Opthalmology

Opthalmology

Opthalmic Infections
1. Endopthlamitis
  1. Organisms: - Often conjunctival “commensals” - Most common is staph epidermidis
  2. - Devastating infection inside of the eye - Post-surgical or endogenous - Painful +++, with decreasing vision - Very red eye - Sight threatening
  3. 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)
2. Chlamydial Conjuctivitis
  1. - 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
  2. topical oxytetracycline (but adults may also need oral azithromycin treament for genital chlamydia infection)
3. Bacteria Conjunctivitis
  1. Neonates: - Staph aureus - Neisseria gonorrhoea - Chlamydia trachomatis
  2. Other ages: - Staph aureus - Strep pneumoniae - Haemophilus influenzae (especially in children)
  3. 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
  4. chloramphenicol (treats most bacteria except Pseudomonas aeruginosa) fusidic acid (treats Staph. aureus) gentamicin (treats most Gram negative bacteria including coliforms, Pseudomonas aeruginosa)
4. Viral Conjunctivitis
  1. Causative organisms: - Adenovirus - Herpes simplex - Herpes zoster
5. Microbial Keratitis
  1. Fungal Keratitis
    1. 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
  2. Virus
    1. 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
    2. 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
  3. Bacteria Keratitis
    1. Need admission for hourly drops - Daily review - Usually in association with other corneal pathology or contact lens wear
    2. 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)
6. Orbital Cellulitis
  1. Causative Organisms: - Staphylococci - Streptococci - Coliforms - Haemophilus influenzae - Anaerobes
  2. 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
7. Chorioretinitis
  1. Haemorrhagic CMV retinitis in AIDS
  2. 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
  3. 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
8. Diagnosis
  1. 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
9. Antibiotics
  1. Chloramphenicol
    1. 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
    2. Side Effects: Allergy Irreversible aplastic anaemia (rare : 1 in 40,000) Grey baby syndrome
  2. Inhibits cell wall synthesis
    1. Penicillins & cephalosporins have common B lactam ring B lactam ring inhibits enzyme which makes bacterial cell wall Without cell wall, bacteria die
  3. Inhibits nucleic acid synthesis
    1. 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
10. Antivirals
  1. Aciclovir inhibits viral DNA synthesis Base analogue (mimics guanine) Topical and systemic Used for dendritic ulcers of the cornea
  2. Do not use steroid drops !!!
Ocular Trauma
1. Mechanism
  1. Burns (chemical)
    1. Alkali - easy, rapid penetration - cicatrising changes to conjuctiva and cornea penetrates intra-ocular structures
    2. Acid - coagulates proteins - little penetration
    3. 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
  2. Penetrating Trauma
    1. Sympathetic Opthalmia
      1. 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
    2. Foreign Bodies
      1. Features: Pupil irregular - Shallow anterior chamber - Localised cataract - Gross inflammation
      2. Intra-ocular Foreign Body (IOFB) - Most often result of fast moving particles (ie. hammer/ chisel injuries) - X-ray
  3. Blunt Trauma
    1. 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
2. The Golden Rules
  1. 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
3. Patient Assessment
  1. 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
1. Sudden Visual Loss
  1. Causes: Vascular aetiology Vitreous haemorrhage Retinal detachment Age related macular degeneration (ARMD) -wet type Closed angle glaucoma Optic neuritis Stroke
  2. Retinal of retinal circulation
    1. Central retinal artery occlusion (CRAO)
      1. 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
      2. Causes: Carotid artery disease; Emboli from heart
      3. 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
    2. Branch retinal artery occlusion
    3. Amaurosis Fugax
      1. 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
    4. Central retinal vein occlusion (CRVO)
      1. Systemic causes (Virchow's triad): Atherosclerosis, Hypertension, Hyperviscosity Ocular causes: raised IOP (venous stasis)
      2. 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
      3. 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
  3. Occlusion of optic nerve head circulation
    1. Also known as ‘Ischaemic optic neuropathy’ Posterior ciliary arteries (PCA) become occluded, resulting in infarction of the optic nerve head (PCA not end arteries)
    2. Arteritic ION
      1. 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
      2. 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
    3. Non-arteritic ION
  4. Haemorrhage
    1. 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)
    2. Vitreous Haemorrhage
      1. Symptoms Loss of vision ‘Floaters’ Signs Loss of red reflex May see haemorrhage on fundoscopy Management Identify cause Vitrectomy for non-resolving cases
  5. Retinal Detachment
    1. 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
  6. Age related Macular Degeneration (AMRD)
    1. Wet AMRD (sudden visual loss)
      1. New blood vessels grow under retina – leakage causes build up of fluid/blood and eventually scarring
      2. Symptoms Rapid central visual loss Distortion (metamorphopsia) Signs haemorrhage/exudate
      3. Treatment: Anti-VEGF treatment – injected into vitreous cavity. Stops new blood vessels growing by binding to VEGF (vascular endothelial growth factor)
  7. Glaucoma
    1. 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)
    2. Closed-angle
      1. 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
2. Gradual Visual Loss
  1. Bilateral – usually Often asymmetrical May present early with reduced VA May present late with decreased field
  2. CAUSES: Cataract Age related macular degeneration (dry type) Refractive error Glaucoma Diabetic retinopathy (not covered in this lecture)
  3. Cataract
    1. Cloudiness of lens
    2. Causes: Age related Congenital – intrauterine infection (importance of checking red reflex in neonates) Traumatic Metabolic – diabetes Drug-induced (steroids)
    3. TYPES: Nuclear cataract; Posterior subscapsular cataract; Christmas Tree (Polychromatic cataract)
    4. 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
  4. Dry ARMD
    1. Symptoms Gradual decline in vision Central vision ‘missing’ (scotoma) Signs Drusen – build up of waste products below RPE Atrophic patches of retina
    2. TREATMENT: No cure – treatment is supportive with low vision aids eg magnifiers
  5. REFRACTIVE ERROR
    1. Eye cannot clearly focus image Myopia (‘short-sighted’) Hypermetropia (‘long- sighted’) Astigmatism (usually irregular corneal curvature) Presbyopia (loss of accommodation with aging)
  6. Glaucoma
    1. Open-Angle type
      1. 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
      2. TREATMENT: aim to preserve vision (by lowering IOP) with eye drops /laser/surgery
In Systemic Disease
1. Inflammatory
  1. Giant Cell Arthritis
    1. Inflammation of middle sized arteries. BLINDING CONDITION Associated with polymyalgia rheumatica.
    2. SIGNS: headache, jaw claudication, malaise, raised PV, blinding condition.
  2. Thyroid Eye Disease
    1. Signs
      1. Extraocular - Proptosis (TED most common cause of U/L & B/L proptosis) - Lid signs: retraction, oedema, lagm pigmentation. - restrictive myopathy
      2. Ocular - Anterior Segment: Chemosis, injection, exposure, glaucoma - Posterior Segment: Choroidal folds, optic nerve swelling.
    2. Swelling of extraocular muscles and orbital fat with a spectrum of severity & potential blinding complications. Autoimmune.
    3. MANAGEMENT: Control of thyroid dysfunction, lubricants & surgical decompression.
  3. Granulomatous Disease
  4. Uveitis
    1. Infective - TB, Herpes zoster, Toxoplasmosis, Candidiasis, Syphillis, Lyme
    2. Non-Infective - HLA-B27, Sarcoidosis, Juvenile Arthritis, Behcet's Disease, Idiopathic Syndromes.
2. Connective tissue
  1. Rheumatoid Arthritis
    1. Dry eyes (Keratoconjunctivitis sicca), scleritis, corneal melt.
      1. SJOGREN'S SYNDROME - keratoconjunctivitis sicca - xerostomia - RA (usually) - infiltration of lacrimal glands
  2. SLE
    1. anti-DNA Ab, ocular inflammation.
  3. Dermatology
    1. drug or food hypersensitivity, maculopapular rash, stomatitis, conjunctivitis.
      1. Erythema Multiforme
      2. 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.
  4. Marfans
3. Cardiovascular
  1. Diabetes
    1. Pathogenesis: Chronic hyperglycaemia --> glycosylation of protein/ basement membrane --> loss of pericytes --> microaneurysm --> leakage/ ischaemia
    2. SIGNS: Microaneurysms, dot blot haemorrhages, cotton wool patches, hard exudate, venous abnormalities, microvascular abnormalities (IRM
      1. Neovascularisation: New vessels grow on the disc (NVD), periphery (NVE) & iris (in severe ischaemia)
    3. Vision loss from: retinal oedema affecting the fovea, vitreous haemorrhage, scarring/ tractional retinal detachment
    4. MANAGEMENT: Laser - PRP, macular grid Surgery - vitrectomy Rehabilitation (blind/partial sighted)
  2. Hypertension
    1. Appearance of fundus correlates to severity of HTN & the state of retinal arteries.
      1. Young people can have extensive retinopathy
      2. Elderly patients with arteriosclerotic vessels often have minimal changes.
    2. SIGNS: cotton wool spots, hard exudates, retinal haemorrhage, optic disc oedema, copper/ silver wiring (attenuated vessels)
    3. ACCELERATED HTN Particularly in young patients, dramatic fundal appearance, may have decreased vision.
  3. Vascular Occlusion
    1. Central Retinal Artery Occlusion
      1. SIGNS: Sudden,painless, profound loss of vision. Retinal nerve fibre layer becomes swollen except at fovea (cherry red spot). Rarely recovers.
    2. Central Retinal Vein Occlusion
      1. SIGNS: Sudden painless visual loss (range). Determine degree of ischaemia (it correlates to degree of visual loss & fundal appearances).
    3. Branch Vein Occlusion
      1. SIGNS: Painless vision disturbance, maybe asymptomatic, may have lost part of field.

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	Created by Jean Yap about 6 years ago