Ophthalmology

Question 1

ptosis paeds 5 causes

Answer 1

horner syndrome (partial, may accompany birth trauma), third nerve palsy (complete w dilated pupil and down/out), myopathies (usually bilat, see in MG, dermatomyositis, myotonic dystrophy), familial (AD inheri), pseudoptosis (upper eyelid drooping due to surrounding pathology eg tumour pressing on eyelid)

Question 2

proptosis causes (4 inc 7 for 1)

Answer 2

best seen from above the pt

infection (periorb cellulitis), thyrotoxicosis, tumours (cap haeman, histiocytosis X, neuroblastoma secondaries, rhabdomyo, optic nerve glioma (look for NF), dermoid cysts, retinoblastoma), and in various syndromes

Question 3

bruising around eye 5 diffs

Answer 3

NAI (fundoscopy for ret h+), bleeding disorder (eg haemophil), leukaemia (maybe subconjunct h+), neuroblastoma, base of skull fracture

Question 4

subconjunctival h+ 5 diffs

Answer 4

trauma, NAI, bleeding disorders inc leuk, whooping cough, spont

Question 5

optic disc atrophy 6 diffs

Answer 5

post-traumatic, raised icp, optic nerve compression, vit B12 def, retinal art thrombosis, syndromes eg leber optic atrophy

Question 6

papilloedema sequence

Answer 6

hyperaemic disc then margins blur (nasal first), then dilatation/engorgement of veins, then optic cup lost, then small flame haemorrhages

initially vision unaffected but then blind spot enlarges, optic atrophy follows

raised icp causes (sol, meningitis, hydroceph, malig htn, benign intracran htn, central retinal vein thrombosis)

Question 7

5 causes of retinitis pigmentosa

Answer 7

infection (congen rubella, measles), cystinosis, refsum disease, abetalipoprotarinamia, congen syndromes)

Question 8

5 causes of corneal clouding

Answer 8

mucopolysaccharidoses, trauma, glaucoma, TORCH syndrome, chronic keratitis

Question 9

coloboma

Answer 9

embryonic fissure of optic cup doesnt complete fuse (in 2nd month), giving shallow cup (like glaucoma one) or sclera visible through normal retina, or an iris with a notch in inferonasal position; may extend to eyelid

Coloboma of the eyelid has a different embryologic origin from a coloboma of the globe. Eyelid colobomas are typically located at the superior medial upper eyelid. Lid coloboma arises from defective eyelid development; either during fusion, occurring during the third and fourth months of embryologic development, or during re-separation, which occurs in the sixth or seventh months

linked to ts13, CHARGE syndrome, rieger syndrome, isolated AD colobomata, goldenhar syndrome)

Anteriorly located coloboma often appears as a defect in the iris tissue, in the shape of a keyhole. They are classified as “typical” if found in the inferonasal quadrant of the affected structure and “atypical” if found elsewhere
Posteriorly located coloboma can involve the optic nerve, retina, and choroid. If the retina is involved, it is reduced to glial tissue with no underlying RPE or choroid. This appears as an area of whitening often with pigment deposition at the junction of the coloboma and normal retina.

Retinal detachment and cataract are the most common complications associated with retinochoroidal coloboma
Complications of eyelid coloboma are mainly due to corneal exposure from large upper eyelid defects resulting in exposure keratopathy and corneal ulceration if left untreated

Eyelid Coloboma
Lubrication should be supplied if there is any evidence of compromised lid closure and corneal protection. Evaluation by oculoplastics is recommended to determine if and how lid reconstruction should occur

Interval monitoring for retinal detachment should be done with a dilated fundus exam approximately every 6-12 months or sooner if indicated for patients with posterior coloboma

Measures such as patching should be taken to maximize visual potential of the affected side as there is often normal retina present and refractive error is often present putting patients at risk for amblyopia

Question 10

paeds uveitis (what it is, sx, 11 causes, mx)

Answer 10

iris, ciliary body or choroid may be inflamed

anterior uve is ant to ciliary body, post uve behind

get pain in eye, photophobia, blurred vision, redness, inc’d lacrimation; may see miosis, erythema

causes: rheum arth, IBD, behcets, sarcoidosis, ank spond, reiter syndrome, toxoplasmosis (commonest cause of post uve), CMV, toxocariasis, TB, syph

local or sys steroids to treat

Question 11

toxocariasis

Answer 11

toxocariasis usually between 2-5yo due to ingesting eggs of nematodes toxocara canis/catis which hatch in intestine then migrate through body; can get fever, cough, wheeze, hepatomeg, chorioretinitis giving granulomatous lesion near macula (diff rb), eosinophilia and raised IgE; serology confirms; recovery oft spont but may need steroids/thiabendazole; deworm pet dogs and cats

Question 12

aniridia

Answer 12

red reflex covers whole corneal diameter

familial forms, sporadic associated with wilm tumour in 20% of cases

Question 13

paeds cataracts (19 causes, mx strat)

Answer 13

get leukocoria

genetic/idiopathic
congen infection (rubella, toxoplasmosis, CMV)
metabolic: DM, galactosaemia, wilson, fabry, hypocalc, hypoparathyroid
ocular disease: chronic uveitis, ret detachment
post trauma
ts 21, ts13, ts18, lowe syndrome, dystrophia myotonica
chronic steroid use

If cataracts are not causing any problems, immediate treatment may not be necessary. Instead, child may only need regular check-ups to monitor their vision. If child’s vision is affected by cataracts, they’ll usually need to have surgery to remove the cloudy lens

if b/l will need congenital cataract genetic panel; also get urinalysis and consider further ix for cause based on clinical need

Question 14

blue sclera causes

Answer 14

normal children but maybe osteogenesis imperfecta or osteopetrosis

Question 15

congen glaucoma

Answer 15

called buphthalmos, eyeball large - often asymetrically so; cornea may be thickened and cloudy due to oedema, pupil fixed and dilated

besides congen may be lowe syndrome, sturge-weber, NF, following chronic uveitis

Question 16

clumsiness, rec sinopulm infections, and telangiectasia on conjunctivae

Answer 16

ataxia telangiectasia

Question 17

causes of lens dislocation

Answer 17

marfans (upwards and outwards) and homocystinuria (downwards and inwards)

Question 18

cause of a dendritic corneal ulcer

Answer 18

herpes simplex keratitis

Question 19

fundoscopic appearance of congen infections

Answer 19

toxoplasmosis - central white/yellow patchy area with periph pigment
CMV - haemorrhages and exudates giving pizza retina
toxocariasis - granulomatous lesion around macula

Question 20

rb causes and presentations

Answer 20

85% sporadic - unilat and presents after 18-24mo
15% inherited - AD, usually bilat and presents before 18mo

may present as strabismus, leukocoria, glaucoma, or hyphaema; will see an elevated mass rising from retina, often white/yellow in colour (diff toxocaria)

Question 21

causes of leukocoria

Answer 21

cataract, corneal clouding, vit haem, toxocariasis, ret detachment

Question 22

retinoblastoma

Answer 22

leukocoria, red/irritated eye, deteriorating vision, faltering growth, maybe squint/strabismus (2nd commonest presenting sign); change in colour of iris; FH; most diagnosed before 5yo
hamartomas, choroiditis, congen cataract (this can cause leukocoria)
urgent referral if suspect
examination under anaesthesia w maximally dilated eye, ocular USS, MRI; genetic counselling
chemo, cryotherapy etc; enucleation if tumour fills over half eye or involvement of other eye structures; radiotherapy may be used
high risk of developing more cancers in future- 250-500x risk of osteosarcoma

Question 23

retinoblastoma and optic glioma

Answer 23

Retinoblastoma arises from the retina, and it may grow under the retina and/or toward the vitreous cavity. Involvement of the ocular coats and optic nerve occurs as a sequence of events as the tumour progresses

Most patients present with leukocoria, which is occasionally first noticed after a flash photograph is taken. Strabismus is the second most common presenting sign and usually correlates with macular involvement. Very advanced intraocular tumours present with pain, orbital cellulitis, glaucoma, or buphthalmos.

As the tumour progresses, patients may present with orbital or metastatic disease. Metastases occur in the preauricular and laterocervical lymph nodes, in the CNS, or systemically

If suspect that your child may have retinoblastoma, referto one of the two specialist centres in the UK for confirmation of the diagnosis and treatment. These centres are in Birmingham and London.

Examination under anaesthetic (EUA) will be performed +/- MRI, OCT, aqueous fluid sampling etc

Treatment will depend on the number, position, and size of tumours; smaller may have cryotherapy, laser therapy; larger or metastasised may supplement with chemo (carboplatin and vincristine common)
If tumour more advanced or vision lost then surgical enucleation

optic nerve glioma:
30% of patients have associated NF1
Malignant gliomas (glioblastoma) are rare & almost always occur in adult males; About 10% of optic pathway tumours are located within an optic nerve. One third of the tumours involve both optic nerve and chiasm, a further third involve predominantly the chiasm itself, and one fourth is predominantly in the hypothalamus

present with slowly progressive visual loss, followed later by proptosis (although this sequence may occasionally be reversed) and RAPD. Acute visual loss due to haemorrhage into the tumour is uncommon; optic nerve head is swollen initially but subsequently becomes atrophic

may be monitored if not growing and good vision; otherwise resection, if not possible (eg chiasm or tract) then RT +/- chemo

Question 24

squint

Answer 24

cover test and eye movements +/- cranial nerve and general exam
check for diplopia, headache, n&v, dizziness (potential neuro causes); exclude leukocoria (retinoblastoma)
refer all to paeds eye service
corrective glasses (plus lenses mean less accomodation thus improve esotropia and neg lenses mean more accomodation thus improve exotropia), patches, eye exercises, corrective surgery may all be considered; botulinum toxin if surgeries fail

Question 25

strabismus

Answer 25

Any complaint of a ‘turning eye’ should be taken seriously even if this cannot be reproduced in a consultation, as the squint may be intermittent.
Intermittent deviation of the eyes is common in healthy neonates and should not cause undue concern in an otherwise healthy baby. However, any constant squint, even in neonates, is significant. Normal binocular coordination is established at about 3 months, and any squint after this age is significant

use corneal light reflex, cover, and cover/uncover tests

Assess for the presence of the red reflex and exclude leukocoria (white or grey pupil)
Squints that may give rise to particular concern about the underlying cause include:
Constant unilateral exotropias.
Any acquired incomitant squint.
Sudden, late-onset (over 3–4 years) esotropia, particularly if there is no family history and no significant hypermetropia

Refer any child with a suspected or confirmed squint to the local paediatric eye service.
A routine referral is indicated for most children. However, the earlier treatment for a squint can be initiated, the better the outcome to prevent amblyopia

Urgent referral if red flags which include:
Limited abduction.
Double vision.
Headaches.
Nystagmus

a child with acquired strabismus or reduced vision may have a primary neurological disorder such as optic nerve glioma,
medulloblastoma, craniopharyngioma or hydrocephalus. This is more likely in the
presence of features such as persistently reduced visual acuity, resistant to
amblyopia therapy, deteriorating visual acuity or an ocular muscle under action. A
careful examination should be performed to exclude an afferent pupil defect,
papilloedema, optic atrophy or other cranial nerve abnormality. The finding of any
abnormal neurological signs should prompt referral to a paediatrician +/- MRI

In many cases, the management of strabismus in children commences with glasses to address any refractive error leading to squint; In all forms of esotropia, full correction of hypermetropia is the treatment of choice, leaving it uncorrected might help in exotropia; A period of refractive adaption is recommended after glasses have been prescribed which may be followed by occlusive therapy managed by orthoptist

botulinum injections and surgical correction are later mx steps

Question 26

amblyopia

Answer 26

amblyopia refers to the reduction of best-corrected visual acuity (BCVA ie glasses worn if required) in one or both eyes that cannot be exclusively attributed to a structural abnormality of the eye It is often referred to as ‘lazy eye’. This is usually a result of an interruption in the visual development during early childhood, from birth to seven years

can be caused by strabismus, hyperetropia, myopia, astigmatism, obstacle obscuring vision (cataract, ptosis, haemangioma etc)

Glasses will be prescribed if there is any significant long or short sightedness, or astigmatism; if the vision remains reduced in the “lazy” eye after glasses have been worn for up to 16 weeks, the usual treatment for amblyopia is to wear a patch over the good eye that will, in turn, stimulate the vision in the poorer sighted eye

Occasionally atropine drops/ointment may be used in the good eye instead. This blurs the vision in the good eye and encourages the vision in the weaker eye to develop. This treatment is usually only used if patching fails.

Question 27

5 red eye diffs (details on endophlamitis - 5x features, mx)

Answer 27

a. acute angle closure glaucoma
b. (infective) endophthalmitis
c. orbital cellulitis
d. trauma i. corneal abrasion ii. corneal / subtarsal foreign body iii. hyphaema iv. chemical injury v. penetrating eye injury
e. “-itises” i. conjunctivitis (viral, bacterial or allergic) ii. anterior uveitis iii. keratitis (herpetic or bacterial) iv. scleritis

endophthalmitis is rare, usually days to weeks postop (for eg cornea) or post trauma; generally if the globe has opened creating a path for infection; pain, red eye, dec’d vision, quite sudden; acute needs emergency admission; vitreous antibiotics needed

Question 28

angle closure glaucoma (8 sx, 4x eye drop drugs, definitive mx)

Answer 28

severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain
an emergency and should prompt urgent referral to an ophthalmologist.

no guidelines for the initial medical treatment emergency treatment. An example regime would be:
combination of eye drops, for example:
a direct parasympathomimetic (e.g. pilocarpine, causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour)
a beta-blocker (e.g. timolol, decreases aqueous humour production)
an alpha-2 agonist (e.g. apraclonidine, dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow)
intravenous acetazolamide
reduces aqueous secretions

Definitive management
laser peripheral iridotomy

Question 29

orbital cellulitis (descrip, 4 risk factors, 7 sx - 3 not seen in preorb, ix - 4 tests and key imaging, mx)

Answer 29

infection affecting the fat and muscles posterior to the orbital septum, within the orbit but not involving the globe. It is usually caused by a spreading upper respiratory tract infection from the sinuses and carries a high mortality rate. Orbital cellulitis is a medical emergency requiring hospital admission and urgent senior review.

periorb cellulitis can progress to orbital cellulitis; also this is mostly kids, mean age 7-12yo; periorb cellulitis, ear/face infection, sinus infection, lack of HiB vaccine are risk factors

Presentation
Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema and ptosis
Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)

Differentiating orbital from preseptal cellulitis
reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis

Investigations
Full blood count – WBC elevated, raised inflammatory markers.
Clinical examination involving complete ophthalmological assessment – Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema.
CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis.
Blood culture and microbiological swab to determine the organism. Most common bacterial causes – Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.

Management
admission to hospital for IV antibiotics

Question 30

ocular trauma and hyphema mx (inc main risk to sight)

Answer 30

Hyphema (blood in the anterior chamber of the eye) - especially in the context of trauma warrants urgent referral to an ophthalmic specialist for assessment and management. The main risk to sight comes from raised intraocular pressure which can develop due to the blockage of the angle and trabecular meshwork with erythrocytes. Strict bed rest is required as excessive movement can redisperse blood that had previously settled; therefore high-risk cases are often admitted. Even isolated hyphema will require daily ophthalmic review and pressure checks initially as an outpatient

Question 31

corneal foreign body (5 sx, 6 inds to refer) and ulcer (4 sx)

Answer 31

foreign body: Features
eye pain
foreign body sensation
photophobia
watering eye
red eye

Indications for referral to ophthalmology
Suspected penetrating eye injury due to high-velocity injuries (e.g. drilling, lawn moving or hammering) or sharp objects (e.g. as glass, knives, pencils or thorns)
Significant orbital or peri-ocular trauma has occurred.
A chemical injury has occurred (irrigate for 20-30 mins before referring)
Foreign bodies composed of organic material (such as seeds, soil) should be referred to ophthalmology as these are associated with a higher risk of infection and complications
Foreign bodies in or near the centre of the cornea
Any red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity
corneal ulcer: more common in contact lens users

Features
eye pain
photophobia
watering of eye
focal fluorescein staining of the cornea

Question 32

conjunctivitis (allergic (5 sx, 2 mx) and infectious (2 sx, 3 mx and school/contacts/towels)

Answer 32

allergic: may occur alone but is often seen in the context of hay fever

Features
Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis)
Itch is prominent
the eyelids may also be swollen
May be a history of atopy
May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)

Management of allergic conjunctivitis
first-line: topical or systemic antihistamines
second-line: topical mast-cell stabilisers
infective: most common eye problem presenting to primary care. It is characterised by sore, red eyes associated with a sticky discharge
bacti is purulent, eyes may be stuck together; viral has serous discharge, maybe recent urti and preauric lymph nodes

mx:
normally a self-limiting condition that usually settles without treatment within 1-2 weeks
topical antibiotic therapy is commonly offered to patients, e.g. Chloramphenicol. Chloramphenicol drops are given 2-3 hourly initially where as chloramphenicol ointment is given qds initially
topical fusidic acid is an alternative and should be used for pregnant women. Treatment is twice daily
contact lens should not be worn during an episode of conjunctivitis
advice should be given not to share towels
school exclusion is not necessary

Question 33

episcleritis (2 sx and mobility/phenylephrine, mx), scleritis (4 sx, 5 associations, mx)

Answer 33

epi:
red eye
classically not painful (in comparison to scleritis), but mild pain may be present
watering and mild photophobia may be present
in episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera. In scleritis, vessels are deeper, hence do not move
phenylephrine drops may be used to differentiate between episcleritis and scleritis. Phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels. If the eye redness improves after phenylephrine a diagnosis of episcleritis can be made

Approximately 50% of cases are bilateral.

Management
conservative
artificial tears may sometimes be used
scleritis:
red eye
classically painful (in comparison to episcleritis), but sometimes only mild pain/discomfort is present
watering and photophobia are common
gradual decrease in vision
associated with autoimmune, msk conditions, hla-B27 conditions, TB, local infection spread from corneal ulcer

should be referred to optho, cause will be identified and managed as well as NSAIDs given

Question 34

anterior uveitis (9 sx, 5 associations, 3x mx)

Answer 34

inflammation of the anterior portion of the uvea - iris and ciliary body. It is associated with HLA-B27 and may be seen in association with other HLA-B27 linked conditions (see below).

Features
acute onset
ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired

Associated conditions
ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen

Management
urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops

longer term steroid sparing agent may be needed eg methotrexate, mycophenolate mofetil, and azathioprine, TNFa inhibitors

Question 35

keratitis - what it is, 8 causes, present (4sx) and 3 mx (inc contact lens wearers), diff from conjunct (4 things) and acute glauc (1 thing)

Answer 35

inflammation of the cornea. Microbial keratitis is not like conjunctivitis - it is potentially sight threatening and should therefore be urgently evaluated and treated

Causes
bacterial
typically Staphylococcus aureus
Pseudomonas aeruginosa is seen in contact lens wearers
fungal
amoebic
acanthamoebic keratitis
accounts for around 5% of cases
increased incidence if eye exposure to soil or contaminated water
parasitic: onchocercal keratitis (‘river blindness’)

Remember, other factors may causes keratitis:
viral: herpes simplex keratitis
environmental
photokeratitis: e.g. welder’s arc eye
exposure keratitis
contact lens acute red eye (CLARE)

Features
red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen
contact lens wearers
assessing contact lens wearers who present with a painful red eye is difficult
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

Management
stop using contact lens until the symptoms have fully resolved
topical antibiotics
typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate

Complications may include:
corneal scarring
perforation
endophthalmitis
visual loss
diff from conjunctivitis can be hard: may be more painful, have cloudy cornea, some photophobia, some blurring of vision; pupil will be normal unlike acute glauc

Question 36

5 gradual deterioration of vision diffs

Answer 36

a. cataract i. age-related ii. pre-senile (steroids, diabetes, trauma, uveitis)

b. age-related macular degeneration i. dry / atrophic ii. wet / neovascular / exudative

c. primary open angle glaucoma

d. diabetic eye disease i. retinopathy (nonproliferative, proliferative) ii. maculopathy (oedematous, ischaemic)

e. presbyopia

Question 37

cataracts 9 causes, 5 sx, 2 ix, mx, 4 subtypes (and what cause goes with each subtype)

Answer 37

Normal ageing process: most common cause

Other possible causes
Smoking
Increased alcohol consumption
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: hypocalcaemia

Patients typically present with a gradual onset of:
Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights

Signs:
A Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.

Investigations:
Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract

Management
Non-surgical: In the early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/contact lens, or by encouraging the use of brighter lighting. These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed.
Surgery: Surgery is the only effective treatment for cataracts. This involves removing the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice. Also whether both eyes are affected and the possible risks and benefits of surgery should be taken into account
subtypes:
Nuclear: change lens refractive index, common in old age
Polar: localized, commonly inherited, lie in the visual axis
Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
any vision impairment is sufficient for an op!

Question 38

ARMD (risk factors, classification, 3 sx, ix, mx)

Answer 38

Risk factors
advancing age itself is the greatest risk factor for ARMD
the risk of ARMD increases 3 fold for patients aged older than 75 years, versus those aged 65-74.
smoking
current smokers are twice as likely as non-smokers to have ARMD related visual loss, and ex-smokers have a slightly increased risk of developing the condition, (OR 1.13).
family history is also a strong risk factor for developing ARMD
first degree relatives of a sufferer of ARMD are thought to be four times more likely to inherit the condition.
other risk factors for developing the condition include those associated with increased risk of ischaemic cardiovascular disease
Traditionally two forms of macular degeneration are seen:
dry macular degeneration
90% of cases
also known as atrophic
characterised by drusen - yellow round spots in Bruch’s membrane
wet macular degeneration
10% of cases
also know as exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries worst prognosis

Recently there has been a move to a more updated classification:
early age-related macular degeneration (non-exudative, age-related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE)
late age-related macular degeneration (neovascularisation, exudative)
Patients typically present with a subacute onset of visual loss with:
a reduction in visual acuity, particularly for near field objects
difficulties in dark adaptation with an overall deterioration in vision at night
fluctuations in visual disturbance which may vary significantly from day to day
they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects

Signs:
distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.

Investigations:
slit-lamp microscopy is the initial investigation of choice
fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therap
combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.
vascular endothelial growth factor (VEGF)
VEGR is a potent mitogen and drives increased vascular permeability in patients with wet ARMD
a number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss
evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible
examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.

Question 39

open angle glaucoma - 3 sx, ix inc 4 fundoscopy signs, whats a big risk factor

Answer 39

POAG may present insidiously and for this reason is often detected during routine optometry appointments. Features may include
peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
decreased visual acuity
optic disc cupping

Fundoscopy signs of primary open-angle glaucoma (POAG):
1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
2. Optic disc pallor - indicating optic atrophy
3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
Investigations:
automated perimetry to assess visual field
slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline
applanation tonometry to measure IOP
central corneal thickness measurement
FH is a big risk factor!

Question 40

open angle glaucoma mx (inc drugs mech + s/e) - 1st line, 2nd line, 3rd line

Answer 40

NICE guidelines:
first line: prostaglandin analogue (PGA) eyedrop
second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
if more advanced: surgery or laser treatment can be tried

Reassessment
important to exclude progression and visual field loss
prost analogue like latanoprost incs uveoscleral outflow, iris may gain brown pigment and eyelashes grow longer
b blocke like timolol reduces aqueous production - avoid in asthmatic/heart block
sympathomimetics do both above mechanisms, avoid if on MAOI/TCAs
carb anyhdrase inhibs reduce aqueous production

Question 41

diabetic eye disease (mech; NPDR (1 mild, 5 mod, 3 severe), 2 PR (more common in which kind?), maculopathy (what and more common in which kind?)

Answer 41

Diabetic retinopathy is the most common cause of blindness in adults aged 35-65 years-old. Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage

Mild NPDR
1 or more microaneurysm

Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots (retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

Severe NPDR aka preprolif
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
Proliferative retinopathy
retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM,
Maculopathy
based on location rather than severity, anything is potentially serious
hard exudates and other ‘background’ changes on macula
check visual acuity
more common in Type II DM

Chronic hyperglycaemia causes blood vessels, including those supplying the retina, to weaken and rupture; the vessel walls may dilate resulting in microaneurysms or small haemorrhages.
The damaged pericytes and erythrocytes increase vascular permeability. Lipoproteins, lipids and other products carried by blood are therefore able to leak out and cluster onto the retina as hard exudates.
As blood flow becomes increasingly compromised, regions of the retina are starved of oxygen. This hypoxia is thought to stimulate the release of mediators such as vascular endothelial growth factor (VEGF) which promotes neovascularization. However, these new vessels are poorly formed and easily rupture resulting in bleeding.
Neovascularization into the vitreous humour may culminate in widespread vitreous haemorrhage causing sudden and complete visual loss. Fibrovascular bundles can lead to fibrosis and, in turn, retinal traction. This can result in retinal detachment and recurrent vitreous haemorrhage.

visual acuity assessed, slit-lamp or fundus photography to classify severity; fluorescein angiography can help you see unclear ischaemia, optical coherence tomography if diabetic macular oedema

lifestyle, glycemic, and BP control; photocoagulation if proliferative or severe nonprolif and high risk eg one eye, pregnant, frequent flyer
In focal photocoagulation, a specific point of leakage is identified and targeted with the laser. comps include worse central vision or scotoma
Pan-retinal photocoagulation (PRP)
The periphery of the retina is targeted with the aim of achieving a global reduction in oxygen demand. so less VEGF; Complications of PRP include a restricted peripheral vision, reduced quality of night vision, ocular pain, worsening macular oedema

Anti-VEGF injections focus on minimising neovascularization and thus are used in proliferative diabetic retinopathy. Aflibercept (Eylea) and Ranibizumab (Lucentis) are two commonly used anti-VEGF agents in the treatment of DR.
Although the mechanism of action is not completely understood, trials have shown intravitreal corticosteroids can also be effective in improving visual acuity and reducing maculopathy.
anti-vegf contra’d if stroke or MI in last 3mo

A potential complication of proliferative DR is bleeding into the vitreous humour, which further increases the risk of retinal detachment. In many cases, waiting for the haemorrhage to settle can allow sufficient view to perform laser therapy.
However, in persistent haemorrhage or in central, sight-threatening tractional retinal detachment a vitrectomy may be performed. This allows for the removal of the vitreous and repair of any scarring/detachment of the retina. Photocoagulation may be used intra-operatively

annual screening once >12yo

retinal detachment/vitreous h+ are main complications, also neovascular glaucoma: Neovascularization can occur within the iris and its trabecular meshwork (rubeosis) causing a narrowing and closure of the drainage angle and therefore increased intraocular pressure.
The typical presentation may include a patient complaining of an acutely painful, red eye

If left untreated, approximately 50% of patients with proliferative DR will lose their vision in 2 years.
Around 90% of affected patients will have lost most of their vision within 10 years.
Those with proliferative DR that undergo treatment can reduce their risk of severe vision loss by 50%.

Question 42

7 sudden/subacute visual loss diffs

Answer 42

a. central retinal artery occlusion (CRAO)
b. anterior ischaemic optic neuropathy i) non arteritic ii) arteritic (i.e. giant cell / temporal arteritis)
c. vitreous haemorrhage
d. wet age related macular degeneration
e. retinal vein occlusion
f. retinal detachment
g. optic neuritis

Question 43

central retinal art (sx, 2 causes, 2 features) and vein occlusion (3 risk factors, feature)

Answer 43

art:
sudden unilateral visual loss
due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
features include afferent pupillary defect, ‘cherry red’ spot on a pale retina
vein: differential for sudden painless loss of vision.

Risk factors
increasing age
glaucoma
polycythaemia

Features
sudden, painless reduction or loss of visual acuity, usually unilaterally
severe retinal haemorrhages are usually seen on fundoscopy

Question 44

vitreous haemorrhage 3 causes, 5 sx, 3 ix (and one if open globe injury)

Answer 44

Common causes (collectively account for 90% of cases):
proliferative diabetic retinopathy (over 50%)
posterior vitreous detachment
ocular trauma: the most common cause in children and young adults

Patients typically present with an acute or subacute onset of:
painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision

Signs:
decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
visual field defect if severe haemorrhage

Investigations:
dilated fundoscopy: may show haemorrhage in the vitreous cavity
slit-lamp examination: red blood cells in the anterior vitreous
ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
fluorescein angiography: to identify neovascularization
orbital CT: used if open globe injury

Question 45

retinal detachment (suspect when (2 things), referral, mx (tear v detachment)

Answer 45

reversible cause of visual loss, provided it is recognised and treated before the macula is affected. If left untreated and symptomatic, retinal detachment will inevitably lead to permanent visual loss

should be suspected if patients complain of new onset floaters or flashes, as these indicate pigment cells entering the vitreous space or traction on the retina respectively. Sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery should also raise suspicion of detachment

Any patients with new onset flashes and floaters should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage

Retinal tears or breaks are treated by laser therapy or cryotherapy

detachment is treated with various surgical approaches

Question 46

optic neuritis - 3 causes, 5 sx, ix of choice, mx - one thing for how long

Answer 46

multiple sclerosis: the commonest associated disease
diabetes
syphilis

Features
unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma

Management
high-dose steroids
recovery usually takes 4-6 weeks
MRI is investigation of choice

Question 47

diplopia diffs (6 diffs)

Answer 47

a. third cranial nerve palsy b. fourth cranial nerve palsy c. sixth cranial nerve palsy d. blow out fracture e. thyroid eye disease f. myasthenia gravis

+hypophos and misc others

Question 48

transient visual symptoms 3 diffs inc detail on retinal migraine (2 sx, timecourse)

Answer 48

a. migraine aura but also retinal migraine: symptoms of retinal migraine may include:
partial or total loss of vision in 1 eye – this usually lasts 10 to 20 minutes before vision gradually returns
headache – this may happen before, during or after the vision attack
It’s unusual for an episode of vision loss to last longer than an hour. The same eye is affected every time in almost all cases.
Vision may slowly become blurred or dimmed, or there may be flashes of light. Some people see a mosaic-like pattern of blank spots (scotomas), which enlarge to cause total loss of vision.
b. amaurosis fugax
c. papilloedema

Question 49

amaurosis fugax (inc 5 causes, mx)

Answer 49

wide differential including large artery disease (atherothrombosis, embolus, dissection), small artery occlusive disease (anterior ischemic optic neuropathy, vasculitis e.g. temporal arteritis), venous disease and hypoperfusion
may represent a form of transient ischaemic attack (TIA). It should therefore be treated in a similar fashion, with aspirin 300mg being given
altitudinal field defects are often seen: ‘curtain coming down’
ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve
can think of amaurosis fugax as transient form of central retinal artery occlusion (as TIA is to stroke)

Question 50

papilloedema - 4sx inc time course, 4 fundo findings, causes

Answer 50

a sign of raised icp
Fleeting vision changes—blurred vision, double vision, flickering, or complete loss of vision—typically lasting seconds are characteristic of papilledema. Other symptoms may be caused by the elevated icp

following features may be observed during fundoscopy:
venous engorgement: usually the first sign
loss of venous pulsation: although many normal patients do not have normal pulsation
blurring of the optic disc margin
elevation of optic disc
loss of the optic cup
Causes of papilloedema
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia

Rare causes include
hypoparathyroidism and hypocalcaemia
vitamin A toxicity

Question 51

blepharitis - path -of post and ant, sx, mx

Answer 51

inflammation of the eyelid margins. It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis)

symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur

Management
softening of the lid margin using hot compresses twice a day
‘lid hygiene’ - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
artificial tears if dry eyes

Question 52

stye (ext vs int) and chalazion (inc mx)

Answer 52

Different types of stye are recognised:
external (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum producing) or glands of Moll (sweat glands).
internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)
management includes hot compresses and analgesia. CKS only recommend topical antibiotics if there is an associated conjunctivitis

A chalazion (Meibomian cyst) is a retention cyst of the Meibomian gland. It presents as a firm painless lump in the eyelid. The majority of cases resolve spontaneously but some require surgical drainage
if the mebomium cyst is persistent, recurrent, causing significant astigmatism, cosmetically unacceptable, or there is uncertainty about the diagnosis, refer the person to an ophthalmologist for further management.
An opthalmologist may consider incision and curettage where appropriate, or intra-lesion injection of steroid (may be preferred in children). For recurrent lesions, biopsy may be indicated to rule out meibomium gland carcinoma.
Otherwise, if the person is being managed in primary care, reassure them that a meibomian cyst is usually self-limiting and rarely causes serious complications. Advise the person to:
Apply a warm compress (for example, a clean flannel that has been rinsed with warm water) to the affected eye for 10–15 minutes up to five times a day. Explain that this will encourage drainage of the cyst contents.
Gently massage the meibomian cyst after application of the warm compress (to aid expression of the cyst contents).
(also random note: remember basal cell carcinoma can be on eyelid, dont mistake that for a stye/chalazion)
stye is on the eyelid margin, chalazion is a bit further away and often central

Question 53

herpes zoster ophthalmicus

Answer 53

reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles.

Features
vesicular rash around the eye, which may or may not involve the actual eye itself
Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement

Management
oral antiviral treatment for 7-10 days
ideally started within 72 hours
intravenous antivirals may be given for very severe infection or if the patient is immunocompromised
ocular involvement requires urgent ophthalmology review

Complications
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia

Question 54

posterior vitreous detachment - path, 3 sx, ix inc timecourse to rule out what comps, mx

Answer 54

separation of the vitreous membrane from the retina. This occurs due to natural changes to the vitreous fluid of the eye with ageing. Posterior vitreous detachment is a common condition that does not cause any pain or loss of vision. However, rarely the separation of the vitreous membrane can lead to tears and detachment of the retina. It is important to rule out retinal tears or retinal detachment in anyone with suspected posterior vitreous detachment

The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)
All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.

Management:
Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this

Question 55

subcon haemorrhage

Answer 55

Subconjunctival haemorrhage — this is due to a bleed into the subconjunctival space. There may or may not be a history of a contributory factor, such as straining with coughing or constipation. It may be associated with hypertension.
On examination, there is an area of localized, well-demarcated haemorrhage in one eye, in the absence of pain, no reduction of visual acuity, normal pupil reactions, and no corneal staining.
usually harmless!

Question 56

choroidal nevus and melanoma

Answer 56

Choroidal nevi are benign melanocytic lesions of the posterior uvea. In the United States, their prevalence ranges from 4.6 percent to 7.9 percent in Caucasians.1 By comparison, choroidal melanoma is rare, manifesting in approximately six in 1 million Caucasian individuals.

Choroidal nevi tend to have clearly defined margins and to be flat or slightly elevated, and they remain stable in size. Over time, choroidal nevi display features such as overlying drusen as well as retinal pigment epithelial atrophy, hyperplasia or fibrous metaplasia.
In contrast, choroidal melanomas are more likely to show signs of activity such as relatively indiscrete margins, irregular or oblong configuration, overlying subretinal fluid and orange pigment, and abruptly elevated edges.
Documentation of growth. Most authorities agree that documentation of growth over a relatively short period of time, such as one to two years, is a convincing characteristic of a mitotically active melanoma. However, it is ideal to detect choroidal melanoma before the recognition of growth

Patients with choroidal nevi who show no suspicious features require no treatment. During the first year, they should be monitored twice; subsequently, they should be evaluated annually as long as the nevi remain stable

Question 57

6 tunnel vision diffs

Answer 57

papilloedema (tho more often enlarged blind spot)
glaucoma (open angle)
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria

Question 58

7 blurred vision diffs and ix (inc how to tell if refractive error or not)

Answer 58

vast majority of patients with blurred vision will have long-term refractive errors

Causes
refractive error: most common
cataracts
retinal detachment
age-related macular degeneration
acute angle closure glaucoma
optic neuritis
amaurosis fugax

Assessment
visual acuity with a Snellen chart
pinhole occluders are a useful way to check for whether the blurred vision is due to a refractive error or not
if the blurring improves with a pinhole occluder then likely cause is a refractive error
visual fields
fundoscopy
if gradual onset, corrected by pinhole occluder and no other associated symptoms then an optician review would be the next step
other patients should be seen by ophthalmology. If there are associated symptoms such as visual loss or pain this should be urgent

Question 59

rapd path and 7 causes

Answer 59

Also known as the Marcus-Gunn pupil, a relative afferent pupillary defect is found by the ‘swinging light test’. It is caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina

Finding
the affected and normal eye appears to dilate when light is shone on the affected
causes:
optic neuritis.
ischemic optic disease or retinal disease.
severe glaucoma causing trauma to optic nerve.
direct optic nerve damage (trauma, radiation, tumor)
retinal detachment.
very severe macular degeneration.
retinal infection (CMV, herpes)

Question 60

horner’s syndrome - symps, causes: 4 central, 3 pregang, 3 postgang

Answer 60

miosis, ptosis, anhidrosis
central has anhidrosis of face/arm/trunk and inc stroke, syringomyelia, MS, tumours
pregang has anhidrosis of face only and inc pancoast tumour, thyroidectomy or other trauma, cervical rib
postgang has no anhidrosis and incs carotid art dissestion or aneurysm, cavernous sinus thrombosis, cluster headache

Question 61

mydriasis causes (5, plus 3x drugs)

Answer 61

Causes of mydriasis (large pupil)
third nerve palsy
Holmes-Adie pupil
traumatic iridoplegia
phaeochromocytoma
congenital

Drug causes of mydriasis
topical mydriatics: tropicamide, atropine
sympathomimetic drugs: amphetamines, cocaine
anticholinergic drugs: tricyclic antidepressants
Holmes-Adie pupil is a benign condition most commonly seen in women. It is one of the differentials of a dilated pupil.

Overview
unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light

Holmes-Adie syndrome
association of Holmes-Adie pupil with reduced/absent ankle/knee reflexes

Question 62

nasolacrimal duct anatomy

Answer 62

lacrimal gland is located anteriorly in the superolateral aspect of the orbit, within the lacrimal fossa – a depression in the orbital plate of the frontal bone.

lacrimal fluid produced by the gland is secreted into excretory ducts, which empty into the superior conjunctival fornix. The fluid is then ‘spread’ over the cornea by the process of blinking

After secretion, lacrimal fluid circulates across the eye, and accumulates in the lacrimal lake – located in the medial canthus of the eye. From here, it drains into the lacrimal sac via a series of canals.

The lacrimal sac is the dilated end of the nasolacrimal duct, and is located in a groove formed by the lacrimal bone and frontal process of the maxilla. Lacrimal fluid drains down the nasolacrimal duct and empties into the inferior meatus of the nasal cavity

Parasympathetic:
Preganglionic fibres are carried in the greater petrosal nerve (branch of the facial nerve) and then the nerve of pterygoid canal, before synapsing at the pterygopalatine ganglion.
Postganglionic fibres travel with the maxillary nerve, and finally the zygomatic nerve.
Stimulates fluid secretion from the lacrimal gland

Question 63

Nasolacrimal duct obstruction

Answer 63

most common cause of watering eyes of new-borns is a delay in the normal
development of the nasolacrimal system. It can affect one or both eyes.

NLD is usually developed by the age of 12 months and the symptoms will often settle by this time. You can encourage tear flow and tear duct development by massaging the area on the inside of the upper lid(s) by firm pressure every day. Stickiness and discharge can be cleared away using
clean water and cotton wool. Antibiotics are not needed unless the eye itself
becomes red

If the symptoms do not get better by 12-18 months of age, then ophtho may perform syringe and probing under general
anaesthetic. This procedure uses a very thin
instrument which is passed into the tear duct to open it.

a few infants with NLDO present within the first few weeks of life with a more severe infection: acute dacryocystitis. Clinical findings include edema and erythema with distension of the lacrimal sac below the medial canthal tendon, and patients may have systemic signs of infection such as fever and irritability. This is a rare complication of isolated congenital NLDO. Acute dacryocystitis can be complicated by preseptal or orbital cellulitis, sepsis, or meningitis and should be treated promptly with systemic antibiotics - will need ophtho discussion ?surgery

Question 64

mucocoele/dacrocoele

Answer 64

Dacryoceles, also known as lacrimal sac mucocele are a rare form of congenital nasolacrimal duct obstruction with both proximal and distal obstruction resulting in lacrimal sac enlargement. Usually presenting at birth, there is significant risk for infection. Probing and excision of an associated intranasal cyst under general anesthesia may be needed

may present in 3% of infants with NLDO

Exam reveals a bluish, cystic mass that is located below the medial canthal tendon in the area of the nasolacrimal sac. The medial canthus can be displaced superiorly. Gentle pressure over the mass can produce mucopurulent discharge from the eyelid puncta

Question 65

excessive tearing ddx

Answer 65

aka epiphora

most commonly due to NLDO

most important ddx is infantile glaucoma: it is important for ophthalmic evaluation of infants who have photophobia and other signs of ocular irritation (eg, excessive eye rubbing) to rule out this possibility

also consider allergic and infectious conjunctivitis, entropion, corneal infection, corneal abrasion, foreign body (inc under eyelid)

Question 66

neonatal conjunctivitis

Answer 66

Ophthalmia neonatorum is conjunctivitis of the newborn occurring within the first 28
days of life.
A sticky eye is a relatively common problem in infancy. It is often simply due to a
blocked lacrimal duct but may also be caused by a variety of bacterial and viral
pathogens

Causes associated with potentially severe outcomes, and which are not detected by
routine bacterial eye swabs:
 Neisseria gonorrhoeae
 Chlamydia trachomatis
 Herpes simplex virus
Ask for maternal Sexually Transmitted Infection’s in history taking

sx:
* Redness (conjunctiva +/- lids)
* Discharge (may be profuse in gonococcal infection)
* Swelling of lids (may be severe)
Symptoms usually bilateral (but may be sequential with few days between onset of
each eye)

gono: Hyperacute conjunctival injection
and chemosis, lid oedema and
severe purulent discharge (incubation 1-3 days), complications corneal ulceration and
perforation
Rarely, disseminated infection
chlam: Unilateral/bilateral watery discharge
which becomes copious and purulent
later on, 5-28 days incubation, Chlamydial pneumonia (10- 20% chance in infants of untreated mothers)

discuss cases with ophtho, take 3 swabs (routine, NAAT, viral) and start chloramphenicol eye drops for all, adding on below if needed
for chlam - PO erythro for 14 days, assess for pneumonitis and admit if any resp involvement, otherwise senior review and discharge
for gon - assess for sepsis; Cefotaxime 100mg/kg IV single dose (max
1g). IM stat dose can be given if baby is
difficult to cannulate; if well home after senior review
for HSV - admit, IV aciclovir

If gonococcal or chlamydial infection confirmed, parent(s) should be referred to
Genito-Urinary Medicine (GUM) clinic

Question 67

congenital glaucoma

Answer 67

pathogenesis of primary congenital glaucoma is unknown and is currently described as a developmental defect with obstruction at the trabecular meshwork

characterized by the clinical triad of epiphora, blepharospasm and photophobia, but these symptoms are often missed. For example, epiphora may be mistaken for congenital nasolacrimal duct obstruction.

The patient usually presents because of corneal clouding and ocular enlargement: glaucoma should be suspected in any child with a corneal diameter greater than 13.0 mm.

needs urgent ophtho referral for IOP measurement, inspection of optic nerve etc

Most infants with primary congenital glaucoma who present between 3 months and 1 year of age will have their IOP controlled by one or two angle surgeries

Question 68

retinal dev and ROP

Answer 68

To function properly, the retina needs
a constant supply of blood to provide
oxygen. The blood vessels that supply this
blood usually develop between weeks 16
and 36 of pregnancy.
If a baby is born early, and the
development of these blood vessels is
incomplete, there will be areas on the
retina that do not receive enough oxygen.
This triggers the production of chemicals
to produce new blood vessels.
These new blood vessels are fragile and
can leak blood causing scarring. This pulls
the retina out of position, affecting the
baby’s ability to see properly

All babies less than 31 weeks gestational age (up to 30 weeks and 6 days)
or less than 1501g birth weight should be screened for retinopathy of prematurity

For infants born before 31+0 book the first screen as soon as both the criteria below are met

Babies must be at least 4 weeks old
Babies must be 31+0 weeks corrected gestational age or more

For infants born from 31+0 (who weight 1500g or less) book the first screen as soon as the infant is:

4 weeks old
OR
Is 36 weeks corrected gestational age

Usually then screen every 1-2 weeks

screening can be stopped when retinal
vascularization has extended into Zone 3

If the baby has a mild form of retinopathy, they will not need any treatment as their condition will resolve itself and the retinopathy will not affect their vision as they grow older

Treat infants in whom a screening examination has detected:
* Zone I any stage ROP with plus disease
* Zone I stage 3 ROP without plus disease
* Zone II stage 2 or 3 with plus disease

ROP in zone I should be treated with an intravitreous injection of an anti-VEGF agent
ROP in zone II should be treated with transpupillary laser