Ophthalmology Flashcards
(153 cards)
1
Q
What is glaucoma?
A
optic nerve damage caused by a rise in intra-ocular pressure by blockage in aqueous humour trying to escape eye
*peripheral vision loss then total
2
Q
What is the path of travel for aqueous humour?
A
- produced by ciliary body
- flows through posterior chamber and around iris into anterior
- drain through trabecular meshwork to canal of schlemm
- eventually entering general circulation
3
Q
What is the normal intra ocular pressure?
A
10-21 mmHg
*created by resistance to flow through trabecular meshwork
4
Q
What is the pathophysiology of acute angle-closure glaucoma?
A
iris bulges forward and seals off trabecular meshwork from anterior chamber, preventing aqueous drainage
5
Q
What is the pathophysiology of open angle glaucoma?
A
gradual increase in resistance to flow through the trabecular meshwork, pressure slowly builds up
6
Q
What are some risk factors of open angle glaucoma?
A
increasing age
family history
black ethnic origin
myopia
7
Q
What are some risk factors of close-angle glaucoma?
A
increasing age
family history
Chinese and was asian ethnic origin
shallow anterior chambers
female
8
Q
What medications might precipitate acute angle-closure?
A
- adrenergic eg: noradrenaline
- anticholinergic eg: oxybutynin and solifenacin
- tricyclic eg: amitriptyline
9
Q
How does closed angle closure present?
A
- severely painful red eye
- blurred vision
- halos around lights
- associated headaches, N+V
o/e - red eye, hazy cornea, decreased visual acuity, mid-dilated pupil not reactive to light, hard eye on gentle palpation
10
Q
How does open angle present?
A
fluctuating pain, headaches, blurred vision, halos around lights, particularly at night
*peripheral loss of vision, arcuate scotomoa, nasal step
11
Q
What are some secondary causes of glaucoma?
A
iatrogenic, lens relates issues like cataracts, medicine related like steroids, neovascular, pigment related
12
Q
How would you investigate suspected glaucoma?
A
- measure intra-ocular pressure with non-contact tonometry or Goldmann
- slit lamp for cup-disk ratio and angle
- visual field
- gonioscopy
13
Q
How do you manage open-angle glaucoma?
A
360 degree selective laser trabeculoplasty
prostaglandin analogue - latanoprost
beta blocker - timolol
carbonic anhydrase inhibitor - dorzolamide
sympathomimetics
trabeculectomy
14
Q
How do you manage closed angle glaucoma?
A
initial - pilocarpine, acetazolamide, other like timolol, latanoprost, analgesia
secondary - pilocarpine, acetazolamide, timolol, brimonidine
*Definitive - laser iridotomy
15
Q
What is uveitis?
A
inflammation of uveal tract, comprising iris, ciliary body and choroid
*commonly uveitis
16
Q
What is anterior uveitis?
A
iritis - which only affects the iris and iridocyclitis affects iris and ciliary body
17
Q
What are some causes of iritis?
A
HLA-B27 conditions - AS, reactive arthritis, IBD
autoimmune - sarcoidosis, vasculitis
infection - herpes, herpes zoster
traumatic
iatrogenic - surgery, bisphosphonates
cancer - leukaemia, malignant melanoma
18
Q
What is intermediate uveitis?
A
inflammation of ciliary body
*no pain, blurring vision, floaters
19
Q
What is posterior uveitis?
A
inflammation of back of eye - retina or choroid
20
Q
How does anterior uveitis present?
A
*over few hours or gradually over several
- bilateral presentation - systemic conditions
- unilateral - idiopathic or herpetic
- painful, red eye with blurring of vision
- photophobia
- tearing
- systemic - joint pain, back pain, flare up of IBD, infective sx
*chronic or intermediate and posterior - painless and decreased vision
21
Q
How is anterior uveitis investigated?
A
general - ciliary injection, irregular pupil, cloudy cornea, hypopyon
slit lamp - ciliary flush, inflammatory cells in anterior chamber, flare, adhesions between lens and pupil
lab - bloods for HLA-B27, ANA, infectious diseases screen
OCT - macular oedema, CXR, spinal XR for AS
22
Q
How is anterior uveitis managed?
A
*can be self limiting
- ophthalmologist referral 24h assessment
- aim to control inflammation, prevent visual loss, minimise long term complications
- topical steroid drops to reduce inflammation
- pupil dilating drops (cyclopentolate) to alleviate sx
- treat underlying
- systemic in severe - steroids and immunosuppressants
23
Q
What are the complications of anterior uveitis?
A
- severe - vision loss
- macular oedema
- secondary cataract
- rise in intra-ocular pressure by inflammation of trabecular meshwork
24
Q
What is conjunctivitis?
A
inflammation of the conjunctiva - thin layer of tissue that covers the inside of the eyelids and the sclera
*bacterial, viral or allergic
25
What is the pathophysiology of conjunctivitis?
- bacterial - staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae
- allergic - when in contact with allergens
- also can be from irritation like smoke, dust, wearing contact lenses longer or without cleaning etc
26
What is the presentation of conjunctivitis?
*no pain, photophobia or reduced visual acuity
- red, blood shot eye
- itchy, gritty sensation
- discharge + blurry vision purulent for bacterial, clear for viral, muco-purulend for chlamydial, swelling of conjunctival sac for allergic
27
How might you investigate conjunctivitis?
- contact lens wearers - topical fluoresceins to identify any corneal staining
- swabs for viral or chlamydial
28
How can you manage conjunctivitis?
*1-2w without tx
- hygiene measures, avoid spread
- clean with cooled boiled water
- chloramphenicol or fusidic acid drops
- antihistamines for allergic
- nO CONTACTS worn
29
When would conjunctivitis be a red flag?
👁️ neonatal - <1m urgent ophthal assessment
- gonococcal infection with permanent vision loss complications
30
What is scleritis?
inflammation of the sclera, which is the outer layer of connective tissue surrounding most of eye, except cornea
*RA, vasculitis like granulomatosis with polyangiitis or less commonly infection
31
How might scleritis present?
- red, inflamed sclera - localised or diffuse
- congested vessles
- severe pain (boring pain)
- pain with eye movement
- photophobia
- epiphoria - excessive tears
- reduced visual acuity
- tenderness to palpation of eye
*white patch on sclera if ischaemia and necrosis
32
How is scleritis managed?
- MDT
- NSAIDs oral
- topical or systemic steroids
- immunosuppression - for underlying condition eg:methotrexate
- antimicrobials for infectious
33
How is episcleritis different?
localised area, outer layer of sclera
*associated with RA and IBD
34
How does episcleritis present?
- localised or diffuse redness - patch in lateral sclera
- triangle of redness
- no pain or mild pain
- dilated episcleral vessels
- injected vessels are mobile when gentle pressure is applied on the sclera
- NO photophobia or discharge and normal visual acuity - SCLERITIS
35
How might episcleritis be investigated?
- apply phenylephrine eye drops - cause blanching of episcleral vessels causing redness to disappear
- will NOT affect scleral vessels and will not impact this redness
36
How is episcleritis managed?
- self limiting in 1-2w
- analgesia like ibuprofen
- lubricating eye drops
- severe - steroid eye drops
37
What is the pathophysiology of a corneal ulcer?
- bacterial
- viral - HSV, HZO, adeno
- other fungal, acanthamoeba
- acathamoeba - tap water bourne
38
How does a corneal ulcer present?
- pain - VERY, pain receptors
- photophobia
- contact lens and tap water contamination
- facial cold sores
- rash and vesicles
- recent injury and abrasions
O/E
- conjunctival injection
- infiltrate
- hypopyon
- fluroscein showing up
39
How is a corneal ulcer managed?
- bacterial - intensive hourly drops of fluroquinolones
- viral - topical acyclovir for a week
- fungal - intensive anti fungal and anti amoebic
40
What is the pathophysiology of herpes keratitis?
viral inflammation of the cornea caused by herpes simplex
- commonly epithelial layer of cornea
- primary or recurrent
41
How does herpes keratitis present?
- primary - mild symptoms of blepharoconjuctivitis - eyelid margins and conjunctiva
- recurrent
- painful red eye
- photophobia
- vesicles
- foreign body sensation
- watery discharge
- reduced visual acuity
42
How is herpes keratitis investigated?
- slit lamp with fluorescein showing dendritic corneal ulcer
- “branching” appearance of ulcer
- corneal scrapings - viral testing
43
How is herpes keratitis managed?
- urgent assessment
- topical or oral antivirals eg: acyclovir
- corneal transplant - treat permanent scarring and vision loss after keratitis
44
What is the common cause of bacterial keratitis?
Pseudomonas
Staphylococcus
45
How does bacterial keratitis present?
- red eye: pain and erythema
- photophobia
- foreign body, gritty sensation
- hypopyon may be seen
46
How might bacterial keratitis be investigated?
an accurate diagnosis can only usually be made with a slit-lamp, meaning same-day referral to an eye specialist is usually required to rule out microbial keratitis
47
How does bacterial keratitis manage?
- topical antibiotics
- typically quinolones are used first-line
- cycloplegic for pain relief
- e.g. cyclopentolate
48
What are the complications of keratitis?
- corneal scarring
- perforation
- endophthalmitis
- visual loss
49
What are some other causes of keratitis?
- Fungal infection (e.g., Candida or Aspergillus)
- Contact lens-induced acute red eye (CLARE)
- Exposure keratitis, caused by inadequate eyelid coverage (e.g ectropion)
50
What is age related macular degeneration?
progressive loss of central vision associated with formation of drusen or angiogenesis and changes in retinal pigmentary epithelium
*dry or wet
51
What is characteristic of dry macular degeneration?
drusen in buch's membrane - undigested cellular debris from degeneration of RPE (retinal pigment epithelium) cells as a part of normal ageing process
*accumulation leads to atrophy of retinal epithelium
52
What characterises wet macular age degeneration?
characterised by choroidal neovascularisation - VEGF (vascular endothelial growth factor) is a protein molecule that has critical role in angiogenesis so in wet AMD causes abnormal angiogenesis and vessel leakage
*fibrous scar tissue and central vision loss and leads to scotoma
53
What are some RF for AMD?
- age
- smoking
- Caucasian ethnicity
- high fat diet
- drugs like aspirin
- co-morbidities like CVS and HTN
- ocular characteristics
- light coloured iris
- hyperopia
- genetics
- complement factor H
- gene variant Y402H (drusen formation link)
54
How would you classify AMD?
early - few medium sized druse, mild pigmentary abnormalities
intermediate - >1 large drusen
advanced - gradual vision loss or advanced wet is rapid vision loss
55
How does dry AMD present?
- visual changes unilateral with
- gradual loss of central vision
- reduced visual acuity
- crooked or wavy appearance to straight lines (metamorphopsia)
- gradually worsening ability to read small text
56
How does wet AMD present?
👁️ wet AMD - more acutely
- visual loss within days and progress to complete within 2-3 years
- often progresses to bilateral disease
57
How is AMD investigated?
- pinhole worsens
- reduced visual acuity - snellen chart
- scotoma - enlarged central area of vision loss
- amsler grid test - assess for distortion of straight lines seen in AMD
- drusen - fundoscopy
- slit lamp - detailed view of retina and macula
- optical coherence tomography - cross sectional view of retina
- fluorescein angiography - fluorescein contrast and photographing the retina to assess the blood supply
- oedema
- neovascularisation in wet AMD
58
How is dry AMD managed?
- no cure, ambler to monitor
- vitamin supplements in early disease
- registration with national centre for blind
- social work involvement, OT, psychology involvement
- informing DVLA if visual acuity poor
59
How is wet AMD managed?
*no cure - maintain functional sight, amsler grid to monitor
- 2w referral for wet AMD
- intravitreal anti-VEGF therapy - monthly
- registration with national centre for blind
- social work involvement, OT, psychology involvement
- informing DVLA if visual acuity poor
60
What may cause gradual vision loss?
corneal abrasion
chemical injury
cataracts
diabetic eye disease
presbyopia
61
What could cause corneal abrasions?
- damaged contact lenses
- associated with pseudomonal infection
- differential with herpes keratitis - antiviral
- fingernails
- foreign body - metal fragments
- tree branches
- makeup brushes
- entropion - inward turned eyelid
62
How might a corneal abrasion present?
- painful red eye
- photophobia
- foreign body sensation
- epiphoria
- blurred vision
63
How would you investigate and manage corneal abrasion?
- fluorescein stain - diagnose
- yellow-orange colour and collects in abrasions or ulcers
- when visualising in cobalt blue light
- uncomplicated - heals in 2-3 days
- complicated - ophthalmology
- remove foreign bodies
- simple analgesia eg:paracetamol
- lubricating eye drops
- antibiotic eye drops eg: chloramphenicol
- close follow up
64
Which type of chemical injury is worse - acid or alkali?
alkali - lipophilic, penetrate corneal stroma and destroy epithelium, releasing proteolytic enzymes which cause further damage
acid - denatures protein, and the coagulated proteins act as a barrier to prevent further penetration (except HCl)
65
How might chemical injuries present and what is a worrying sign?
stinging, burning, redness, pain, swelling of eyelids, blurring of vision
*red eye, except for pallor of vessels in a certain patch - suggestive of limbal ischaemia → corneal scarring and limbal deficiency
66
How would you manage chemical injuries?
- IRRIGATION! to achieve physiological pH
- remove foreign bodies
- medically augment collagen synthesis
- antibiotics, atropine, artificial tears
- surgical debridement
67
What is the role of the lens and ciliary body?
68
What is a cataract?
progressively opaque eye lens which reduces light entering eye and visual acuity
*can be congenital or progressive
69
What are some causes of cataracts?
- age related
- pre-senile
- steroids
- DM
- trauma
- uveitis
- congenital
70
What are some risk factors of developing cataracts?
- increasing age
- smoking
- alcohol
- DM
- steroids
- hypocalcaemia
71
How does cataracts present?
*asymmetrical
- change in glasses prescription - myopic shift with short sighted first as light converges as cataract hardens
- slow reduction in visual acuity
- progressive blurring of vision
- colours more faded - brown or yellow
- starbursts around lights at night especially
*loss of red reflex
72
How are cataracts managed?
- phacoemulsification - if vision 6/12 with sub-tenon block
*important to treat as prevents detection of other pathology like AMD, DM retinopathy etc
73
What is a complication of cataracts?
endophthalmitis - inflammation of vitreous and aqeous humour
mx: intravitreal abx
74
What is the blood supply to the retina?
carotid → ophthalmic → central retinal and posterior ciliary artery
75
What is the pathophysiology of diabetic retinopathy?
- chronic hypoglycaemia damages retinal small vessels and endothelial cells
- increases vascular permeability -> leaks and blot haemorrhages + hard exudates
- neovascularisation etc
76
What are some characteristic features of diabetic retinopathy?
hard exudates
micro-aneurysms and venous beading
cotton wool spots
intra-retinal microvascular abnormalities
neovascularisation
77
What are the stages of diabetic retinopathy?
background retinopathy
pre-proliferative
proliferative
diabetic maculopathy
ischaemic diabetic maculopathy
78
What is background diabetic retinopathy? and what does this mean for management?
micro-aneurysms
dot and blot haemorrhages
cotton wool spots
hard exudates
*no tx indicated, annual screening with digital photography
79
What is pre-proliferative stage and what's the management?
extensive blot haemorrhages and intra-retinal microvascular abnormalities (ischaemia)
*4-6m follow up with digital fundus colour photos + retinal laser tx
80
what is proliferative stage and what is the management?
neovasuclarisation and vitreous haemorrhages
*pan retinal photocoagulation targeting new vessels, retinal laser
81
Differentiate between diabetic maculopathy and ischaemic diabetic maculopathy and what is the management?
diabetic - exudates within macula and macular oedema!
ischaemic - angio needed to diagnose, occlusions within vessels
*mx - anti-VEGF bevacizumab, ranibizumab, intravitreal dexamethasone implant to reduce macular oedema
82
What are some risk factors for diabetic retinopathy?
- duration of diabetes - 50% at 7 years duration and 90% at 17-50
- poor glycaemic control
- hypertension
- dyslipidaemia
- obesity
- pregnancy
83
How might diabetic retinopathy present?
asymptomatic and most present with severe disease
- floaters
- blurred vision and distortion if macula affected
- decreased visual acuity - gradual, painless reduction in quality
- loss of vision - severe haemorrhage in results in sudden complete and painless vision loss
- blindness in untreated and uncontrolled
84
What is the diabetic eye screening programme?
- for anyone with diabetes
- every 1-2 years
- depends on previous 2 scans
85
How is diabetic retinopathy investigated?
- visual acuity - logMAR
- gold: fundoscopy with slit lamp or through fundus photography
- OCT: non invasive and infrared
- Fundus fluorescein angiography
- dye into arm to see retinal blood vessels
86
What is the general management options available for non-proliferative diabetic retinopathy?
- close monitoring and careful diabetic control
- pre-proliferative: 4-6m follow up with digital fundus colour photos
- retinal laser treatment given if,
- only one good eye left
- attendance to clinic poor
- prior cataract surgery
87
What is the management for proliferative DM retinopathy?
- Pan-retinal photocoagulation (PRP) - extensive laser treatment across the retina to suppress new vessels
- aim to kill ischaemic retina so hypoxic drive and oxygen demand is lessened and supply focused to central retina
*complications - visual field defects, impaired night vision, accidental macular burn
- anti VEGF - medication intravitreal injection
- bevacizumab, ranibizumab
- surgery - vitrectomy in severe disease
- macular oedema
- intravitreal implant containing dexamethasone
88
What is presbyopia?
age related nearsightedness - begins at 40 year old
- secondary to loss of elasticity of the crystalline lens
- results in decreased accommodating power when seeing objects at arm’s length or closer
- image focuses behind retina
*presents as gradual loss of near vision eg: reading
89
How is presbyopia managed?
- corrective lenses
- convex lenses
- bifocal - bottom lens refracts light for close up vision, top refracts light to allow you to see distant objects
- multifocals
- corrective surgery
- refractive surgery to achieve monovision
- corneal inlays
90
what conditions cause sudden loss of vision?
retinal detachment
central retinal artery occlusion
central retinal vein occlusion vitreous haemorrhage (due to diabetic retinopathy)
91
what causes amaurosis fugax?
temporary loss of vision caused by a temporary interruption to the blood supply
92
what is the pathophysiology of central retinal artery?
obstruction to blood flow through the central retinal artery, which was a brach of ophthalmic artery which is a brach of ICA
*cause atherosclerosis, GCA, vasculitis hence CVS RF
93
how does central artery occlusion present?
- sudden painless loss of vision: curtain coming down
- RAPD
94
what is relative afferent pupillary defect?
- pupil in affected eye constricts more when light shone in other eye than when shone in itself
- input not sensed by ischaemic retina when testing direct but sensed in consensual
95
how is retinal artery occlusion investigated?
- fundoscopy: pale retina with cherry red spot (fovea) due to lack of perfusion
- GCA: ESR, temporal artery biopsy
*refer immediately
96
how is central artery occlusion managed?
- GCA: potentially reversible so high dose prednisolone +/- IV Methylpred
- attempt to dislodge blockage: ocular massage, anterior chamber paracentesis, inhaled carbogen, IV acetazolamide+mannitol etc
- secondary prevention of CVS, treat reversible RF
97
what is the pathophysiology of central vein occlusion?
thrombus forms in retinal veins and obstructs the venous drainage from retina
- central retinal vein run through the optic nerve - responsible for draining retinal capillaries
- atherosclerotic thickening of central retinal artery leading to vein compression
- causes retinal tissue ischaemia, infarction, vessel leakage and neovascularisation
98
what are some risk factors for central vein occlusion?
- age
- FHx of vascular
- atherosclerosis
- open angle glaucoma
- inflammatory: sarcoidosis, Lyme
- hyper coagulable state
- myeloproliferative states
99
what is the presentation of central vein occlusion?
- sudden, painless unilateral visual loss (more gradual than artery occlusion)
- relative afferent pupillary defect - ischaemia
- visual field defect
100
what is a differential for CRVO?
branch retinal vein occlusion (BRVO) - this occurs when a vein in the distal retinal venous system is occluded
101
how is retinal venous occlusion investigated?
- fundoscopy: widespread hyperaemia, severe retinal haemorrhages, macular oedema, cotton wool spots
- BP
- FBC, glucose, ESR
- fundal photo
- fundus fluorescein angio
102
how is CRVO managed?
- immediate ophthal referral
- control BP
- treatment aim to control complications
- macular oedema: anti-VEGF, intravitreal steroid implant, laser
- neovascular complications: pan-retinal photocoagulation
103
what is a complication of CRVO?
- Ischaemic carries poorer prognosis
- retinal non-perfusion, capillary closure, retinal hypoxia which increases neovascularisation risk
- may resolve spontaneously, cause vitreous haemorrhages or cystoid macular oedema
104
what is retinal detachment?
involves the neurosensory layer of retina (containing photoreceptors and nerves) separating from the retinal pigment epithelium (base later attached to choroid)
105
what is the consequence of a retinal detachment?
- due to retinal tear -> vitreous fluid to get under the neurosensory retina and fill the space
- neurosensory retina relies on blood vessels of the choroid for its blood supply
- detachment disrupts this causing permanent damage to photoreceptors -> sight threat
106
what are some RF for retinal detachment?
- lattice degeneration (thinning of retina)
- posterior vitreous detachment
- trauma
- diabetic retinopathy
- retinal malignancy
- family history
107
how does retinal detachment present?
- painless
- peripheral vision loss - sudden, shadow coming across vision
- blurred vision or distorted vision
- flashes and floaters
- RAPD if optic nerve involved
- fundoscopy: red reflex might be lost
108
how is retinal detachment managed?
- aim to create adhesions between retina and choroid with laser and cryo
- aim to reattach retina: vitrectomy, scleral buckle, pneumatic retinoplexy
109
what is optic neuritis?
inflammatory condition of the optic nerve that leads to acute, unilateral, central loss of vision (over hours to days)
- common in females 20-40
110
what is the pathophysiology of optic neuritis?
- immune-mediated demyelination of the optic nerve as an isolated incident or part of wider disorder
- acute version of MS
- also associated with DM, syphillis
111
what is the presentation of optic neuritis?
- acute, central vision loss - unilateral over hours to days
- poor discrimination of colours - red desaturation
- pain worse of eye movement
- photopsia - flashes of light
- relative afferent pupillary defect
- visual field defects - central scotoma
- optic atrophy - chronic
112
how is optic neuritis investigated?
- swinging light test: RAPD
- ophthalmoscopy: mildly swollen disc
- MRI brain and orbits with contrast: confirm demyelinating optic neuritis
- LP: elevated protein, lymphocytes,oligoclonal bands
113
how is optic neuritis managed?
- high dose IV steroids - methylprednisolone
- disease modifying therapies - MS?
- recovery usually 4-6w
114
what is the pathophysiology of third nerve palsy?
- posterior communicating artery aneurysm
- microvascular, pupil sparing DM, HTN
- other: trauma, neoplasm, infection, migraine, congenital
115
how does third nerve palsy present?
- affects all EOM except lateral rectus and superior oblique
- these act unopposed to give exotropia and hypotropia ie. down and out
- dilated pupil + accommodation paralysis
116
how is third nerve palsy investigated?
- check BP
- cranial nerve examination
- fundoscopy - retinopathy and optic disc swelling
- temporal artery examination
- lid fatigue
- eye movements and cover test - orthoptics
- fasting glucose
- CT, MRI if pupil sparing
- MG antibodies
117
how is third nerve palsy managed?
- treat amblyopia in children <8 → prisms help in isolated muscles
- surgery - achieves limited area of binocular single vision at best
- occlusive contact lens - residual diplopia
118
what is the pathophysiology of fourth nerve palsy?
- acquired - head trauma, trochlear or orbital injury, ENT surgery, sinus infections or vascular
- can be idiopathic or associated with HTN, DM, rarely demyelination, GCA, tumours and aneurysms
119
how does fourth nerve palsy present?
- vertical diplopia: defective downwards gaze
*prominent when looking down
- contralateral head tilt
- ipsilateral hypertropia
120
how is trochlear palsy managed?
- prisms may control small deviations
- hyperdeviation - surgery
- SO tendon tuck etc
121
what is the pathophysiology of a abducens palsy?
- adults - microvascular HTN, DM, MS, neoplasm, head trauma, infection, raised ICP, GCA and idiopathic
- children - microvascular unlikely, transient in neonates, benign palsy of childhood 1-3w after febrile illness
122
what is the presentation of abducens palsy?
- horizontal diplopia - greater when looking to affected side and distance
- diplopia may be constant
- head turn to same side
123
how is abducens palsy investigated?
- check for other CN signs - present when Pons (CN 7), cavernous sinus (CN 3,4, 5 trigeminal division) affected
- orthoptic testing - prism cover test
- hess chart
- blood tests
- MRI, CT → false localising signs in raised ICP
124
how is abducens palsy managed?
- childhood - resolve spontaneously
- stable and symptomatic post 6m consider surgery
- surgery selected based on abduction status (past midline)
125
what is the pathophysiology of orbital floor fracture?
usually as a result of a direct blow to the orbit, typically involving the floor and or medial wall but with orbital rim intact
- this leads to sudden increase in intraorbital pressure
126
what are the types of orbital floor fractures and the anatomical components involved?
- inferior: most common, orbital fat prolapses into maxillary sinus, inferior rectus too?
- medial: orbital fat, medial rectus into ethmoid air cells
- superior: uncommon
- lateral: associated with orbital rim, craniofacial injuries
127
how does orbital blow out fracture present?
*excessive soft tissue swelling
- diplopia, restricted ocular motion
- enophthalmos
- diplopia as EOM entrapment
- orbital emphysema
- malar region numb: infraorbital nerve injury
- hypoglobus
128
how might you manage an orbital blow out fracture?
*CT
- ice for swelling, decongestants to aid drainage, avoid nose blowing, steroids for swelling, abx
- surgery to release trapped tissue within 24-48h
129
what is the significance of thyroid diseases in relation to ophthalmology?
autoimmune condition resulting in inflammation and swelling of extra-ocular muscle, fatty tissue and connective tissue within orbit
*follows acute phase for 6m to 2y where damage happens, inactive phase when sx remain
130
how might thyroid related eye disease present?
- excessive watering
- ‘gritty’ sensation
- photophobia
- eye pain
- ask - red eye, blurred vision, pressure sensation
- systemic - pretibial myxoedema, goitre, acropachy
131
what might thyroid eye disease exemption show?
- eye lid retraction
- proptosis
- lig lag - von Graefe’s sign
- lid oedema
- diplopia due to restriction of inferior rectus
- incomplete eyelid closure
- strabismus
132
what investigations are carried out for thyroid related eye disease?
- measure proptosis
- assess optic disc
- visual acuity, colour vision, RAPD
- TFT
- antibody test
- anti-thyroid peroxidase, anti-TSH
- USS extra-ocular muscles
- CT orbit - nerve involvement
- MRI orbits
133
how is thyroid related eye disease managed?
- compressive optic neuropathy - Urgent IV methylprednisolone
- Ophthal + endo review
- correct thyroid hormone levels
- smoking cessation
- steroids to reduce swelling
134
what are some complications of thyroid related eye disease?
*compressive optic neuropathy - reduced visual acuity, colour vision → sight-threatening
- globe subluxation
- gaze abnormalities
- raised IOP → glaucoma
135
what is the pathophysiology of amaurosis fugax?
result of ischaemia to the retina, choroid, or optic nerve from an arterial embolus, usually in the retinal artery (from ipsilateral carotid artery disease)
136
what are some RF for amaurosis fugax?
- over 50
- vascular RF
- HTN, HPL, smoking, previous TIA or stroke
137
how does amaurosis fugax present?
- transient vision loss in one or both eyes
- abrupt, maximum severity within seconds lasting to minutes
- full recovery
- negative visual phenomenon - blackout or ‘greying out’ of vision
- normal ophthal exam
138
how is amaurosis fugax investigated?
- inflammatory markers - rule out GCA
- carotid imaging for stenosis
- cardiac investigations - AF other stroke RF
- neuro-imaging is needed
139
how is amaurosis fugax managed?
- 300mg of aspirin unless contraindicated
- urgent TIA referral within 24h
- secondary prevention - statin, antiplt, optimising BP etc
140
what is blepharitis?
inflammation of the eyelid margins
- due to meibomian gland dysfunction (common, posterior bleph), or seborrhoeic dermatitis/ staphylococcal infection (less common, anterior bleph)
141
how does blepharitis present?
- bilateral symptoms
- grittiness and burning discomfort - around lid margins
- eyes sticky in the morning
- results in dry eye which could cause redness
- foreign body sensation
- margins may be red - swollen in staphylococcal blepharitis
- styes and chalazions common in these
- secondary conjunctivitis
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what does blepharitis look like on examination?
- anterior - eyelash deformity and depigmentation and loss
- posterior - dilated and obstructed Meibomian glands
143
how is blepharitis managed?
diagnosis - history, examination
- slit lamp
- swabs maybe done for cultures
hot compress
lid hygiene
artificial tears
abx
ophthal referral if painful
144
how is lid hygiene done for blepharitis?
- lid hygiene - mechanical removal of debris from margins
- cotton wool buds dipped in mix of cooled boiled water and baby shampoo often used
- alternative is sodium bicarb, teaspoonful in cup of cooled water recently boiled
145
what is a meibomian cyst?
- lipo-granulomatous lesion that forms in obstructed meibomian gland
- non-infectious and associated with blepharitis and acne rosacea
146
how does meibomian cyst present and how is it managed?
- painless red eyelid cysts
- in internal eyelid
- when infected becomes internal hordeolum
- not painful or tender to touch
- resolves spontaneously
- warm compress of eye lid to loosen gland
- eyelid massage to express content 2x a day
- if persistent referral for incision and curettage
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what is a subconjuctival haemorrhage?
- small blood vessels within the conjunctiva ruptures, releasing blood into the space between the sclera and conjunctiva
- after strenuous activity like coughing, weight lifting or straining
- or trauma to eye
- commonly idiopathic in otherwise healthy
148
what are some risk factors for subconjuctival haemorrhage?
*may predispose
- HTN
- bleeding disorders - thrombocytopenia
- whooping cough
- medications eg: anti-plt, DOACs, warfarin
- non-accidental injury
149
how does subconjuctival haemorrhage present?
- patch of bright red blood underneath conjunctiva - covering white of eye
- painless
- does NOT affect vision
- precipitating event!
150
how is subconjuctival haemorrhage investigated and managed?
- simple history and examination, BP, INR - if on warfarin
- spontaneous resolution
- 2 weeks
- lubricating eye drops - mild irritation
151
what is the pathophysiology of posterior vitreous detachment?
- vitreous body comes away from retina - common in older age
- vitreous humour is gel inside the vitreous chamber of eye, maintain structure of eyeball and keeps retina pressed on choroid
- with age, less firm and less able to maintain shape
152
how does posterior vitreous detachment present?
- painless
- can be asymptomatic
- floaters
- flashing lights
- blurred vision
153
How is posterior vitreous detachment managed?
*exclude retinal detachement
- brain adjusts overtime
- safety net for retinal detachment as predisposes
