Ophthalmology Flashcards
1
Q
Where do orbital fractures usually occur?
A
Medial + inferior walls as thinner
- Orbital rim#: usually at sutures of bones
- Blowout#: partial herniation of orbital contents into ethmoid/maxillary sinus, usually blunt trauma, if blood goes into maxillary sinus is better than accumulating in eye as less chance of optic nerve compression from raised IOP
- Orbital floor #; usually blow from an object e.g. tennis ball, often a/w soft tissue injury, vertical diplopia, enophthlamos, infraorbital anaesthesia
2
Q
What is the role + innervation of the extra-ocular muscles?
A
- Levator palpebrae superioris: superior tarsal part innervated by CNS (is activated in fight or flight so eyes go wide) and rest by CN III
- Superior rectus - elevation, some adduction + MR, CN III
- IR - depression, some adduction + LR, CN III
- MR - adduction, CN III
- LR - abduction, CN VI
- SO - angular, depression abduction + MR, CN IV
- IO - angular, elevation abduction LR CN III
3
Q
How does a CN III palsy present and what are the causes?
A
- Complete: ptosis (unopposed orbiculares oculi as LPS inhibited), down and out position of eyes (+diplopia) and mydriasis (dilated pupil-sphincter pupillae-PNS fibres carried on the CN III)
- Partial: any of the features
- Pupil involvement indicates compression from outside as these fibres are carried peripherally
Painful palsy - indicates an intracranial event, non-painful indicates a medical cause like DM or HTN
4
Q
Outline the structure of the eyeball
A
- Supplied by ophthalmic artery (from ICA)
- Fibrous layer (sclera [attachment of muscles] + cornea [central, refraction])
- Vascular layer: choroid, ciliary body iris (contains S+D pupillae muscles)
- Retina
- Lens between VH + pupil
- Vitreous humour behind lens
- Anterior + posterior chamber - contain aqueous humor
5
Q
What is exophthalmos?
A
Eyeball protrudes - eyelids open more to accommodate - more sclera visible
E.g. in thyroid eye disease
6
Q
What is the effect of RICP on the eye?
A
Raised CSF pressure in subarachnoid space - optic nerve surrounded by meninges so gets compressed - affects the veins and then the arteries
7
Q
Outline the structure of the eyelids
A
- Skin and loose CT tissue (no fat-easily distended by oedema), glands (ciliary glands of Moll + sebaceous glands of Zeis)
- Orbicularis oculi: CN VII, closes eyelids + drains tears
- Tarsal plates: attachment for LPS, has the Meiobiam/tarsal glands which secret lipid to stop eyelids sticking
- Levator apparatus: LPS + superior tarsal muscle
- Conjunctiva: thin MM called palpebral conjunctiva, reflected onto sclera (bulbar conjunctiva)
8
Q
Meiobiam cyst vs stye
A
- Meiobiam cyst/chalazion: blockage of the M gland which makes the oil layer of the tear film; deeper, last ~6m, treat with warm compress or in younger child may do surgery if interfering with vision due to risk of amblyopia or astigmatism
- Stye/hordeolum: acute infection of a gland of Moll/Zeiss/eyelash follicle, ducts of ciliary glands become obstructed causing a painful swelling in lid margin. M-topical fusidic acid
9
Q
Outline the structure of the lacrimal glands
A
- Lacrimal gland in lacrimal fossa in supers-lateral part, goes through ducts and blinking spreads over cornea
- Lacrimal apparatus to drain: conjunctival sac - lacrimal lake at medial eye - lacrimal canals - lacrimal sac - nasolacrimal duct - inferior meatus of nasal cavity - nasopharynx - swallowed
10
Q
What is epiphora?
A
Overflow of tears due to obstruction in the lacrimal system. Stagnant tears predispose to infection
11
Q
What is in tears?
A
- Smooth surface for refraction, lubrication and antibacterial
- Surface lipid layer from Meiobian glands, middle aqueous layer from lacrimal gland + inner mucous layer from goblet cells
12
Q
What is the cause of dry eyes?
A
Usually describing mild tear film instability due to blepharitis - focus on cause not artificial tears. True dry eyes can be v painful + threaten vision
- CF: burning, itch, blurred vision if in cornea, mucus strands
- Aqueous deficiency: Sjogren’s syndrome (primary or due to RA/SLE etc), lacrimal gland deficiencies (age, congenital, ablation, denervation), lacrimal duct obstruction e.g. erythema multiforme, reflex hypo secretion like CL wear/DM/CNVII damage, systemic drugs
- Evaporative: Meibomian oil deficiency, drugs, low blink rate, vit A deficiency, topical drugs, CL wear, ocular surface disease
13
Q
What is the structure and function of the cornea?
A
Avascular structure in the centre to maintain transparency, protect the eyes (physical + corneal reflex) and refraction of incoming light - is the main refracting surface as first thing light enters
Innervated by CNV1
Layers: epithelium of non-keratinised stratified squamous epi (only layer that regenerates), Bowman’s membrane (acellular), collagenous stroma, descemet’s membrane (like a basement membrane) and endothelium (for hydration, simple squamous)
14
Q
Infective keratitis?
A
Infection of the cornea due to disruption to the epithelial surface
RF: contact lenses, trauma, dry eyes, immunocompromise
CF: severe pain, peri-corneal vascularity + red eye, watery discharge/epiphora, reduced visual acuity (surface + tear film disrupted + oedema), photophobia, may have a mucho-purulent DC, corneal infiltrate (white deposit), hypopyon (pus behind cornea in AC), ‘cells’ (leucocytes) and ‘flare’ (protein) in AC due to leaking bv in iris
15
Q
What is the sclera?
A
An opaque white tissue continuous with the cornea at the limbus, where the extra-ocular muscles are attached and the optic nerve enters
16
Q
How is the intra-ocular pressure formed?
A
- Aqueous humour produced by ciliary processes of the ciliary body
- AH drained through the trabecular meshwork + canal of Schlemm
- Balance of production and drainage
17
Q
What topical agents are used to lower IOP and how do they work?
A
- Beta blockers e.g. timolol - reduce production of aqueous humour by the ciliary body (beta stimulation causes production)
- Alpha agonists e.g. apraclonidine or brimonidine - reduce production of AH (as alpha agonists reduce production) + small increase in drainage
- Carbonic anhydrase inhibitors e.g. dorzolamide - reduce production of AH
- Parasympathomimetics [muscarinic agonist] e.g. pilocarpine - contract ciliary muscles to open trabecular meshwork so increase outflow of AH
18
Q
What does the lens do?
A
Between the vitreous and the iris, function is to refract light (less power than cornea) + accommodation (changes its shape to vary amount it refracts - needed for near vision)
19
Q
What is presbyopia?
A
Reduced ability of the lens to accommodation due to reduced elasticity + atrophy of the ciliary muscle
20
Q
What is the uveal tract?
A
- Iris: divides eye into AC+PC and controls amount of light entering eye by varying pupil size
- Ciliary body: has ciliary muscle for accommodation and ciliary processes which make AH
- Choroid: covers the posterior part of the eye and separates the retina from the sclera, has a rich capillary bed and is involved in nutrient supply/waste removal to the retina
21
Q
How does the pupil dilate and constrict?
A
- Mydriasis (dilation) in low light/SNS activation - dilator pupillae contracts
- Miosis (constriction) in bright light/PSNS carried on CN III
- Age also causes meiosis as dilator pupillae atrophies + sphincter pupillae fibroses
22
Q
What is the anterior chamber?
A
Space between the cornea + iris that is filled with AH, supplies nutrients + oxygen to cornea
23
Q
What is the vitreous?
A
Between he lens + retina and fills 2/3 volume of eye - holds retina in place + supports the lens
A water-based substance with collagen in
24
Q
What is vitreal detachment?
A
Fluid fills the potential space between the vitreous and retina - vitreous detaches from retina
This can predispose to retinal detachment especially in parts where the V-R attachments are firmer
25
Describe the structure of the retina
* Outer pigmented epithelium, attached to Bruch's membrane
* Neural retina: receives light and transforms into impulses which travel along axons in optic nerve to reach visual cortex.
* Early in embryology these fuse but can separate in retinal detachment as only really firmly attached at the optic nerve head
* Macula - central retina just lateral to the optic disc, yellowish colour. Depression (fovea) has a high concentration of photoreceptors so where high acuity vision is, supplied by central artery of retina
* Optic disc - where optic nerve enters, no photoreceptors
* Fundus - posterior part of retina
26
What is the blood supply to the retina?
* Inner 2/3 - central retinal artery, with branches as end-arteries. Retinal arteries overlie the veins so this is why in HTN you see AV nipping where they cross
* Macula - v dense capillary network
* Fovea - capillary free zone
* Outer 1/3 - from the choroid
27
What is retinal detachment?
Separation of the pigmented + neural retinal layers
CF: flashing lights, floaters, visual field defects (due to disrupted neural pathways)
28
What is retinal artery occlusion?
Obstruction to flow = in the artery p/w painless sudden loss of vision
Irreversible changes occur quickly
29
Outline the visual pathway
* Light goes in a straight line so light striking the temporal retina comes from the nasal visual field
* Temporal + nasal fibres merge at optic nerve and travel to optic chiasm
* At chiasm the nasal retinal fibres (from the temporal VF) decussate forming optic tracts
* Right optic tract has temporal retinal fibres from the right eye and nasal retinal fibres from the left eye - i.e. right optic tract as all the information from the left visual field
* Optic tract synapses at lateral geniculate nucleus
* Optic radiations arch through temporal lobe (inferior radiations) and parietal lobe (superior radiations) - inferior radiations carry info from superior visual field and vv
30
Why do injuries to the central cornea heal more slowly than those at the sides?
Stem cells are found peripherally in the cornea so regeneration takes longer for cells to move to the centre
31
What is the role of the tonometer?
Measures IOP by the force needed to flatten the corneal surface. Higher force=higher pressure
32
What drugs can affect pupil size?
* Mydriasis: tropicamide (anti-muscarinic), phenylephrine (sympathomimetic)
* Miosis: pilocarpine (muscarinic agonist)
33
What are the photoreceptor cells?
* Rods: sense contrast + motion rather than details, monochrome, useful in dark
* Cones: sense fine detail + colour vision
Highest concentration at the fovea (central part of the macula) for high acuity vision, absent at the optic disc (where the optic nerve enters)
34
How would you work out where a visual field defect arose from?
*Retinal lesions - monocular. Sudden onset in vascular/detachment, ARMD macular affected first with peripheries spared
*Pre-chiasmal: monocular, ipsilateral eye. Often affects acuity
*Chiasmal: bitemporal hemianopia
*Post-chiasmal: homonymous (matching) and image reversal means that right optic tract problem causes left visual field defect
-HH without macular sparing-main optic radiation
-Superior homonymous quadrantonopia - temporal radiation
-Inferior homonymous quadrantonopia - parietal radiation
"PITS-patietal inferior, temporal superior". Tho in studies most quadranopias are from occipital lobe!
-Visual cortex - contralateral homonymous hemianopia with macular sparing
-Occipital lobe: if both cortical impairment (may still act like that have vision?), or just on one side a loss of visual perception from contralateral visual field
35
How is visual image projected?
Projected through lens onto retina upside down + laterally reversed
Information from each eye split at chasm:
* Medial fibres (temporal visual field) cross to opposite side
* Lateral fibres (nasal visual field) pass to ipsilateral optic tract
* This ensures info from both eyes about same part of VF passes to same part of visual cortex e.g. left half of VF in right optic tract
36
Differentials for painless loss of vision
* Cataract
* Open angle glaucoma
* Retinal detachment/PVD/vitreous haemorrhage
* CRV/CRA occlusion
* Diabetic retinopathy
* Posterior uveitis
* ARMD
* Optic nerve compression e.g. pituitary tumour
* Cerebral vascular disease e.g. amaurosis fugal, TIA, stroke
* Refractive error
* Corneal dystrophy
* Drugs - methanol, hydroxychloroquine, isoniazid, isotretinoin, tetracycline, ethambutol
37
Differentials for painful loss of vision
* Acute angle closure glaucoma
* GCA
* Optic neuritis
* Uveitis
* Scleritis
* Keratitis
* Shingles
* Orbital cellulitis
* Trauma
38
Differentials for the acute painful red eye
* Scleritis
* Uveitis
* Corneal abrasion
* Corneal ulcer
* Viral keratitis
* Acute angle closure glaucoma
* Endophthalmitis
* Foreign body
* Chemical injury
39
Differentials for the acute painless red eye
* Subconjunctival haemorrhage
* Episcleritis
* Conjunctivitis
* Dry eye
40
Scleritis
* CF: dull boring pain, headache, eye watering, painful movements, reduced VA (late), deep pink colour, tender, may have dilated superficial vessels
* Causes: rheumatological conditions (50%); may also be due to ocular surgery or infection
* Recurrent causes thinning
* M: treat the cause e.g. high dose steroids or Abx, all need urgent ophthalmology referral
41
Anterior uveitis
* CF: photophobia, red painful watering eye, VA often mildly reduced; hypopyon (pus), irregular pupil shape (due to posterior synechiae [iris attaching to lens capsule]), cloudy (cells in the AH + corneal oedema), injection around cornea, slit lamp may show flare + cells
* Causes: idiopathic young white males, systemic a/w HLA-B27 conditions (e.g. psoriatic arthritis, ankylosing spondylitis), IBD, sarcoidosis, Behcet's disease, infections
* M: control inflammation, prevent visual loss + minimise long term comps (e.g.topical steroids + cytoplegics, may need immunosuppression or antimicrobials)
42
Corneal abrasion
A break in the corneal epithelium usually trauma e.g. gusts of wind or FB, common
* CF: v painful (exposed nerve endings), red watering eye, photophobia, blepharospasm (unable to open eye), FB sensation, VA may be mildly reduced if in visual axis. Stains with fluorescein drops + blue light
* Need to evert upper lid to check a FB isn't lodged underneath
* M:
- Small: chloramphenicol ointment (reduce risk of bacteria + lubricant) + ocular lubricants + oral analgesic, avoid contact lenses until healed
- Large/VA affected refer
* Comps: microbial keratitis, recurrent erosions
43
Corneal ulcer
Emergency -can cause permanent scarring + significant LoV
* CF: v painful red eye photophobia, worsening VA, may see an epithelial defect + haziness
* Causes: usually an infected abrasion from extended contact lens wear, with respiratory pathogens or Pseudomonas (if tap water in CL) or acanthaemoeba from standing water. Haemophilus + Neisseria can penetrate without an initial insult
* M: if severe may need admission for Abx + mydriatic eye drops (e.g. every 30m)
44
Viral keratitis
* CF: pain, watering, photophobia, reduced VA, dendritic epithelial defect
* Causes: herpes simplex e.g. from cold sore or varicella zoster (may come with shingles w V1 distribution)
* M: refer to ophthalmology, topical antivirals
45
Acute angle closure glaucoma
Acutely raised IOP a/w physical obstruction in the AC
* CF: pain, headache, N+V, reduced VA, photophobia, hazy cornea, mid-dilated unreactive pupil
* M: lie flat on back to help open angle, IV/oral acetazolamide (reduce pressure), topical agents like BB (reduce AH production)/pilocarpine (constrict pupil to open angles), peripheral iridotomy (laser hole through iris to allow separate AH drainage route)
46
Endophthalmitis
Emergency!
* Causes: endogenous, from severe infection like endocarditis or exogenous e.g. after cataract surgery/intravitrela injection
* CF: severe pain, photophobia, rapidly progressive vision loss, hypopyon, injection, corneal oedema
* M: urgent ophthalmology, systemic + intravitreal Abx, biopsy vitreous for culture
47
Foreign body-low speed e.g. paint, dust, gravel
* CF: irritation, red/watering eye, FB sensation even after cleared, photophobia, minor visual changes if near visual axis, use fluoroscein to look for abrasions + evert upper eyelid - FB may have gone, be under upper eyelid, embedded in cornea/conjunctiva
* M: LA drops, remove FB with cotton bud, Abx drops for abrasions, lubricants to reduce FB sensation
48
Foreign body-high speed
More potential for damage like corneal lacerations or globe penetration
* CF: pain, watering, photophobia, VA changes, flashes + floaters (retinal), ferric FBs often leave an orange rust ring, corneal oedema
* Signs of penetrating: hyphaema (blood in AC), visible holes in iris/distortion, reduced IOP from AH leakage, 'plugged' wound from prolapses, fluorescein to look for leaks of AH
* M: emergency surgery, may do orbital XR/US if can't see the FB. DO NOT PUT DROPS IN, plastic shield to minimise further trauma
49
Chemical injury
* Causes: accidental e.g. cleaning products, deliberate. Alkalis worse than acids as cause liquefactive necrosis so propagate deeper, acids coagulative necrosis so impede their own progress
* CF: severe eye pain, watering, reduced VA, skin blistering, corneal abrasion, blanching of the limbus (join between conjunctiva + cornea)
* White eye indicates v ischaemic eye and that the stem cells are dead-will need corneal graft
* Severity: alkali, duration of contact, corneal involvement, limbal involvement (where stem cells are), other injury like blunt trauma
* M: IRRIGATE (water, saline, Hartmann's), test pH of the fluid, urgent r/v, topical anaesthetic, topical steroids to reduce inflammation + Abx to prevent infection + cytoplegics (e.g. cyclopentolate) paralyse iris to reduce pain, analgesia, acetazolamide if raised IOP
* Comps: conjunctival burns, limbal ischaemia, full thickness burns affecting retina etc, poor corneal healing, corneal opacification
50
Subconjunctival haemorhage
Common complaint that can cause FB sensation/grittiness
* Causes: trauma, sudden rise in intrathoracic pressure e.g. lifting, rubbing eye
* RF: HTN, anticoagulants/plts
* M: nothing, lubricants if feels gritty, adv will go in a few weeks (may go a faint yellow colour first); if secondary to trauma consider a FB or occult globe rupture
51
Episcleritis
* CF: feels uncomfortable but not frank pain, sectoral area of hyperaemia + dilated superficial vessels (moveable with a swab pressed gently on cornea), blanches with phenylephrine (vasoconstrictor)
* Usually no underlying cause but can be a/w autoimmune e.g. UC
* M: self limiting, analgesia + topical lubricants, sometimes topical steroids/NSAIDs
52
Conjunctivitis
Inflammation over the sclera (bulbar) + inner (tarsal) eyelids, usually b/l due to symmetrical pathologies (eye drops, allergy) or cross-infection. Common CF are general discomfort, watering, gritty, discharge, crusted eyes shut in morning, injection, chemises, debris
May be viral, bacterial, STI or allergic
53
Dry eye
B/L ocular irritation worsened with exposure e.g. to wind/excessive screen time
May be evaporative meaning that tears evaporate so eyes water in response e.g. blepharitis, or tear deficiency e.g. Sjogren's syndrome
CF in blepharitis: irritated margins with capping, crusting + matted eyelashes, may also see chalazions
M of blepharitis: good lid hygiene, warm compresses with lid massage, ocular lubricants (thin in day, ointment at night), in severe causes occlusion of the puncta is used to reduce drainage + improve lubrication
54
Causes of tunnel vision
* Papilloedema
* Glacuoma
* Retinitis pigmentosa
* Choroidoretinitis
* Optic atrophy in tabes dorsalis
* Psychological
55
Causes of mydriasis
* Third nerve palsy
* Holmes-Adie pupil (usually u/l constriction of a pupil with slow accommodation + poor light reflex)
* Traumatic iridoplegia
* Phaeochromocytoma
* Congenitla
* Topical mydriatics-tropicamide, atropein
* Sympathomimetic drugs-amphetamines, cocaine
* Anticholinergic drugs-TCAs
56
What is RAPD and what causes it?
aka Marcus-Gunn pupil
detected by swinging light test - paradoxical dilation of affected pupil when light shines into it. usually first time constricts as normal then when swing it dilates (and normal pupil also dilates-consensual) - relative as compared to the other pupil
Due to a lesion to the retina or optic nerve
57
What is the normal pathway for the pupillary light reflex?
afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
58
What causes optic atrophy?
* Acquired: MS, chronic papilloedema, raised IOP, retinal damage e.g. ischaemia, toxins e.g. arsenic, nutritional deficiencies e.g. B1/2/6/12
* Congenital: Friedreich's ataxia, mitochondrial disorders, DIDMOAD (Wolfram syndrome)
59
What does cupping of the optic disc mean and what causes it?
Neuro-retinal rim thins which causes the cup to disc ratio to be enlarged (cup > half the disc diameter); defined as enlarged when cup to disc ratio is >0.7 (suspect glaucoma)
Usual cause is glaucoma - death of optic nerve axons + glia, so the rim thins and the support structure goes so the cup part looks bigger
60
What actually is the cup vs the disc of the optic nerve?
* Cup: central portion of the disc, usually quite small compared to entire disc
* Disc: optic nerve head, mostly filled with axons, fibres grouped around it in a rim
61
Why should you never give steroids for an undiagnosed red eye?
If is on HSV keratitis will cause a geographic ulcer as you have impaired the immune response
62
What is the difference between herpes simplex and herpes zoster keratitis?
* HSV: primary periocular infection usually occurring in children, looks like a branching ulcer (like HZ) but has terminal bulbs (unlike HZ), cause a patchy iris defect
* Herpes zoster ophthalmicus: segmental iris defect, Hutchinson's sign (rash on nose indicates in cornea, as both are supplied by the nasociliary branch of CNV1)
63
What's the difference between scleritis and episcleritis?
* Scleritis: 50% have underlying cause e.g. RA. Vessels don't blanch with phenylephrine, dull pink areas of inflammation, v painful, dull pinkish area may have overlying bright red vessels that aren't moveable, sight-threatening, if recurs causes thinning of the area so choroid more exposed (so looks darker), diffuse + can have areas of necrosis
* Episcleritis: 30% a/w systemic conditions like UC. Dilated vessels are moveable and blanch with phenylephrine (a vasoconstrictor), not acutely painful may be sore/gritty, redness in sectors, usually self-limiting but may recur (but won't cause thinning)
64
Viral conjunctivitis
* Adenovirus main pathogen
* V contagious -can cause epidemics
* 50% u/l
* CF: eye watering, coryzal sx, pre-auricular lymphadenopathy, corneal inflammation
* M: lubricants, cold compress, hygiene. Topical steroids if cornea involved. Adv may take weeks
* Herpes simplex type - usually UL, cutaneous vesicles on skin, burning/FB sensation, high risk of dendritic ulcer so give topical aciclovir
* Molluscum type - papule on lid margin, excise the lesions. Chronic course
65
Bacterial conjunctivitis
* Resp pathogens like S pneumonia and Haemophilus
* Usually b/l
* CF: extensive conjunctival injection + DC
* M: topical chloramphenicol drops/ointment or fusidic acid, hand washing, f/u if worsens or persists, not sharing towels, don't use contact lenses during the infection
66
Chlamydial conjunctivitis
Typically u/l conjunctivitis with serous DC, PCR for diagnosis, needs systemic Abx (e.g. doxycycline) + refer to GUM, can cause scarring
67
Gonorrhoeal conjunctivitis
Severe swelling, hyper-purulent DC.
Refer to GUM -- systemic Abx
Comps include corneal ulcer + scarring
68
Allergic conjunctivitis
Common, h/o atopy, occurs on exposure to allergen. Seasonal (S+S) or perennial (peak autumn) type, type I hypersensitivity a/w mast cells
* CF: itch, swelling of lids/conjunctiva, pink-red eyes, watering, stringy discharge, occ chemosis, coryzal sx.
* M: cold compress, topical or oral antihistamines, wash face after exposure, for more severe topical mast cell stabilisers (e.g. sodium cromoglicate-but they need longer time for therapeutic benefit for several weeks), lower allergen load, ocular lubricants (dilute allergen)
69
Thermal burns
* CF: keratopathy or burns to lids
* M: burins specialists, IV fluids if >10-15% of BSA affected, use non-adherent dressings, simple emmolients, irrigate with cool liquid, topical cytoplegics+lubricants, analgesia, steroids if oedema
* Comps: loss of lid tissue, lid cicatrization (fibrous tissue contraction), epiphora, conjunctival burns, limbal ischaemia
70
CF of orbital #
Periorbital bruising, oedema or haemorrhage
Surgical emphysema
Abnormal globe position
Abnormal pupil responses or RAPD
Subconjunctival haemorrhage
Dysmotility
Associated injuries to head, neck or teeth
71
Corneal foreign body
Usually metallic so rarely cause infection, microbes more likely in stone/ceramic/organic matter
* CF: photophobia, pain, injection, lacrimation, blurred vision, FB, rust ring, anterior uveitis
* M: only remove under slit lamp, give LA drops and topical Abx + NSAID
72
What is hyphaema?
Blood in anterior chamber - causes include blunt trauma, surgery and haematological disease
Usually apparent on slit lamp but if extensive may see with naked eye
Comps: corneal staining, red cell glaucoma
M: bed rest, globe protection, avoid aspirin/antiplt/NSAID, cytoplegic e.g. atropine, topical steroid
73
What is retrobulbar haemorrhage?
Compartment syndrome of the eye socket
* Causes-trauma, surgery
* CF: tight swollen eyelid, u/l fixed+dilated pupil, reduced eye movements, profound LoV. If no movement/pupil unreactive optic nerve must be v compressed - needs urgent lateral canthotomy + cantholysis (make hole at the side, not in the globe, to allow blood out)
74
What are the causes of orbital cellulitis?
* Causes: S pneumonia, S aureus, S progenies, H influenzae (less since HiB vaccine)
* RF: sinus disease, dental/facial infection, dacryocystitis, trauma, surgery to orbit/lacrimal/vitreoretinal, endogenous spread in immunocompromised pt
75
How does orbital cellulitis present and what is the management?
* CF: fever, malaise, periocular pain, inflamed lids, chemises, proptosis, painful restricted movements, diplopia, lagophthalmos, optic nerve dysfunction (reduced VA/RAPD/reduced colour)
* CT orbit sinus brain - may see sinus opacity, orbital infiltrate or abscess
* M:
76
What may cause orbital inflammation?
Orbital cellulitis, preseptal cellulitis, myositis, dacryoadenitis (lacrimal gland), thyroid eye disease, granulomatosis with polyangiitis, sarcoidosis
77
What cystic lesions may arise on the orbit?
* Dacryops: lacrimal duct cyst, painless blue-grey areas in superolateral fornix
* Dermoid cyst - may disturb orbit or cause recurrent inflammation, need excision
* Mucocele: blocked sinus opening so secretions cause a collection, need ENT to sort sinus out
78
What is the difference between orbital cellulitis + preseptal (periorbital) cellulitis?
* Preseptal: more limited disease, but in young children is serious because the orbital septum isn't fully developed so it can spread to orbit. Causes fever pain + swollen lid, but eye movements + conjunctiva + optic nerve unaffected
* OC has proptosis, restricted eye movements, reduced A, RAPD
79
Name some common eyelid disorders
* Trichiasis (misdirected lashes) - causes irritation, can cause corneal changes so if severe may need lash removal/surgery
* Lash infestations with head lice or crab lice - causes itch, blepharitis, conjunctivitis
* Madarosis - partial/complete loss of lashes. Local causes e.g. chronic blepharitis or systemic e.g. alopecia/psoriasis/hypothyroidism
* Entropion - lid margin rolls inwards so lashes cause irritation + red eye, usually need surgery
* Ectropion - lid margin rolls out, lacrimal sac in wrong place so watery eye, more likely in CN VII palsy, usually surgery
* Blepharitis - inflammation of lid margins
80
Blepharitis
* Causes: Meibomian gland dysfunction, seborrhoea, S aureus infection (linked to many conditions inc preseptal cellulitis)
* CF: asymptomatic or itchy burning eyes, crusty scaly deposits on lashes, may see Meibomian glands plugged with secretions/evidence of chalazion
* M: lid hygiene to reduce bacteria + unblock MG, mechanical removal of debris from lid margins (e.g. cotton wool in cooled boiled water mixed with baby shampoo), topical chloramphenicol/fusidic acid, oral doxycycline if severe/suspect acne rosacea
* Artificial tears for sx relief
81
Common lid lumps and their management
* External hordeolum (stye): abscess in lash follicle in gland of Zeis (sebum) or Moll (sweat), usually Staph, M-warm compress and topical Abx only if there is conjunctivitis
* Internal hordeolum (stye): abscess within a MG, usually Staph tender lump, M-warm compress, oral Abx if cellulitis, chronic-incise, may leave a chalazion
* Chalazion (Meibomian cyst): commonest lump, chronic inflammation of a MG, a/w chronic blepharitis/rosacea/seborrheic dermatitis. Firm and painless. M-hot compress to drain, if symptomatic may remove or in children if obstructing vision (as blocks development so amblyopia risk)
* Cyst of Moll and Zeis: chronic cysts
* Xanthelasma: SC lipid deposits in medial area
* Molluscum contagiosum: pearly umbilicate nodules caused by poxvirus, may remove if causing issues
* Benign tumours like papillomas, seborrheic keratosis or capillary haemangiomas
* Malignant tumours like basal cell carcinoma (deffo remove if near eye as can be locally invasive + destructive), SCC (higher risk of mets)
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Give some causes of acquired ptosis
* Involution: disinsertion of LPS a/w age + surgery, may cause high upper lid crease + compensatory brow lift. Can have surgery
* Neurogenic: CN III palsy (complete ptosis from los of LPS, usually down + out and sometimes dilated pupil if affected the PNS), Horner's syndrome (partial ptosis, may also have meiosis + lower lid elevation + anhidrosis)
* Myasthenia gravis: fatiguable eyelid, consider when skin crease is normal
* Myopathy: b/l + symmetrical, restricted ocular movement
* Mechanical from masses or oedema
* Pseudoptosis: brown ptosis (frontalis dysfunction), dermatochalasis (upper eyelid skin hangs in folds in elderly pt), blepharochalasis (abnormal lid elastic tissue)
83
What causes a watery eye?
* Increased production: autonomic disturbance, drugs, chronic lid disease, local irritants, aberrant regeneration after CNVII palsy
* Lacrimal pump failure: lid laxity, orbiculares weakness, ectropion
* Reduced drainage: punctal obstruction like stenosis in the elderly, canalicular obstruction like idiopathic/from 5-FU, lacrimal sac obstruction from sarcoid/granuloma/papilloma, nasolacrimal duct obstruction eg. nasal #
84
Dacryocystitis
Inflammation of the lacrimal sac - causes painful lump at side of nose next to lower lid
Causes:
* Acute: causes tender erythematous lump inferior to medial canthus, need Abx to prevent abscess which can lead to fistula.
* Chronic: recurrent ipsilateral conjunctivitis, mucocele
M: oral Abx, watch for cellulitis, refer to ophthalmology as may have an underlying cause e.g. mucocele that needs surgery
85
Neonatal conjunctivitis
* Chlamydia trachomatis commonest cause . Check for otitis media + pneumonia, M-oral erythromycin. Onset ~2w after birth
* 30-50% accounted for by Staph, Strep Haemophilus, Pseudomonas. Topical therapy or oral in Pseudomonas
* Viral infections less common in neonate
* Gonorrhoea <1% nowadays. Onset within days, hyperacute injection + chemosis + lid oedema + severe purulent discharge, may have corneal ulceration + perforation. Need hourly saline lavage and IM/IV ceftriaxone.
Purulent/mucopurulent discharge, conjunctival injection, swelling; may have systemic signs
86
Why do you use oral erythromycin for neonatal Chlamydial conjunctivitis?
Topical not sufficient
and
if its in eyes its likely to also be in the respiratory tract
87
What is chemosis?
Conjunctival oedema
88
Vernal keratoconjunctivitis
Uncommon but serious, affects 5-15yo with atopic history usually, lasts 5-10y
* CF: itch, thick mucus, tarsal giant papillae, limbal papillae or white dots, keratitis. Causes corneal scarring
* M:
- Acute: intensive topical steroids + antihistamines
- Steroids spared where poss cos of cataract risk
- Chronic: topical mast cell stabiliser, cyclosporin, mucolytics e.g. acetylcysteine
- Surgical debridement may be needed
89
Atopic keratoconjunctivitis
Eczema of lids + staphylococcal lid disease --> keratitis, anterior blepharitis, limbal hyperaemia, chemosis
A/w keratoconus + cataract
90
Cicatricial conjunctivitis
Conjunctival inflammation a/w scarring, rare, sight-threatening
Causes include physical damage, infections like trachoma, oculocutaneous disorders such as bulllous pemphigoid or SLE, rosacea, Sjogren's, IBD, graft vs host disease, drug-induced from anti-glaucoma meds
91
What are the causes of keratitis?
* Commonest - gram + like S aureus/epidermidis or S pneumoniae
* G negs like Pseudomonas (a/w CL), H influenza, N gonorrhoea
* Herpes simplex virus - cells lyse forming a dendritic ulcer, more likely in immunosuppression, virus lies dormant in CN V ganglion, M-aciclovir ointment
* Contact-lens related: not common but can cause infective corneal ulcers
* Blepharitis
92
RF for keratitis
Trauma causing abrasions, extended CL wear, poor hygiene e.g. rinsing in tap water- Acanthamoeba
93
How does keratitis present?
FB sensation, pain, photophobia, lacrimation, reduced vision, discharge, injection, white opacity
Comps: limbal + scleral extension, corneal perforation, endophthalmitis (rare unless certain things like fungi)
94
How do you manage keratitis?
* Send scrapes + contact lenses for MCS
* Topical Abx intensive sterilisation
* In healing phase add steroids + lubricants
* Stop CL wear, report to Yellow Card scheme if CL-associated
95
Herpes simplex keratitis
* Usually blepharitis but can spread to cornea using dendritic erosion (branching, terminal bulbs) + geographic ulcers in areas of de-epithelialisation
* Superficial punctate keratitis, pseudodendrites
* Need systemic antivirals, topical lubricants
96
Herpes zoster ophthalmicus
* Reactivation of VZV in area supplied by CNVa
* CF: viral prodrome, preherpetic neuralgia, rash (papules-vesicles-pustules-scabs), Hutchinson's sign, cornea more vulnerable to bacteria + fungi
* M: oral antivirals, IV if severe/immunocomrpomised
* Comps: episcleritis, anterior uveitis, ptosis, post-herpetic neuralgia
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Keratoconus
A common progressive cone-shaped bulge that affects vision leading to astigmatism + myopia. Mostly in younger people
RF: FH, allergic diseases causing chronic rubbing, CT disease causing abnormal corneal structure, Apert's syndrome
CF: worse prognosis the earlier the onset, usually b/l but asymmetrical, irregular astigmatism with reduced VA, usually stabilises by mid-30s
Comps: rupture of Descemet's membrane causing oedema, corneal scar
M: glasses/soft CL to correct vision, corneal cross-linking procedure, corneal transplant
98
Corneal dystrophy
* Endothelial e.g. Fuch's corneal dystrophy. Gradual onset, blindness in 40-60s if don't do a transplant
* Epithelial
* Stromal
99
What is a penetrating keratoplasty?
A corneal transplant - full or partial thickness
* Inds: keratoconus, corneal thinning, perforation, Fuch's endothelial dystrophy
* Post-op need topical steroid + Abx for infection risk and rejection for minimum 2y but poss lifelong
100
What is a cataract?
An opacity in the lens that reduces its transparency
101
What are the types of cataracts?
* Nuclear: central, commonest type. CF include gradually reducing contrast + colour intensity, difficulty seeing number plates/golf balls/recognising faces, a/w myopia
* Cortical: in outer layer of lens, may not have sx unless on visual axis. CF include light scatter, problems with glare when driving, reading reduced
* Subscapular: directly under lens capsule, may cause glare/near vision issue, a/w steroids
* Childhood: congenital from birth to 1y, developmental or traumatic
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What are the causes of cataracts in adults?
* Age: commonest. Protein aggregates deposited + pigment accumulate in lens
* Secondary to other eye disease e.g. high myopia or fundal dystrophies like retinitis pigmentosa
* Metabolic e.g. poorly controlled DM, galactosaemia, hypocalcaemia, Wilson's disease
* Drug-induced: steroids, miotics, amiodarone
* Traumatic like post surgery or radiation
* Inflammatory-uveitis
* A/w disorders like T21 and NF2
* In developing world - malnutrition, acute dehydration, excessive UVB exposure
103
What are the CF of cataracts?
* Painless gradual deterioration of vision
* Glare problems - in bright light
* Reducing perception of colour intensity
* Frequently changing prescription as more refractive error
* Monocular diplopia
* Red reflex reduced or with a dark defect
* If VA improved with pinhole implies refractive error
104
Outline the management for adult cataracts
* Changes in glasses prescription for early correction
* Surgery - lens extraction + replacement, phacoemulsification commonest type
* Incise sclera, make round hole in lens capsule, US probe liquefies the lens nucleus + extracts it and soft lens fibres are aspirated, and put a replacement lens in. Heals without sutures
* Criteria include vision impairment caused by cataract affecting pt life (no set level), co-morbidity meaning will benefit form surgery e.g. reducing falls risk, and if they have DM but cataract means can't do retinal screening properly
* After surgery the usually need glasses even if they didn't need them before
105
What are the causes of congenital cataracts?
* Unilateral - usually idiopathic + non-hereditary
* Bilateral: may be idiopathic, or have a cause --> hereditary, intrauterine infection, genetic syndromes like T21, metabolic conditions like galactosaemia
106
What are the benefits and risks of cataract surgery?
* Benefits: improved VA (90% get vision to meet driving requirements), improved clarity + colour
* Early comps: bruising (common + resolves), post-op raised IOP (rare with modern techniques), posterior capsule rupture, iris trauma, AC/vitreous haemorrhage, infective endophthalmitis (severe painful infection can cause sight loss)
* Late comps: posterior capsule opacification (healing response taking m-y, laser can correct), risk of inadequate correction, cystoid macular oedema (mild, inflammatory fluid in retina), retinal detachment (a/w high myopia), uveitis, glaucoma (<1%)
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What will happen during cataract surgery? In pt friendly way
* Surgery is to replace the cloudy lens (a see through bit at front of eye) with an artificial one
* Before: assessment, if both eyes being done have 6-12w apart
* During: takes 30-45m, usually day case, LA drops, make tiny cut in eye to replace the lens, then monofocal lens put in
* After: go home with a pad/shield for the day to protect, feeling returns n a few hours, vision may take a few days to be completely returned, normal to have grittiness/waterying/blurred vision/double vision/red eye for a few days (up to 6w) but seek help if severe or painful
* Use eye shield at night for a week, use eye drops as instructed, use eye shield when showering, do normal things like watching TV but dont go swimming for 4-6w/allow anything into eye/drive until dr says ok, avoid strenuous things like housework for at least 4w, dont wear eye make up for 4w, dont fly without advice
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What are the CF of cataracts in children and how is this managed?
* CF: poor vision, white/grey pupil (leucokoria), nystagmus, strabismus, sensitivity to light, reduced red reflex, lens opacity
* Refer urgently to minimise amblyopia; same day if have leucocoria/absent red reflex to rule out retinoblastoma
* Surgery: do before 6w for congenital, may need father treatment like patching as need to avoid deprivation amblyopia
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What advice would you give a pt with cataracts or post-cataract surgery regarding driving?
* Contact DVLA if uncertain
* Dont drive + contact DVLA if cannot read a number plate at 20m, or if Snellen VA is less than 6/12 [larger vehicles different requirements]
* Document this advice
110
Define glaucoma.
A group of eye diseases causing progressive optic neuropathy, where IOP may or may not be raised (but is a modifiable RF)
Leads to visual field defects + changes to the optic nerve head
111
What is the normal range for IOP?
10-21 mmHg
112
What is open angle glaucoma and what are the different types?
The angle between the iris + the cornea is normal, but something reduces outflow causing raised IOP
* Most common=primary open angle glaucoma aka chronic simple glaucoma
* Other types include normal pressure glaucoma (normal IOP but nerve fibres still damaged) and secondary causes (e.g. pigmentary, neovascular in diabetic retinopathy, uveitis inflammatory deposits, steroid-induced)
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What are the features of primary open angle glaucoma?
* Usually b/l + raised IOP
* Asymptomatic then insidious painless loss of peripheral vision e.g. nasal scotomas, reduced VA
* Optic disc cupping
* Optic disc atrophy
* Bayonetting of the vessels (breaks as they disappear into deep cup + re-appear at base)
* Disc haemorrhages
* Cup notching
* Or on tonometry screening identify raised IOP
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What is angle closure glaucoma?
The iris between the iris + cornea is at least partially closed. May be acute or intermittent or chronic
* Primary angle closure glaucoma commonest, peripheral iris comes into contact with trabecular meshwork
* Can also have secondary causes e.g. a subluxated lens
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What happens in acute angle closure glaucoma?
Sudden rise in IOP with reduced AH drainage as iris pushed forwards against TM due to a blockage in the trabecular meshrwokr
Risk of irreversible partial or complete LoV due to raised IOP compressing supply to optic nerve head
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Who is most at risk of acute angle closure glaucoma?
Hypermetropes (shorter eye), women (shallow anterior chamber), Asian ethnicity, age (size of lens increases which crowds the anterior chamber), FH in some, pupillary dilation
117
CF of acute angle closure glaucoma
* Sudden onset red painful eye
* Blurred vision, halos around lights
* Headache, eye pain, tender eye
* Conjunctival injection esp peri-limbal
* Eye feels hard
* Hazy/dull cornea
* Semi-dilated pupil, non-reacting pupil
* Worse with mydriasis e.g. watching TV in a dark room, and worse in semi=prone position
* May have systemic like N+V, abdo pain
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What is the management of acute angle closure glaucoma?
* Immediate ophthalmologist referral
* Lie flat with face up
* Oral or IV acetazolamide (reduce AH production)
* Topical pilocarpine to constrict pupil (prevent iris adhesion)
* Analgesia + anti-emetics
* Specialists may give oral glycerol or IV mannitol
* Definitive treatment - laser/surgical iridotomy (at peripheral iris in both eyes as prophylaxis) --> hole in iris allows AH to flow without passing through pupil which reduces pressure difference + allows angle to open
119
RF for primary open angle glaucoma?
Age, myopia, family history 1st degree relative, black ethnicity, corticosteroids, T2DM
120
What is ocular hypertension?
Consistently elevated IOP >21 mmHg, but without signs of glaucoma (i.e. no optic neuropathy)
Give agents to lower the IOP
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What is the NICE guidelines for management of primary open angle glaucoma?
1. Prostaglandin analogue e.g. latanoprost
2. Beta blocker, carbonic anhydrase inhibitor (topical or oral), alpha agonists (often combined as adjuncts or with a PGA)
3. Selective laser trabeculoplasty - usually lasts 1-5y, for refractory cases
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Prostaglandin analogues mech + s/e (POAG)
E.g. latanoprost
* Increase AH outflow via the uveoscleral route
* S/e: brown pigmentation of iris, increased eyelash length (so higher risk of trichiasis)
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Beta blockers mech + s/e (POAG)
E.g. timolol (usually Top can have oral)
* Reduce AH production
* CI in asthma/bronchospasm + heart block
* S/e of top: eye discomfort or inflammation
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Carbonic anhydrase inhibitors mech + s/e (POAG)
E.g. brinzolamide (top), dorzolamide (Top), acetazolamide (oral-most potent)
* Oral acts on the kidney causing diuresis, topical reduces AH production
* CI in sulphonamide allergy as may cause a sulfonamide-like reaction (like a rash), also CI in adrenocortical insufficiency + hyperchloraemic acidosis
* S/e include eye discomfort + nausea
125
Alpha agonists mech + s/e (POAG)
E.g. brimonidine
* Reduce AH production + increase outflow
* S/e: dry eye, eye discomfort, hyperaemia, FB sensation, altered taste
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Pilocarpine mech + side effects
Muscarinic receptor agonist - cause pupil constriction which increases AH outflow
* S/e: meiosis, headache, blurred vision
* CI in uveitis
127
What screening is offered for glaucoma?
* >60y every 2y
* >70y every 1y
* >40y if FH of glaucoma in a 1st degree relative or if black ethnicities
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How is the cup to disc ratio affected in glaucoma?
Normally ratio is about 0.2, in glaucoma is typically 0.7 or more -- neuroretinal rim is thinner so cup looks larger, as there is a loss of the support structures
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What are the causes of uveitis?
* Infection: bacterial, viral, fungal, parasitic
* Non-infectious with systemic associations like RA, SLE, AS, sarcoid, HIV, TB, GPA, IBD, Reiter's syndrome, Lyme disease, MS, etc etc
* Masquerade: neoplastic or non-neoplastic
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What are the general features of uveitis?
Blurred vision, pain, redness, photophobia, floaters, small fixed oval pupil, ciliary flush (ring of red spreading out from the cornea)
131
What are the possible complications of uveitis?
Cataract, cystoid macular oedema (inflammatory fluid in retina), glaucomatous optic neuropathy, band keratophy, vitreous debris, retinal detachment, macular scar, macular hole, sub retinal fibrosis
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Anterior uveitis
* commonest - iritis/iridocystitis (I+CB)
* acute onset photophobia, red, pain
* may have reduced VA, pus + inflammatory cells in AC, posterior synechiae (pupil adhere to lens), IOP may be raised
* may have irregular small pupil
* may be asymptomatic
* HLA-B27 associated eg. ankylosing spondylitis, IBD, reactive arthritis, Behcet's
* M: topical steroids + pupil dilation with cytoplegics like atropine/cyclopentolate (reduce pain + prevent posterior synechiae + allow fundoscopy), treat IOP if raised
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Intermediate uveitis
* affects vitreous
| * photopsia (floaters, light flashes etc), reduced VA [red+photophobia unusual)
134
Posterior uveitis
* affects choroid/optic nerve head/retina (includes chorioretinitis etc)
* reduced VA, photopsia, scotomas
* painless!
* often a/w systemic disease like RA, Behcets, AS, reactive arthritis, psoriasis, IBD, sarcoidosis
* occ a/w infections like HZV, toxoplasmosis, TB, Lyme disease
* M: oral or intravitreal steroids, may need 2nd line immunosuppression
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Panuveitis
Whole uveal tract inflamed
136
Central retinal vein occlusion causes + management
* RF: HTN, age, CV disease, DM, glaucoma, blood dyscrasias, vasculitis
* Can be atherosclerotic, polycythaemia, glaucoma, inflammation, oral contraceptives, eye causes (glaucoma, trauma, optic disc drusen)
* Thrombus obstructs outflow - raised pressure, dilated veins, retinal haemorrhage, CWS, abnormal fluid leakage, oedema
* M: refer to monitor, if macular oedema may need intravitreal steroids/anti-VEGF
137
How does central retinal vein occlusion present?
Profound sudden painless LoV, +/- RAPD
* non-ischaemic type: milder, metamorphopsia (straight lines look curvy), dilated tortuous veins with retinal haemorrhages, mild disc oedema
* ischaemic: severely reduced VA, RAPD, more extensive haemorrhages + cotton wool spots
Comps: retinal ishaemia leading to neovascularisation of iris + retina, risk of a type of glaucoma
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Central retinal artery occlusion causes + presentation
Emergency - can lead to infarction of inner 2/3 of retina (outer 1/3 supply by choroid)
*Usually due to atherosclerotic thrombosis but may also be embolic like from carotids or inflammation like GCA
CF: sudden severe painless LoV, pale oedematous retina, cherry red spot at fovea (the choroid vasculature), RAPD, visible emboli
Comps: neovascularisation, rubeotic glaucoma, optic atrophy
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Central retinal artery occlusion management
Emergency!
* Reduce pressure with IV acetazolamide + ocular massage
* Breathing into paper bag builds up CO2 to vasodilator to dislodge embolus (really?)
* corneal paracentesis drain off some AH
* oral aspirin
* protect other eye - e.g. systemic steroids for GCA
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What is the fundoscopic difference between CRVO and CRAO?
* CRVO: severe retinal haemorrhages, cotton wool spots
| * CRAO: cherry red spot on a pale retina, may see emboli, oedematous retina
141
What is the pathology of retinal detachment?
Tear in the retina - fluid collects in potential space between pigment + neural layer
142
How does retinal detachment present?
* 'Curtain' field defect that stays in one place [wherreas AF it goes away]; dense shadow starting peripherally and moving centrally
* May have flashes/floaters, metamorphopsia, reduced VA, central visual loss
* M: surgical
143
How does posterior vitreal detachment present?
* Photopsia (flashes) in peripheral field
| * Floaters, often on temporal side of the central vision
144
How does vitreous haemorrhage present?
Acute or subacute onset
* Sudden visual loss - large bleed
* Numerous dark spots - moderate bleeds
* Floaters - small bleeds
* May have haze, red hue in vision, visual field defect if severe
Ix: dilated fundoscopy, slit lamp (RBCs in anterior vitreous), US to rule out retinal tear/detachment, fluorescein angiography, orbital CT if open globe injury
145
What are retinal breaks?
Tears (U-shaped defect, due to PVD) or holes (U-shaped defect), can predispose to retinal detachment. Often a/w surgery, myopia or systemic things like EDS/Marfan's
146
What is posterior vitreous detachment + how do you manage it?
A break in the vitreous causing fluid to separate the vitreous + retina
Occurs when vitreous becomes more liquefied (age, trauma, myopia, inflammation, CT disorders) - less shock absorption - breaks more likely
CF similar to retinal detachment, floaters usually seen as rings/cobwebs, occasionally haemorrhages, 10% a/w retinal tear
M: reassure, adv urgent help if sx of RD (new sx, curtain field defect, drop in vision)
147
What is vitreous haemorrhage?
Bleeding into the vitreous humour - range of disruption to vision varies
Occur due to disrupted vessels i the retina or extension through the retina from other areas
148
What causes vitreous haemorrhage?
* Proliferative diabetic retinopathy commonest cause
* Posterior vitreous detachment
* Ocular trauma (commonest in younger people)
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What is retinitis pigmentosa and what diseases is it a/w?
Inherited disease causing progressive dysfunction + atrophy of the retina, eventually leads to blindness
A/w Refsum disease (cerebellar, peripheral neuropathy, deafness), Usher syndrome, Alport syndrome ..
150
What are the CF of retinitis pigments and how is it managed?
CF: reduced peripheral vision leading to tunnel vision, progressive loss of night vision, spicule deposits + attenuated vessels + mottling of the pigment epithelium
M: high dose vitamin A may slow progression
151
Cystoid macular oedema
A common response to ocular insults like surgery, retinal vascular disease, nicotinic acid/topical adrenaline
CF: asymptomatic or reduced VA/metamorphosia/scotomas, loss of foveal contour, retinal thickening, central yellow spot, small haemorhrages
M: things like topical steroids
152
What might excessive near vision work lead to?
Degenerative myopia - axial length doesnt stabilise so get degenerative changes and PVD at a young age, may lead to macular hole
153
What drugs can cause toxic retinopathies?
So many
E.g. hydroxychloroquine, phenothiazines, quinine, ritonavir, ahminoglycosides, prostaglandin analogues (but you give for POAG?), glitazones, tamoxifen, nitrofurantoin, topiramate
154
What is age-related macular degeneration?
Changes in the central areas of the retina (macula) of photoreceptors causing drusen in people aged 55+. Usually b/l
Commonest cause of vision impairment in people >50 in developed world
155
What are the RF for ARMD?
* Advancing age - biggest RF
* Smoking - also v sig, 2x risk of vision loss with it + higher risk of getting it too
* FH: 4x in 1st degree relatives
* Other: CV disease like HTN/DM/dyslipidaemia
156
What is the prognosis for ARMD?
* Visual impairment + blindness - a/w visual hallucinations (Charles Bonnet syndrome, lasts up to 18m), depression, falls, limited ADL
* Early AMD has low progression to advanced
* Advanced: geographic atrophy severe gradual loss, if neovascular type severe loss within weeks-months if untreated
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What pathological changes are seen in ARMD?
* Drusen: lipid-protein stuff beneath the RPE within Bruch's membrane, pale yellow spots. due to age
* Hypo/hyperpigmentation of the RPE
* Geographic atrophy of the RPE
* Neovascular AMD (exudative) - new BVs made beneath
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What is the classification of ARMD?
* No AMD: no/few small drusen (doesnt always progress)
* Early AMD: multiple small drusen, mild abnormalities of RPE (used to be non-exudative/dry). 90% are this type
* Intermediate AMD
* Advanced AMD: used to be exudative/wet type. 10%, worst prognosis. Abnormal sub-choroidal neovascularisation around macula causing severe central VL, leakage of fluid + blood
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What are the CF of ARMD?
* Sx: reduced VA esp near, difficulties in dark adaptation, fluctuations in vision day to day, photopsia (flashing lights), glare around objects. Central field loss most obvious
* Signs: distorted perception on Amsler grid testing, drusen (yellow pigment in macula, confluent in late forming a macular scar), in neovascular well-demarcated red patches of intra/sub-retinal fluid leak or haemorrhage
160
What Ix are done in suspected ARMD?
* Slit lamp microsocpy-to see pigementary, exudative or haemorrhage changes
* Colour fundus photography-baseline to see changes over time
* Fluorescein angiography -if neovascular suspected to guide anti-VEGF therapy
* Optical coherence tomography - visualise retina in 3D
161
What is the management of ARMD?
* Adv if worsening sx/in other eyes see someone urgently, driving advice (need to check if eyesight is acceptable legally by optometrist), inform about possibility for visual hallucinations (Charles Bonnet)
* Consider registering as sight impaired for support/benefits
* Stop smoking
* Zinc with vitamins A, C + E some evidence reduce disease progression so might as well (but not if smoker cos of higher risk lung cancer)
* Geographic atrophy/early sort - no specific treatments
* Anti-VEGF - reduces progression of neovascular AMD by blocking the angiogenic growth factor --> about 1/3 improve, 1/10 don't respond and the rest maintain (so quite good)
* Laser photocoagulation - they used to do this but not used really now due to risk of acute visual loss after treatment
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What are the typical features in ARMD?
* Subacute painless blurring of central vision 55+
* Geographic atrophy usually gradual deterioration e.g. difficulty reading
* Neovascular can happen quickly e.g. suddenly unable to read/drive/see facial features
* Sometimes only obvious when second eye becomes affected
* Metamorphopsia – distorted vision where straight lines appear wavy
* Scotoma – black/grey patch centrally
163
How does retinoblastoma arise?
Loss of function of the Rb tumour suppressor gene
* Somatic type (most) - a single developing retinal cell loses one copy of Rb gene, then a random event causes a 2nd hit so get a tumour. Always unilateral + unifocal
* Genetic type (10%) - autosomal dominant, can be u/l multifocal or b/l, every cell is missing a copy of Rb gene
164
What are the CF of retinoblastoma?
* Average age 18m, rarely >6y
* Absent red reflex + leukocoria
* Strabismus
* Visual problems like reduced VA
* May be inflamed like acute red eye, excess watering
* Possible for it to invade optic nerve, CNS, anterior segment causing glaucoma
165
How is retinoblastoma managed?
* >95% cure rate
* Do not do diagnostic biopsy as can disseminated it!
* Enucleation - advanced uniocular (used to be main option but usually avoid now), put in an implant
* Intravitreal chemotherapy
* External beam radiotherapy
* Surveillance with regular EUA to detect new tumours and can use like laser etc to remove small ones
* Metastasise if untreated
* protective eye wear
* Genetic counselling
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What is the commonest cause of blindness in the UK?
>65y ARMD
| <65y diabetic retinopathy
167
What are the ocular complications of diabetes?
* Cataracts at an earlier age due to denatured proteins
* Refractive variability from fluctuating blood glucose-osmotic changes in lens
* Diabetic retinopathy + maculopathy (maculopathy causes severe sight loss)
* Ocular nerve palsies: usually painless CN III palsy (usually pupil spared) or CN VI palsy, usually recover in 3-6m
* Reduced corneal healing, orbital infection
* Anterior uveitis, AION
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What is the cause of diabetic retinopathy?
Increases with length had diabetes + control of BG, so like T1DM usually get it after 20y
Hyperglycaemia --> increased retinal blood flow + abnormal metabolism in vessel walls --> endothelial cell damage -- > more permeability so get exudates, micro aneurysms, neovascularisation as growth factors produced in response to retinal ischaemia
169
How does diabetic retinopathy present?
* Asymptomatic on screening
| * Reduced VA, distortion, floaters
170
What screening is in place for diabetic retinopathy?
Annual acuity + retinal photography for people with diabetes aged over 12
171
How is diabetic retinopathy managed?
* Tight HbA1c + BP control e.g. 6.5-7.5% HbA1c, BP<130, consider statins
* Proliferative retinopathy: laser photocoagulation directed at the new vessels, laser burns to peripheral retina, VR surgery if needed like for fibrosis or vitreous haemorrhage
* Maculopathy: laser photocoagulation to remove rings of exudates around fovea sometimes used but now mostly the new things
* New things: anti-VEGF drugs like bevacizumab for retinopathy + maculopathy
172
What can accelerate retinopathy?
Rapid improvement in glycemic control, pregnancy, nephropathy
173
What happens in diabetic retinopathy?
Changes in the peripheral part of the retina
* Small BV damage causes microaneurysms
* Superficial/blot haemorrhages when BV walls breached
* BV leak fluid into retina - goes into veins - lipid + protein left behind - hard exudates
* Cotton wool spots - debris
* Venous beading - damage to walls
* Neovascularisation due to VEGF release in response to ischaemia
* Predisposes to vitreous haemorrhage + rubeotic glaucoma
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What happens in diabetic maculopathy?
Damage in the central retina. Fluid doesnt clear as well hear so may get oedema which can distort central vision. Can't see on retinal photography or fundoscopy, can see oedema with OCT
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What are the stages of diabetic retinopathy?
* Background R1 (low risk): capillary micro aneurysms, blot haemorrhages, hard exudations, occasional cotton wool spots/cytoid bodies(macrophages)
* Pre-proliferative R2 (high risk): venous bearing, deep haemorrhages, multiple CWS
* Proliferative R3: neovascularisation, preretinal/subhyaloid/vitreous haemorrhage
* Advanced retinopathy: retinal fibrosis, traction retinal detachment
* M1-maculopathy. Hard exudates (bright white-yellow colour, irregular), micro aneurysms, retinal haemorrhages, leaks, oedema, retinal thickening. All happen near the macula. More in T2DM
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How does hypertension affect the eye?
Narrowing of arterioles in the retina + choroid
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What is malignant HTN?
Severe acute damage leading to fibrinoid necrosis:
* Headache
* Eye: scotoma, diplopia, eye pain, photopsia, reduced VA, choroidal infarcts, optic neuropathy, macular star
* Other end organ damage
Need antihypertensives + emergency admission - don't reduce BP too quickly as could cause cerebral/retinal/renal ischaemia
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What are the fundoscopic changes + severity of hypertensive retinopathy?
Grade 1: tortuous arteries, increased reflectiveness (silver wiring)
Grade 2: AV nipping (thickened retinal arteries pass over veins w compression of venules), focal narrowing
Grade 3: flame-shaped haemorrhages + CWS + hard exudates
Grade 4: the above plus papilloedema, aka malignant HTN
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What is the NICE guidelines for HTN management?
* Lifestyle for stage I initially (up to 160)
* Pharm: if >140/90 offer if have target organ damage (e.g. retinopathy), or if other RF like DM:
1. <55 ACEi/ARB or >55 or black use CCB
2. Add the CCB or ACEi/ARB
3. Add a thiazide like diuretic
4. Add more diuretic or alpha blocker or beta blocker
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What are the manifestations of thyroid eye disease?
Usually a/w Graves' disease
* Acute progressive optic neuropathy: emergency, need immunosuppressive +/- decompression
* Exposure keratopathy: because of proptosis + lid retraction. M is lubricants, taping, immunosuppression
* Eye sx like irritation, ache, red eyes, pain on movement, cosmetic, diplopia
* Signs like exophthalmos, lid retraction, lid lag on downgaze, conjunctiva injection, keratopathy, orbital fat prolapse, restrictive myopathy, optic neuropathy
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How is thyroid eye disease managed?
Endocrine + orthoptist involvement. Control TFTs, explain the sx, ocular lubcricants, nocturnal eyelid taping, immunosuppression in active disease, surgery as acute decompression or lid surgery
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What atopic eye diseases are there?
* IgG4-orbitopathy: proptosis, lid swelling, restiricted movements. Good steroid response
* Allergic conjunctivitis
* Vernal keratoconjunctivtiis (children)
* Atopic keratoconjunctivitis (adults)
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Urogenital eye disease
* Chlamydia + gonorrhoeal conjunctivitis
* Phthirus pubis
* HIV: CMV retinitis sight-threatening, anterior uveitis, higher infection risk
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Sjögren syndrome
Dry eye syndrome, also may affect the mouth/skin/vagina/salivary glands and cause fatigue. Can be primary or secondary to other autoimmune things
M: symptomatic with artificial tears/saliva, hydroxychloroquine for fatigue + arthralgia
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Eye problems a/w rheumatoid arthritis
Sjogren syndrome, scleritis, episcleritis
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Eye problems a/w granulomatitis with polyangitis
Occur in 50% and involve eye pain, proptosis, restrictive myopathy, disc swelling, reduced VA, epi/scleritis, uveitis, vasculitis
Most are c-ANCA positive
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Eye problems a/w ankylosing spondylitis
Acute anterior uveitis - 30%
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What is giant cell arteritis and how does it present?
Inflammatory granulomatous arteritis of medium+large cerebral vessels, in pt >50y and a/w polymyalgia rheumatica
CF: severe headache, tender scalp/temple, jaw claudication, tender swollen temporal/occipital arteries (non pulsatile), sudden painless LoV in one eye [ophthalmic artery], systemic features like tiredness/fever/night sweats
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How is GCA diagnosed + treated?
Need 3 out of: aged >50, new headache, temporal artery abnormality, ESR > 50 or positive temporal artery biopsy
Do the biopsy just before treating (to avoid delay) or if not within 7d as need to prove is GCA to justify long steroids
M: high dose steroids to reduce irreversible vision loss (if 1 eye lost vision you are trying to save the other one), usually 24-48h to improv then reduced gradually to a daily dose for ~2y (w calcium + vit D supplements and bisphosphonates in some)
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What blood diseases can affect the eyes?
* Haemoglobinopathies (thal and sickle cell): retinopathy, periorbital swelling from infarctions or haematomas, comma shaped conjunctival capillaries
* Anaemia: retinopathy, optic neuropathy if low B12
* Leukaemia: acute retinopathy (Roth's spots, CWS, venous tortuosity), direct infiltration, spontaneous haemorrhage
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What renal problems can affect the eyes?
* Alport syndrome: defect in type 4 collagen can cause fleck retinopathy + macular thinning
* Membranoproliferative glomerulonephritis: drusen like deposits but VA unaffected
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Ocular albinism
Reduced VA (foveal hypoplasia), photophobia, nystagmus, strabismus, iris hypo pigmentation
M: correct ametropia with tinted lesions + prevent amblyopia, consider surgery for strabismus
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What causes optic neuritis?
* MS (other ocular CF include INO, isolated VF defects, uveitis + nystagmus)
* Diabetes
* Syphilis, SLE, sarcoid etc
* Clinically-isolated syndrome
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Atypical vs typical optic neuritis
* Typical: acute demyelinating, a/w MS, usually females aged 20-50, usually b/l
* Atypical: need investigations for compressive lesion/serious pathologies
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How may optic neuritis present?
* U/L reduction in VA over hours-days
* Red desaturation: poor discrimination of colours
* Pain worse on movement of eye, retrobulbar pain
* RAPD
* Central scotoma
* Swollen disc in 1/3 (but it shouldn't be pale)
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How is optic neuritis managed?
* High dose steroids
* Should start to improve in 2w and recovered in 4-6w, may have remaining issues like contrast sensitivity or colour perception
* Atypical-refer on day
* All others-refer for MS workup (MRI with >3 WM lesions means 50% chance of MS within 5y)
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Causes of optic atrophy (pale disc)
* Inherited
* Compression from tumour e.g. craniopharyngioma extrinsic or optic nerve glioma intrinsic
* Vascular
* Inflammation e.g. acute optic neuritis
* Infection e.g. Lyme disease
* Nutritional e.g. thiamine deficiency
* Toxic e.g. amiodarone, ethambutol, methanol, isoniazid, lead, carbon monoxide
* Other: trauma, disc oedema, retinal disease
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What is papilloedema?
Disc swelling due to RICP - transmitted fro SAS via optic nerve sheath - disc oedema
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What causes papilloedema?
* Masses - tumour, bleed
* Increased CSF production e.g. choroid plexus tumour
* Reduced CSF drainage e.g. meningitis damage, IIH
* Other: malignant hypertension, hypercapnia
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What are the CF of papilloedema?
* Visual obscurations, diplopia, VF defects
* Headache worse lying down/straining, N+V, pulsatile tinnitus
* Disc swelling-usually b/l but may not swell if the disc sheath is already abnormal e.g. optic atrophy
* Venous engorgement, blurring of optic disc margin, loss of venous pulsation, loss of optic cup, elevation of optic disc, Paton's lines (concentric retinal lines from disc)
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What are the types of disc swelling?
* Papilloedema: true swelling, due to RICP
* Local swelling: true, due to things like optic neuritis, granulomas, leukaemia, CRVO, trauma
* Pseudopapilloedema - no true disc swelling just appears this way like cos of disc drusen or hypermetropic/myopic discs
202
How do migraine visual auras typically present?
Central then does temporally, form a positive scotoma (flickering/shimmering lights), trailing edge negative, may get foggy vision, heatwaves, tunnel vision, complete LoV
203
What is internuclear ophthalmoplegia?
Lesions of the MLF (connect III and contralateral VI nerve nuclei) --> no ipsilateral adduction --> overshoot of contralateral eye. May have upbeat torsional nystagmus, los of vertical smooth pursuit, abnormal VOR, skew deviation
204
Give some drug causes of optic neuritis
amiodarone, ethambutol, methanol, isoniazid, lead, carbon monoxide
205
What are the causes of a third nerve palsy?
* Aneurysms - usually PCA
* Microvascular ischaemia
* Trauma
* Demyelination
* Vasculitis
* Congenital
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How do third nerve palsies present?
* Pain - only in compressive lesions or ischaemia, or SAH
* Complete: diplopia (due to ophthalmoplegia), complete ptosis, eye abducted + depressed
* Partial: any of the above e.g. just ptosis
* Aberrant regeneration a/w longstanding lesions, e.g. pupil constriction on adduction/depression
* May involve pupil (midriasis) or spare it
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Sixth nerve disorders
Causes: idiopathic, micovascular ischaemia, tumours, RICP, basal skull #, demyelination, meningitis, cavernous sinus thrombosis
CF: neurogenic strabismus, abduction deficit, horizontal diplopia, esotropia
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Seventh nerve disorders
Causes: many. Idiopathic (Bell's palsy, majority but diagnosis of exclusion. a/w Dm + pregame's, peak in 40s, most start to recover in 3w, steroids), Ramsay-Hunt syndrome (VZV infection), trauma, parotid gland mass, sarcoidosis etc etc
CF: u/l weakness not sparing forehead, lagophthalmos, lower lid ectropion, corneal surface exposure
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Horner's syndrome CF
Unilateral partial ptosis, miosis, enophthalmos (sunken eye), anhidrosis (unless post-ganglionic lesion)
Normal light + near reaction
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Horner's syndrome causes
Disruption to the sympathetic trunk
* Central: stroke, syringomyelia, MS, tumour, encephalitis
* Pre-ganglionic: Pancoat's tumour, thyroidectomy, trauma, cervical rib
* Post-ganglionic: carotid artery dissection, carotid aneurysm, cavernous sinus thrombosis, cluster headache
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Aniosocoria
Means unequal pupils
Causes: physiological, iris pathology from surgery/trauma, pharmacological (fixed pupils, no reactions), Horner's syndrome, parasympathetic chain pathology e.g. Adie's pupil
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Holmes-Adie pupil
U/l in 80%
* Due to damage to PNS innervation from viral/bacterial infection
* Dilated pupil
* Once pupil constricts it remains small for an abnormally long time
* Slowly reactive to accommodation, doesn't really react to light
* A/w absent knee/ankle reflexes, F>M
213
Argyll Robertson pupils
B/L irregular miosed pupils that accommodate but don't react to light
A/w neurosyphilis so now rare, also a/w severe diabetic retinopathy
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Define nystagmus
Abnormal slow movement away from fixation corrected by a fast movement/another slow movement
Causes: idiopathic, sensory deprivation from retinal/optic nerve disease, fusion maldevelopment
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Ocular signs of myasthenia gravis
Autoantibodies against post-synaptic ACh receptors
Variable diplopia/ptosis (usually worsens in evening/with exercise), ocular motility disturbance, spontaneous twitching
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Amaurosis fugax
Ischaemic cause of sudden LoV - typically painless transient monocular blindness with description of a 'black curtain coming down'
* Causes: large artery disease (thrombosis, embolus, dissection), small artery disease (AION, temporal arteritis), venous disease, hypo perfusion
* May be a form of TIA - 300mg aspirin
* Often see altitudinal field defects ' curtain coming down'
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Fourth nerve disorders
Causes: congenital, trauma, microvascular infarction, iatrogenic like ENT surgery, tumours, demyelination, vasculitis, cavernous sinus lesions
CF: diplopia (worse on downgaze), head tilt to compensate to other side, ipsilateral hypermetropia etc
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What is Hutchinson's pupil?
U/L dilated pupil, unresponsive to light
Due to compression of CN III on same side by an intracranial mass
219
What is Marcus-Gunn pupil?
RAPD - pupils constrict less so appear to dilate when light swung from unaffected to affected eye, most commonly due to damage to optic nerve or severe retinal disease
220
What is a refractive error and what are the causes?
Any abnormality in the focussing mechanism of the eye (not opacities) causing a blurred image
Either physiological (usually altered length of eye with normal corneal power) or pathological like trauma/corneal transplant
221
What is myopia?
Short-sighted - distant objects blurred. Can start form 6y
Usually because the eye is too long so light comes in a bit in front of retina with normal cornea (tho can be high power cornea with average length)
Minus prescription to push focus backward
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What is hypermetropia?
Long sighted: can see distant objects but closer out of focus, usually people >40 but can affect kids. Low degrees may be asymptomatic as can compensate with accommodation
Usually eye is too short with average cornea, tho can be average length eye with low power cornea
Plus prescription - moves focus forwards
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What is astigmatism?
Refractive error with different degree of refraction in different bit of curvature
Because cornea is more like a rugby ball than a football - has 2 axes of curvature - affects power as there are 2 foci
Leads to blurred vision
224
What is presbyopia?
Old age causes reducing amplitude of accommodation due to changes in ciliary muscle - problems with near vision have to hold things further away to read them
Can have reading glasses for near vision, or bifocals/varifocals where they correct near + distance vision
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Outline the paediatric visual milestones
6w: fix + follow light source, responsive smile
3m: fix + follow a slow target, converge
6m: reaches out for toys accurately
2y: picture matching
3y: letter matching of single letters
5y: Snellen
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Why do newborns have poor vision and how does it improve?
Fovea is immature + optic nerve unmyelinated - need well-focussed images on retina to allow VA development
This is why cataracts affect long term viision if not fixed
227
How may visual impairment in a child present?
* Obvious malformation
* Absent red reflex or leukocoria
* Not smiling by 6w
* Concerns e.g. poor eye contact
* Roving eye movements
* Nystagmus
* Squint
* Screening at pre school age
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What is amblyopia and how may it present?
Developmental defect of central visual processing causing reduced vision due to unbalanced foveal images
permanent if not reversed by 7-8y
main focus for preschool screening as often asymptomatic until too late
cf: reduced VA despite correction of refractive errors, exaggerated crowding phenomenon, tolerate a neutral density filter
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What causes amblyopia?
Any form of competitive disadvantage between the two eyes, so usually u/l problems:
* No/reduced image like congenital cataracts --> deprivation amblyopia
* Refractive errors causing blurred vision anisometropic (asymmetrical, e.g. cos of a chalazion) or ametropic (big symmetrically error)
* Abnormal binocular interaction e.g. strabismus
230
How is amblyopia managed?
* Spectacles for refractive correction
* Occlusion (patching) [cover the 'good' eye]
* Penalisation with atropine - useful when there's a hypermetropic error
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Outline the aspects of care for a child with vision loss
* MDT: optometrists, paeds, orthoptists, GP, teachers, specialist nurses
* Disabilities: vision loss +/- other disability/developmental problems
* Treatment: ensure best potential but be realistic
* Equipment e.g. Braille, large print, where wold be best for school
* Social: practical + financial help, effects on family dynamics, genetic counselling
* Prognosis: stationary or progressive
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What are the causes of severe vision impairment in children?
* Genetic: cataract, albinism, retinoblastoma
* Antenatal + perinatal: TORCH, retinopathy of prematurity, HIE, cerebral abnormality, optic nerve hypoplasia
* Postnatal: trauma, infection, JIA
233
What is strabismus?
Misalignment of the visual axis ie both eyes not directed on an object at the same time
due to incoordination preventing focus of gaze
234
Pseudostrabismus?
appearance of a squint in an ormolu child e.g. prominent epicanthic folds, asymmetry of face/globes, abnormal inter-palpebral distance
235
How are squints classified?
By where eye deviates:
* nose-esotropia
* temporal-exotropia
* superior-hypertropia
* Inferior-hypotropia
Or
* concomitant (non-paralytic): commonest, usually refractive error, glasses often correct the squint, usually turns inwards (convergent) but can be divergent or vertical
* paralytic (rare): paralysis of motor nerves so varies with gaze direction
236
What causes strabismus?
* usually idiopathic
* refractive errors esp hypermetropia
* sensory squint e.g. retinoblastoma or cataract
* amblyopia (they cause each other)
* neurodevelopmental conditions + syndromes
* congenital abnormalities of extra ocular muscles
237
What are the possible complications of strabismus?
* amblyopia
* loss of or failure to develop binocular vision so poor depth perception
* compensatory head postures
* poor eye contact
* social/psychological things
238
How are squints diagnosed?
* parents notice turning eye
* always check red reflex-RB rare cause
* inspection, corneal light reflex (hold light 30cm from face see if light reflects symmetrically off the pupils), cover tests (focus on object, cover one eye, observe movement of uncovered eye, if fixing eye covered the squinting eye moves to take up fixation, do at near + distance), range of eye movements
239
How is strabismus treated?
* in up to 3m neonates intermittent eye deviation normal as they're not coordinated
* orthoptist + ophthalmologist
* corrective glasses-usually hypermetropic kids see ok but accomodate to compensate which causes the squint
* occlusion patching or penalisation with atropine (blur normal eye, when occlusion not complied with)
* surgery to alter point of insertion of an EOM into sclera which reduces size of squint
240
What refractive errors occur in children?
usually hypermetropia - accommodation compensates for mild degrees otherwise plus lenses
myopia doesnt really occur until adolescence, minus lenses
astigmatism: minor common, if u/l can cause amblyopia, abnormal corneal curvature
amblyopia: reduction in VA that hasn't received a clear image, usually u/l. causes include squint, RE, cataracts. treat cause + patching for specific periods of day to force 'lazy' eye to work
241
Nasolacrimal duct obstruction
Commonest cause of persistent watery eye in the neonate, due to imperforate membrane
M: ask parents to massage lacrimal duct, majority resolved by 1y otherwise they consider probing under light GA
242
Atropine
Cytoplegic- Anticholinergic (acts on PNS) - blocks iris sphincter muscles + accommodative muscles in CB - lasts 1-2w
CI in HTN + closed angle glaucoma
243
Cyclopentolate
Cytoplegic, anticholinergic to stop iris sphincter + accommodation
works over about half an hour, recovery 6-24h
CI: closed angle glaucoma
244
Tropicamide
A mydriatic, blocks PNS, anticholinergic to stop sphincter muscles
works in about 20m, recovery 4-8h
CI: closed angle glaucoma
245
Phenylephrine
sympathetic agonist - stimulates dilator muscle in iris
lasts 3-6h
CI in children + closed angle glaucoma
246
Side effects of mydriatic drops?
* whitening of eyelids from vasoconstriction (during use)
* atropine can cause red warm face
* stinging during instillation
* blurred vision can't drive till worn off
247
Fluorescein drops
Used to see defects in corneal epithelium or when doing tonometry
temporarily stains any cell it enters so marks damaged areas
may stain skin fora bit
248
How do you instil eye drops in a patient?
- Prep: bottle of drops, tissue, wash hands, consent inc about not driving , dilation + stinging, check for allergies + Cis
- Application: look up, pull inferior eyelid down to form a well, apply one drop from a vertical position, allow patient to blink, wipe away any excess
- Documentation: record type of drops, which eye, how many drops, time of instillation. Time, date and sign
249
What is used for conjunctivitis in pregnant women?
Topical fusidic acid
250
How may you differentiate glaucoma from uveitis in painful red eye?
* Glaucoma - severe pain, halos, semi dilated pupil
| * Uveitis: small fixed oval pupil, ciliary flush, may have HLA-B27 associations
251
What are the two main types of squint?
Concomitant - main type, imbalance in extra ocular muscles. Convergent more common than divergent
Paralytic - paralysis of extra ocular muscles
