Ophthalmology Flashcards
What is Horner’s syndrome
Causes
Ptosis, Miosis (constricted pupil) and Anyhdrosis
Causes
(1) Central: - anhydrois of face, arm and trunk
- MS
- Wallenburg Lateral Medullary syndrome?
(2) Pre-ganglionic (neck) - anhiydrosis of face
- Pancoast’s tumour: T1 nerve root lesion
- Trauma: CVA insertion or CEA
- Thyroidectomy
(3) Post-ganglionic (no anhydrous)
- Cavernous sinus thrombosis
- Carotid artery dissection
- Carotid aneurysm
- Usually secondary to spreading facial infection via opthalmic veins
- CN 3, 4, 5, 6 palsies
Optic atrophy/optic neuropathy
Features
Causes
Features
- Reduced acuity
- Reduced colour vision (especially red)
- CENTRAL SCOTOMA
- Pale optic disc
- RAPD
Causes: CAC VISION
- Commonest: MS and glaucoma
Congenital
- HMSN/CMT
- Freidrich’s ataxia
- Retinitis pigmentosa
- DIDMOAD
Alcohol and other toxins
- Ethambutanol
- Lead
- B12 deficiency
Compression
- Neoplasia: Optic glioma, pituitary adenoma
- Glaucoma
- Paget’s
Vascular: DM, GCA or thromboembolic
Inflammatory: Optic neuritis - MS, Devic’s, DM
Sarcoid/other granulomatous
Infection: Herpes zoster, TB, Syphilis
Oedema: Papilloedema
Neoplastic infiltration: Lymphoma, Leukaemia
Pupils Afferent defect
features
Causes
Features
- No direct response but intact consensual response
- Cannot initiate consensual response in contralateral eye
- Dilation on moving light from normal to abnormal eye
Causes
- Total CN II lesion
RAPD = Marcus-Gunn pupil
Features
Causes
Features
- Minor constriction to direct light
- Dilation on moving light from normal to abnormal eye
Causes
- Optic neuritis
- Optic atrophy
- Retinal disease
Pupils efferent defect
Features
Causes
Features
- Dilated pupil does not react to light
- Initialtes consensual response in contralateral pupil
- Opthalmoplegia + ptosis
Cause
- 3rd nerve palsy
(Pupil often spared in a vascular lesion e.g. DM as pupillary fibres run in the periphery)
Differentials of a fixed dilated pupil
1) Mydriatices e.g. tropicamide
2) Iris trauma
3) Acute glaucoma
4) CN3 compression: Tumour, coning
Red eye history essentials
What to check O/E
Signs of serious disease
Vision
- Blurring
- Diplopia
- Flashes/floaters
- Field defect/scotoma
Sensation
- Itching
- Pain
- Irritation
- Photophobia
- Foreign body?
Appearance
- Red
- Lumpy
- Puffy lids
Discharge
- Watering
- Sticky
- Stringy
O/E
- Inspect anterior to posterior
- Is acuity affect?
- Is globe painful?
- Pupil size and reactivity
- Cornea: Intact, cloudy? Use fluorescein
Signs of serious disease
- Poor vision
- Photophobia
- Corneal fluorescein staining
- Abnormal pupil
Acute closed angle glaucoma
Definition
Risk factors
Symptoms
Examination
Management
Blocked drainage of aqueous humour from the anterior chamber via the canal of Schlemm - increases the pressure inside the eye, sufficiently increased to damage the optic nerve + results in visual field defects
IOP rises from 15-20 –< >60mmHg
Risk factors
- Hypermetripia
- Shallow ant chamber
- Female
- FH
- Age
- Drugs: Anti-cholinergics, sympathomimetics, TCAs, Anti-histamines
- MYDRIATIC DROPS WTF
Symptoms - Rainbow haloes around lights at night, severe pain with N&V, Decreased acuity and blurred vision - Sudden onset red, painful eye with blurred eye O/E - Cloudy cornea - Fixed dilated, irregular pupil - Increased IOP makes eye feel hard - Worse at night (as eyes dilated)
Acute management: Refer to ophthalmologist
- Pilocarpine 2-4% drops stat: mitosis opens blockage
- Azetozolamide 500mg IV stat: reduced aqueous formation
- Topical BB e.g. timolol (decreases aqueous formation)
- Analgesia and antiemetics as required
Subsequent management
- Bilateral YAG peripheral iridotomy once IOP decreased medically (making a hole in periphery of iris of both eyes by laser to surgery)
NB: Accounts for 50% of blindness caused by glaucoma WW even though much less prevalent than POAG
What is astigmatism
Refractive error of the eye where there is a different degree of refraction in the different meridians of curvature
- May be myopic in one plane and hypermetropic or emmetropic in the other plane
What is presbyopia
Solution
Normal ageing of the lens, which leads to a change in the refractive state of the eye. As the lens ages, it becoemes less able to alter its curvature and this causes difficulty with near vision, especially reading
Solution
- Convex lenses
Eye anterior and posterior segments
Cornea
Sclera
Conjunctiva
Uveal tract - parts and function
Anterior = smaller space between the cornea and the iris
- Transparent and coated by cornea
- Radius ~ 8mm
- Filled with aqueous humour - produced by ciliary body - provides nutrients and oxygen to the avascualar cornea
Posterior = larger
- Coated by the opaque sclera
- Radius ~12mm
Cornea
- Clear transparent structure - provides 78% of focusing power of the eye
Sclera
- Opaque white structure covering 4/5 of the globe
- Continuous with the cornea at the limbus
- The 6 extra ocular muscles are attached to the sclera and the optic nerve perforates it posteriorly
Conjunctiva
- Covers the anterior surface of the sclera
- Richly vascularised and innervated mucous membrane
Uveal tract = Iris, Ciliary body, choroid
- Iris = coloured part of eye
- Ciliary body = muscles control the accommodation of the lens, and the secretory epithelium produces the aqueous humour
- Choroid = highly vascular lining the inner aspect of the sclera and upon this lies the retina
The lens location
Vitreous cavity location
Retina - structure and composition
Lens
Lies immediately posterior to the pupil and anterior to the vitreous humour
- Transparent convex structure responsible for 22% of the refractive power of the eye
- Loses its ability to change shape with time
Vitreous cavity
- Fills the cavity between the retina and the lens
The retina
- multilayered structure with 2 types of photoreceptor
- 6 million cones (mainly confined to macula) = responsible for detailed central colour vision
- 125 million rods responsible for peripheral vision
Blood supply to the eye
Motor innervation of the eye
Blood supply to the eye
- Ophthalmic artery
- Venous return through central retinal and ophthalmic veins
Local lymphatic drainage is to pre-auricular and submittal nodes
Motor innervation of the eye
- 3rd n. - Medial, Superior, Inferior rectus and inferior oblique
- 4th n. - Superior oblique
- 6th n. - Lateral rectus
Lateral rectus - abduction
Medial rectus - adduction
Superior rectus - elevates + medially turns the eye
Inferior rectus - Depresses eye + turns it medially
Superior oblique - Down and out
Inferior oblique - Up and out
3rd nerve palsy
Deviated down and out
Dilated
Ptosis
Paralysis of accommodation
Anterior uveitis
Pathophysiology
Symptoms
O/E
Associations
Management
Pathophysiology
Iris + ciliary body = anterior uvea
- Iris inflammation involves ciliary body too
Symptoms
Triad of: (1) Redness (2) Pain (3) Photophobia
BLURRY VISON
O/E
- Small pupil initially, irregular later
- Circumcorneal injection
- Hypopyon (pus in anterior chamber)
- Whte (Keratic) precipitates on back of corea
- Pain on convergence (Talbot’s test)
Associations (most have none)
- Seronegative arthritis
- Still’s, JIA
- IBD
- Sarcoidosis
- Behcet’s
- Infections: TB, leprosy, syphilis, HSV, CMV
Management
- Refer to ophthalmologist
- Steroid drops (dexamethasone 0.1%) +
- 1% Cyclopentolate drops: dilates pupils and prevents adhesions between iris and lens (mydriatic)
Corneal abrasion
Definition
Cause
Symptoms
Epithelial breech w/o keratitis.
Cause: trauma
Symptoms
- Pain (severe)
- Photophobia
- Blurred vision
- Blepharospasm
Investigation
Must evert upper eyelid
- Slit lamp: Fluorescein stains defect green
Management
- Chloramphenicol ointment for infection prophylaxis (QDS 5x/day)
- Pack eye for 24h after ointment
Corneal ulcer and keratitis
Define keratitis
Keratitis = Corneal inflammation
Causes
- Bacteria, herpes, fungi, protozoa
- Dendritic ulcer = Herpes simplex
- Contact lens wearers
Presentation
- Pain, photophobia
- Conjunctival hyperaemia
- REDUCED ACUITY
- White corneal opacity
Investigations
- Green with fluorescein on slit lamp
Management - REFER immediately
- Scraping of ulcer - smear and culture
- Abx drops (oral/topical acyclovir 5x/d for 2 weeks)
Complications
- Scarring and visual loss
Conjunctivitis
Common features
Types and management
Complications
Common features - Soreness/gritty/sore - Redness - Discharge NO CHANGE TO VISIION OR PUPIL RESPONSE
(1) Bacterial conjunctivitis
- Invariably bacterial
- Suspect gonococcal if rapid, copious discharge, ocular inflammation includes lid oedema
- Less acute: H.influenzae, S.pneumoniae
- Chronic: S.aureus, Moraxella lacunnata
Management:
- Gonoccocal (gram stain quickly confirms presence of diplococci) - Prompt PO and topical penicillin]
- Empirical treatment for subacute + chronic = chloramphenicol 0.5% drops for 5 days
Discharge: mucopurulent; Pre-auricular node -ve; corneal involvement +ve gonococos; Rapid onset
(2) Chlamydial conjunctivitis
- Cause: Direct contact with genital secretions but can be shared cosmetics
- Onset slow. Conjunctival swabs + NAAT before Rx
- Rx: Tropical erythromycin BD
Discharge: watery; +ve pre-auricular node, +ve corneal involvement, genito-urinary discharge
(3) Viral conjunctivitis
HSV: Typically unilateral, cutaneous vesicles on eyelids + around skin, >50% develop dendritic corneal ulcer. Rx: topical acyclovir
Adenovirus: High contagious, largely self limiting.
Rx: Lubricants, cold compress, strict hygiene. if cornea involvement - topical steroids
(4) Allergic conjunctivitis
Rx: Cold compress, eye wash, tear substitutes.
Medical Rx:
- Antihistamine drops e.g. Azelastine + Emadestine
- Olapadine (BD) v effective
- PO anti-histamines
Discharge: stringy; -ve pre-auricular node; +ve corneal involvement; itchiness
Prognosis
- Viral: Resolves in 7 days w/o
- Bacteria: Resolve in 5-10 days w/o Rx
Complications:
1) Keratoconjunctivits (inflammation of conjunctiva + cornea)
2) Trachoma is a chronic keratoconjunctivitis found mostly in sub-Saharan Africa. It is due to recurrent infection with Chlamydia trachomatis in childhood and can cause scarring of the eyelid, conjunctiva and cornea.
Topical fluorescein does not identify any corneal staining and the person does not require referral to ophthalmology:
Advise them to immediately stop contact lens use.
Advise regular bathing/cleaning of the eyelids with cotton wool soaked in sterile saline or boiled and cooled water to remove any discharge.
Advise that contant lenses should be kept out until all symptoms of the infection have gone.
Treat and arrange follow up as described above.
Primary open angle glaucoma
Cause
SYMPTOMS
SIGNS
MANAGMENT
Cause Increasing age Genetics: first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease Myopia = near sightedness HTN, Migraines DM, CVD CORTICOSTEROID USE
Symptoms
Slow rise in intraocular pressure: symptomless for a long period
Typically present following an ocular pressure measurement during a routine examination by an optometrist
Signs
Increased intraocular pressure
Visual field defect - peripheral visual defect (superior nasal first) - Central field intact
Pathological cupping of the optic disc
Investigations
- Automated perimetry to assess visual field
-Slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline - may be cupping
- TONOMETRY to measure IOP: 21 or more
- Central corneal thickness measurement
- Gonioscopy to assess peripheral anterior chamber configuration and depth
Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy
Management - NICE guidelines:
If treatment is recommended by an ophthalmologist, a target IOP is established, and first-line treatment is usually either:
- A topical prostaglandin analogue or prostamide e.g. latanoprost
- A topical beta-blocker e.g. Timolol
Lifetime monitoring is usual once treatment is commenced.
If a 1st line Rx unsuccessful, or not tolerated, 2nd line options that may be considered by the ophthalmologist include:
- Switching to a drug in the other first-line drug class.
- Combining a topical prostaglandin analogue or prostamide with a topical beta-blocker.
- Switching to, or adding in, a second-line drug treatment which are: a topical sympathomimetic, or a topical carbonic anhydrase inhibitor, or a topical miotic.
- Laser or surgical procedures.
