and nerve disorders

Question 82

Consequence of untreated strabismus?

Answer 82

• May be distressing for child and parent
• Amblyopia is a significant long-term consequence

Question 83

How can strabismus present itself in thyroid eye disease?

Answer 83

• Presents as hypotropia or esotropia because the inferior rectus and the medial rectus muscles are the most commonly involved extraocular muscles

Question 84

What is amblyopia?

Answer 84

• Amblyopia is a condition of reduced visual acuity in the absence of any obvious structural abnormality or ocular disease
• Usually unilateral but can be bilateral
  
  • Not necessarily an inherent problem with the eye itself
  • Diagnosis of exclusion; other explanation for visual loss should always be sought
  • Amblyopia is not improved by correcting any refractive error or pathological obstacle to vision eg cataract
• During visual development, permanent neural connections between the eye and visual cortex are established. When there is a problem focussing in early childhood: the brain is not stimulated to develop correctly

Question 85

What can amblyopia be caused by?

Answer 85

• Most common cause- strabismus
• Anisometropia (interocular difference in refractive error)
• Refractive error, particularly if asymmetrical (anisometropia)
• Stimulus deprivation- due to obscuration of the visual axis (ptosis, congenital cataract)
• High Astigmatism

Question 86

In a child, strabismus and amblyopia can be the sign of a serious problem. Which causes are of concern?

Answer 86

• Retinoblastoma
  
  • If missed can cause blindness, loss of eye, death
• Congenital cataract
  
  • If missed can cause blindness
• To rule these out- all children are examined for red reflex at birth
  
  • If dark or white- something is blocking the light, refer to Ophthalmology immediately

Question 87

Describe the different types of diplopia?

Answer 87

• Monocular double vision/ blurry vision
  
  • Overlapping images with blurring
• Horizontal binocular double vision
  
  • 2 identical images next to each other
• Vertical binocular double vision
  
  • 2 identical images on top of each other
• Oblique binocular double vision
  
  • 2 identical images at an angle to each other

Question 88

Why do people with childhood squints not have diplopia?

Answer 88

• Due to retinal suppression: the cortical inhibition of the visual sensation from 1 eye, when both eyes are open
• The image is never consciously perceived the suppressed area of the retina
• Depending on whether the patient is esoptropic or exotropic, either the nasal half or temporal half of the retina is suppressed
• Essentially making pts operate monocularly

Question 89

How can strabismus in childhood be treated?

Answer 89

• Correct any refractive error- glasses
• Reverse the amblyopia- part-time occlusion of the better seeing eye forcing the amblyopic eye to take up fixation and see
  
  • Non-compliance is a significant problem: if the amblyopia is severe, the occlusion may not be tolerated
• Orthoptic management- may help control intermittent and latent deviations
• Surgery- altering the pull of extraocular muscles for cosmetic reasons or for relief of abnormal head position (surgery won’t improve vision or reverse amblyopia and recurrence of squint later in life can happen)

Question 90

What are the branches of the oculomotor nerve?

Answer 90

• Superior branch- LPS, superior rectus
• Inferior branch- MR, IR, IO

Question 91

What happens to the eye in an oculomotor nerve palsy?

Answer 91

• Most extraocular muscles are affected, besides superior oblique and lateral rectus
  
  • Inability to elevate, depress and adduct the eye
• Affected eye is abducted (lateral rectus) and depressed (superior oblique)
• ‘Down and out’
  
  • Superior oblique and lateral rectus act to give an unopposed exotropia and hypotropia plus a dilated pupil with paralysis of accommodation
• Partial ptosis
• Pupil may be involved and dilated- emergency- compressive pathology

Question 92

Causes of third nerve palsy?

Answer 92

• Can be congenital, but most often acquired
• Microvascular- diabetes, htn- pupil-sparing third nerve palsy
• PCA aneurysm- painful, unilateral 3^rd nerve palsy- neuro emergency
• SoL
• Trauma
• Migraine
• Demyelinating disease
• Infection
• GCA (rare)

Question 93

What can a painful, unilateral 3^rd nerve palsy suggest? What to do in this situation?

Answer 93

• Posterior communicating artery aneurysm- emergency neurological referral!

Question 94

How to treat third nerve palsy?

Answer 94

• Treat amblyopia in children <8 years old. Prisms may help in isolated muscle cases
• Surgery only achieves a limited area of binocular single vision at best, the main aim is to improve the appearance.
• Residual diplopia can be treated with an occlusive contact lens

Question 95

What happens to the eye in a trochlear nerve palsy?

Answer 95

• Superior oblique is affected only (SO is responsible for depressing and intorting the eye)
• Diplopia
• Head tilt away from site of lesion

Question 96

Causes of 4^th nerve palsy?

Answer 96

• The trochlear nerve is the only nerve to leave brainstem backwards, before curling around and projecting anteriorly; this makes it increasing susceptible to damage from head trauma- back of head trauma eg RTA, horse riding accident, fall from height
• Microvascular- DM, htn
• Demyelinating disease
• Tumour
• Aneurysm
• Congenital

Question 97

What happens to the eye in an abducens nerve palsy?

Answer 97

• Lateral rectus muscle paralysed (responsible for abduction of the eye)
• Affected eye adducted by resting tone of medial rectus
  
  • Esotropia = inturned eye
• If 6^th nerve palsy + disc swelling or papilloedema à order emergency neuro imaging to rule out raised ICP

Question 98

Causes of 6^th nerve palsy?

Answer 98

• The abducens nerve exits the pons and runs over the petrous temporal ridge, making it susceptible to damage from raised ICP
• Microvascular- diabetes, htn
• SoL
• Trauma
• Demyelinating disease
• Infection (bacterial or viral)

Question 99

How to treat 6^th nerve palsy?

Answer 99

• Most microvascular palsies and childhood post-viral palsies resolve spontaneously so offer prisms or occlusion for large incomitant deviations
• If stable & symptomatic for >6 months, consider surgery

Question 100

What is Duane’s syndrome?

Answer 100

• A congenital strabismus due to abnormal development of the 6^th cranial nerve
• Anomalous innervation of the lateral rectus muscle, together with retraction of the globe, and narrowing of the palpebral fissure on adduction
• Basically there are problems with abduction & adduction

Question 101

What symptoms occur in Horner’s syndrome and why?

Answer 101

• Partial ptosis- denervation of superior tarsal muscle
• Miosis (pupillary constriction)- denervation of dilator pupillae muscle
• Anhidrosis on ipsilateral side of face- denervation of sweat glands

Question 102

Why might patients with thyroid eye disease experience diplopia? How can you manage this aspect of thyroid eye disease?

Answer 102

• Due to inflammatory changes that is then followed by extraocular muscle fibrosis
• Diplopia is commonly intermittent, vertical and is either up-gaze or primary position
• Treatment- stop smoking as this worsens TED, prisms may help diplopia in the primary position, occlusion of one eye may be necessary in large strabismus

Question 103

Describe the lymphatic drainage of the eyelids?

Answer 103

• Lateral 2/3 of the lids drain to superficial parotid nodes
• The medial lids drain to submandibular nodes

Question 104

Causes of eyelid lumps?

Answer 104

• Stye
• Chalazion (Meibomian cyst)
• Benign lid lesions, such as-
  
  • Epithelial lesions- squamous papilloma, epidermoid cyst
• Vascular lesions eg capillary hemangioma- superficial strawberry ‘naevi’
• Pigmented naevi
• Xanthelasma- medial eyelids, middle-aged adults, hyperlipidaemia
• Eyelid neurofibroma- isolated or associated w/ neurofibromatosis type I
• Conjunctival granuloma
• Neoplastic lid lesions
  
  • Pre-malignant disease eg acitinic keratosis (progresses to SCC), Bowen’s disease, lentigo maligna
  • Primary eyelid malignant disease: basal cell carcinoma

Question 105

Clinical features of orbital disease?

Answer 105

• Although a wide range of diseases can affect the orbit, they share many common features, by occupying volume within a confined space and damaging orbital structures
• Hence the main clinical features of orbital disease are not specific to the underlying pathology
  
  • Proptosis
  • Visual loss
  • Double vision
  • Pain

Question 106

Key things to ask in a history when exploring orbital pathology?

Answer 106

• The P’s
  
  • Proptosis- bulging, prominent eye?
  • Pain- causes include inflammation, infection, acute pressure changed eg haemorrhage, bony/ neural invasion
  • Progression- symptoms may occur over minutes (eg haemorrhage), hours-days (inflammation, weeks-months (malignancy), months- years (benign tumour)
  • PMH- thyroid disease, malignancy, trauma, sinusitis
  • Perceptual visual changes- diplopia, blurring, altered colour perception, refractive change
  • Palpable or visible mass
  • Periorbital abnormalities- including sensory- paraesthesia, numbness, facial weakness, redness, tenderness, watering, lid anomalies

Question 107

What are the main causes of disease affecting the orbit?

Answer 107

• Thyroid eye disease
• Orbital cellulitis
• Trauma
• Vascular abnormalities
• Idiopathic inflammation

Question 108

Differentials for acute red eye? (common exam Q)

Answer 108

• Painless red eye
  
  • Conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage
• Painful red eye
  
  • Glaucoma
  • Anterior uveitis
  • Scleritis
  • Corneal abrasions or ulceration
  • Keratitis
  • Foreign body
  • Traumatic or chemical injury

Question 109

What is blepharitis?

Answer 109

• Common chronic inflammatory disorder of the margin of the lids which may cause persistent and annoying symptoms of irritation, watering and redness
• Anterior blepharitis- inflammation of the base of the eyelashes- 2 main types that may co-exist:
  
  • Staphylococcal blepharitis- due to infection of the lid margins by staph aureus/ epidermidis
  • Seborrheic dermatitis
• Posterior blepharitis- inflammation of the meibomian glands
  
  • = Meibomian gland dysfunction blepharitis
• Mixed anterior & posterior blepharitis can occur

Question 110

Describe clinical features of blepharitis and how to manage it?

Answer 110

• Characteristic clinical features- burning, itching, erythema, crusting of eyelids, worse in morning
• Mx-
  
  • Eyelid hygiene measures and warm compress
    
    • Cotton tip buds to rub away scales, crusts, meibum and to reduce the bacterial load
    • Plugged meibomian glands should be express by pressure with a warm compress such as cotton wool balls or a soft cloth soaked in warm water or heatable masks
  • Topical abx- chloramphenicol if hygiene measures fail
  • Artificial tear drops for relief of symptoms, when necessary
  • Steroid eye drops for inflammatory side, used very sparingly

Question 111

What are some conditions commonly associated with blepharitis?

Answer 111

• Dry eye syndrome
• Seborrheic dermatitis
• Rosacea

Question 112

Differentials for blepharitis?

Answer 112

• Malignant tumours of eyelid- scc, bcc
• Eczema
• Infection
• Infestation- pubic lice
• Autoimmune- pemphigoid

Question 113

Suggest some causes of contact dermatitis of the eyelids?

Answer 113

• Makeup
• Skin cleansers
• Hair shampoo/ sprays

Question 114

Features of contact dermatitis on the eyelids?

Answer 114

• Erythema, swelling, scales of eyelid skin

Question 115

What are the types of stye? How do they resolve/ how to manage in GP?

Answer 115

• Acute onset painful localised swelling near the eyelid margin that develops over several days
• Hordeolum externum- infection of glands of Zeis (sebaceous glands at base of eyelashes) or glands of Moll (sweat glands at base of eyelashes)
• Hordeolum internum- infection of Meibomian glands- deeper, more painful, may point inward towards the eyeball under the eyelid
• Symptoms resolve within 5-7 days once the stye spontaneously ruptures or been drained
• Mx in GP setting- pluck eyelash from infected follicle to facilitate drainage, I&D by someone with suitable expertise
• Admit to hospital if suspecting periorbital or orbital cellulitis

Question 116

What is a chalazion? How to treat?

Answer 116

• Meibomian gland becomes blocked and swells up
• Painless swelling of eyelid
  
  • Can be tender or red
  • More common on upper eyelid than lower eyelid
  • Usually 2-8mm in diameter
  • One or both eyes can be affected
  • More than one cyst can be present
• Treatment- hot compress twice daily, analgesia
• Rarely if this fails- surgical I&D

Question 117

What is ptosis and what causes it?

Answer 117

• Droopy upper eyelid- ptosis describes a low position of the upper lid on the globe
• It is in a diagnosis
• Entropion (turning inwards) and ectropion (turning outwards) both cause watering, as a result of eyelashes irritating the ocular surface (entropion) or impairment of tear collection by the eyelid puncta (ectropion)
• May be unilateral or bilateral
• Causes-
  
  • Congenital Horner’s syndrome
  • Myasthenia gravis
  • Trauma
  • Oculomotor nerve disease
  • Pseudoptosis- aberrant facial nerve regeneration, enophthalmos, hypotropia, hyperglobus

Question 118

What is entropion? What are the causes and management?

Answer 118

• Entropion is a turning inward of the lid margin such that normal eyelashes abrade the eyeball
• May affect upper or lower lid
• Causes
  
  • Involutional (aging) changes
  • Conjunctival scarring (cicatricial)
  • Spasm of orbicularis oculi
• Mx
  
  • Initial- taping down eyelid to prevent eye drying out
  • Regular eyedrops
  • Surgical intervention- lid tightening

Question 119

What is ectropion? What are the causes & management?

Answer 119

• Ectropion is turning outwards of the eyelid margin
• Causes
  
  • Aging (due to collagen laxity)
    
    • Age-related ectropion is common, but exclude other causes
  • Paralytic: facial nerve palsy
  • Eyelid skin scarring eg from eczema or from previous lower lid surgery
  • Mechanical: lower lid mass eg meibomian cyst or bulky eyelid tumours
• Mx- surgery

Question 120

What is trichiasis? How to treat?

Answer 120

• Inward growth of eyelashes
• Results in pain and can result in corneal damage and ulceration
• Mx- specialist removes the eyelash (epilation)
• Rare cases may require electrolysis, cryotherapy, laser treatment to prevent the lash regrowing

Question 121

What is necrotising fasciitis of the eyelid, risk factors for developing NF, and how to manage?

Answer 121

• A destructive microbial infection of the soft tissue which can cause precipitous tissue destruction, septicaemia, DIC and death
• Causative organisms eg neg bacilli, strep, staph
• Risk factors- advancing age, injury eg insect bite, immunosuppression including diabetes
• Mx- immediate IV benzylpenicillin 2.4g qds and IV clindamycin 600mg qds
• Debride necrotic tissue down to a healthy (bleeding) bed
• Repeat as necessary
• Send tissue for culture & sensitivity
• Subsequent reconstructive approaches

Question 122

What is conjunctivitis?

Answer 122

• Inflammation of the conjunctiva
• 3 main types- bacterial, viral, allergic

Question 123

How does conjunctivitis present?

Answer 123

• Unilateral or bilateral
• Red eyes
• Bloodshot
• Itchy or gritty sensation
• Discharge from eyes
• None of the following: pain, photophobia, reduced VA (blurry vision due to discharge but when the discharge is cleared the vision is normal)
• Bacterial- purulent discharge, inflamed conjunctiva, typically worse in morning when the eyes may be stuck together, starts in 1 eye and can spread to the other, highly contagious
• Viral- common, clear discharge, other viral features- dry cough, sore throat, blocked nose. Tender pre-auricular lymph nodes. Contagious
• Allergic- swelling of conjunctival sac and eye lid, significant watery discharge, itchy

Question 124

How to manage the different types of conjunctivitis?

Answer 124

• Usually resolves within 2 weeks without treatment
• Advice- good hygiene to avoid spreading (don’t share towels or rub eyes, and regular hand washing), avoid contact lenses use, clean the eyes with cooled boiled water and cotton wool to help clear the discharge
• Bacterial- consider abx eye drops (although not always required)- chloramphenicol, fusidic acid eye drops
• Allergic- oral/ topical antihistamines, topical mast-cell stabilisers (require several weeks before showing benefit)

Question 125

You have a 1-month-old patient with conjunctivitis, what will you do & why?

Answer 125

• Pts < 1 month- urgent ophthalmology review because neonatal conjunctivitis can be associated with gonococcal infection and cause loss of sight and serious complications such as pneumonia

Question 126

What is episcleritis? Who is affected?

Answer 126

• Benign, self-limiting inflammation of the episcleral, the outermost layer of the sclera
• Episcleral is just underneath the conjunctiva
• Often associated with inflammatory disorders such as rheumatoid arthritis, IBD

Question 127

How does episcleritis present?

Answer 127

• Acute onset unilateral symptoms
• Typically painless/ mild pain
• Segmental redness (rather than diffuse)
  
  • Patch of redness on lateral sclera
• Foreign body sensation
• Dilated body sensation
• Watering of eye
• Discharge

Question 128

How to manage pts with episcleritis?

Answer 128

• Usually self-limiting & resolves within 1-4 weeks
• Lubricating eye drops may aid symptoms
• Simple analgesia
• Cold compress
• Safety net advice
• Systemic NSAIDs- naproxen or topical steroid eye drops in severe cases

Question 129

What is scleritis?

Answer 129

• Inflammation of the full thickness of the sclera
• More serious than episcleritis

Question 130

What systemic conditions is scleritis associated with?

Answer 130

• Rheumatoid arthritis
• SLE
• IBD
• Sarcoidosis
• Granulomatosis with polyangiitis

Question 131

How do pts with scleritis present?

Answer 131

• Acute onset of symptoms, ~50% bilateral
• Severe ocular & periocular pain (in comparison to episcleritis- painless or mild pain)
  
  • Particularly bad at night
• Pain w/ eye movement
• Redness
• Photophobia
• Eye watering
• Reduced VA
• Abnormal pupil reaction to light
• Globe tenderness to palpation of the eye

Question 132

How to manage scleritis?

Answer 132

• Emergency referral if in GP
• NSAIDs
• Steroids
• Immunosuppression in relation to systemic disease

Question 133

Causes of subconjunctival haemorrhage?

Answer 133

• A bleed into the subconjunctival space
• Most idiopathic
• Ask about htn, Valsalva (coughing. Constipation, heavy lifting, bleeding, anticoagulants, antiplatelets, trauma

Question 134

Name some factors that can contribute to developing a subconjunctival haemorrhage?

Answer 134

• Hypertension
• Bleeding disorders eg thrombocytopenia
• Whooping cough
• Medications- warfarin, NOACs, antiplatelets
• Non-accidental injury

Question 135

What does a subconjunctival haemorrhage look like O/E?

Answer 135

• Area of localised, well-demarcated haemorrhage in one eye
• May be a hx of a precipitating event eg coughing fit or heavy lifting
• No pain
• No reduction of VA
• Normal pupil reactions
• No corneal staining

Question 136

Do we treat pts with sub conjunctival haemorrhage?

Answer 136

• No
• Reassure the haemorrhage will fade over 2 weeks
• If there is a foreign body sensation lubricating eye drops may help with the symptoms

Question 137

What are corneal abrasions?

Answer 137

• Scratches or damage to the cornea
• A shearing force breaches the epithelium to expose the subepithelial nerve plexus

Question 138

Symptoms of corneal abrasion?

Answer 138

• Painful red eye
• Photophobia
• Foreign body sensation
• Tearing
• Watering eye
• Hx of contact lenses or FB
• Blurring vision
• Photophobia

Question 139

Causes of corneal abrasion?

Answer 139

• Contact lenses
• Foreign body
• Fingernails
• Eyelashes
• Entropion (inward turning eyelid)

Question 140

How to diagnose a corneal abrasion?

Answer 140

• Fluorescein stain- yellow orange colour- collects in abrasions or ulcers, highlighting them
• Slit light examination for more significant abrasions

Question 141

How to manage corneal abrasion?

Answer 141

• Simple analgesia
• Lubricating eye drops
• Abx eye drops eg chloramphenicol
• Bring the pt back after 1 week to check it has healed
• Cyclopentolate eye drops to dilate the pupil & improve significant symptoms such as photophobia- not usually necessary

Question 142

How long do corneal abrasions take to heal?

Answer 142

• Approx. 2-3 days if they are uncomplicated

Question 143

What is keratitis?

Answer 143

• Inflammation of the cornea

Question 144

What causes keratitis?

Answer 144

• Viral infection- herpes simplex
• Bacterial infection- pseudomonas or staphylococcus
• Fungal infection- candida or aspergillus
• Contact lens acute red eye (CLARE)
• Exposure keratitis caused by inadequate eyelid coverage eg eyelid ectropion

Question 145

What is the most common cause of keratitis?

Answer 145

• Herpes simplex infection

Question 146

What happens in Herpes keratitis and how do patients present?

Answer 146

• Can occur as a primary infection (first eye manifestation) or recurrent
• May affect one or more of the 3 corneal layers
  
  • Epithelial layer- most common
  • Stromal layer
    
    • Complications- stromal necrosis, vascularisation, scarring, corneal blindness
• Presentation-
  
  • Painful red eye
  • Photophobia
  • Vesicles around the eye
  • FB sensation
  • Watering eye
  • Reduced VA (can be subtle or significant)
  • A hazy cornea or cream opacity (suggests stromal keratitis)
  • Reduced corneal sensation

Question 147

How to diagnose herpes keratitis?

Answer 147

• Staining with fluorescein- shows a dendritic corneal ulcer (branching and spreading of the ulcer)
• Slit lamp exam to find and diagnose keratitis
• Corneal swabs or scrapings used to isolate the virus using viral culture or PCR

Question 148

How to manage herpes keratitis?

Answer 148

• Epithelial HSV- debride loose epithelium using topical anaesthetic and a cotton wool swab
• Acyclovir- topical or oral
• Ganciclovir eye gel
• If there is ulceration of the cornea, then treat prophylactically with topical chloramphenicol
• Topical steroids may be indicated for stromal keratitis (not epithelial)
• Corneal transplant may be required for scarring of the cornea from stromal keratitis

Question 149

Describe some complications of ocular HSV?

Answer 149

• Corneal scarring and visual impairment
• Corneal perforation
• Secondary infection with bacteria or fungi
• Systemic infection such as aseptic meningitis, encephalitis, or hepatitis

Question 150

Suggest some complications of wearing contact lenses

Answer 150

• Bacterial keratitis
• Other types of keratitis
• Corneal abrasion
• Contact kens associated red eye (CLARE)
• 3 and 9 O clock staining
• Inferior closure stain

Question 151

What is the uvea? What is uveitis?

Answer 151

• The pigmented middle layer of the eyeball
• 3 segments: the iris, ciliary body and choroid
• Uveitis is inflammation of the uveal tract
  
  • Inflammation of nearby tissues eg retina, optic nerve, vitreous humour can also occur

Question 152

How is uveitis classified?

Answer 152

• Anterior uveitis- anterior segment
  
  • Pain, redness, photophobia
• Intermediate uveitis- inflammation of vitreous
  
  • Floaters, blurry vision, vitreous opacities, snowballs (aggregates of inflammatory cells in the vitreous humour posterior to the lens)
• Posterior uveitis- inflammation of retina or choroid
• Panuveitis- anterior chamber, vitreous and retina or choroid

Question 153

What is anterior uveitis?

Answer 153

• Primary site of inflammation: anterior chamber of the uvea
• The anterior chamber becomes infiltrated by neutrophils, lymphocytes, macrophages
  
  • O/E: deposits of white blood cells are often seen in the anterior chamber
• Causes- usually autoimmune, infection, trauma, ischaemia, malignancy
• Acute or chronic

Question 154

What is acute anterior uveitis associated with?

Answer 154

• Ankylosing spondylitis
• Inflammatory bowel disease
• Reactive arthritis

Question 155

What is chronic anterior uveitis associated with?

Answer 155

• Sarcoidosis
• Syphilis
• Lyme disease
• Tuberculosis
• Herpes virus

Question 156

How does uveitis present?

Answer 156

• Pain or dull ache
• Red eye
• Diminished or blurred vision
• Watering of the eye
• Photophobia- due to ciliary muscle spasm
• Flashes or floaters
• Unreactive or distorted pupil
• Ciliary flush- a ring of red spreading from the cornea outwards
• Excessive tear production
• Abnormally shaped pupil due to posterior synechiae (adhesions)

Question 157

How does anterior uveitis present?

Answer 157

• Onset over hours or days of redness, pain, photophobia
• Usually unilateral but may be bilateral

Question 158

Differentials for uveitis?

Answer 158

• Acute glaucoma
• Keratitis
• Scleritis
• Ocular trauma

Question 159

How to treat uveitis?

Answer 159

• Steroids-topical drops
  
  • Systemic steroids may be a possibility if pts recur
• Cycloplegic-mydriatic medications eg cyclopentolate or atropine eye drops- antimuscarinics, block the action of the iris sphincter muscles & ciliary body. Dilate pupils and reduce pain associated with ciliary spasm by stopping the action of the ciliary body
  
  • Cycloplegic = paralysing ciliary muscles
  • Mydriatic = dilating pupil
• Suspecting infection- topical abx (chloramphenicol)
• Immunosuppressants eg DMARDs and TNF inhibitors
• Laser therapy, cryotherapy, surgery (vitrectomy) are also options in severe cases

Question 160

What are some possible problems affecting the front of the eye in the ICU?

Suggest how we can recognise and manage them.

Answer 160

• Direct injury to cornea- most often a superficial corneal abrasion
  
  • Red eye, seen using fluorescein eye drops and a blue light
  • Give chloramphenicol ointment for 5-7 days qds
• Exposure keratopathy
  
  • Dryness of the cornea due to incomplete lid closure allowing tear evaporation & consequent failure of the tears to spread adequately across the eye surface
  • Red eye
  • Lid taping if there is unwanted corneal exposure
• Chemosis (conjunctival swelling)
  
  • Risk factors- compromise venous return from ocular structures (eg from tight endotracheal tube taping), states of generalised oedema (eg fluid overload), incomplete eyelid closure can also predispose chemosis
  • Chemosis can cause impaired eyelid closure
• Microbial conjunctivitis and keratitis
  
  • Respiratory secretions are thought to be the major source of ocular surface infection, with aerosols from tracheal suctioning and direct contact from suction catheter both being implicated
  • If endotracheal suctioning is done from the side of the pt (rather than at the head) and with the eyes covered, pseudomonas infection rates can be reduced
  • Conjunctivitis: look for a red sticky eye, take swabs of the eye discharge, remove discharge by bathing eyelids with warm water, using a separate gauze for each eye. Use chloramphenicol ointment (rather than drops to aid lubrication) qds for 5-7 days
  • Microbial keratitis: the damaged cornea is especially vulnerable to bacterial invasion which can occur rapidly. Most cases are due to bacteria & appear as a red eye, corneal ulcer. Seek urgent ophthalmology referral

Question 161

How to identify those at greatest risk of corneal injury in the ITU? How to protect the eyes of ITU pts?

Answer 161

• Assess eyelid closure- is the lid completely closed, or is there some conjunctival exposure (any white bit visible) or any corneal exposure (even a tiny amount)?
• Protective measures-
  
  • Manual closure of the eyes or taping the eyes shut- although this can be distressing to relatives and repeated removal of tape can cause facial skin or eyelid injury or irritation so try not to use tape
  • Liberal use of lubricants into the eye- ointment > drops, because drops don’t last long enough

Question 162

Describe the causes of sudden loss of vision

Answer 162

• Vascular- AION (Anterior Ischaemic Optic Neuropathy), retinal venous and arterial occlusion
  
  • Amaurosis fugax, may represent a form of TIA (give 300mg aspirin)
  • Altitudinal field defects are often seen- ‘curtain coming down’
  • Ischaemic optic neuropathy due to occlusion of the short posterior ciliary arteries, causing damage to optic nerve
  • CRVO: severe retinal haemorrhages often seen on fundoscopy
  • CRAO: due to thromboembolism (atherosclerosis) or due to arteritis (GCA), cherry red spot on pale retina, afferent pupillary defect
• Retinal detachment
  
  • Features of vitreous detachment, floaters or flashes or light
• Vitreous haemorrhage
  
  • Sudden visual loss, dark spots
  • Diabetes, bleeding disorders, anticoagulants
• Wet Age-Related Macular Degeneration (ARMD)

Question 163

State some causes of chronic visual loss

Answer 163

• Cataract
• Dry ARMD
• Glaucoma

Question 164

Suggest some ocular manifestations of child abuse?

Answer 164

• Periorbital trauma- ecchymosis, lid oedema, orbital fractures
• Anterior segment trauma- iris prolapse, corneal laceration, cataract
• Posterior segment trauma- vitreous haemorrhage, retinal detachment, optic nerve avulsion
• Associated brain injury resulting in nystagmus, cortical blindness, encephalopathy, cranial nerve palsies

Question 165

Features of shaken baby syndrome?

Answer 165

• Triad: retinal haemorrhages, subdural haematoma, encephalopathy
• Retinal haemorrhages are the cardinal manifestation
• Splitting of the retinal layers
• Retinal haemorrhages may subside over time so prompt retinal photography is recommended at the time of discovery of retinal haemorrhage on dilated fundoscopy to record findings as a baseline for future comparison

Question 166

What is a retinoblastoma?

What is the average age of diagnosis, and briefly describe the pathophysiology?

Answer 166

• The most common ocular malignancy found in children
• Average age of diagnosis is 18 months
• Pathophysiology-
  
  • Autosomal dominant
  • Caused by a loss of function of the retinoblastoma tumour suppressor gene on chromosome 13
  • ~10% cases hereditary

Question 167

When to suspect a retinoblastoma in GP?

Answer 167

• Absent red reflex
  
  • Replaced by a white pupil (leukocoria) from a large posterior retinal tumour mass
• Strabismus
• Visual problems

Question 168

How to manage retinoblastoma?

Answer 168

• Local therapy
  
  • Enucleation for advanced local tumours or after treatment failure
• Systemic chemotherapy- multi agent chemotherapy used alone or with local treatments as primary or salvage therapy
• External beam radiotherapy now abandoned due to long-term morbidity and mortality risks

Question 169

What is hypertensive retinopathy?

Answer 169

• Describes the damage to the small blood vessels in the retina relating to systemic hypertension
• This can be a result of years of chronic htn or can develop quickly in response to malignant htn

Question 170

Describe the signs of hypertensive retinopathy?

Answer 170

• Silver wiring or copper wiring where the walls of the arterioles become thickened & sclerosed causing increased reflection of the light
• Arteriovenous nipping where the arterioles cause compression of the veins where they cross, again due to sclerosis & hardening of the arterioles
• Cotton wool spots- due to ischaemia & infarction in the retina causing damage to nerve fibres
• Hard exudates- caused by damaged vessels leaking lipids into the retina
• Retinal haemorrhages- damaged vessels rupture & release blood into retina
• Papilloedema- ischaemia to the optic nerve resulting in optic nerve oedema & blurring of the disc margins

Question 171

How to manage hypertensive retinopathy?

Answer 171

• Control BP
• Control other risk factors such as smoking and blood lipid levels

Question 172

Most common form of ocular involvement in HIV?

Answer 172

• HIV retinopathy

Question 173

Causes of optic neuritis?

Answer 173

• Multiple sclerosis- the commonest associated disease
• Diabetes
• Syphilis

Question 174

Who is typically affected by MS-associated optic neuritis?

Answer 174

• Young women- average age 31
• Who spent their childhood in temperate latitudes
• Those with MS

Question 175

How does MS associated optic neuritis present?

Answer 175

• Unilateral decrease in VA over hrs or days
• Poor discrimination of colours, ‘red desaturation’
• Pain worse on eye movement
• Relative afferent pupillary defect
• Central scrotoma

Question 176

How to manage optic neuritis?

Answer 176

• High dose steroids
• Recovery usually takes 4-6 weeks
• Prognosis-
  
  • MRI: if >3 white matter lesions, 5 year risk of developing MS is 50%

Question 177

What is sarcoidosis?

Answer 177

• A systemic granulomatous disease commonest in Asian and Afro-Caribbean pts
• Multiple sites affected- in particular, lungs, lymph nodes, skin, liver, eyes
• The eyes are affected in 30-60% of cases

Question 178

Describe some ocular pathologies that sarcoidosis can cause?

Answer 178

• Sarcoidosis can lead to a number of ocular pathologies- mainly uveitis (bilateral)
  
  • Anterior- pain, redness, photophobia
  • Intermediate- inflammation of ciliary body, floaters, blurry vision
  • Posterior- choroiditis- may involve retinal vasculitis, floaters, visual loss
• Keratoconjunctivitis sicca
• Adnexal granuloma
• Secondary glaucoma

Question 179

How to manage patients with sarcoidosis with ocular involvement?

Answer 179

• Steroids as appropriate
• Neovascularisation secondary to ischaemia or inflammation may occur; so laser or steroids may be used

Question 180

What is ocular TB? Give some examples of ocular manifestations of TB

Answer 180

• Defined as an infection by MTB in the eye, around the eye or on its surface
• Not usually associated with clinical evidence of pulmonary TB
• The conjunctiva, cornea, sclera are sites of primary ocular involvement
• Ocular manifestations of TB are varied and include scleritis, interstitial keratitis, corneal infiltrates, anterior chamber and iris nodules, anterior uveitis

Question 181

What is thyroid eye disease?

Which gender does it predominantly affect?

Answer 181

• Idiopathic autoimmune disorder resulting in an active orbital inflammatory phase (months-years) and subsequent inactive fibrotic phase, largely involving extraocular muscles and orbital fat/ connective tissues
• Affects more women than men

Question 182

Clinical features of thyroid eye disease?

Answer 182

• Symptoms-
  
  • Gritty or watery eyes
  • Puffy eyelids
  • Ocular pressure or pain
  • Angry looking eyes
  • Bulging eyes
  • Diplopia
  • Visual loss
  • Field loss
  • Dyschromatopsia- colour vision problems
  • Depression
• Signs-
  
  • Proptosis- unilateral reflecting the asymmetric muscle involvement
  • Lid lag on downgaze (von Graefe sign)
  • Lid oedema
  • Increased IOP- glaucoma may result from decreased episcleral venous outflow, because of restrictive myopathy, intraocular pressure may rise >8mmhg on up-gaze
  • Strabismus- hypotropia or esotropia because the inferior rectus and medial rectus muscles are the most commonly involved extraocular muscles
  • Optic nerve compression may occur with seemingly mild proptosis – often without visible optic nerve oedema
    
    • Document visual acuity, colour vision, presence/ absence of a relative afferent pupillary defect during each visit

Question 183

What diseases is Graves’ disease associated with?

Answer 183

• Pernicious anaemia
• Diabetes- very important due to steroid treatments
• Autoimmune adrenal insufficiency
• Vitiligo
• Systemic sclerosis
• Sjogren syndrome
• Rheumatoid arthritis
• SLE

Question 184

How to assess patients with thyroid eye disease?

Answer 184

• General health
• Ocular health
• Hx- Fhx, SMOKING, occupation, hyper/hypothyroid, compliance to meds, which meds and how often they take them, symptoms, old images
• Examination- VA, istihara colour vision assessment, exophthalmometry, orbital tension, assess lid lag, lid retraction, corneal exposure- ulcer?
• Orthoptic assessment- field of binocular single vision, field of uniocular fixation, Hess chart, visual field study, take pictures

Question 185

Describe the approach to management of thyroid eye disease?

Answer 185

• Clinical activity score- done when you first see them and when you see them again to see improvements/ decline
  
  • Pain- painful oppressive feeling on or behind globe, pain on attempted up/ down/ side gaze
  • Redness- of eyelids or conjunctiva
  • Swelling- of lids, chemosis, swollen caruncle, increase in proptosis of >2mm in 1-3 months
  • Impaired function- decrease in eye movements of 5 degrees in 1-3 months, or decrease in VA on Snellens or 1 or more lines in 1-3 months
• > or including 4= benefit from immunosuppression
• <4= risks outweigh the benefits of immunosuppression
• Immunosuppression options:
  
  • IV or oral corticosteroids if active inflammation coexists with moderate or severe TED
• Optimise endocrine control
• STOP SMOKING
• Avoid radioiodine
• Lubricants
• Ocular hypotensives
• Radiotherapy
• Surgery- orbital decompression firstly, strabismus surgery, lid surgery (upper/ lower retractions)

Question 186

Imaging for stroke?

Answer 186

• Non-contrast CT

Question 187

What is giant cell arteritis?

Answer 187

• Sight-threatening vasculitis
• Characterised by granulomatous inflammation of medium and large-sized arteries (vessel walls)
  
  • Granulomas present on microscopy- collection of macrophages

Question 188

How do pts with GCA present?

Answer 188

• Symptoms-
  
  • New headache
  • Scalp tenderness
  • Loss of appetite
  • Weight loss
  • Limb girdle pain (worse in morning, relieved by movement)
  • Ischaemic jaw pain on chewing
  • Prodromal episodic transient visual loss, often on standing due to poor perfusion, occurs in 10%
  • Ophthalmoplegia may occur (paralysis/ weakness of extraocular muscles)
• Signs-
  
  • Thickened temporal arteries, may be non pulsatile & tender
  • RAPD
  • Pale disc swelling +/- flame haemorrhages
  • VA < count fingers
  • Central retinal artery occlusion (pale retina w/ cherry red spot) and retinal cotton wool spots may occur
  • Optic nerve ischaemia may be retrobulbar

Question 189

How is a diagnosis of giant cell arteritis made?

Answer 189

• When 3 of the following criteria are met-
  
  • Age at disease on set >50
  • New headache
  • Temporal artery abnormality
  • Elevated ESR (>50)
  • Abnormal temporal artery biopsy

Question 190

How to manage giant cell arteritis?

Answer 190

• High dose corticosteroids
  
  • With visual symptoms: 60-100mg one off dose prednisolone until further ophthalmic assessment. Alternatively, IV methylprednisolone 500-1000mg for 3 days then oral prednisolone ~60mg daily
  • Without visual symptoms: 40-60mg prednisolone daily
• If there isn’t a rapid response to steroids, re-assess the diagnosis of GCA
• Steroid-related complications- steroid-induced hyperglycaemia, mood changes, insomnia, GI bleeding, immunosuppression, weight gain, Cushingoid appearance, osteoporosis, adrenal cortex suppression
• Review at 1 week and then monthly w/ repeat ESR
• When pt is asymptomatic & the ESR has significantly fallen- start a steroid-reducing regimen

Question 191

Describe the main complications of GCA?

Answer 191

• The major one is visual loss: 20% pts, little chance of recovery once lost
• Larger arterial complications: aortic aneurysm, aortic dissection, large artery stenosis
• CVD
• Steroid-related complications

Question 192

Describe some broad groups of eyelid injury?

Answer 192

• Lacerating trauma
• Blunt trauma
• Chemical injury

Question 193

Suggest 4 questions to ask when taking a history from a patient with eyelid trauma?

Answer 193

1. The time & nature of alleged assault or foreign body as well as the distance and trajectory
2. The foreign body material and structure and whether all parts have been recovered
3. Other ocular symptoms
4. ENT symptoms including epistaxis, CSF rhinorrhoea

Question 194

What is the most common orbital injury?

How do you confirm the diagnosis?

Answer 194

• Blowout fracture
  
  • Typically involving the floor or medial wall
• X-ray of the face is a first line ix
• A definitive diagnosis is confirmed by CT scan of the orbit

Question 195

Key diagnostic features of an orbital blowout fracture?

Answer 195

• Diplopia on upward gaze
• Derangement of globe position
• Intercanthal distance increased
• Oculovagal symptoms- bradycardia, hypotension, N&V)
• Visual disturbance
• Peri-orbital ecchymosis (bruising)
• Peri-orbital oedema
• Nerve sensory loss- numbness over cheek, lower eyelid, upper lip and upper teeth and gums on affected side

Question 196

What sort of chemicals can harm the eye?

Answer 196

• Alkalis penetrate ocular tissue and are the most harmful eg ammonia, lye in drain cleaner, caustic potash, Mg(OH)2 from sparklers, lime in wet plaster, cement and mortar
• Acids usually produce more superficial damage but concentrated acids may produce effects where you can’t distinguish from alkali damage

Question 197

How might an eye look after chemical trauma is sustained?

Answer 197

• Lids- burned or oedematous
• Conjunctiva- epithelial loss, chemosis, haemorrhage

Question 198

How to treat chemical trauma to the eye?

Answer 198

• Treat as an emergency even before vision testing
• Immediate management-
  
  • Measure the pH of both eyes- normal pH is 7.3-7.6
  • Instil topical anaesthetic and eyelid speculum and irrigate the eye copiously with saline or Ringer’s lactate solution delivered via IV tubing for at least 30mins
  • Pull down lower lid and double evert the upper lid to irrigate the fornices and remove any matter
    
    • Rarely this requires a GA
  • Continue irrigating until normal pH
• Subsequent treatment
  
  • Review after 1-2 days for ischaemia
  • Debride clearly necrotic corneal and conjunctival epithelium
  • Use preservative free eye drops
  • Surgical interventions may be required

Question 199

Is orbital cellulitis an emergency?

Answer 199

• YES
• THREAT TO LIFE if it spreads to intracranial space

Question 200

Possible sources of infection for orbital cellulitis?

Of these which is the most common source of infection?

Also what is the most common causative microorganism of orbital cellulitis?

Answer 200

• Paranasal sinuses (most common)
• Oropharynx including teeth
• Foreign bodies
• Skin
• Trauma including iatrogenic
• Haematogenous spread
• Bacteria most common cause- strep or staph

Question 201

Describe the difference between periorbital and orbital cellulitis?

Which one has more severe complications?

Answer 201

• Periorbital = pre-septal cellulitis
  
  • Within eyelid tissue, superficial to orbital septum
  • Secondary to superficial infections eg from bites, wounds
  • Ocular function- eye movements and vision- unaffected
• Orbital = post-septal cellulitis
  
  • Infection within the orbit, posterior or deep to orbital septum
  • Sight-threatening
  • Potential route
  • Features- proptosis/ exophthalmos, reduced or painful eye movements, reduced visual acuity
  • There’s potential for infection to spread intracranially because orbital veins drain to cavernous sinus, pterygoid venous plexus and facial veins- resulting in cavernous sinus thrombosis or meningitis

Question 202

Clinical features of orbital cellulitis?

Answer 202

• Pre-septal cellulitis- fever, peri-ocular pain, swelling, ptosis, tenderness, redness
• Orbital cellulitis- similar to the above however with chemosis, conjunctival infection, reduced eye movements, +/- diplopia, vision loss, RAPD (relative afferent pupil defect), proptosis

Question 203

Suggest 4 key Qs to ask in a hx when suspecting orbital cellulitis?

Answer 203

• Sinus disease
• Trauma
• Skin infection, dental infection
• Immunocompromise, diabetes

Question 204

What to do when examining orbital cellulitis pt?

Answer 204

• Mark the skin inflammation to determine if it’s improving or worsening later on

Question 205

How to manage pre-septal cellulitis?

Answer 205

• Mild: amoxicillin/ clavulanate or flucloxacillin. 10 days
  
  • Then every 2-7 days till improvement
• Severe: admit for ceftriazone IV daily in divided doses until responding then treat as mild disease

Question 206

How to manage orbital cellulitis?

Answer 206

• Admit into hospital
• Monitor orbital and visual functions 2-3 times daily
• Give ceftriaxone IV plus flucloxacillin IV qds
• Consider vancomycin, clindamycin, teicoplanin or other abx for MRSA
• In pts >10 years old or those with chronic sinonasal disease, add metronidazole
• Consider IV treatment 3-5 days, provided condition improves
• Request CT, blood glucose, FBC, blood culture
• Refer sinus disease to ENT
• Repeat CT to exclude abscess if any deterioration occurs
• Urgent neurosurgical referral if there is neurological deterioration or intracranial abscess
• Change to oral abx when there is definite improvement
• Review every 2-5 days after discharge until complete resolution

Question 207

Describe the use of vital dyes to aid diagnosis of ocular disease?

Answer 207

• Dyes are used for diagnostic purposes-
  
  • In clinic
  • During procedures/ surgeries
• Preservative free dyes are not recommended- due to contamination of pseudomonas aeruginosa
• Eg fluorescein- orange, water soluble dye, emits a yellow green light. Some uses include:
  
  • To look at the cornea- eg see corneal ulcers or abrasions
  • Goldmann tonometer (intraocular pressure)
  • FFA

Question 208

Describe the use of mydriatics in diagnosis of ocular disease?

Answer 208

• Antimuscarinics dilate the pupil & paralyse the ciliary muscle
• Short acting weak mydriatics eg tropicamide (action lasts up to 6hrs)- facilitate examination of the fundus of the eye

Question 209

What is optic coherence tomography?

Answer 209

• A non-invasive diagnostic test which uses a low powered laser to scan and image the inner layers of the retina
• OCT can help diagnose various eye diseases- ARMD, macular oedema, glaucoma

Question 210

What is fundus fluorescein angiography used for?

Answer 210

• FFA is a technique for examining the circulation of the retina and choroid using a fluorescent dye and a specialised camera
• Dilation drops may be required to enlarge pupils

Question 211

How are visual fields assessed? Including imaging techniques

Answer 211

• Sit directly opposite the pt, ~1metre
• Ask pt to cover 1 eye with their hand, you mirror them and cover the opposite eye on yourself
• Ask pt to focus on your nose and not move their head or eyes. You also focus on their face
• Ask pt is any part of your face missing or distorted- this screens for central visual field loss or distortion
• Position the hatpin at an equal distance between you ant the patient
• Assess the pt’s peripheral visual field, start from the periphery and slowly move towards the centre, asking the pt to report when they first see it- if you see it and the pt cannot, then they have a reduced visual field

Question 212

What are some types of visual field defects?

Answer 212

• Bitemporal hemianopia
  
  • Central tunnel vision
  • Typically due to optic chiasm compression by tumour (eg pituitary adenoma)
• Homonymous field defects
  
  • Affect the same side of the visual field in each eye
  • Commonly due to stroke, tumour, abscess
  • Half the vision is affected
• Scrotoma
  
  • Area of absent or reduced vision surrounded by areas of normal vision
  • Many possible aetiologies- eg demyelinating disease (MS) and diabetic maculopathy
• Monocular vision loss
  
  • Total vision loss in 1 eye secondary to optic nerve pathology (eg anterior ischaemic optic neuropathy) or ocular diseases (eg central retinal artery occlusion, total retinal detachment)

Question 213

What is optical biometry & when is it used?

Answer 213

• A highly accurate non-invasive automated method for measuring anatomical characteristics of the eye
• Accurate measurements are required for determining the correct power of an intraocular lens before it is implanted during cataract surgery
• The corneal curvature, axial length, focimetry (or refraction) are all measured

Question 214

What is optical biometry & when is it used?

Answer 214

• A highly accurate non-invasive automated method for measuring anatomical characteristics of the eye
• Accurate measurements are required for determining the correct power of an intraocular lens before it is implanted during cataract surgery
• The corneal curvature, axial length, focimetry (or refraction) are all measured

Question 215

Briefly describe what happens in cataract surgery?

Answer 215

• Removing the cloudy lens & replacing with the artificial one
• Mostly local anaesthetic
• Corneal incision

Question 216

Briefly, what is a retinal laser used for?

Answer 216

• Treatment of proliferative diabetic retinopathy
• Treatment of diabetic macular oedema
• Branch and central retinal vein occlusion
• ARMD

Question 217

When are intravitreal injections required? What are some risks of intravitreal injections?

Answer 217

• Gold standard for treatment of many retinal diseases, such as-
  
  • Neovascular AMD
  • Diabetic macular oedema/ non proliferative or proliferative diabetic retinopathy
  • Retinal vein occlusions
  • Uveitis
• Risks-
  
  • Pain/ FB sensation
  • Bleeding- subconjunctival, vitreous haemorrhage
  • Retinal tear/ detachment
  • Cataract- from inadvertently hitting the lens
  • Infection- endophthalmitis
  • Uveitis

Question 218

Describe the visual requirements for driving? (visual acuity and visual field)

Answer 218

• You must be able to read with glasses or contact lenses if necessary, a car number plate made after 1^st September 2001 from 20 metres
• You also must have a visual acuity of at least 0.5 (6/12) measured on Snellen scale (with glasses or contact lenses if needed) using both eyes together or one eye only if you only have one eye
• You must have adequate field of vision- horizontal field of vision of at least 120 degrees

Question 219

What are low visual aids?

Answer 219

• Items such as reading stands, anti-glare spectacles and task lights help to aid function during more visual tasks

Question 220

Briefly, what Is Charles Bonnet syndrome?

Answer 220

• Characterised by persistent or recurrent complex hallucinations (usually visual or auditory), occurring in clear consciousness
• Generally this is against a background of visual impairment
• Insight is usually preserved
• Risk factors- advanced age, peripheral visual impairment, social isolation, sensory deprivation, early cognitive impairment

Question 221

What are some causes of monocular diplopia?

Answer 221

• Abnormal refraction
• Abnormal cornea
• Abnormal lens
• Abnormal iris
• Normal examination- not diplopia

Question 222

What are some causes of monocular diplopia?

Answer 222

• Intermittent/ variable
  
  • Myasthenia gravis
  • Intranuclear ophthalmoplegia
  • GCA
• Persistent:
  
  • Neurogenic- cranial nerve palsies
  • Myogenic- congenital (rare) or acquired (thyroid)

Question 223

What are causes of a red eye + reduced vision?

Answer 223

• Normal IOP:
  
  • Corneal abrasion
  • Keratitis
  • Endophthalmitis
• Increased IOP:
  
  • Acute glaucoma
  • Anterior uveitis

Question 224

What is myasthenia gravis?

Answer 224

• Autoimmune disease, characterised by weakness and fatigability of skeletal muscle
• Antibodies against post-synaptic Ach receptors (AChR-Ab), bind to ACh at the neuromuscular junction, preventing binding of Ach and subsequent depolarisation needed for muscular contraction
• Any age, but has bimodal distribution- peaks about 20 years and 60 years
• Commoner in females

Question 225

Describe the ocular and systemic features of myasthenia gravis?

Answer 225

• Ocular: variable diplopia/ ptosis/ ophthalmoplegia- weakness to eyelids extraocular muscles- usually worsening towards evening/ with exercise
  
  • Pupillary sparing- no evidence of abnormally small or large pupils and react to light normally
• Systemic: fatigable weakness of limbs, speech, chewing, swallowing, breathing

Question 226

What are the investigations and treatment for myasthenia gravis?

Answer 226

• Ix-
  
  • Serum antibodies: anti-Ach receptor is present in >90% of pts with generalised MG, BUT only 50% of ocular myasthenia
  • MuSK antibodies- found in a small % of pts
  • Electromyography
  • Thymus scanning- CT/ MRI
• Mx-
  
  • Anticholinesterases- pyridostigmine
  • Prednisolone
  • Immunosuppression- azathioprine
  • Thymoma is an indication for thymectomy

Question 227

What are the key things to ask in an ophthalmology history?

Answer 227

• Sudden or gradual?
• Painful or painless?
• Transient or persistent?
• One or both eyes?
• Blurred vision- centrally or centrally + peripherally
• Associated distortion or double vision?
• Symptoms there all the time?

Question 228

How are the pupils assessed?

Answer 228

• Inspect pupils- size and symmetry
• Light reaction- observe constriction in the illuminated pupil (direct response) and the constriction of the shielded pupil (consensual pupil)
• Swinging light test- pen torch beam passed rapidly from one eye to the other, the normal response is sustained constriction of both pupils
  
  • If one pupil dilates upon illumination there is a relative afferent pupillary defect in that eye
  • Simple test of optic nerve function
• Accommodation reflex- ask pt to look at distant object and then at an object close to his face, both pupils should constrict and dilate again when distant gaze is resumed

Question 229

How do you assess eye movements?

Answer 229

• H-test- ask pt to keep head still, and with both eyes open, follow your finger (you make a H shape)
  
  • Pause when they look laterally to look for nystagmus (cerebellar pathology)
  • If there is a complex ophthalmoplegia, ask them to look straight up while counting down from 20 (fatigability – myasthenia gravis)

Question 230

How is colour vision assessed?

Answer 230

• Istihara plates- colour perception test for red-green colour deficiencies

Question 231

How are visual fields assessed?

Answer 231

• Ask pt to cover 1 eye with their palm and cover your eye on the same side too
• Ask them to stay focussed on your open eye
• Select a white visual fields pin and bring it in from the periphery, keeping it mid-distance from you and the pt
• Ask them to tell you when they can see it
• Move in a diagonal direction into each of the 4 quadrants

Question 232

What sort of visual field abnormalities may be identified?

Answer 232

• Monocular field loss = intra-ocular pathology or ipsilateral optic nerve lesion
• Bitemporal hemianopia = optic chiasm compression
• Left/ right homonymous hemianopia = contralateral optic tract/ radiation lesion, or occipital cortex if macular sparing if present

Question 233

How to examine for visual inattention?

Answer 233

• While the pt keeps both eyes open and focussed on you, hold out your hands in each of their outer visual fields, ask them to point to the hand which you are opening or closing
  
  • Inattention to one side = contralateral parietal lesion

Question 234

What is visual acuity?

Answer 234

• A measure of the ability of the eye to distinguish shapes and the details of objects at a given distance
• One eye is assessed at a time

Question 235

How is visual acuity assessed in adults?

Answer 235

• Snellen chart
  
  • Sit pt 6m away from chart
  • Ask pt to cover 1 eye and read lowest line
  • Record the line
    
    • eg 6/6 (= 20/20). If they read the 6/6 line but get 2 letters incorrect, record as 6/6 (-2)
  • Use a pinhole to see if vision improves- if it does, then this suggests a refractive error
  • If pt unable to read the top line of the Snellen chart at 6m even with pinhole, reduce distance to 3m (record as 3/denominator), then 1m (record as 1/denominator), assess if they can count the number of fingers you’re holding up (record as CF- counting fingers), assess if they can see gross hand movements (record as HM- hand movements), assess if they can detect light from a pen torch shone into each eye (record as PL- perception or light- or NPL- no perception of light)
• (Assess near vision- fine print reading in a book or newspaper (with 1 eye closed))

Question 236

How is visual acuity assessed in children?

Answer 236

• Preferential looking test- based upon the turning of the head or eyes towards the pattern rather than a uniform field
• Children with better vision can see finer grating and turn toward it

Question 237

At what level of vision do most people undergo surgery for their cataracts?

Answer 237

• The threshold is 6/12 in the worst eye
• However, NICE states that measurement of visual acuity can fail to detect vision problems that may benefit from cataract surgery such as glare and loss of colour vision
• The decision should include consideration of a pt’s quality of life and symptoms such as difficulty with reading, night driving, work or home activities, glare and loss of contrast, despite appropriate optical correction

Question 238

How would you consent someone for cataract surgery?

Answer 238

• Explain the benefit and complications
• Benefits-
  
  • Improved quality of vision
  • Improved fundal view to monitor or treat posterior segment disease
  • Reduced spectacle dependence (a reading correction is usually required)
• Complications-
  
  • Most complications are infrequent, and most can be treated
  • Risk of blindness is 1 in 1000, with the risk of losing the eye as a result of surgery is 1 in 10,000
  • Immediate: endophthalmitis (bacterial or fungal infection of the intra-ocular fluid)- intravitreal abx required, can lead to loss of vision and the eye
  • Delayed: retinal detachment, macular degeneration, posterior capsule opacification

Question 239

What is the commonest cause of registration as blind in the UK?

Answer 239

• Age related macular degeneration

Question 240

Can drusen ever be normal?

Answer 240

• Small hard drusen- less than 63 micrometres, can be normal
• When there is 63 micrometres or more, there is risk of progression to AMD

Question 241

Describe the changes that occur in wet ARMD?

Answer 241

• Neovascular (exudative) AMD- new blood vessels in choroid, easily bleed, leak, resulting in distortion & scarring of retina

Question 242

What 2 investigations can be used to investigate a diagnosis of age-related macular degeneration?

Answer 242

• A diagnosis of dry AMD is made using slit-lamp fundus examination alone
• Optical coherence tomography (OCT) for wet AMD
• If OCT doesn’t exclude neovascular disease, then fundus fluorescein angiography (FFA) is used

Question 243

What is the most common systemic association of paediatric uveitis?

Answer 243

• Juvenile idiopathic arthritis
• It is defined as inflammation of 1 or more joints of unknown aetiology, that begins before the age of 16 and persists for at least 6 weeks

Question 244

What long-term ophthalmological complications may develop as a result of uveitis?

Answer 244

• Higher incidence of vision threatening complications eg cataract, macular oedema, glaucoma- which may cause irreversible visual loss

Question 245

What is the tear film?

Answer 245

• Tears wet the ocular surface and a tear film is regenerated every time blinking occurs
• Tears provide a smooth ocular surface for light rays to be refracted uniformly and to provide lubrication
• The tear film has 3 components
  
  • Surface lipid layer- secreted by meibomian (tarsal) glands- prevents evaporation of the underlying aqueous component
  • Middle aqueous layer- secreted by lacrimal gland and accessory lacrimal glands
  • Inner mucus layer- secreted by goblet cells of the conjunctiva and the epithelial cell surface
• Prevents the ocular surface from drying out

Question 246

What symptoms would a patient experience with dry eyes and what are the mechanisms of a dry eye?

Answer 246

• Grittiness and discomfort of the eye
• Deficiency of tarsal glands eg obstruction to their openings will lead to increased evaporation of tears
• Reduced production of tears- consider systemic disease- Sjogren’s or drugs- antihistamines

Question 247

Describe the chambers of the eye

Answer 247

• 2 chambers- filled with aqueous humour
  
  • Anterior chamber- the space between the cornea and iris
  • Posterior chamber- the space between the iris and the ciliary body and the lens
• Vitreous chamber- The cavity behind the lens is filled by vitreous humour (transparent, jelly-like substance), supports the lens & holds the retina in place

Question 248

What are the functions of the cornea?

Answer 248

• Maintaining transparency à clear window through which we can see
• Ocular protection (including corneal reflex)
• Retraction of incoming light (+ overlying tear film)

Question 249

What are the 5 layers of the cornea?

Answer 249

• Epithelium
  
  • Non-keratinised stratified squamous layer, 5-7 cells layers thick
  • When damaged, cells from the basal layer must migrate to here to cover the wound
  • Regeneration of the corneal epithelium takes around 3-14 days
• Bowman’s membrane
  
  • Acellular layer
  • Separates the overlying epithelium from the underlying stroma
  • Trauma below this level will result in scarring of the cornea because only the epithelium is regenerated
• Stroma
  
  • Connective tissue layer, forms the bulk of the cornea
  • Predominantly type 1 collagen fibres w/ keratinocytes (fibroblasts) between the collagen fibres
  • Corneal oedema: visible lines in the stroma (striae)
• Descemet’s membrane
  
  • Separates the corneal stroma anteriorly from the endothelium posteriorly
  • Acts as a basement membrane to the endothelium
• Endothelium
  
  • Main function is to maintain hydration in order for the cornea to remain transparent
  • A layer of simple squamous endothelium that does not regenerate
  • Cellular loss may be accelerated by trauma, surgery and exposure to UV radiation

Question 250

Describe why the following symptoms occur in keratitis: pain, red eye, reduction in visual acuity

Answer 250

• Loss of epithelium exposes free nerve endings causing severe pain
• The inflammation also leads to increased circumcorneal vascularity and a red eye
• Corneal surface and tear film is disrupted along with possible corneal oedema causing a resultant reduction in visual acuity

Question 251

What might an examination of the eye of a patient with keratitis reveal?

Answer 251

• White deposit in the cornea (corneal infiltrate)
• Collection of pus behind the cornea in the anterior chamber (hypopyon)
• Looking at the anterior chamber more closely may reveal cells and flare which are leucocytes and protein derived from the leaky iris blood vessels responding to the infection

Question 252

Describe the autonomic control of intraocular pressure?

Answer 252

• Via adrenergic receptors
• Alpha 2 receptors- stimulation reduces the IOP by reducing aqueous production and may increase uveo-sacral outflow
• Beta 2 receptors- stimulation increases IOP by increasing aqueous production

Question 253

What are some causes of cataract in younger patients?

Answer 253

• Trauma- direct injury to lens (penetrating), electric shock/ lightening, blunt trauma
• Drugs- steroids (systemic and topical), amiodarone, phenothiazines
• Systemic disease- diabetes mellitus, myotonic dystrophy, neurofibromatosis type 2

Question 254

What are the 3 morphological types of cataract?

Answer 254

1. Subscapular
   
   1. Directly under the lens capsule, granular or plaque-like appearance
   2. Near vision is affected more than distance as opacity at nodal point of eye
2. Nuclear
   
   1. Involving lens nucleus. Yellowish-brown due to deposition of urochrome pigment
   2. Pt becomes myopic due to increase refractive index of lens, colours appear less well saturated and more yellow/ brown
3. Cortical
   
   1. Cortex of lens, radial spokes in the periphery
   2. Give risk to astigmatic changes, pts troubled more in dark when pupil dilates and exposes more of cataract

Question 255

Describe the functions of the iris?

Answer 255

• The iris controls the amount of light entering the eye by varying the size of the aperture in the middle of the iris- the pupil
• In conditions of low light/ sympathetic activation- the pupil dilates = mydriasis, allows more light into the eye
  
  • Dilator pupillae muscle allows the pupil to dilate
• Bright light- pupil constricts = miosis
  
  • Sphincter pupillae muscle allows the pupil to constrict
  • Stimulated via parasympathetic activation, the fibres of which are carried in the inferior division of the 3^rd nerve

Question 256

List some of the important functions of the choroid?

Answer 256

• Allows nerves and vessels to reach the anterior eye by passing through the choroid
• Removes waste product from the outer retina
• Supplies essential nutrients to the outer half of the retina
• Absorbs any light passing through the retina, thus preventing it from reflecting back and interfering with vision

Question 257

How is the choroid attached to the retina?

Answer 257

• Basement membrane called Bruch’s membrane

Question 258

Describe the blood supply to the retina?

Answer 258

• Highly metabolically active hence requires a good blood supply to meet demands
• Inner 2/3 supplied by central retinal artery
• Outer 1/3 supplied by the choroidal blood supply
• The central retinal artery divides into 4 and each supplies a segment of the retina
  
  • These arteries are end arteries

Question 259

Describe the pupillary reflex?

Answer 259

• Afferent pupillary fibres travel with the rest of the retinal fibres but leave the visual pathway just before the lateral geniculate nucleus (LGN)
• After leaving the visual pathway they synapse with the pretectal nucleus
• From here fibres travel to both Edinger-Westphall nuclei (3^rd nerve nucleus)
• This is important as it demonstrates why stimulation of pupillary afferent fibres in 1 eye causes a bilateral motor pupillary response
• Efferent fibres leave the 3^rd nerve nucleus, travel to the ciliary ganglion (via the inferior division of the oculomotor nerve) and finally to the sphincter pupillae à pupillary constriction

Question 260

List the steps of an eye examination?

Answer 260

• Check visual acuity
• Check visual fields with the confrontation test
• Observe both eyes- look for discharge, ptosis, lid lesions
• Examine corneal reflexes and carry out a cover test to detect any misalignment, check the eye movements in all positions of gaze
• Examine the pupils and look for any opacity within the normally black pupil, look for irregularity or distortion of the pupil that could be caused by damage to pupil or adhesions between the iris and the lens, check for a relative afferent pupillary defect
• Examine each eye with pen torch looking for generalised or circumcorneal redness, corneal opacity such as a foreign body or abscess, any fluid level of blood or pus in the anterior chamber, and any distortion or irregularity of the pupil
• Use a direct ophthalmoscope to examine the red reflex in each eye to check opacities in the ocular media such as those caused by corneal oedema or other opacity, cataract, or vitreous haemorrhage
• Examine the optic disc, macula and retina with the direct ophthalmoscope, taking care to document both normal and abnormal findings (this is easier when the pupils are dilated)

Question 261

What are the uses of fluorescein drops?

Answer 261

• Diagnostically to highlight defects in the corneal epithelium
• Diagnostically to assess tear drainage in children with congenital nasolacrimal duct obstruction
• Can be used as an investigation when measuring the intraocular pressure (tonometry)
• Can be administered combined with a local anaesthetic as a 0.25% solution with oxybuprocaine HCl or proxymetacaine HCl

Question 262

What is RAPD caused by?

Answer 262

• It is caused by a lesion anterior to the optic chiasm ie optic nerve or retina
  
  • Retina: detachment
  • Optic nerve: optic neuritis (MS)

Question 263

What is Relative Afferent Pupillary Defect?

Answer 263

• A condition where pupils respond differently to light stimuli shone in one eye at a time due to unilateral or asymmetrical disease of the retina or optic nerve
• It is found by the swinging light test

Question 264

Describe how partial damage to the right optic nerve can cause RAPD?

Answer 264

• Stimulation of R afferent pupillary fibres causes bilateral pupillary constriction- if the R optic nerve is severed there’s no afferent conduction so there’s no direct or consensual response from shining a light in the right eye
• When light is shone into the left eye a consensual pupillary response would still occur because the efferent system is still intact and can still be innervated by afferent fibres from the L eye innervating both R and L 3^rd nerve nuclei
• If the R optic nerve was damaged only partly, there would be a sluggish pupillary response when light is shone into the R eye and a normal response when light is shone into the L. This can be exaggerated by swinging light from the R eye to the L and back again- the R eye will dilate (rather than constrict)

Question 265

What are some causes of vision loss that lasts a few seconds?

Answer 265

• Unilateral:
  
  • GCA
  • Optic disc swelling- infection, inflammation
  • Impending central retinal vein occlusion
• Bilateral:
  
  • Disc swelling due to idiopathic intracranial hypertension (visual obscurations)

Question 266

What are some causes of vision loss that lasts a few minutes?

Answer 266

• Unilateral:
  
  • Amaurosis fugax
  • GCA
• Bilateral:
  
  • Vertebrobasilar artery insufficiency
• Migraine- lasts up to 1 hr

Question 267

State some causes of painful sudden/ recent loss of vision

Answer 267

• Abnormal cornea- keratitis
• Abnormal disc- optic neuritis
• Abnormal uvea- anterior uveitis
• Normal fundus- retrobulbar optic neuritis

Question 268

What is papilloedema?

Answer 268

• Optic disc swelling caused by raised ICP
• Almost always bilateral

Question 269

What features are observed during fundoscopy that suggest papilloedema?

Answer 269

• Venous engorgement (usually first sign)
• Loss of venous pulsation- although normal pts may not have a pulsation
• Blurring of the optic disc margin
• Elevation of optic disc
• Loss of optic cup
• Paton’s lines: concentric/ radial retinal lines cascading from the optic disc

Question 270

What causes papilloedema?

Answer 270

• SoL: neoplastic, vascular
• Malignant hypertension
• Idiopathic intracranial hypertension
• Hydrocephalus
• Hypercapnia
• Rarer causes- hypoparathyroidism, hypocalcaemia, vitamin A toxicity

Question 271

How to manage papilloedema?

Answer 271

• Urgent CT head or MRI
• Referral to neurosurgeons
• If CT head doesn’t show SoL or anything to increase ICP, can consider LP

Question 272

Causes of tunnel vision?

Answer 272

• Papilloedema
• Glaucoma
• Retinitis pigmentosa
• Choroidoretinitis
• Optic atrophy