Zusammenfassung der Ressource
Opthalmology
- Opthalmic Infections
- Endopthlamitis
- Organisms: - Often conjunctival “commensals” - Most
common is staph epidermidis
- - Devastating infection inside of the eye -
Post-surgical or endogenous - Painful +++, with
decreasing vision - Very red eye - Sight threatening
- Treatment: - Intravitreal amikacin/ ceftazidime/ vancomycin
and topical antibiotics - EVS (is the main body of evidence
but at that time 4th gen fluoroquinolones which have
better penetration of blood ocular barrier were not
available)
- Chlamydial Conjuctivitis
- - Often chronic history - Unresponsive to treatments - Suspect in bilateral conjunctivitis in
young adults - May or may not have symptoms of urethritis, vaginitis - Need contact tracing
- topical oxytetracycline (but adults may also need oral
azithromycin treament for genital chlamydia infection)
- Bacteria Conjunctivitis
- Neonates: - Staph aureus - Neisseria
gonorrhoea - Chlamydia trachomatis
- Other ages: - Staph aureus - Strep pneumoniae -
Haemophilus influenzae (especially in children)
- Treatment: - Swab - Topical antibiotic usually chloramphenical qds - Drops vs ointment - Avoid chloramphenicol if
history of aplastic anaemia or allergy - Be aware of chloramphenicol allergy if worsening sympooms
- chloramphenicol (treats most bacteria except Pseudomonas aeruginosa) fusidic acid (treats Staph. aureus) gentamicin
(treats most Gram negative bacteria including coliforms, Pseudomonas aeruginosa)
- Viral Conjunctivitis
- Causative organisms: -
Adenovirus - Herpes
simplex - Herpes zoster
- Microbial Keratitis
- Fungal Keratitis
- 1. Contact lenses - Acanthamoeba - Pseudomonas aeruginosa 2. Fungal keratitis
with hypopyon - More indolent course than microbial keratitis -Usually a history
of trauma from vegetation - Takes a long time to heal
- Virus
- Herpetic keratitis - Very painful - Can be recurrent - recurrences eventually result in reduced corneal
sensation - If treated with steroids can cause a corneal melt and perforation of the cornea
- Adenovirus - Bilateral - Usually follows an URTI - Contagious - Can
give topical AB to prevent secondary infection - May affect vision -
Can require steroids to speed up recovery if becomes chronic
- Bacteria Keratitis
- Need admission for hourly drops - Daily review - Usually in association with other
corneal pathology or contact lens wear
- Treatment: A 4-quinolone (Ofloxacin) (treats most Gram negative bacteria
including coliforms, Pseudomonas aeruginosa, Haemophilus influenzae.
Not active vs. Strep. pneumoniae) Gentamicin and cefuroxime (the
combination will treat most Gram positive and Gram negative organisms)
- Orbital Cellulitis
- Causative Organisms: - Staphylococci - Streptococci
- Coliforms - Haemophilus influenzae - Anaerobes
- Painful (especially on eye movements) - Proptosis - Often associated with paranasal sinusitis -
Pyrexial - Sight threatening - Cared for by ENT and Ophthalmology - CT scan to identify orbital
abscesses - Direct extension from sinus - Extension from focal orbital infection (infected
chalazion, dacryocystitis) - Post-operative - Need to differentiate between preseptal and orbital
- If any suggestion there is restriction of muscles or optic nerve dysfunction then scan - Broad
spectrum AB and monitor closely - Sometimes an abscess will require drainage
- Chorioretinitis
- Haemorrhagic CMV retinitis in AIDS
- Toxoplasmosis: Protozoan infection toxoplasmosis gondii; Cats and raw meat; Mild flu like
illness; Rarely causes any further problems In immunocompetent patients it enters latent
phase with cysts forming; Very common- 10% of USA sample had toxoplasmosis specific IgG;
Can reactivate; Requires systematic treatment if sight threatening
- Toxocara canis (Worm): Parasitic nemotode (roundworm) Affects cats or
dogs Unable to replicate in humans Remains an immature form of the
worm (larvae) Often self limiting as they cannot replicate Form granulomas
which can cause irreversible visual loss
- Diagnosis
- Swabs for culture – bacterial, chlamydial, viral Corneal scrapes in bacterial keratitis Aqueous/vitreous
for culture in endophthalmitis Microscopy/culture for acanthamoeba Serology for toxoplasma and
toxocara
- Antibiotics
- Chloramphenicol
- Most commonly used topical antibiotic Ointment or drops
Inhibits peptidyl transferase enzyme (therefore stops
bacterial protein being made) Bacterocidal for strep and
haemophilus Bacterostatic for staph
- Side Effects: Allergy Irreversible
aplastic anaemia (rare : 1 in
40,000) Grey baby syndrome
- Inhibits cell wall synthesis
- Penicillins & cephalosporins have common B lactam ring
B lactam ring inhibits enzyme which makes bacterial cell
wall Without cell wall, bacteria die
- Inhibits nucleic acid synthesis
- Quinolones e.g. ofloxacin, inhibit DNA gyrase, an
enzyme that compresses bacterial DNA into
supercoils Inhibition of DNA gyrase leads to
unwinding of supercoils and cell death
- Antivirals
- Aciclovir inhibits viral DNA synthesis Base analogue (mimics guanine) Topical and systemic Used for
dendritic ulcers of the cornea
- Do not use steroid drops !!!
- Ocular Trauma
- Mechanism
- Burns (chemical)
- Alkali - easy, rapid penetration - cicatrising
changes to conjuctiva and cornea penetrates
intra-ocular structures
- Acid - coagulates proteins - little penetration
- Management: - Assessment of chemical injury occurs
after thorough irrigation ◦Quick history- Nature of
chemical, when, irrigation at event; Beware Lime /
Cement ◦Check Toxbase if available ◦Check pH
◦Irrigate +++ (minimum of 2l saline, or until pH
normal) ◦Then assess at slit lamp
- Penetrating Trauma
- Sympathetic Opthalmia
- Penetrating injury to one eye - exposure of
intra-ocular antigens - auto-immune
reaction in both eyes - Inflammation in
both eyes - May lead to bilateral blindness
- Foreign Bodies
- Features: Pupil irregular - Shallow anterior
chamber - Localised cataract - Gross
inflammation
- Intra-ocular Foreign Body (IOFB) - Most often
result of fast moving particles (ie. hammer/
chisel injuries) - X-ray
- Blunt Trauma
- Blow out fracture - Traumatic uveitis -
Hyphaema (blood in anterior chamber - Tearing
of intra-ocular structures - Dislocated lens -
Retinal detachment - Choroidal tear - Commotio
Retinae "Bruised retina" - Optic nerve avulsion -
Severe intra-ocular desruption
- The Golden Rules
- 1. History is KEY 2. Always record visual acuity 3.
Don't forget Fluorescein 4. Handle suspected
globe rupture with care 5. X-ray orbits if
suspicion of Intra-Ocular Foreign Body (IOFB) 6.
Immediate irrigation of chemical injuries
- Patient Assessment
- 1. Good history of incident 2. Visual acuities 3.
Examination of eye: lids, conjunctiva, cornea,
anterior segment, pupils, fundus 4. Use Fleorescein
drops (to identify area of epithelial loss)
- Visual Loss and Blindness
- Sudden Visual Loss
- Causes: Vascular aetiology Vitreous
haemorrhage Retinal detachment Age
related macular degeneration (ARMD)
-wet type Closed angle glaucoma Optic
neuritis Stroke
- Retinal of retinal circulation
- Central retinal artery occlusion (CRAO)
- Remember: CRA supplies inner 2/3 retina (outer 1/3 supplied by choroid) Symptoms of CRAO: Sudden
visual loss Profound (CF or less- remember CRA is ‘end artery’) Painless Signs RAPD (relative afferent
pupil defect) Pale oedematous retina, thread-like retinal vessels
- Causes: Carotid artery disease; Emboli from heart
- Management: Ophthalmic management If presents within 24 hours, Ocular massage (try to convert CRAO to
BRAO) Vascular management Establish source of embolus – carotid doppler Assess and manage risk factors
- Branch retinal artery occlusion
- Amaurosis Fugax
- Symptoms transient painless visual loss ‘like a
curtain coming down’ lasts~5mins with full
recovery Signs Usually nothing abnormal to see on
examination Urgent referral Stroke clinic Aspirin
Other cause of TVL: Migraine – visual loss usually
followed by headache
- Central retinal vein occlusion (CRVO)
- Systemic causes (Virchow's triad): Atherosclerosis, Hypertension,
Hyperviscosity Ocular causes: raised IOP (venous stasis)
- Symptoms: Sudden visual loss Moderate to severe
visual loss (6/9 – P of L) Signs: Retinal
haemorrhages Dilated tortuous veins Disc
swelling and macular swelling
- Treatment: Monitor : may develop complications due to development of new vessels
(laser treatment may be required to avoid complications from these vessels eg vitreous
haemorrhage) More recently, anti- VEGFs used (VEGF = vascular endothelial growth
factor) Address underlying risk factors eg hypertension, diabetes
- Occlusion of optic nerve head circulation
- Also known as ‘Ischaemic optic neuropathy’
Posterior ciliary arteries (PCA) become
occluded, resulting in infarction of the optic
nerve head (PCA not end arteries)
- Arteritic ION
- Giant cell arteritis (GCA) Medium to large sized arteries inflamed (multinucleate giant cells) Lumen of
artery becomes occluded (posterior ciliary arteries) Visual loss from ischaemia of optic nerve head
- Giant Cell Arteritis (GCA)
- Visual symptoms Sudden visual loss Profound (CF – NPoL)
Irreversible blindness Important as diagnosis and
immediate treatment may prevent bilateral visual loss
- Headache (usually temporal) Jaw claudication Scalp tenderness (painful to comb
hair) Tender/enlarged scalp arteriesAmaurosis fugax Malaise Very High ESR , PV
and CRP Temporal artery biopsy may help diagnosis
- Treatment: High dose steroid
- Non-arteritic ION
- Haemorrhage
- Haemorrhage often occurs into the vitreous cavity – known as a ‘vitreous haemorrhage’
Bleeding occurs from abnormal vessels - associated with retinal ischaemia and new
vessel formation eg after retinal vein occlusion or diabetic retinopathy Bleeding occurs
from normal retinal vessels (usually associated with a retinal tear)
- Vitreous Haemorrhage
- Symptoms Loss of vision ‘Floaters’ Signs Loss
of red reflex May see haemorrhage on
fundoscopy Management Identify cause
Vitrectomy for non-resolving cases
- Retinal Detachment
- Symptoms Painless loss of vision Sudden onset of
flashes/floaters (mechanical separation of sensory retina
from retinal pigment epithelium) Signs May have RAPD May
see tear on ophthalmoscopy Management usually surgical
- Age related Macular Degeneration (AMRD)
- Wet AMRD (sudden visual loss)
- New blood vessels grow under retina –
leakage causes build up of fluid/blood and
eventually scarring
- Symptoms Rapid central visual loss Distortion
(metamorphopsia) Signs haemorrhage/exudate
- Treatment: Anti-VEGF treatment – injected into vitreous cavity. Stops new blood vessels growing by
binding to VEGF (vascular endothelial growth factor)
- Glaucoma
- Progressive optic neuropathy Pathogenesis not
fully understood (high *IOP may be a factor)
Many different types of glaucoma (open-angle vs
closed-angle) Ultimately result in optic nerve
damage (and therefore, visual loss)
- Closed-angle
- Aqueous humour encounters increased resistance through iris/lens channel Increased pressure
gradient causes peripheral iris to bow forward, obstructing trabecular meshwork – pressure
increases May be acute (ophthalmic emergency) Patient presents with painful, red eye/visual
loss/headache/nausea/vomiting Need to lower IOP with drops/oral medication to prevent patient
going blind, then do laser iridotomy
- Gradual Visual Loss
- Bilateral – usually Often
asymmetrical May present
early with reduced VA May
present late with decreased
field
- CAUSES: Cataract Age related macular
degeneration (dry type) Refractive error
Glaucoma Diabetic retinopathy (not
covered in this lecture)
- Cataract
- Cloudiness of lens
- Causes: Age related Congenital – intrauterine infection
(importance of checking red reflex in neonates) Traumatic
Metabolic – diabetes Drug-induced (steroids)
- TYPES: Nuclear cataract; Posterior subscapsular cataract; Christmas Tree (Polychromatic cataract)
- SYMPTOMS: Gradual decline in vision (‘hazy’ /
‘blurred’) that cannot be corrected with glasses
May get glare (can be very disabling at night
when driving) Management is surgical removal
with intra-ocular lens implant if patient is
symptomatic
- Dry ARMD
- Symptoms Gradual decline in vision
Central vision ‘missing’ (scotoma) Signs
Drusen – build up of waste products
below RPE Atrophic patches of retina
- TREATMENT: No cure – treatment is supportive with low vision aids eg magnifiers
- REFRACTIVE ERROR
- Eye cannot clearly focus image Myopia (‘short-sighted’)
Hypermetropia (‘long- sighted’) Astigmatism (usually irregular
corneal curvature) Presbyopia (loss of accommodation with aging)
- Glaucoma
- Open-Angle type
- In open angle type, angle is ‘open’ but there is resistance to outflow of aqueous in trabecular
meshwork Symptoms Often NONE Optician may discover it Signs Cupped disc Visual field defect
May/may not have high IOP
- TREATMENT: aim to preserve vision (by
lowering IOP) with eye drops /laser/surgery
- In Systemic Disease
- Inflammatory
- Giant Cell Arthritis
- Inflammation of middle sized arteries. BLINDING CONDITION
Associated with polymyalgia rheumatica.
- SIGNS: headache, jaw claudication,
malaise, raised PV, blinding condition.
- Thyroid Eye Disease
- Signs
- Extraocular - Proptosis (TED most common cause of U/L
& B/L proptosis) - Lid signs: retraction, oedema, lagm
pigmentation. - restrictive myopathy
- Ocular - Anterior Segment: Chemosis, injection,
exposure, glaucoma - Posterior Segment:
Choroidal folds, optic nerve swelling.
- Swelling of extraocular muscles and orbital
fat with a spectrum of severity & potential
blinding complications. Autoimmune.
- MANAGEMENT: Control of thyroid dysfunction,
lubricants & surgical decompression.
- Granulomatous Disease
- Uveitis
- Infective - TB, Herpes zoster, Toxoplasmosis,
Candidiasis, Syphillis, Lyme
- Non-Infective - HLA-B27, Sarcoidosis, Juvenile Arthritis,
Behcet's Disease, Idiopathic Syndromes.
- Connective tissue
- Rheumatoid Arthritis
- Dry eyes
(Keratoconjunctivitis sicca),
scleritis, corneal melt.
- SJOGREN'S SYNDROME -
keratoconjunctivitis sicca -
xerostomia - RA (usually) -
infiltration of lacrimal glands
- SLE
- anti-DNA Ab, ocular inflammation.
- Dermatology
- drug or food
hypersensitivity,
maculopapular rash,
stomatitis,
conjunctivitis.
- Erythema Multiforme
- Steven-Johnson Syndrome
- Disorder of your skin and mucous
membranes - usually a reaction to a
medication/ infection. - Often begins
with flu-like symptoms, followed by a
painful red or purplish rash that
spreads & blisters
- Symblepharon - occlusion of
lacrimal glands - corneal ulcers
- A symblepharon is a partial or complete adhesion of
the palpebral conjunctiva of the eyelid to the bulbar
conjunctiva of the eyeball.
- Marfans
- Cardiovascular
- Diabetes
- Pathogenesis: Chronic hyperglycaemia
--> glycosylation of protein/ basement
membrane --> loss of pericytes -->
microaneurysm --> leakage/ ischaemia
- SIGNS: Microaneurysms, dot blot
haemorrhages, cotton wool patches, hard
exudate, venous abnormalities,
microvascular abnormalities (IRM
- Neovascularisation: New vessels grow on the disc (NVD),
periphery (NVE) & iris (in severe ischaemia)
- Vision loss from: retinal oedema
affecting the fovea, vitreous
haemorrhage, scarring/ tractional
retinal detachment
- MANAGEMENT: Laser - PRP, macular grid
Surgery - vitrectomy Rehabilitation
(blind/partial sighted)
- Hypertension
- Appearance of fundus correlates to
severity of HTN & the state of retinal
arteries.
- Young people can have
extensive retinopathy
- Elderly patients with arteriosclerotic
vessels often have minimal changes.
- SIGNS: cotton wool spots,
hard exudates, retinal
haemorrhage, optic disc
oedema, copper/ silver
wiring (attenuated vessels)
- ACCELERATED HTN Particularly in young
patients, dramatic fundal appearance, may
have decreased vision.
- Vascular Occlusion
- Central Retinal Artery Occlusion
- SIGNS: Sudden,painless, profound loss of
vision. Retinal nerve fibre layer becomes
swollen except at fovea (cherry red spot).
Rarely recovers.
- Central Retinal
Vein Occlusion
- SIGNS: Sudden painless visual loss (range). Determine
degree of ischaemia (it correlates to degree of visual
loss & fundal appearances).
- Branch Vein
Occlusion
- SIGNS: Painless vision
disturbance, maybe
asymptomatic, may have
lost part of field.