Ophthalmology AS Flashcards
What is an afferent defect?
No direct response but intact consensual response
Cannot initiate consensual response in contralateral eye
Dilatation on moving light from normal to abnormal eye.
Due to a total CN II lesion.
What is a relative afferent pupillary defect?
Marcus-Gunn Pupil
Features
- Minor constriction to direct light
- Dilatation on moving light from normal to abnormal eye
- RAPD = Marcus Gunn Pupil
Damage to the affect pathway (retina or optic nerve). Due to consensual pupillary relaxation response form healthy eye.
Due to:
optic neuritis
Optic atrophy
retinal disease
Afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
What is the efferent defect?
Features
- Dilated pupil does not react to light
- Initiate consensual response in contralateral pupil
- Ophthalmoplegia + ptosis
What is the cause of an efferent defect?
3rd nerve palsy
- The pupil is often spared in a vascular lesion as pupillary fibres run in the periphery.
Differential for a fixed dilated pupil?
Mydriatics - tropicamide
Iris Truma
Acute Glaucoma
CN3 Compression: tumour, coning.
Features of Holmes- Adie Pupil?
Young women with sudden blurring of near vision.
Initially unilateral and then bilateral pupil dilatation
Dilated pupil has no response to light and sluggish response to accommodation
- A tonic pupil
Investigations
- Iris shows spontaneous wormy movements on slit-lamp examination
- Iris streaming
Cause of a holmes-adie pupil?
Damage to postganglionic parasympathetic fibres
- Idiopathic: may have viral origin
Holmes-Adie Syndrome?
Tonic pupil + absent knee/ankle jerks + decreased BP.
Horner’s syndrome features?
Damage to sympathetic nerves
Ptosis: partial
Enophthalmos
Anhydrosis
Small pupil
Ptosis + constricted pupil = Horner’s
Causes of horner’s syndrome?
Distinguishing cause
- Heterochromia (difference in iris colour) in congenital Horner’s.
- Anhidrosis
Central = Anhidrosis in face, arm and trunk.
- Syringomyelia
- MS
- Wallenberg’s Lateral Medullary Syndrome
- Tumour
- Encephalitis
Pre-ganglionic - Anhidrosis of face
- Pancoast tumour: T1 nerve root lesion. Presents with shoulder and arm pain due to Brachial plexus invasion. Check smokign history.
- Trauma: CVA insertion or CEA
- Thyroidectomy
- Cervical rib
Post-ganglionic
- Cavernous sinus thrombosis
- Usually 2ndry to spreading facial infeciton via the ophthalmic vein
- CN 3, 4, 5, 6 palsies.
- Cluster headache
- Carotid artery dissection
What is an Argyll robertson pupil?
Features
- Small, irregular pupils
- Accommodate but doesn’t react to light. Prostitute.
- Atrophied and depigmented iris
Caused by
- DM
- Quaternary Syphilis
What are the features of optic atrophy?
Decreased acuity Decreased colour vision Central scotoma Pale optic disc RAPD
Causes of Optic atrophy?
MS and glaucoma most common.
Congenital: Leber’s hereditary optic neuropathy
Hereditary motor + Sensory neuropathy
Friedrich’s ataxia
retinitis pigmentosa
- EtOH
- Ethambutol
- Lead
- B12 deficiency
Compression
- Neoplasia: optic glioma, pituitary adenoma
- Glaucoma
- Paget’s
Vascular: DM, GCA Inflammatory: MS, Devic's Sarcoid/other granulomatous Infection: herpes zoster Oedema: papilloedema Neoplastic infiltration: lymphoma, leukaemia
Visual history - Red eye history, exam and differential?
Vision
- Blurred
- Distorted
- Diplopia
- Field defect/Scotoma
- Floaters
Sensation
- Irritation
- Pain
- Itching
- Photophobia
- FB
Appearance
- Red? Distribution
- Lump
- Puffy lids
Discharge
- Watery
- Sticky
- Stringy
Key examination questions for red eye?
Inspect from anterior to posterior Is acuity affected Is the globe painful Pupil size and reactivity Cornea: intact, cloudy? Use florescein
Signs of serious disease in red eye?
Photophobia
Poor vision
Corneal fluorescein staining
Abnormal pupil
What are the differentials for the eyelid?
Mechanical - ectropion (lower eyelid sags) , entropion (sages inwards) , trichiasis (eyelashes rubbing eyes)
Inflammation - Blepharitis, Chalazion (blockage of mebobian gland)
Infection
- Preseptal cellulitis
- Orbital cellulitis
What are the differentials for conjunctiva?
Mechanical - Sub conjunctival haemorrhage
Inflammation - allergic conjunctivitis
Infection - Conjunctivitis
What are the differentials for the sclera
Mechanical - Perforation
Inflammation - chemical burn, episcleritis, scleritis
Infection
What are the differnetials for the cornea?
Foreign body
Abrasion
Keratitis - infection
What are the differentials for anterior chamber?
Acute Glacuoma
Iritis/Uveitis
Endophthalmitis
How does acute glaucoma present?
- Very painful
- NO photophobia
- Decreased acuity - loss of peripheral vision first.
- Hazy/cloudy cornea
- Pupil is large
- very increased IOP
Systemic upset may be seen, such as nausea, vomiting and abdo pain.
How does anterior uveitis present?
Painful photophobia Decreased acuity normal cornea small pupil Normal IOP
How does conjunctivitis present?
- a little pain
- Photophobia
- Normal acuity
- normal cornea
- normal pupil
- normal IOP
What is acute closed angle glaucoma?
Blocked drainage of aqueous humour from anterior chamber via the canal of Schlemm
Pupil dilatation (e.g at night) worsens the blockage
Intraocular pressure rises from 15-20 –> >60mmHg.
Risk factors of ACAG?
- Hypermetropia (long-sightedness)
- Shallow anterior chamber
- Female
- FH
- Increased Age
Drugs
- Mydriatic drops
- Anti-cholinergics
- Sympathomimetics
- TCAs
- Anti-histamines
Symptoms of ACAG?
Prodrome: rainbow haloes around lights at night-time
- Severe pain with n/v
- Decreased acuity and blurred vision
Examination of ACAG?
Cloudy cornea with circumcorneal injection
Fixed, dilated, irregular pupil. DILATED!
Increased IOP makes eye feel hard.
Investigations of ACAG?
Tonometry: increased IOP (>40)
Acute management for ACAG?
Refer to ophthalmologist
- Pilocarpine: 2-4 drops stat: miosis opens blockage. Miosis is constricting the pupil.
- Topical B-B: timolol decreased aqueous formation
- Acetazolamide 500mg IV stat: decreased aqueous formation.
Analgesia and antiemetics.
Subsequent management of ACAG?
Bilateral YAG peripheral iridotomy once IOP decreased medically.
A Yag capsulotomy is a special laser treatment used to improve your vision after cataract surgery. It is a simple, commonly performed procedure which is very safe.
What is the pathophysiology of anterior uveitis?
Uvea is pigmented part of eye and includes: iris, ciliary body and choroid
Iris + ciliary body = anterior uvea
Iris inflammation involves ciliary body too
Symptoms of anterior uveitis?
Acute pain and photophobia Blurred vision (Aqueous precipitates)
Examination of eye in anterior uveitis?
Small pupil initially, irregular later. May be small, fixed oval shaped. Circumcorneal injection Hypopyon: pus in anterior chamber White precipitates on back of cornea Talbots test: increased pain on convergence
Associations with uveitis?
Seronegative arthritis: AS, psoriatic, Reiter’s
HLA-B27
Still's/JIA IBD Sarcoidosis Behcet Infection: TB, leprosy, syphilis, HSV, CMV.
Management of anterior uveitis?
Refer to ophthalmologist
prednisolone drops
Cyclopentolate drops: Dilates pupil and prevents adhesions between iris = atropine too! = mydriatic
Stay on TROP = Big/wide.
piLOWcapine = Small
Steroid eye drops.
What is episcleritis?
PAINLESS = Episcleritis
Inflammation below the conjunctiva in the episclera
Presentation
- Localised reddening; can be moved over sclera
- watering and mild photophobia.
- Painless/mild discomfort
- Acuity preserved
Causes of episcleritis?
Usually idiopathic
May complicate RA or SLE
Management: Topical or systemic NSAIDs.
What is scleritis?
Painful = SCLERA
Vasculitis of the sclera
Presentation
- Severe pain: worse on eye movement
- Generalised scleral inflammation
Vessels wont’ move over sclera
- Conjunctival oedema.
What are the causes of scleritis?
WEgener’s
RA
SLE
Vasculitis
Management of scleritis?
Refer to specialist
Most need corticosteroids or immunosuppressants
Complications of scleritis?
Scleromalacia - globe perforation
What is conjunctivitis?
Presentation
- Often bilateral with purulent discharge
Bacterial: Sticky (staph, strep, haemophilus)
Viral: watery
- Discomfort
- Conjunctival injection: Vessels may be moved over the sclera.
- Acuity, pupil responses and cornea are unaffected.
Causes of conjunctivitis?
Viral: adenovirus. Serous discharge, recent URTI, preauricular lymph nodes.
Bacterial: staph, chlamydia, gonococcus. Eyes may be stuck together in morning.
Allergic
Manangement of conjunctivitis?
Don’t share towels, school exclusion not necessary.
Bacterial: chloramphenical 0.5% ointment. Given 2-3hrly initially where as ointment is given qds initially.
Use fusidic acid in pregnant women.
Allergic: anti-histamine drops e.g emedastine
What is a corneal abrasion ?
Epithelial breech without keratitis
- Cause: trauma
Symptoms
- Pain
- Photophobia
- Blurred vision
Investigations
- Slit lamp: fluorescein stains defect green.
Management
- Chloramphenicol ointment for infection prophylaxis.
Causes of a Corneal ulcer + keratitis (corneal inflammation)
Causes
- Bacterial, herpetic, fungal, protozoea, vasculitic (RA).
Due to steroid eye drop which leads to fungal infection leading to corneal ulcer. Not causative
May get a dendritic ulcer = Herpes Simplex. This leads to herpes simplex keratitis. Gold crusted lesions = Herpes.
Acanthamoeba: Protazoal infection affecting contact lens wearers swimming in pools.
Presentation of corneal ulcer?
- Pain, photophobia
- Conjunctival hyperaemia
- Decreased acuity
- White corneal opacity.
Risk factor of corneal ulcer?
Contact lens wearer
Investigations for corneal ulcer?
Green with fluorescein on slit lamp.
Management of corneal ulcer?
Refer immediately to specialist who will
- Take smears + Cultures
- Abx drops, oral/topical aciclovir
- Cycloplegics/mydriatics ease photophobia
- Steroids may worsen symptoms: professional only
Can lead to scarring and visual loss.
What is ophthlamic shingles ? - Herpes Zoster Ophthalmicus
20% of all shingles
Presents with pain in CNV1, dermatome precedes blistering rash
40% –> keratitis, iritis.
Hutchinson sign - nose-top zoster due to involvement of nasociliary nerve also supplies globe. Likely to have ocular involvement.
if this is present there is risk of ocular development therefore MUST be referred to ophthalmology.
Ophthalmic involvement
- Keratitis + corneal ulceration (fluorescein stains)
± iritis.
- Post-herpetic neuralgia
Management
- Oral antiviral treatment for 7-10 days.
- ideally started within 72hrs.
- IV antivirals given for very severe infection.
Key questions in sudden vision loss?
Sudden painless loss of vision
- Ischaemic/vascular (thrombosis, embolism, temporal arteritis). Included recognised syndromes (Occlusion of central retinal vein + occlusion of central retinal artery). Amaurosis fugax (can be large or small artery occlusion). Can be from a TIA therefore give aspirin 300mg.
Curtain coming down.
Central retinal vein occlusion
Central retinal artery occlusion
Vitreous haemorrhage
Retinal detachment
- Dense shadow that starts peripherally progresses towards the central vision
A veil or curtain over the field of vision
Straight lines appear curved
Central visual loss
Vitreous haemorrhage
- Large bleeds cause sudden visual loss
Moderate bleeds may be described as numerous dark spots
Small bleeds may cause floaters
Headache associated: GCA
Eye movement hurt: optic neuritis
Lights/flashes preceding visual loss: detached retina
Like curtain descending: TIA, GCA
Poorly controlled DM: vitreous bleed from new vessels.
What is anterior ischaemic optic neuropathy?
- Optic nerve damaged if posterior ciliary arteries blocked by inflammation or atheroma.
Pale/swollen optic disc.
What can cause anterior ischaemic optic neuropathy?
Arteritic AION: Giant cell arteritis
Non-arteritic AION: HTN, DM, Increased lipids, smoking.
What is optic neuritis?
- Unilateral loss of acuity over hrs-days usuallynot immediately.
- decreased colour discrimination (Dyschromatopsia) - red desaturation
- Eye movement may hurt
Signs of optic neuritis?
- Decreased acuity
- Decreased colour vision
enlarged blind spot - Optic disc may be: normal, swollen, blurred.
- Afferent defect
- Central scotoma.
Causes of optic neuritis?
MS (45-80% over 15yrs) if >3 white matter lesions.
DM
Drugs: ethambutol, chloramphenicol
Vitamin Deficiency
Infection: zoster, lyme disease, syphilis.
Management of optic neuritis?
High-dose methyl-pred IV for 72hrs
Then oral pred for 11/7.
What is a vitreous haemorrhage?
Bleeding
- From new vessels: DM
- Retinal tears/detachment/trauma
RF: Diabetes, trauma, anticoagulants, severe short sightedness.
Presentation for vitreous haemorrhage?
Small bleeds –> Small black dots/ring floaters. Red tinged vision along with dark spots.!!!!
Large bleed can obscure vision –> No red reflex, retina can’t be visualised.
Patients present with cobwebs in the eye, which are floaters. Past medical history of DM, 50% due to proliferative diabetic retinopathy.
Investigations of vitreous haemorrhage?
May used B scan US to identify cause
Management of vitreous haemorrhage?
VH undergoes spontaneous absorption
Vitrectomy may be performed in dense VH/
Central retinal artery occlusion?
- Dramatic unilateral visual loss in seconds
- Afferent pupil defect (may precede retinal changes)
- Pale retina with cherry-red macula. Very pale with bright red macula.
Causes of CRAO?
GCA
Thromboembolism: clot, infective, tumour
Management of central retinal artery occlusion?
If seen within 6hr aim is to return retinal blood flow by decreased IOP.
- Ocular massage
- Surgical removal of aqueous
- Anti-hypertensive (local and systemic)
Central Retinal vein occlusion?
Central
- commoner than arterial occlusion
Causes : arteriosclerosis, Increased BP, DM, Polycythaemia
Presentation: Sudden unilateral visual loss with RAPD
Fundus: Stormy sunset appearance/Pizza.
- Tortuous dilated vessels
- haemorrhages
- Cotton wool spots
Complications
- Glaucoma - can be due to glaucoma.
- Neovascularization
Prognosis: possible improvement for 6mo-1yr.
Branches of the retinal vein occlusion?
Present - Unilateral visual loss
Fundus: segmental fundal changes
Complication: Retinal ischaemia –> VEGF release and neovascularization (management: laser photocoagulation) .
Retinal detachment presentation and management?
Holes/tear in retina allow fluid to separate sensory retina from retinal pigmented epithelium.
- May be secondary to cataract surgery, trauma, DM.
- Floaters: Numerous, acute onset, ‘spiders-web’
- Flashes
- Field loss
- Fall in acuity
- Painless
- Curtain down the wall.
Fundus: grey, opalescent retina, ballooning forwards.
Management of retinal detachment?
Urgent surgery + referral ot ophthalmologist.
Vitrectomy + gas tamponade with laser coagulation to secure the retina?
Causes of transient visual loss?
Vascular: TIA, migraine
MS
Subacute glaucoma
Papilloedema
What is the cause of gradual visual loss?
Common
- Diabetic retinopathy
- Age related macular degeneration
- Cataracts
- Open-angle glaucoma
Rarer causes of gradual visual loss?
Genetic retinal disease: retinitis pigmentosa
HTN
Optic atrophy
What is age-related macular degeneration (ARMD)
Commonest cause of blindness >60
30% of >75yr old will have dry AMD
Risk factors for ARMD?
Smoking
increased age
Genetic factors
What is the presentation of ARMD?
Elderly pts
central visual loss
Loss of vision of near field objects.
Blurring of small words and straight lines appearing curvy.
Difficulties in dark adaption.
Fluctuations in visual disturbance which may vary significantly from day to day.
Photopsia
Dry ARMD: geographic atrophy?
Drusen: fluffy white spots around macula. D for Dry
Degeneration of macula
Slow visual decline over 1-2 yrs.
Wet ARMD: subretinal neovascularitisation?
Aberrant vessels grow into retina from choroid and –> haemorrhage
Rapid visual decline (sudden/days/wks) with distortion.
Fundoscopy shows macular haemorrhage –> scarring.
Amsler grid detect distortion
Investigations for gradual visual loss?
Fluorescein angiography = neovascular ARMD is suspected. Guide intervention with anti-VEGF therapy. May see choroid neovascularization.
OCT: optical coherence tomography
Gives high resolution images of the retina.
Management of wet AMRD?
Wet
- Intravitreal VEGF inhibitors
- Bevacizumab (Avastin)
- Ranibizumab
This is for dry! Vitamins, photodynamic then photocoagulation. Antioxidant vitamins (A,C,E, K) + zinc may help early ARMD.
Chronic simple (open-angle glaucoma)
Pathogenesis
- Depends on susceptibility of pts retina and optic nerve to increased IOP damage.
- Trabecular network functionally offers an increased resistance to aqueous outflow, causing increased IOP.
Here- iris is clear of meshwork.
IOP >21mmHg –> decreased blood flow and damage to optic nerve –> optic disc atrophy + cupping.
Presentation of CS (open-angle) glaucoma?
Peripheral visual field defect: superior nasal first.
Central field is intact therefore acuity maintained until late
- Presentation delayed until optic nerve damage is irreversible.
Screening for CS glaucoma?
- > 35
- Afro-Caribbean
- FH
- Drugs: Steroids
- Co-morbidities: DM, HTN, - migraines
- Myopia (different to hypermetropia in acute closure glaucoma).
If there is a family history - screen form 40yrs. Normally at opticians.
Investigtions for CS glaucoma?
Tonometry: IOP >24 mmHg
Fundoscopy: cupping of optic disc.
- Optic disc cupping >0.7. Occurs as loss of disc substance makes optic cup widen and deepen.
- OPtic disc pallor - indicating optic atrophy.
- Bayonetting of vessels - breaks as they disappear into deep cup.
Visual field assessment: peripheral loss
Corneal thickness measurement
- Gonioscopy to assess peripheral anterior chamber
Management of CS glaucoma?
Life-long f/up.
Eye-drops to decrease IOP?
1st line: Prostaglandin analogues
- Latanoprost, travoprost
- Increased uveoscleral outflow. once a day. Post so after so increase outflow.
SE: increased eyelash length iris pigmentation and periocular pigmentation.
2nst line: b-blockers
- Timolol, betaxolol
- Decreased aqueous production
- Caution in asthma, heart failure
alpha2-agonist
- Brimonidine, apraclonidine
- decreased aqueous production and increased uveoscleral outflow
- AVOID if taking MAOI or tricyclic antidepressant.
Carbonic anhydrase inhibitors
- Dorzolamide, acetazolamide
Miotics
- Pilocarpine
Non-medical options for open-angle glaucoma?
Laser trabeculoplasty
-Surgery (trabeculectomy) is used if drugs fail
New channel allows aqueous to flow into conjunctival bleb.
Commonest cause of blindness worldwide?
Trachoma Cataract Glaucoma Keratomalacia: vitamin A deficiency Onchocerciasis Diabetic Retinopathy
The problem with diabetes in the eye?
DM is the leading cause of blindess up to 60yrs
30% have ocular problems @ presentation
BP<130/80 and normoglycaemia –> Decreased diabetic retinopathy
How does DM increase risk of cataract?
DM accelerates cataract formation
Lens absorbs glucose which is converted to sorbitol by aldose reductase
How does DM increase risk of retinopathy?
- Microangiopahty –> occlusion
- Occlusion –> ischaemia –> new vessel formation in retina
Bleed –> vitreous haemorrhage
Carry fibrous tissue with them –> retinal detachment
Occlusion also -> cotton wool spots (ischaemia)
Vascular leakage -> Oedema and lipid exudates
Rupture of microaneurysms –> blot haemorrhages
Screeening for diabetic retinopathy?
All diabetics should be screened annually
Fundus photography
Refer those with maculopathy, NPDR and PDR to ophthalmologist
Investigation for DM in eye?
Fluorescein angiography
Management of DM in eye?
Good BP and glycaemic control
Rx concurrent disease: HTN, dyslipidaemia, renal disease, smoking, anaemia
Laser photocoagulation
- Maculopathy: focal or grid
Nice concentric circles.
- Proliferative disease: pan-retinal (Macula spread).
CN palsies in diabetes?
CN 3 (pupil may be spared) and 6 Palsies may occur
Fundoscopy findings in background retinopathy?
Background retinopathy: Leakage
- dots: Microaneurysm
- Blot haemorrhages
- Hard exudates: yellow lipid patches
Fundoscopy findings in pre-proliferative retinopathy?
Cotton-wool spots (infarcts - soft exudates)
Venous beading
Dark haemorrhages
Intra-retinal microvascular abnormalities
Severe preproliferative = widespread microaneurysms and dot-and-blot haemorrhages, venous beading in 2 or more and IRMA in at least one quadrant.
Mild = Only microaneurysm
Moderate PPDR = Not severe.
Findings on proliferative retinopathy?
New vessels
Pre-retinal and vitreous haemorrhage
REtinal detachment
Maculopathy?
Caused by macular oedema
Decreased acuity may be only sign
Hard exudates within one disc width of macula
What is the presentation of cataracts?
- Increasing myopia (near sightedness)
- Blurred vision –> gradual visual loss
- Dazzling in sunshine/bright lights
- Monocular diplopia
A defect on red reflex - reddish orange reflection through ophthalmoscope when light is shone on retina.
Types of cataracts
- 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
Causes of cataracts?
Age: 75% of >65yrs old DM Steroids - especially subcapsular. Located behind the capsule. Often present with glare from bright lights. Congenital - Idiopathic - Hypocalcaemia - DM - Downs - Long-term steroids - Infection: rubella - Metabolic: Wilson's - Myotonic dystrophy = dot cataracts. - myopia = nuclear cataracts - Allopurinol = less strong associated with subcapsular.
Investigation of cataracts?
Visual acuity
Dilated fundoscopy
Tonometry
Blood glucose to exclude diabetes
Conservative management of cataracts?
Glasses
Mydriatic drops and sunglasses may give some relief
Surgery for cataracts?
Consider if symptoms affect lifestyle or driving
NICE - refer to surgery dependent on whether a visual impairment is present + impact on quality of life. Therefore even if there is minor affect on visual acuity refer.
Day case surgery under LA
- Phacoemulsion + lens implant
1% risk of serious complications
- Anterior uveitis/iritis
- VH
- Retinal detachment
- Secondary glaucoma
- Endophthalmitis
Post-op capsule thickening is common - manage with laser capsulotomy.
Retinal detachment
Posterior capsule rupture
Endophthalmitis
Post-op eye irritation is common and requires drops.
What is the retina?
- Outer pigmented layer in contact with the choroid
- Inner sensory layer in contact with vitreous
- At centre is fovea
Optic disc colour?
Should be pale pink
Paler in optic atrophy
Contour of optic disc?
- Margins blurred in papilloedema and optic neuritis
Cup of the optic disc?
Physiological cup lies centrally and should occupy 1/3 of disc diameter
Cup widening and deepening in glaucoma.
Retinitis pigmentosa?
Most prevalent inherited degeneration of the macula
Various modes of inheritence
- Mostly AR
- AD has good prognosis
Presentation
- night blindness
- Decreased visual fields - tunnel vision
- Most are registrable blind by mid 30s (<3/60).
Fundoscopy
- Pale optic disc: optic atrophy
- Peripheral retina pigmentation: spares the macula.
- Bone spicule appearance with thinner, blacker lines.
= Mottling of the retinal pigment epithelium .
Associations of retinitis pigmentosa?
Friedrich's ataxia Refsum disease Usher's syndrome Lawrence-Moon-Biedl syndrome Kearns-Sayre syndrome Alports
Retinoblastoma?
Comonest intraocular tumour in children
- Hereditary type differers.
5% occurs with pineal or other tumours
- Increaed risk of osteosarcoma and rhabdomyosarcoma
Signs
- Stabismus
- Leukocoria (white pupil) –> no red reflex
Rx
- depends on size
- Options include: chemo, radio,enucleation
What is a stye?
Abscess or infection in a lash follicle which points outwards
- Local abx - fusidic acid
- External: (hordeolum externum) infection of gland of Zeis or glands of Moll (sweat)
- Internal (hordeolim internum): infection of Meibomian glands leaving residual chalazion
- Management = Hot compression and analgesia.
What is a chalazion?
Abscess of the meibomian gland which points inwards onto conjunctiva
- Sebaceous gland of eyelid
Most resolve spontaneously but some require surgical drainage.
What is blepharitis?
Chronic inflammation of eyelid
Causes: Seborrhoeic dermatitis, staphs - dry skin of the eyes. Also common with patients with rosacea.
Meibomian gland secrete oil to prevent rapid evaporation of tear film.
Features
- Red eyes
- Gritty/itchy sensation
- Scales on lashes
- Often associated with rosaea
Management - Clean crusts of lashes with warm soaks
May need fusidic acid drops.
Lid hygiene - mechanical removal of debris from lid margins. Artificial tears.
Styes and chalazions more common.
Entropion?
Lid inversion –> corneal irritation
Degeneration of lower lid fascia
If left untreated this patient may develop a corneal ulcer.
Definitive management of entropion is surgical although eye lubircants + tap may be used whilst waiting for surgery.
Ectropion?
Low lid eversion –> watering and exposure keratitis
Associated with ageing and facial nerve palsy.
Ptosis?
Ture ptosis is intrinsic LPS weakness - Levator palpebrae superioris
Causes of bilateral ptosis?
Congenital
Senile
MG
Myotonic dystrophy
Causes of unilateral ptosis?
3rd nerve palsy
Horner’s syndrome
Mechanical: xanthelasma, trauma.
Lagophthalmos
Difficulty in lid closure over the globe which may –> Exposure keratitis
Causes: exophthalmos, facial palsy, injury.
Management - Lubricate eye with liquid parafinn ointment
Temporary tarsorrhaphy may be needed if corneal ulcers develop
Pinguecula?
yellow vascular nodules either side of cornea
Pteryguim?
Similar to pinguecula but grows over the cornea - decreased vision
Benign growth of conjunctiva
Associated with dusty, wind-blown lifetyles, sun exposure.
What is orbital cellulitis?
Infection from paranasal sinuses, eyelid or external eye
Staph, pneumococcus, GAS.
Presentation of orbital cellulitis?
Usually a child with inflammation of the orbit + lid swelling
Pain and decreased range of eye movement
Exophthalmos
Systemic signs - fever
± tenderness over the sinuses
NB: reduced visual acuity, proptosis, ophthalmoplegia, pain with eye movements are NOT consistent with periorbital cellulitis.
Management of orbital swellings?
when suspected - contrast enhanced CT scan of the orbits, sinuses and brain should be considered to support the diagnosis and to search for possible complications.
Medical emergencies.
IV Abx: Cefuroxime
Complications
- Local extension –> Meningitis and cavernous sinus thrombosis
- Blindness due to optic nerve presure
What is a carotico-carvernosus fistula?
May follow carotid aneurysm rupture with reflux of blood into cavernous sinus
Causes: spontaneous, trauma
Presentation - engorgement of eye vessels
- Lid and conjunctival oedema
- Pulsatile exophthalmos
- Eye bruit
Manage with oral antiviral: aciclovir
Exophthalmos/Proptosis?
Protrusion of one or both eyes
Graves disease - Anti-TSH abds –> retro-orbital inflammation and lymphocyte infiltration –> swelling.
Orbital cellulitis
Trauma
Other causes of exophthalmos?
Idiopathic orbital inflammatory disease Vasculitis: Wegeners - Neoplasm - Optic glioma lyphoma
Carotico-carvernous fistula
Myopia?
Short sightedness
Distant objects are focussed too far forward
Causes
- Genetic
- Excessive close work in the early decades
Solution
- Concave lenses
Astigmatism?
Cornea or lens doesn’t have same degree of curvature in horizontal and vertical planes
- Image of object is distorted longitudinally or vertically
Need correcting lenses
Hypermetropia- long-sightedness
Eye is too short
When eye relaxed and not accomodating, objects behind the retina.
Need convex lenses.
What is esotropia?
Convergent squint
- Commonest type in children
Towards the nose.
When covering left eye will move laterally from nasal to take up fixation.
Features ambylopia
What is exotropia
Divergent squint
- Older children
Towards to temporals.
Superiorly = Hypertropia Inferiorly = Hypotropia.
Ambylopia. Don’t normally have double vision as they adapt.
Non-paralytic squint
Concomitant = imbalance in extraocular muscles.
Corneal reflection: should fall centrally and symmetrically over each cornea
Cover test: movement of uncovered eye to take up fixation demonstrates manifest squint.
Management of non-paralytic squint?
Refer to ophthalmologist and orthoptist.
Optical: correct refractive errors
Orthoptic: patching good eye encourages use of squinting eye
Operations: e.g resection + recession of rectus muscle - help alignment
What is a paralytic squint?
Diplopia is most on looking in direction of pull of paralysed muscles
Eyes won’t fixate on covering
Cover each eye in turn: which ever eye sees the outer image is malfunctioning
CNIII
Ptosis (LPS)
Fixed dilated pupil (no parasympathetic)
Eye looking down and out
Causes
- Medical: DM, MS, infarction
- Surgical: Increased ICP, cavernous sinus thrombosis, posterior communicating artery aneurysm
CNIV
Diplopia especially on going down stairs
Head tilt
Test: Can’t depress in adduction
- Cause
Peripheral: DM, trauma, compresion
Central: MS, vascular, SOL
CNVI
Eye is medially deviated and cannot abduct Diplopia in the horizontal plane Causes - Peripheral: DM, compression trauma - Central: MS, vascular, SOL
Managment: botulinum toxin can eliminate need for surgery
What is orbital blowout frature?
Blunt injury –> Sudden increased in orbital pressure with herniation of orbital contents into maxillary sinus
Presents
- Ophthalmoplegia + diplopia
Tethering of inferior rectus + inferior oblique
- Loss of sensation to lower lid skin = Infraorbital nerve injury
- Ipsilateral epistaxis: Damage to anterior ethmoidal artery
Decreased acuity
Irregular pupil that reacts slowly to light.
Management of orbital blowout fracture?
Fracture reduction + muscle release necessary
Chemical injury to eye?
Alkalmine solutions are really bad.
Manage = copious irrigation
Specialist referral.
What are floaters?
Small dark spots in the visual field
Sudden shower of floaters in one eye may be due to blood or retinal detacment
Causes of floaters?
Retinal detachment VH Diabetic retinopathy Old retinal branch vein occlusion Syneresis
Flashes cause?
Either from intraocular or intracerebral pathology
Headache, n/v, migraine
Flashes and floaters: retinal detachment
Haloes?
Usualyl just diffractive phenomena
May be caused by hazy ocular media –> Cataract, corneal oedema, acute glaucoma
Haloes + Eye pain - Acute glaucoma.
jagged haloes which change shape are usually migrainous .
Allergic eye disease - seasonal allergic conjunctivits?
50% of allergic eye disease
Small papillae on tarsal conjunctiviae (Bulging)
- Management: Antazoline - antihistamine drops topically.
Cromoglycate: inhibitis mast cell degranulation need to be applied for several weeks to attain optimal prophylactic benefit.
Perennial allergic conjunctivitis?
Symptoms all year with seasonal exacerbation
- Manage with olopatadine (antihistamine + mast cell stabiliser)
Giant papillary conjunctivitis?
Iatrogenic FBs: Contact lension, sutures
Giant papillae on tarsal conjunctivae therefore remove FB/
Management of allergic eye disease?
Remove allergen General measurs - Cold compression - Artificial tears - Oral antihistamines: Loratadine
Eye drops
- ANtihistamines: antazoline
- Mast cell stabilisers: cromoglycate
- Steroids - dexamethasone
- NSAIDS: diclofenac
What is a trachoma?
Caused by chlamydia trachomatis
spread by flies
- inflammatory reaction under lids –> scarring –> lid distortion –> entropion –> Eyelashes scatch cornea
–> ulceration –> blindness
Management = tetracycline 1% ointment.
What is onchocerciasis (river blindness)
Caused by nematode Onchocerca
- spread by flies
Invades eye, leads to fibrosis, corneal opacitiies and synechiae
Ivermectin as management
What is xerophthalmia and keratomalcia?
Manifestations of Vitamin A deficiency
- Night blindness + dry conjunctivae (xerosis)
- Corneal ulceration + perforation
Manage with Vitamin A palmitate reverses early corneal changes.
What are the stages of hypertensive retinopathy?
- Tortuosity and silver wiring
- AV nipping
- Flame haemorrhages + soft/cotton wool spots. If they just have cotton-wool spots makes it 3.
- Papilloedema
SAFE
- Silver wiring + Tortuosity. Arteriolar narrowing.
- AV nipping
- Flame and cotton wool
- Papilloedema.
Which granulomatous disorders causes uveitis and choriodoretinitis?
TB, Sarcoid, Toxo, leprosy, brucella
Which inflammatory diseases cause conjunctivitis
SLE, reactive arthritis, IBD
Which inflamamtory diseases cause scleritis/epislepritis?
RA, vasculitis, SLE, IBD
Which inflammatory disease cause iritis?
Ank Spond
IBD
Sarcoid
Which inflammatory disease can cause retinopathy?
Dermatomyositis
What is keratoconjunctivitis Sicca?
Sjogrens
- Decreased tear production (Schirmer’s <5mm in 5m ins
- Dry eyes and dry mouth
- Primary or secondary: SLE, RA, Sarcoid
Management with artificial tears or saliva
Amaurosis fugax?
GCA
Carotid atheroemboli
Microemboli of the eye?
Roth spots
Infective endocarditis
Kayser-fleisher rings
Wilsons
Exophthalmos
Graves
Corneal calcification
HPT
HIV eye related disease?
CMV retinitis: Pizza-pie fundus + flames
HIV retinopathy: cotton wool spots
What are mydriatics?
Eye dilators
Anti-muscarinics
- Tropicamide
Duration: 3hr
Cyclopentolate
- duration:24hr (paediatrics)
Used in pupil dilatation
Cyclopelgia –> blurred vision
Sympathomimetics
- Para-hydroxyamphetamine
- may be used with tropicamide
- Don’t affect the light reflex.
Indications
- Eye examination
Miotics?
Effects
- Constrict pupil
Pilocarpine
- Muscarinic agonist
Used in –> Acute closed-angle glaucoma
Papilloedema?
Optic disc swelling that is caused by increased intracranial pressure. Almost always bilateral.
- On fundoscopy =
venous engorgement,
the loss of venous pulsation.
Blurring of optic disc margin. elevation of optic disc.
Loss of optic cup.
Paton’s lines: concentric/radial retinal lines cascading from optic disc.
Causes of papilloedema
- SOL
- Malignant HTN
- Idiopathic intracranial HTN
- Hydrocephalus
- Hypercapnia
Therefore hypocapnia via hyperventilation can be used to reduced ICP. Increased PaCO2 leads to arterial vasoconstriction lowing cerebral blood flow.
Hutchinson’s pupil?
Unilateral dilated pupil is unresponsive to light. A result of compression of the oculomotor nerve of the same side. By an intracranial mass.
Nasolacrimal duct obstruction?
Persistent watery eye in an infant. Caused by imperforate membrane.
Usually at the lower end of the lacrimal duct.
teach parents to massage the lacrimal duct
symptoms resolve in 95% by the age of one year. Unresolved cases should be referred to an ophthalmologist for consideration of probing, which is done under a light general anaesthetic
Tunnel Vision?
Papilloedema Glaucoma retinitis pigmentosa Choroidoretinitis Optic atrophy secondary to tabes dorsalis hysteria
Causes of mydriasis?
Third nerve palsy Holmes-Adie Pupil Traumatic iridoplegia Phaechromocytoma Congenital
Drugs
- Topical: tropicamide, atropine
Sympathomimetic drugs: amphetamines, cocaine
- Anticholinergic drug: tricyclic antidepressants.
Macular hole?
Similar to age-related macular degeneration.
Well-defined round or oval lesions in the macular with yellow deposits at the base.
No choroidal neovascularisation
Differentials for red eye?
Acute angle closure glaucoma
- severe pain (may be ocular or headache)
- decreased visual acuity, patient sees haloes
- semi-dilated pupil
- hazy cornea
Anterior uveitis
- acute onset
- pain
- blurred vision and
- photophobia
- small, fixed oval pupil, ciliary flush
Scleritis
- Severe pain and tenderness
(episcleritis = painless)
Conjunctivits
- Purulent discharge or clear if viral
Subconjunctival haemorrahge
- history of trauma or coughing bouts
Endophthalmitis
- Typically red eye, pain and visual loss following intraocular surgery.
Babies with minor purulent discharge?
Take swab samples to detect chlamydia and gonococcus.
Must take swabs first.
Posterior vitreous detachment
Natural changes to the vitreous fluid of the eye with ageing. Not associated with pain or loss of vision. Can ead to tear of the membrane. Therefore need to rule this out.
Highly myopic (near sighted) patients have an increased risk.
vitreous shrinks and pulls away from retina. 10% of patients with PVD develop retinal tear.
- Flashes of light (photopsia) - in the peripheral field of vision
Floaters, often on the temporal side of the central vision
Weiss ring on ophthalmoscopy.
Investigations
- patients must be seen by ophthalmologist within 24hrs.
Management
- Normally does not need treatment as improves and not associated with permanent loss of vision.
