Opthalmology Flashcards
What is present in background diabetic retinpathy
Microaneurysms, blot hemorrhages, hard exudates, cotton wool spots
What questions should be asked when taking an opthalmic history?
- Did the problem start suddenly or gradually?
- Painful or painless?
- Transient of persistent?
- Unilateral or bilateral?
- Is the vision blurred: centerally or both centerally and peripherally
- Is there and associated distortion or double vision
- Are the symptoms there all the time?
Causes of an acute red eye?
Conjuntivities
Scleritis
Keratitis
Anterior uveitis
Corneal forigen body
Episcleritis
Subconjunctival haemorrhage
An acute red eye is usually painful or uncomfotable, what might be the cause if it is not?
Subconjunctivial haemorrhage
Vision in conjunctivitis?
Normal
Vision in scleritis?
Either normal or reduced
Vision in keratitis?
Reduced
Vision in anterior uveitis?
Normal or reduced
Vision in episcleritis?
Normal
Will a corneal forigen body reduce vision?
Sometimes, depedning on where the FB is
Vision in subconjuncitival haemorrhage?
Normal
What might be the cause of reduced vision and red eye in a patient found to have normal IOP?
Corneal abrasion
Keratitis
Endophthalmitis
What might be the cause of reduced vision and red eye in a patient found to have increased IOP?
Acute glaucoma
Anterior uveitis
What might cause a sudden, painless loss of vision, of a few seconds of duration?
Unilateral:
Giant cell arteritis
Optic disc swelling (infectious, inflammatory)
Impending central retinal vein occlusion
Bilateral:
Disc swelling due to idiopathic intracranial hypertension (visual obscurations)
What might cause a sudden, painless loss of vision, of a few minuites of duration?
Unilateral:
Amaurosis fugax
Giant cell arteritis
Bilateral:
Vertebrobasilar artery insufficiency
How long might visual loss from migraine aura last?
Up to 1 hour
What is visual obscurations?
Disc swelling due to idiopathic intracranial hypertension
What might cause a painful sudden loss of vision?
CORNEAL ABNORMALITY - Keratitis
DISC ABNORMALITY - optic neuritis
UVEA ABNORMALITIY - anterior uveitis
NORMAL FUNDUS - retrobulbar optic neuritis
Generalised causes of gradual visual loss?
Refractive error
Cataract
Central causes of gradual visual loss?
Abnormal macula (e.g. age related macular degeneration, macula oedema, diabetic maculopathy)
Abnormal optic disc (optic neuritis)
Peripheral or pathy causes of gradual loss of vision?
Abnormal choroid/retina (e.g. posterior uveitis)
Abnormal optic disc (e.g. glaucoma)
Causes of monocular diplopia?
Due to pathology from affectsed eye
Abnormal refraction
Abnormal cornea
Abnormal lens
Abnormal iris
(Normal examination - not diplopia)
e.g. cataract, corneal abrasion, eyelid cyst
What might cause binocular diplopia?
Pathology in the nerves, neurmuscular junction or muscles
Intermittent/variable:
Myasthenia gravis (NMJ)
Intranuclear opthalmoplegia
Giant cell arteritis
Persistent:
Neurogenic - cranial nerve palsies
Myogenic - congenital (rare) or acquired (e.g. thyroid)
Ocular clinical features of myasthenia gravis?
Variable diplopia/pstosis - usually worsening towards evening/with exercise
What determines IOP?
Balance of aqueous production and aqeous drainage
How is glaucoma treated?
Aim: stop or slow progression.
Only option is aim to lower the pressure - by reducing production or increasing drainage
- Drugs: topical or oral - production/drainage?
- Laser (irodotomy) - production/drainage
- Surgery: trabeculectomy (less common) -drainage
NB. pressure is a risk factor not a given
What drugs can be used to decrease IOP in glaucoma and how do they act?
Drops:
- Alpha agonists: reduce aqueous production and increase drainage
- Beta blockers: reduce aqueous production only
- Carbonic anhydrase inhibitors: reduce aqueous production only
- Prostaglandin analogues: increase aqueous drainage only
Tablets:
Carbonic anhydrase inhibitors
What is a trabeculectomy and how is it utilised in glaucoma?
Sclera incised, new channel (bleb) through which aqueous fluid can drain is created.
Restoring the eye’s ability to drain aqeuous humour reduced IOP
How does acute angle closure glaucoma typically present?
Patients over 50, usually female
Unilateral eye pain
Watering eye
Bad headache
Typically starts in evening
Progression to N&V
Patients may report collapsing ‘‘off legs’’
Reduced vision
Red eye
Corneal odeama
Fixed mid dilated pupil
High IOP
What is the 7th cranial nerve responsible for?
Motor: Facial expression
Sensory: taste and sensation in the mouth
Parasympathetic: salivary & lacrimal glands
What will be effected in a proximal facial nerve palsy, at point of nerve root?
Motor, parasympathetic and sensory function
Paralysis of nerves of facial expression
Loss of taste and sensation in mouth
Dry mouth and eyes
What will be affected in a facial nerve palsy just distal to the geniculate ganglion?
Chorda typania nevre paraysis - loss of taste on anterior two thirds of tounge
Loss of parasympathetic innervation to the salivary glands - dry mouth
Loss of motor innervation enterirely: facial muscle and stapedius muscle paralysis
Intact: Sensory innervation to the soft palate (taste buds) (greater pretosal nerve), parasympathetic innervation to the lacrimal gland and glands of the nasal mucosa, sensory innervation to the skin of external ear (wuth vagus)
What will happen in a facial nerve palsy at the level of the stylomastoid foramen?
Paralysis of facia muscles (temporal zygomatic buccal mandibula and cervical branches compromised)
Loss of sensation to skin of external ear
Rest of sensory innervation and the paraysympathetics are intact (taste and sesnation in mout intact, salivary and lacrimal glands still inverated)
Causes of facial palsy?
Bells palsy (75%)
Viral - HSV/VZV (VZV+ramsey hunt syndrome)
Chronic otitis media
Iatrogenic
Tumour - cerbellopontine angle
Cerebrovascular (brainstem or supranuclear)
Rare; DM, MS, lyme disease
What is Ramsay Hunt syndrome?
An acute peripheral facial neuropathy that occurs as a complication of shingles. It causes hearing loss and facial paralysis.
Symptoms of Ramsay Hunt syndrome?
A painful red rash with fluid-filled blisters on, in and around one ear
Facial weakness or paralysis on the same side as the affected ear
Ear pain
Heating loss
Tinitus
Difficulty closing one eye
Vertigo
Change or loss of taste
Dry mouth
Dry eyes
What are the opthalmic manefestations of Ramsay Hunt syndrome?
Lagophthalmos (can’t close eye)
Dry eye
What are the opthalmic manefestations of Ramsay Hunt syndrome?
Lagophthalmos (can’t close eye)
Dry eye
Symptoms of facial nerve palsay?
Unilateral facial weakness
Rapid onset
Dribbling from mouth
Sore, red eye
(Be suspicious if pain or other cranial nerves involved)
Opthalmic manefestations of facial nerve palasy?
Bell’s phenomenon - rolling up of eye onclosure - present in 80% of population but detoriorates with age
Lagophthalmos - failure of lids to meet on closure, can be measured in mm, needs to be assesed with Bell’s phenomenon
What should be checked (in terms of the eye) in facial nerve palsay, to establish risk of corneal ulceration and scarring?
Corneal sensation - if absent this significantly increased the risk of corneal ulceration & scarring
How can acute eye protection be provided in management of facial nerve palsy?
Lubricant ointment: lacrilub or simple eye ointment
Cross taping if needed (no patching)
When might you further investigate facial nerve palsy?
Worring features or slow recovery
MRI brain, brainstem and facial nerve
Electroneurography if available
How is facial nevre palsy managed?
Acute eye protection (drops, taping)
Acyclovir PO for 7 days if ?viral aetiology
Prednisolone
Referral: eye casualty or OPD, ENT, facial nerve clinic
Recovery of Bells plasy?
85% recovery starts within 3 weeks
16% wil be left with a perminent deficity and &% with have a recurrent epidose
How is Ramsay-Hunt syndrome different in its presentation compared to other facial nerve palsies?
Pain is a prominent deature
Prognosis of Ramsay Hunt Syndrome
60% full recovery
Why should pathcing be avoided in facial nerve palsy?
Causes corneal alcers
Acute eye management in facial nerve palsy?
Copuous lubrucant ointment
What causes an afferent pupillary defect?
Complete potent nerve lesion
What is found in an afferent pupillary defect?
Affected pupil is stimulated neither eye reacts
When the normal pupil stimulated both eyes react
Involved eye is blind
What is RAPD
Relative afferent pupil defect/ Marcus Gunn pupil
Defect caused by an incomplete optic nerve lesion
What is found in a relative afferent pupil defect
The affected side will react to light more Weasley when compared to the normal side
The difference between the level of function between these nerves can be exploited by the swinging flashlight test
What is the normal reaction to swinging flashlight test?
Both pupils constrict when light shone into non-tested side
Flashlight off both eye temporarily as swings - pupils start to dilate
Light shone to the tested side - pupils constrict
What will happen in swinging flashlight test in RAPD
both pupils constrict when light shone into non tested eye
Flashlight off both eye temporarily swings - pupils start to dilate
Both pupils continue to dilate when swung to tested side
Causes of relative afferent pupillary defect?
Optic nerve aetiology:
Optic neuritis
Optic nerve tumours (glioma, meningioma)
Trauma to optic nerve ie. Surgery
Pressure on optic nerve (TED)
Advanced unilateral glaucoma
Retinal aetiology:
Sever retinal pathology: retinal detachment, CRVO, CRAO
What is the action of the EOM lateral rectus, and which nerve is it innervated by?
aBduction
CN 6 Abducens
What is the action of the EOM medial rectus, and which nerve is it innervated by?
ADuction
CN3 occulomotor
What is the action of the EOM superior recuts, and which nerve is it innervated by?
Elevation (and aduction and intorsion)
CN 3
What is the action of the EOM inferior rectus, and which nerve is it innervated by?
Depression (Aduction, extortion)
CN3
What is the action of the EOM superior oblique, and which nerve is it innervated by?
Depression (abbduction, intorsion)
CN4 trochlear
What is the action of the EOM inferior oblique, and which nerve is it innervated by?
Elevation (aBduction, extorsion)
CN3 occulomotor
Which EOMs does the Abducens nerve, CN6, supply?
Lateral recuts
Which EOMs does the occulomotor nerve, CN3, supply?
Medial rectus
Inferior rectus
Superior rectus
Inferior oblique
Which EOMs does the trochlear nerve, CN4, supply?
Superior oblique
What might be seen in a nerve palsy of CN6 (abducens)
Esotropia in primary postion
Inability to aBduct the eye
No issues with aDuction
Symptoms of CN6 (abducens) nerve palsy?
Binocular Diplopoda (images side by side)
Worse in direction of impaired muscle
Pt may turn their head into the direction of the impaired field
Causes of CN6 (abducens) nerve palsy?
Most common: microvascular: DM, HTN
Stroke
Acoustic neuroma
Acute petrositis
Raised cranial pressure
Differentials for CN6 (abducens) nerve palsy?
Medial wall #
Myasthenia
Features of CN4 (trochlear) nerve palsy?
Vertical diplopia (difficulty walking downstairs, looking down and in)
Left hypertropia
WOOG - hypertropia worse on opposite gaze
BOOT - better on opposite tilt
Causes of CN4 (trochlear) nerve palsy?
Common: vascular, trauma
Uncommon: aneurysm, tumour
What does the occulomotor nerve (CN 3) innervate?
Ocular muscles (SR, IR, MR, IO) (all except LR and SO)
Levator palpebrae superioris
Spinchter pupillae (parasympathetic)
Symptoms of CN3, occulomotor nerve palsy?
Opthalmoplegia
Affected eye down and out
Pupil size (dilated)
Lid droop
Ptosis
Causes of dilated pupil?
Pupil involved - aneurysm (post communicating artery), tumour, cavernous sinus lesion, pituitary apoplexy
Pupil sparing - ischemia micro vascular disease (common) GCA
Symptoms associated with papiloedema?
Transient visual field loss
Enlarged blind spot
Headaches
n and v
What are the most important causes of papilodema to exclude?
Intracranial tumours
Other masses - brain abscess
Meningitis/encepahilitis
Most common cause of paipilodema?
Idiopathic intracranial hypertension
Risk/associated factors for IIH (idiopathic intracranial hypertension)
Obesity
Weight gain
Pregnancy
OCP
Tetracylcines
How is idiopathic intracranial hypertension diagnosed?
Normal MRI V
INcreased opening pressure on lumbar puncture
How is IIH treated?
Diamox (acetylzolamide)
Optic nerve decompression
Neurosurgical shunts
How might optic neuritis present?
Unilateral gradual visual loss
Loss colour vision
Pain on extraocular movements
Causes of optic neuritis?
MS most common
Viral infections
Granulomatosis inflammation - TB sarcoidosis syphlis
What is internuclear ophthalmoplegia? (INO)
Weakness of aDuction of affected eye and horizontal jerk Nystagmus of aBducting other eye
Caused by lesion in the medial longitudinal fasciculus (connects 3rd and 6th nerves on opposite sides)
Most common cause is MS
What could cause loss of red reflex and leucokoria?
Cataracts
Retinoblastoma
Pseudoleukocoria
Retinal detatchment
ROP
Coats disease
Warrents urgent referral - retinoblastoma is fatal if mets, cataracts can cause amblyopia
What can cause cataracts in childhood?
Intrauterine infection - rubella, varicella
Metabolic - galastosaemia, hypocalcaemia, diabetes
Trauma
Radiation
Inherited - autosomal dominant, recessive or X-linked
Chromosomal - trisomy 21, trisomy 13
How should childhood cataracts be investigated?
Urinalysis: for glucose and also urinary reducing substances in younger children
Infants: blood calcium and glucose, test for galactokinase deficiency
Referal to paediatricians and geneticists should be considered
What is coloboma?
Eye abnormality caused by failure of closure of optic fissure.
Can occur in isolation or be associated with lens and retinal coloboma
If optic disc coloboma involves macula area, vision is poor, nystagmus and strabismus may be present. Can also be associated with microphthalmos?
What causes ptosis in children?
Congenital (most common, due to dystrophy or dsygenesis of levator muscle)
Neurogenic (third nerve palsy, marcus Gunn jaw-winking, Horner syndrome)
Trauma
Myogenic (progressive external opthalmoplegia, myasthenia gravis)
Pseudoptosis (excess skin from resolving haemangioma, enophthalmos, hypotropic eye)
How can coloboma be managed in young adults?
Cosmetic contact lenses
When can congenital ptosis be managed surgically?
Once the child is able to cooporate with local anesthesia, as young as 9 or 10
What should be looked for in significant ptosis in children with congenital ptosis?
Early signs of amblyopia
Clinical features of Horners syndrome?
Miosis – anisocoria greatest in the dark (failure of dilator pupillae muscle)
Ptosis – mild (1 to 2mm)
Ipsilateral anhidrosis
Heterochromia (light irides on affected side)
What will be found in pharmacological testing in horners syndrome with cocaine?
Normal pupil will be dilated by 10%, abnormal will not
Causes of horners syndrome in children?
Neuroblastoma
Syringomyelia
Trauma
What should all children with anisocoria which is not physiological undergo?
Urinary catecholamine analysis (VMA - vanilymandelic acid)
Causes of Horner syndrome in adults?
Pancoast tumour - lung apex
Trauma
Mets
Internal carotid dissection
What are myelinated nerve fibres associated with?
Gorlin syndrome
Retinal dystrophy with night blindness
Limb deformities
Extensive unilateral myelination can be associated with high myopia amblyopia
What is CHRPE?
Congenital hypertophy of retinal pigment epithelium
Usually have no visual or systemic problems
What is important to exclude in patients with congenital hypertrophy of retinal pigment epithelium (CHRPE)?
Gardner syndrome (adenomatous polyposis of colon and extracolonic manifestations)
Ocular findings to exclude in congenital toxoplasmosis?
Microphthalmos, cataracts, panuveitis, optic atrophy
What can be associated with congenital toxoplasmosis?
Chorioretinitis
Epilepsy
Hydrocephalus
Microcephaly
Intracranial infection
How can you demonstrate a shallow anterior chamber?
Oblique flashlight test
What should be included in a history from a patient with a red eye?
Onset
Location (unilateral/bilateral/sectoral)
Pain/discomfort (gritty, FB sensation, itch, deep ache)
Photosensitivity
Watering +/- discharge
Change in vision (blurring, halos)
Trauma
Contact lens wear
Previous ocular history
PMH
What might cause localized eyelid tenderness?
Hordeolum
Chalazion
Opthalmic causes of photophobia?
Cornial abrasions
Iritis
Acute glaucoma
Causes of halo vision?
Corneal edema (acute glaucoma, contact lens overwear)
How to examine a patient with a opthalmic complaint?
► Inspect whole patient
► Visual acuity- each eye - WITH GLASSES/CONTACT LENSES TO MEAUSRE CORRECTED ACUITY (IF FOR DISTANCE) + pinhole
► Eye movement (ask about double vision)
►Visual fields (arms width apart max, level with pt eyeline)
► Symettry positions of eyballs (hypoglobus)
► Eyelids (lid retraction, ptosis, blepharitis, eczema, etc)
► Conjunctiva (bulbar and palpebral, diffuse or local redness, injection, haemorrhage)
► Cornea (clarity, staining with fluorescein, sensation, localised opacity)
► Anterior chamber (depth) - with slit lamp
► Pupils shape/ reaction to light / accomodation / RAPD
►Lense
►Vitreous
►Fundus - fundoscopy (retina)
►Optic nerve
What is ciliary flush and when might it be seen?
Injection of deep conjuncitval vessels and episcleral vessels surrounding the cornea
Seen in iritis and acute glaucoma - not seen in simple conjuncitvits
What is conjunctival hyperemia?
Engorgement of more superficial vessels
Nonspecific sign
Lid related causes of acute red eye?
blepharitis
marginal keratitis
trichiasis
chalazion
stye
sub tardal foreign body
dacrocystitits
Conjunctiva related causes of red eye?
bacterial conjuncitvitis
gonococcal conjunctivitis
chlamydial conjunctivitis
viral conjunctivitis
allergic conjunctivitis
subconjuncitvital haemorrhage
episcleritis vs scleritis
Cornea related causes of red eye?
bacterial keratitis
herpetic keraitits
forigen body
Anterior chamber related causes of red eye?
anterior uveitis/iritis vs viritis
What is blepharitis
Inflammation of the lid margin
Characterized by: lid crusting, redness, telangectasia, misdirected lashes
Styes and conjunctivitis are often associated
Often caused by staphylococcus and other skin flora major causes
Often meibomian gland abnormality
Older patients may have dry eye
Symptoms of blepharitis?
Forigen body sensation/gritty
Itching
Redness
Mild pain
How is blepharitis treated?
Lid hygiene
Topical antibiotics
Lubricants
Doxycycline - meibomian gland disease and rosacea
What is marginal keratitis?
Hypersensitivity to staphylococcal exotoxins
Associated with chronic stahplococcal blepharitis
Subepithelial marginal infiltreate separated from the limbus by a clear zone
FB sensation
How is marginal keratitis treated?
Short course of topical low dose steroids
Treat associated blepharitis
What is trichiasis?
Inward turning lashes
Idiopathic/secondary to chronic blepharitis/herpes zoster opthalmicus
Presents with FB sensation and tearing
Treated with lubricants epilation, electrolysis (few lashes), cryotherapy - many lashes
What is an internal hordeolum and how is it treated?
Acute chalazion
Staphylococcal infection of the meibomian (tarsal) gland
Tender nodule within the tarsal plate
May be associated cellulititis
Treated with hot compress, topical antibiotic ointment, incision and drainage once the infection subsides
What is an external hordeolum and how is it treated?
Stye or hordeolum
Staphylococcal abscess of lash follicle and its associated glands of Zeiss or Moll
Tender nodule in the lid margin pointing through the skin
Treated with a hot compress, epilation of lash associated with the infected folicle and topical antibiotic ointment
How do you manage a subtarsal forigen body?
Evert eyelid while patient looks downwards and removed with cotton bud
Stain with flourescein for abrasion
+/- abx
Common causeative organisms bacterial conjuncitvitis?
Staph aureus
Staph epidermis
Strep pneumoniae
Haemophilus influenzae
How is bacterial conjunctivitis aquired?
Direct contact with infected secretions
Symptoms of bacterial conjunctivitis?
Subacute onset
Redness
Grittiness
Burning
Mucopurulent discharge
Often bilateral
(No photophobia)
Signs of bacterial conjuncitivits?
Crusty lids
Conjunctival hyperaemia
Mild papillary reaction
Lids and conjuncitiva may be odematous
How would you manage bacterial conjuncitvitis?
Swab if uncertain
Topical antibiotics, effective in 2 to 7 days (except in very severe infections)
Chloramphenicol or fusidic acid are a appropriate first line treatments
What is chlamydial conjunctivitis?
Veneral infection - chlamydia trachomatis serotypes D to K
Sexually active patients
Chronic with a mild keratitis
How does chlamydial conjunctivitis?
Usually unilateral
FB sensation
Lid crusting with sticky discharge
Follicles
No response with topical antibiotics
How is Chlamydial conjunctivitis managed?
Swab/smear: direct monoclonal flourescent antibody microscopy, PCR
Treat with topical tetracycline/oral doxycycline/azithromycin
Contact trace
GUM referral
What causes viral conjunctivitis?
Most commonly adenoviral
Adenovirus types 3, 4 and 7 - pharyngoconjunctival fever (PCF)
Adenovirus types 8 and 9 -epidemic keratoconjunctivitis
Symptoms of viral conjunctivitis?
Acut onset
Bilateral
Watery discharge
Grittiness
Soreness, FB sensation
Often no photophobia
History of URTI
Associated: follicles, haemorrhages, inflammatory membranes, lymphadenopathy (preauricular node), keratitis
How is viral conjunctivitis managed?
Self resolving up to two weeks
Advice - very contagious
Topical steroids for keratitis if risk of scarring
Symptoms/signs of allergic conjunctivitis?
Itchy
Bilateral
wattery discharge
Chemosis (odema)- swollen conjunctive
Papillae (can be giant cobblestone in chronic cases)
Viral vs allergic conjuncitvitis?
Viral not typically itchy
Management of allergic conjunctivitis?
► Investigation
Exclude infection (generally viral is NOT itchy)
IgE levels ? Patch testing
► Treatment (severity dependent)
- cold compresses
- remove (reduce) allergen
- NSAIDS
- antihistamines oral/ topical (olapatanol)
- mast cell stabilizers (sodium cromoglycate)
- topical corticosteroids
- Immunosuppressants (cyclosporin) for steroids
How does spontaneous subconjunctival haemorrhage present and how is it managed?
Painless red eye w/o discharge
VA not affected
Clear borders
Masks conjunctival vessels
Check BP
No treatment (lubricants)
10-14 days to ressolve
Clotting and FBC to be done if recurrent
What is episcleritis, how does it present and how is it managed?
► Episcleral inflammation
► Localized (sectoral) or diffuse
► Symptoms/Signs:
Often asymptomatic
Mild tearing/ irritation
Tender to touch but not particularly painful
Vessels blanch with phenylephrine
► Self-limiting (may last for months)
► Treatment
Lubricants
NSAIDS (Froben po 100mg tds)
Rarely low dose steroids (predsol)
What is scleritis, how does it present?
Scleral inflammation with maximal
congestion in the deep vascular plexus
RED EYE
► Symptoms/Signs:
Pain (often severe boring)
Significant ocular tenderness to movement
and palpation
Watering and photophobia
Appearance bluish-red
► Localized
► Diffuse
► Nodular
What causes scleritis and what is it commonly associated?
Usually immune rather than infectious, most commonly with RA
How is scleritis managed?
Underlying condition managed
NSAIDs
Corticosteroids
Immunosupression
What is pterygium?
Fibrovascular growth from the conjunctiva onto the cornea
How is pterygium managed?
Excision of pterygium - covering of defect with a conjunctival autograft or amniotic membrane
Adjuvant mitomycin - reduce recurrence
Corneal abrasion/foreign presentation and management
History
► Severe pain esp with blinking
► Watering ++
► Remove FB with cotton bud if
able under topical anaesthetic
► Chloramphenicol ointment,
cyclopentolate, double pad
► Abrasion crossing visual axis
refer
► High impact history hammering/
grinding with out protective eye
wear- exclude intraocular
foreign body
Causative organisms of bacterial keratitis?
Staph aureus
Strep pyogenes
Strep pneumoniae
Pseudomonas aeruginosa
Risk factors for bacterial keratitis?
Contact lense wear (extended, soft lenses)
Pre existing chronic corneal disease e.g. neurotrophic keratopathy
Bacterial Keratitis: signs and symptoms
Ocular pain
Watering discharge
Foregin body sensation
Descreased vision
Photophobia
Corneal lesion (ulcer) - can spread rapidyly
Corneal oedema
Hypopyon - pus level (sterile) seen in eye
How do you investigate bacterial keratitis?
Culture - blood agar, chocolate agar, sabran agar
How is bacterial keratitis managed?
Treated with ofloxacin
Initially hourly, subequently 2 hrly (waking hours)
Tapered
Cyclopentolate tds
Steroids when cultutres become sterile and evidence of improvement (7-10 days initiation of treatment)
What is herpes simplex keratitis?
Reactivation of laternt herpes simplex virus type 1 (which lies dormant in the trigeminal ganglion)
Migrates down branch of the trigeminal nerve to cornea
Form of corneal blindness
Pts have a hx of cold sores, run down, stress
Signs/symptoms of HSV keratitis?
Tearing (epiphoria)
Light sensitivity
Pain hyperaemia
Corneal sensation reduced
Geographic amoeboid ulcer esp if incorrect use of steroid
Under slit lamp examination with fluorescein applied, dendritic ulcers may be seen, which are pathogonomic of the infection
How is herpes simplex keraititis managed?
Topical aciclovir ointment 5X/day 10-14 days
Cyclopentolate
Topical steroids to minimise scarring
Aciclovir PO for up to a year
Corneal scarring may cause blindness if untreated
How does hepres zoster present and how is it treated?
► Reactivation
► Crusting and ulceration of skin
innervated by 1st division of
trigeminal nerve
► Lesions to tip of noseHutchinson’s sign, increased
chance ocular involvement
► Tx
1. Oral aciclovir within 48hrs of
onset of vesicles 800mg 5x day
for 7 days (No effect if later)
2. Aciclovir ointment within 5/7 of
onset of vesicles
Ocular complications include
conjunctivitis, uveitis, keratitis,
scleritis, optic neuritis
What is anterior uveitis (iritis)?
Inflammation of the anterior uveal tract
Idiopathic (70%)
Associated with systemic disease: sarcoid, ankylosing spondilitis, IBD, Reiter’s syndrome, Psoriatic arthritis, Juvenile Chronic arthritis, HLA B27
What can cause uveitis?
Idiopathic (70%)
Infection: bacteria - TB syphillis, leprosy, viral: HSV, HZV, HIV, fungal (candida), protozoa: toxopasmosis, infestation (most vascular structure in the body hence why infection can cause uveuitus),
Autoimmune: sarcoid, SLE, MS bechets, vogt koyanagi
Drugs: Bisphiosphonates, rifabition, cidofovir (antiviral)
Post-trauma:
Sympathetic opthalmia
Lens induced
Post-op
Retinoblastoma, lymphoma
How does anterior uveitis (iritis) present?
Pain (ache)
Photophobia - due to cillary muscle spasam
Blurred vision
Reduced visual acuity
Floaters (cell clumps in vitreous body)
Perilimbal conjunctival injection
Pupil miotic/poorly reactive (sphincter muscle contraction constricts pupil)
Lacrimation (excessive tear production)
Abnormally shaped pupil due to posterior synechiae (adhesions) pulling the iris into abnormal shapes
A hypopyon is a collection of white blood cells in the anterior chamber, seen as a yellowish fluid collection settled in front of the lower iris, with a fluid level
Cillary flush
Slit-lamp examination of anterior uveitis (iritis) - what is seen and why?
Flare (protein) in AC - (can’t see beam in non inflamed eye)
Cells in AC
Keratic precipitates (WBC on the back of the cornea)
Hypopyon - level of sterile pus vidable
Iris inflammed
Odema of iris leaky
WBC leak anteriorly into aqueous humour (cells visable on slit lamp)
Number of cells determines the severity
How is anterior uveitis (iritis) managed?
Steroids (oral, topical or intravenous) May need sub conjunctival steroid if very severe. Initially topical steroids can be as often as half hourly in severe cases
Cycloplegic-mydriatic medications such as cyclopentolate or atropine eye drops. Cycloplegic means paralysing the ciliary muscles. Mydriatic means dilating the pupils. Break synechiae, comfort.
Cyclopentolate and atropine are antimuscarinic medications that blocks to the action of the iris sphincter muscles and ciliary body. These dilate the pupil and reduce pain associated with ciliary spasm by stopping the action of the ciliary body.
Immunosuppressants such as DMARDS and TNF inhibitors
Laser therapy, cryotherapy or surgery (vitrectomy) are also options in severe cases.
How might you investigate repeated attacks of anterior uveitis?
CXR
Lumbar XR
Autoimmune serology
HLA B27
Full blood count
U and E
LFT
Q Gold
Treponemal antibody
Specific test based on aetiolofy (PCRs, HLA B27, MRI (MS), HLA b51 (bechets), Anti DsDNA (SLE) Satcoid - ACE, X ray, vitreous biopsy
Bilateral or severe cases
Why is acute angle closure an opthalmic emergency?
Needs immediate treatment to prevent irreversible glaucomatous damage from raised intraocular pressure
How is aqueous humour produced and drained?
Produced by the ciliary body in the posterior chamber of the eye
It diffuses from the posterior chamber, through the pupil, and into the anterior chamber
From the anterior chamber, the fluid is drained into the vascular system via the trabecular meshwork and Schlemm canal contained within the angle
Aetiology of acute angle closure?
Peripheral iris blocking the outflow of aqueous humour
What might predispose to acute angle closure?
Anatomical factors: relatively anterior location of iris-lens diaphragm (plateau iris), shallow anterior chamber, floppy iris
Female (anterior chamber is shalloweer)
Asian
Hypermetropia
Fhx
Avg. age 60 years
Signs and symptoms of acute angle closure?
Severe ocular pain
Headache
Nausea and vomiting
Decreased vision
Coloured haloes around lights
Photophobia
Semi-dilated non reactive pupil
Cilary injection
Corneal oedema
Shallow AC
Flare in AC
Raised IOP
Tense on palpation
How is acute angle closure treated?
IF delay in admission:
Lie patient on their back without a pillow
Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
Give acetazolamide 500 mg orally
Given analgesia and an antiemetic if required
Medical: to lower the pressure IOP
Topical steroid
Iopidine
Pilocarpine
Acetazolamide (oral or IV)
Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in the eye
Timolol is a beta-blocker that reduces the production of aqueous humour
Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour
Brimonidine is a sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow
Surgical: Laser iridotomy - curative, prophylactically to unaffected eye
Pre-septal vs orbital cellulitis
Prespetal - infection of the subcutaneous tissues anterior to the orbital septum. CONFINED TO SOFT TISSUES ANTERIOR TO ORIBTAL SEPTUM
Usually follows periorbital trauma or dermal infection
Systemic illness rare
Orbital - infection and inflammation within the orbital cavity producing orbital signs and symptoms
Most commonly secondary to ethmoidal sinusitis
Proptosis, chemosis, opthalmoplegia, decreased visual acuity
(Both: bacterial infection usually resultss from local spread of adjacent URTI
Erythema, induration, tenderness of eyelid
Swelling so sevre pt cannot open eye)
What is the orbital septum?
Fibrous membrane that originates from the orbital periosteum and inserts into the anterior surface of the tarsal plate of the eyelid
Seperates the eyelid into preseptal and post septal areas
Preseptal cellulitis caustive ogranisms
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus
Orbital cellulitis causative organisms
Strep pneumoniae and pyogenes,
Staph aureus
Haemophilus influenzae,
anaerobes
What should be acertained in a history from a patient with either orbital cellulitis or preseptal cellulitis?
Recent URTI
Trauma
Sinus disease
Recent dental work or infection
Systemic symptoms - fever
CNS symptoms - headache, neck stiffness
How is pre-septal cellulitis managed?
Mild: augmentin or first generation cephalosporin, warm compress, topical antibiotics for concurrent conjunctivitis
Failure to respond withing 48-72hrs conside iv abx
How is orbital cellulits managed?
Immediate referral
Admit for IV abx
+/- imaging
Risks associated with orbital cellulitis?
Raise intraocular pressure
Endopthalmitis
Optic neuropathy
Meningitis
Cavernous sinus thrombosis
Superiosteal/orbital infections
Different severities of ocular blunt trauma?
Mild to moderate: bruise ocular tissues, eyewall intact
Moderate to severe - ruptured eye wall, severe consequences
Types of ocular trauma?
Foreign bodies
Corneal abrasions
Disruption of globe
Introcular FB
Hyphemas
Orbital wall fractures
Chemical injury
How is acid injury to the eye limited?
Damage occurs due to denaturation and coagulation of protein, but is often limited by neutralisation of the buffering action of the tissues, damage is limited to the area of contamination
Why are alkaline injuries to the eye serious?
Penetrate ocular tissues rapidly and produce intense ocular reactions.
Damage is widespread, uncontrolled and progressive
Often results in epithelial loss, corneal opacification, scarring, severe dry eye, cataract, galucoma and blindness
Management of chemical injury to the eye
Complete and copious irrigation, should be insitiuted within minuites
Instil topical anestethic
Use eye irrigation solutions and normal saline IV drip
Squeeze copious amounts of solution into the eye and direct towards the temple, away from the unaffected eye
Irrigate under the lids
After several minuites or irrigation, check the pH of the eye by placing litmus paper into the inferior fornix
Continue until pH neutralized, check pH after 30 mins as may rise again after irrigation stopped
Remove any visable particulate mater and urgently refer to an opthalmologist
What is hyphema?
Blood in anterior chamber of the eye
Usually associated with trauma
Requires urgent referal to an opthalmologist for treatment
How is hyphaema treated?
Strict bedrest
Topical steroids
Topical cyloplegic agents
Admit to hosptial if youn or concerned about follow-up/compliance
Need exams for 5 days including mesaurement of IOP
Sickle-cell prep (pts with sickle cell trait need more aggresive management of elevated IOP)
What might follow a orbital floor fracture?
Muscle entrapment
Common minor eye injuries?
Corneal abrasion
Corneal foreign body
Chemical splash
Traumatic iritis
What is the uvea?
Pigmented part of the eye
Iris
Ciliary body
Choroid (most vascular part of the body)
Why is uveitis sight threatenting
Retina is directly anterior to the choroid (part of uvea) - rods and cones get blood supply from choroid, so if effected when uvea inflamed, hence why uveitis is sight threatening.
Types of uveitis by location?
Anterior - iritis - iris
Intermediate: cyclitis - cillary body
Posterior - choroiditis - choroid
Why can dots be seen on the cornea in uveitis?
Keritic precipitates adhere to the cornea
Granulomatous and non-granulomatous
Signs in uveitis?
Keratic precifitates
Cells in anterior chamber
Fibrin in anterior chamber
Posterior synechae (pupil has an abnormal shape), circumcorneal congestion - iris bludges forward (pushed forward by aqueous humour which is unable to flow out via pupil as lens is stuck)
Cells in viteros
Choroiditis lesions
Macular odeama
HIGH INTRAOCULAR PRESSURE
Anatomical location of the iris?
Lens is posteior
In close proximity to conjunctivia
Cornea is anterior
How can a posterior synachea be broken?
Cataract laser eye surgery
Pupil dilation
Symptoms of intermediate uveitis?
Blurring of vision
Floaters
Signs of intermediate uveitis
Cells in vitreous
Snow balls (fundoscpoy)
Snowbanking (fundoscopy)
Sheating of blood vessels (seen on fundoscopy)
Macula odeama (fudoscopy or OCT)
How can TB cause uveitis?
- Formation of granulomas
- Immune reaction to TB protein
Management of intermediate and posterior uveitis?
Local treatment:
Periocular steroids
Intravitreal steroid implants
TOPICAL STEROIDS NOT SUITABLE
Systemic treatment:
Pulse therapy
Oral steroids
Immunosuppression
Aetilogy specific antibiotic/antifungal/antiviral
Infections associated with chronic anterior uveitis?
Sarcoidosis
Syphilis
Lyme disease
Tuberculosis
Herpes virus
Side effects of topical steroids in opthalmology?
Cataracts
Increased intraocular pressure (can lead to glaucoma and blindness)
What is an Ozurdex implant?
Steroid implant (for the eye)
Oral steroid sparing
Anterior uveitis complications?
Posterior synechiae
Pupillary Membrane
Ocular HTN/glaucoma
Hypotony (low IOP) - cillary body produces less aqeous humour - greater worry than high IOP
Cataract
Cystoid Macular Odema
Complications of posterior uveitis?
Inflammation and infection in the posterior chamber may lead to retinal scarring and irreversible visual compromise
Complications of posterior uveitis?
Inflammation and infection in the posterior chamber may lead to retinal scarring and irreversible visual compromise
Complications of intermediate uveitis?
Glaucoma: A condition that can cause blindness due to higher intraocular pressure
Cataracts: When the lens of the eye becomes clouded and cause vision loss
Macular edema
Retinal detachment: An eye condition wherein the retina gets separated from the eye structures that holds the retinal layers together
Over time and due to a lack of proper treatment, the condition can affect other surrounding eye structures such as the lens, optic nerve, vitreous fluid, and retina
In a patient with congenital absence of the zygomatic bone, what opthalmic abnormality would be present?
Proptosis, oulsitile
Which muscle opens the eye and what nerve supplies it?
Levator palpabre superioris - elevates the upper eyelid
Occularmotor nerve
Where do the recti muscles
What might a unilateral fixed dilated pupil in and injured (eye) patient?
Retrobulbar haemorrage, causing compatment syndrome
Why is there only partial ptosis in Horners syndrome
Sympathetic innervation to superior tarsal muscle (Mullers muscle) only is compromised
Where would a lesion cause non-axial proptosis?
Extra conal lesion
Where would a lesion cause an axial proptosis?
Intra conal lesion
(In muscle cone)
Why are many patients with autoimmune conditions such as GPA and RA at risk of eyeball rupture?
Thinning of the sclera increased susceptibility to injury (blue sclera)
Where is the blind spot in a healthy person and why?
Temporal visual field
Optic nerve head as no photoreceptors here
What is OCT?
Optical coherence tomography (OCT) is a non-invasive imaging test that uses light waves to take cross-section pictures of your retina
Can view retina at cellular level
Where would pathology likely arise from if a patient is complaining of an ache or pressure in their eye?
Pain from the orbit
Where would pathology likely arise from if a patient is complaining of an itchiness or grittiness in their eye?
Surface of eye
What is photopsia and how might it differ per cause?
Flashing lights
Migraine: bilateral, may be coloured
Retinal detachment or tare : unilateral, yellow or white
Blephirits vs eczema
Both erythematous dry painful eyelid
Blephritis involvement of eyelash, treat with warm compress
Eczema look for skin thickening and fissures in other area, do not use warm compress
Bacterial vs allergic bs viral conjunctivitis**
Bacterial: purulent discharge
Viral: systemically unwell (fever, sore throat) haemorrhages visible, clear discharge
Allergic: clear discharge
Causes of unilateral photophobia
Corneal abrasion
Corneal ulcer
Anterior uveitis
What might cause pressure sensation with nausea and vomiting
Acute angle closure glaucoma
Juvinielle artheritis vs RA eye problems
Scleritis - RA
Uveitis - Juvinielle arthritis
Most important cause of nausea vommiting and pressure sensation in eye to exclude?
Acute angle glaucoma
What sight threatening condition is jaw claudication indicative of?
GCA
Differs from artheritis as more anterior and worsens with eating (rather than improving)
Diplopia in 6th nerve palsy?
Horizontal
Vision loss in papilodema?
Intermittent visual loss
Conditions which may cause generalised eye blurring?
Usually means a reduction in the clarity of the entire field of vision
Astigmatisim (reffractive error)
Side effects of medications such as ORAL steroids
Cataracts
Causes of central visual blurring?
Age related macular degeneration (preceeded by complaints of distorion)
Diabetic maculopathy
Optic disc swelling
How to tell difference between floaters and a scotoma (blind spot)
Floaters - can move into and out of view, ‘slosh about with eye movements’. Suggest pathology in the vitreous e.g. posterior vitreous detatchment,vitritis, blood
Scotoma- moves with vision. Suggests vascular occlusion or retinal detatchment.
What might cause ‘curtain vision’ and how can you differentiate between the causes?
Retinal detachment - curtain constant - progressive
Amaurosis fugax -curtain is transient
Central retinal artery occlusion - sudden, may improve as associated swelling foes down
Central retinal vein occlusion - comes on more gradually and progressive
What might you see with an opthalmoscope in retinal detatchment?
Section of retina unable to focus on and section that you can
Key questions in history (diplopia)
One or both eyes
- Usually due to misalignment of eyes
- Monocular (rare, catracts or corneal deformity), double vision remains when one eye covered
What does red desaturation indicate?
Red desaturation - paler shade of red in eye of concern - suggestive of optic nerve disease
What medical conditions can cause eye pathology?
Diabetes – retinopathy, cranial nerve palsies, infection, vascular occlusion
Hypertension – hypertensive retinopathy, cranial nerve palsies, vascular occlusion
Thyroid disease – lid retraction, lid lag, exophthalmos, dry eye, ocular motility restriction, optic neuropathy
Ankylosing spondylitis- anterior uveitis and side effects from treatment e.g. oral steroids
Arthritis – rheumatoid arthritis, reactive arthritis
Which patients can be registered as blind or partially sighted?
Visual field defects in BOTH eyes with low visual acuity
How is the fundus imaged?
Direct opthalmoscopy
Indirect opthalmoscopy
Slit lamp bimicroscopy
Photography
Optical coherence tomography
Florescein angiography
Clinical tests to asses opthalmology patient
Snellen visual acuity
Near vison acuity test
Amsler grid
Ishihara
Eye movement examination
Cranial nerve examination
What is glaucoma?
Group of conditions with characteristic progressive optic nerve damage associated with visual field damage +/- raised intraocular pressure
V**ISUAL FIELD PATHWAY
How is open-angle glaucoma managed?
Management of glaucoma aims to reduce the intraocular pressure. Treatment is usually started at an intraocular pressure of 24 mmHg or above. Patients are followed up closely to assess the response to treatment.
Prostaglandin analogue eye drops (e.g. latanoprost) are first line. These increase uveoscleral outflow. Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning).
Other options:
Beta-blockers (e.g. timolol) reduce the production of aqueous humour
Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour
Sympathomimetics (e.g. brimonidine) reduce the production of aqueous fluid and increase uveoscleral outflow
Trabeculectomy surgery may be required where eye drops are ineffective. This involves creating a new channel from the anterior chamber, through the sclera to a location under the conjunctiva. It causes a “bleb” under the conjunctiva where the aqueous humour drains. It is then reabsorbed from this bleb into the general circulation.
Name the infection
Subarachnoid haemorrhage
Monocular double vision
Overlapping images with blurring
Usually in one eye but can be both
Will remain when one eye is covered
Eyes will appear straight
Horizontal binocular double vision
2 identical images seen next to each other
Horizontal misalignment
Occurs when the eyes become misaligned - nerve palsy, trauma
Brain projects images from two different positions
Resolves when one eye is converged
Vertical binocular double vision
Two identical images on top of each other
Vertical misalignment
Occurs when the eyes become misaligned - nerve palsy, trauma
Brain projects images from two different positions
Resolves when one eye is converged
Implication of CN3 palsy on ocular movement
• Left complete upper lid ptosis. • Left exotropia (divergent eye). • Anisocoria – Left pupil larger than Right.
• Pupil involvement indicating compressive
aetiology.
Implications of trochlear nerve (CN4) palsy?
o Hypertropia (greater at near) slight esodeviation.
o CHP Head tilt to unaffected side, chin depression (adaptation to correct diplopia)
o Diplopia vertical (with torsional and horizontal components)
o Torsion
Implications of CN6 (abducens nerve) palsy?
o Esodeviation (larger in the distance).
o CHP – Face turn towards affected side.
o Horizontal diplopia (greater in distance and looking towards affected side, normal looking towards unaffected side)
o Limited abduction.
Esotropia in primary postion towards affected side
What is an orbital blow out fracture?
Break in orbital wall whilst orbital rim remind intact
Secondary to assault of sporting injury, occuring as the orbital floor breaks acting as a crumple zone to protect the globe from rapid increase in intraocular pressure
Orbital contents may drop downwards into the maxillary sinus
May cause IR compression (trap door mechanism)
Contents of the optic tracts
Left optic tract – contains fibres from the left temporal (lateral) retina, and the right nasal (medial) retina.
Right optic tract – contains fibres from the right temporal retina, and the left nasal retina.
episcleritis vs scleritis
Scleritis involves inflammation of the full thickness of the sclera.
Episcleritis is benign and self-limiting inflammation of the episclera, the outermost layer of the sclera. The episclera is situated just underneath the conjunctiva.
Scleritis is more serious than episcleritis.
Like episcleritis, scleritis an inflammatory condition - It is not usually caused by infection.
Both have links to AID - RA, IBD (both) and SLE sarcoidosis GPA (more so scleritis) but episcleritis more l
Presenting features different
Scleritis: Severe pain and pain with eye movement, deep boating pain
Episcleritis: mild or no eye pain - more of grittiness/FB sensation
S: photophobia (absent in E)
Both eye watering
S: can be bilateral (E usually unilateral)
S: tenderness to palpation of the eye
S:reduced visual acuity
S: abnormal réaction to light
S: diffuse red eye, E: segmental
E: dilated episcleral vessels
S: does NOT blanch with phenylephrine drops E does
Which is episcleritis and which is scleritis
What is the orbit and what are its borders and anatomical relations?
Orbit is the pyramidal cavity in the facial skeleton which contains the eyeball and its associated muscles, and a number of nerves and vessels.
Roof/superior wall: frontal bone and lesser wing of sphenoid
Floor: Maxilla, zygomatic and palatine bones
Medial: Ethomid, maxilla, lacrimal and sphenoid bones
Apex: Located at the opening to the optic canal, the optic foramen
Base: opens out into the face, bounded by eyeball. Is also known as orbital rim.
What are the three main pathways into the orbit and what do they contain? What are the minor openings?
Optic canal (optic nerve and ophthalmic artery)
Superior orbital fissure (lacrimal, frontal, trochlear, oculomotor, nasocillary and abducens nerves, superior opthalmic vein)
Inferior orbital fissure: transmits the zygomatic branch of the maxillary nerve, the inferior ophthalmic vein and sympathetic nerves
Minor openings: nasolacrimal canal (drains tears from eye to nasal cavity, supra orbital foramen, infraorbital canal)
What is this?
Orbital blowout fracture
Partial herniation of the orbital contents through one of its walls. This usually occurs via blunt force trauma to the eye.
The medial and inferior walls are the weakest with the contents heniating into the ethmoid and maxillary sinuses respectively.
Why does orbital fracture cause exophthalmos?
Raised intraorbital pressure
What clinical sign is this?
Exophthalmos
What is this
Stye/Hordeolum/External hordoleum
- resulting from acut infection of a gland of Moll, Zeiss or he eyelash folicle.
What is this
Chalazion/Internal hordelum/Eyelid cyst
Swelling involving tarsal (meibomian) gland
What does the lacrimal apparatus consist of?
Lacrimal glands
Lacrimal ducts
Lacrimal canaliculi
What do the lacrimal glands produce and what is the pathway of this fluid?
Gland secretes one of the component of tears
Lies in a fossa on the upper part of the orbit
Lacrimal fluid entering the conjunctival sac through the lacrimal ducts passes into the lacrimal lake (at medial angle of eye)
Lacrimal fluid drains from lacrimal lake to lacrimal sac
Fluid passes through nasal cavity through the nasolacrimal duct
Passes from nasolacrimal duct into the nasopharynx where it is swollowed
The three layers of the eyeball?
Outer, protective layer: Sclera and the cornea. Fibrous, provides attachments for the extra ocular muscles.
Middle: Choroid, cillary body and iris. Rich network of vessels.
Inner layer: retina, consisting of optic and non visual parts
What is this iris?
Lies on anterior surface of lense
Thin contractile diaphragm with a central apeture (pupil) to allow for transmission of light.
Two musclrs (sphincter and dilator pupillae) control pupil size
What are these, and when are they seen?
Microaneurysms
Microaneurysms are localised outpouchings of capillaries that leak plasma constituents into the retina. They may be clinically indistinguishable from small dot and blot haemorrhages
Seen in background diabetic retinopathy
What are these, and when are they seen?
Dot and blot haemorrhages
Dot and blot haemorrhages arise from bleeding capillaries in the middle layers of the retina.
They may look like microaneurysms if small enough. It is not particularly important to be able to distinguish between small haemorrhages and microaneurysms as they are both parts of background diabetic retinopathy.
What are these, and when are they seen?
Cotton wool spots appear as small, fluffy, whitish superficial lesions.
They are accumulations of dead nerve cells from ischaemic damage.
The presence of retinal ischaemia represents a progression from background diabetic retinopathy to the pre-proliferative stage.
What are these, and when are they seen?
NVE - Neovascularisation elsewhere
Insufficient retinal perfusion results in the production of vascular endothelial growth factor (VEGF) which results in the development of new vessels on the retina (neovascularisation).
Proliferative diabetic retinopathy
What are these, and when are they seen?
NVD- Neovascularisation at the disc
Insufficient retinal perfusion results in the production of vascular endothelial growth factor (VEGF) which results in the development of new vessels on the retina (neovascularisation).
Proliferative diabetic retinopathy
What is this and why might it be present?
Pan-retinal photocoagulation is the primary treatment for proliferative diabetic retinopathy.
The rationale behind the treatment is to reduce the production of VEGF by reducing the oxygen demand from the peripheral retina.
Clinically it is seen as clusters of burn marks on the retina which have been created by the laser used in the treatment process.
What are these and in which condition are they seen?
Hard exudates
Hard exudates are waxy yellow lesions with relatively distinct margins arranged in clumps or rings, often surrounding leaking microaneurysms.
They are called “hard exudates” to distinguish them from “soft exudates”, an older term for cotton wool spots
They are seen in diabetic maculopathy
What is this and when is it seen?
AV nipping
Grade 2/3 hypertensive retionpathy
What is this clinical sign and when is it seen?
The image shows extensive haemorrhages, cotton wool spots, optic disc swelling and a ring of exudates around the macula (macular star).
Mallignant hypertension
How is hypertensive retinopathy graded?
Grade 1 disease: the changes of early hypertensive retinopathy are subtle, with generalised arteriolar narrowing.
Grade 2 disease: development of areas of focal narrowing, and compression of venules at sites of arteriovenous crossing (AV nipping).
Grade 3 disease: development of features similar to those of diabetic retinopathy, namely retinal haemorrhages, hard exudates and cotton wool spots.
What is seen her and what condition does it occur in?
Cupping - increased vertical cup-to-disc ratio
Glaucoma results in irreversible loss of nerve fibres, leading to an appearance of “cupping” or an increased vertical cup-to-disc ratio (C/D ratio).
What is seen here
Papillodema/optic disc swelling
Optic disc margins appear blurred and small haemorrhages may be noted.
Chlaky, white patches visible on the tympanic membrane, but it does not appear inflamed and is not bulging - suggestive of what
Tympanosclerosis
May present with hearing deterioration, history of grommets and recurrent otitis media
Periorbital vs orbital cellulitis features?
Fundoscopy findings in retinitis pigmentosa?
Characteristic fundoscopy findings include
peripheral bone-spicule pigmentation, optic disc
pallor and retinal vessel attenuation.
Age related macula degeneration is the leading causes of blindness in the UK, what key finding appears in fundoscopy in both wet and dry ARMD? What other features do both have i. common?
A key finding associated with macular degeneration is drusen seen during fundoscopy.
Atrophy of the retinal pigment epithelium
Degeneration of the photoreceptors
Layers of the macula
The macula is made of four key layers.
At the bottom, there is the choroid layer, which contains blood vessels that provide the blood supply to the macula.
Above that is Bruch’s membrane.
Above Bruch’s membrane there is the retinal pigment epithelium and above that are the photoreceptors.
What are these called and when are they seen?
Drusen are yellow deposits of proteins and lipids that appear between the retinal pigment epithelium and Bruch’s membrane.
Some drusen can be normal. Normal drusen are small (< 63 micrometres) and hard. Larger and greater numbers of drusen can be an early sign of macular degeneration. They are common to both wet and dry AMD.
Wet AMD pathophysiology
In wet AMD there is the development of new vessels growing from the choroid layer into the retina.
These vessels can leak fluid or blood and cause oedema and more rapid loss of vision.
A key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF) and this is the target of medications to treat wet AMD.
Where is the choroid found and what is it’s function?
The choroid is found lining the posterior part of the eye, extending from the ciliary body to the optic nerve lying between the retina and the sclera. As with the iris and ciliary body it too is a pigmented structure. The choroid has several important functions:
1. Allows nerves and vessels to reach the anterior eye by passing through the choroid
2. Removes waste product from the outer retina (area closest to choroid)
3. Supplies essential nutrients to the outer half of the retina
4. Absorbs any light passing through the retina, thus preventing it from reflecting back and
interfering with vision
Chambers of the eye
Chambers of the eye
Chambers of the eye
Examination of a patient with acute angle glaucoma might reveal what?
Red-eye
Teary
Hazy cornea
Decreased visual acuity
Dilatation of the affected pupil
Fixed pupil size
Firm eyeball on palpation
Clinical signs in hypertensive retinopathy
Silver wiring or copper wiring is where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light.
Arteriovenous nipping is where the arterioles cause compression of the veins where they cross. This is again due to sclerosis and hardening of the arterioles.
Cotton wool spots are caused by ischaemia and infarction in the retina causing damage to nerve fibres.
Hard exudates are caused by damaged vessels leaking lipids into the retina.
Retinal haemorrhages are caused by damaged vessels rupturing and releasing blood into the retina.
Papilloedema is caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins.
What is a Holmes Adie pupil?
A Holmes Adie pupil is a unilateral dilated pupil that is sluggish to react to light with slow dilation of the pupil following constriction.
Over time the pupil will get smaller. This is caused by damage to the post-ganglionic parasympathetic fibres. The exact cause is unknown but may be viral.
Holmes Adie Syndrome is where there is a Holmes Adie pupil with absent ankle and knee reflexes.
How does corneal abrasion tend to present?
History of contact lenses or foreign body
Painful red eye
Foreign body sensation
Watering eye
Blurring vision
Photophobia
How does herpes keraitits present?
Painful red eye
Photophobia
Vesicles around the eye
Foreign body sensation
Watering eye
Reduced visual acuity. This can vary from subtle to significant.
What is posterior viterous detatchment?
The vitreous body is the gel inside the eye that maintains the structure of the eyeball and keeps the retina pressed on the choroid.
The vitreous body is made up of collagen and water. With age it becomes less firm and less able to maintain its shape.
Posterior vitreous detachment is a condition is where the vitreous gel comes away from the retina. It is very common, particularly in older patients.
Retinal detachment presentation
Retinal detachment is a painless condition that can present with:
Peripheral vision loss. This is often sudden and like a shadow coming across the vision.
Blurred or distorted vision
Flashes and floaters
What might be seen on examination in CRVO?
Fundoscopy examination is diagnostic of retinal vein occlusion. It give characteristic findings:
Flame and blot haemorrhages
Optic disc oedema
Macula oedema
How does CRAO present?
Blockage of the central retinal artery causes sudden painless loss of vision.
There will be a relative afferent pupillary defect. This is where the pupil in the affected eye constricts more when light is shone in the other eye compared when it is shone in the affected eye. This occurs because the input is not being sensed by the ischaemic retina when testing the direct light reflex but is being sensed by the normal retina during the consensual light reflex.
Fundoscopy will show a pale retina with a cherry-red spot. The retina is pale due to a lack of perfusion with blood. The cherry-red spot is the macula, which has a thinner surface that shows the red coloured choroid below and contrasts with the pale retina.
