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.
Latanoprost
MOA
Use
Adverse effects
Prostaglandin analogue used for glaucoma - 1st line in primary open angle
- Increases uvoscleral outflow
Adverse effects
- Browning of iris
- Increased eyelash length
timolol, betaxolol
MOA
Use
Adverse effects
Beta blockers
Reduces aqueous production for glaucoma
Should be avoided in asthmatics and patients with heart block
Dorzolamide
MOA
Use
Adverse effects
Carbonic anhydrase inhibitors
Reduces aqueous production for glaucoma
Systemic absorption may cause sulphonamide-like reactions
pilocarpine
MOA
Use
Adverse effects
Miotics ( a muscarinic receptor agonist)
Increases uveoscleral outflow for glaucoma
Adverse effects
Constricted pupil, headache and blurred vision
Causes of tunnel vision
Papilloedema Glaucoma Retinitis pigmentosa Choroidoretinitis Optic atrophy secondary to tabes dorsalis Hysteria
Causes of papilloedema
Space-occupying lesion: neoplastic, vascular Malignant hypertension Idiopathic intracranial hypertension Hydrocephalus Hypercapnia
Cataracts causes
Cataracts = Age related opacification of the lens
Most commonc ause of visual impairment with 30% of >65yo having acuity (Snellen <6/12 - needed for driving)
Normal ageing process = most common Smoking Increased alcohol consumption Trauma Diabetes mellitus Long-term corticosteroids Radiation exposure Myotonic dystrophy Metabolic disorders: hypocalcaemia
Classification
Nuclear: change lens refractive index, common in old age
Polar: localized, commonly inherited, lie in the visual axis
Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
Blepharitis
Inflammation of the eyelid margins.
Cause
It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis). Blepharitis is also more common in patients with rosacea
The meibomian glands secrete oil on to the eye surface to prevent rapid evaporation of the tear film. Any problem affecting the meibomian glands (as in blepharitis) can hence cause drying of the eyes which in turns leads to irritation
Features
Symptoms are usually bilateral
Srittiness and discomfort, particularly around the eyelid margins
Eyes may be sticky in the morning
Eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
Styes and chalazions are more common in patients with blepharitis
Secondary conjunctivitis may occur
Management
Softening of the lid margin using hot compresses twice a day
Mechanical removal of the debris from lid margins - cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used*
Artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
Episcleritis
Define
Presentation
How to differentiate with scleritis
Management
Inflammation below conjunctivae in the episclera
Presentation
- Red eye
- Classically not painful (in comparison to scleritis), but mild pain may be present
- Watering and mild photophobia may be present
Phenylephrine drops may be used to differentiate between episcleritis and scleritis. Phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels. If the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
Approximately 50% of cases are bilateral.
Management
- Conservative - topical/systemic NSAIDs
- Artificial tears may sometimes be used
Vitreous haemorrhage
Risk factors
Symptoms/signs
Risk factors Diabetes Trauma Anticoagulants Coagulation disorders Severe short sightedness
Patients typically present with an acute or subacute onset of:
painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision - cobwebs
Signs:
decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
visual field defect if severe haemorrhage
Diabetic retinopathy stages
Mild NPDR
1 or more microaneurysm
Moderate NPDR microaneurysms blot haemorrhages hard exudates cotton wool spots, venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
Severe NPDR
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
Proliferative retinopathy
retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years
What’s the normal flow of aqueous humour
Upper range for pressure in the aqueous humour compartment
Aqueous humour produced by ciliary body and is present between cornea and iris (anterior compartment)
Ciliary body produces it and it flows into the anterior chamber and then it drains via the trabecular meshwork and canal of Schlemm
Extrao-occular muscle nerve supply
Occulomotor (3rd CN): MR, IO, SR, IR
Abducens (6th CN): Lateral rectus
Trochlear (4th CN): Superior oblique
Glaucoma definition
Group of eye diseases that cause progressive optic neuropathy, and in which intraocular pressure (IOP) is a key modifiable factor.
Glaucoma is commonly associated with raised IOP and is characterized by:
Visual field defects.
Changes to the optic nerve head such as pathological cupping or, as a late sign, pallor of the optic disc.
Central retinal vein occlusion features on fundoscopy
Clinical symptoms
Fundoscopy
1) Tortuous dilated vessels
2) Diffuse haemorrhages
3) Cotton wool spots
Clinical symptoms
- Painless sudden loss of vision in eye
Complications
- Glaucoma
- Neovascularisation
Investigations
- Medical History
- BP measurement
- Serum glucose estimation
- Request laboratory investigations for FBC and ESR
Age related macular degeneration
Symptoms
Fundoscopy
Risk factors
Management
Symptoms
- Gradual loss of central vision in dry
- Rapid visual decline (sudden/days/weeks) in wet
Commonest cause of vision loss in elderly in developed world
- PAINLESS
Fundoscopy:
- DRY ARMD (90%): Drusen (fluffy white spots around macula)
- WET ARMD: Aberrant vessels grow into the retina from corrhoid –> haemorrhage –> scarring.AMSLER grid detects distortions
Risk factors
- Age
- Smoking
- FH
- IHD risk factors
Management
Age related macular degeneration
Drusen: fluffy white spots around macula
Painless central vision loss
Management:
- Dry ARMD: zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third.
- Wet ARMD: anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection
Causes of gradual vision loss
Common
- Diabetic retinopathy
- ARMD
- Cataracts
- POAG
Less common
- Retinitis pigmentosa
- HTN
- Optic atrophy
What is retinitis pigmentosa
Symptoms
Fundoscopy
Management
peripheral retina pigmentation that spares the macula
= Inherited degeneration of macula (mostly AR)
Tunnel visison; Night blindness
Leads to blindness – usually <30
Fundoscopy
- Pale disc: Optic atrophy
- Peripheral retina pigmentation spares the maula (bone spicule deposition
Management = Isn’t any but
- High dose vitamin A supplementation may slow progress
Cataracts symptoms
management
Symptoms
- Increasing myopia
- Blurred vision –> gradual visual loss (PAINLESS)
- Dazzling in sunshine/bright lights
- Monocular diplopia
Conservative - initially correctible
- Glasses
- Mydriatic drops + sunglasses may provide relief
Surgery - eventually will be needed
NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice. Also whether both eyes are affected and the possible risks and benefits of surgery should be taken into account. Prior to cataract surgery, patients should be provided with information on the refractive implications of various types of intraocular lenses. After cataract surgery, patients should be advised on the use of eye drops and eyewear, what to do if vision changes and the management of other ocular problems. Cataract surgery has a high success rate with 85-90% of patients achieving 6/12 corrected vision (on a Snellen chart) postoperatively.
= Day case phaecoemulsion + lens implant
Complications of cataract surgery (Only 1%)
Posterior capsule opacification: thickening of the lens capsule - Rx with laser capsulotomy (easy)
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour –> Blindness in 0.1%
What is retinal detachment
Symptoms
Fundoscopy
Management
Retinal detachment
Holes/tears in retina allow fluid to separate sensory retina from retinal pigmented epithelium
4 F’s 1) Floaters 2) Flashes 3) Field loss (painless and progressive) 4) Fall in acuity Dense shadow that starts peripherally progresses towards the central vision; A veil orcurtainover the field of vision; STRAIGHT LINES APPEAR CURVED; Central visual loss
Fundus
Grey, opalescent retina, ballooning forwards
Management
Urgent surgery
Central retinal artery occlusion
Clinical symptoms
Fundoscopy
Causes
Fundoscopy: Pale retina + cherry red macula
Presentation
Unilateral visual loss in seconds
Afferent pupil
Causes
GCA
Thromboembolism: clot, infective, tumour
Management
- Ocular massage
- Surgical removal of aqueous +/- acetozolamide
- Anti hypertensives (local and systemic)
What is orbital cellulitis
Cause
Risk factors
Presentation
Investigations
Management
Complications
Result of an infection affecting the fat and muscles posterior to the orbital septum, within the orbit but NOT INVOLVING THE GLOBE.
Cause
Usually spreading URTI from the sinuses and carries a high mortality rate. Orbital cellulitis is a medical emergency requiring hospital admission and urgent senior review. Periorbital (preseptal) cellulitis is a less serious superficial infection anterior to the orbital septum, resulting from a superficial tissue injury (chalazion, insect bite etc…). Periorbital cellulitis can progress to orbital cellulitis.
Epidemiology
Mean age of hospitalisation 7-12 years.
Risk factors
- Childhood
- Previous sinus infection
- Lack of Haemophilus influenzae type b (Hib) vaccination
Recent eyelid infection/ insect bite on eyelid (Peri-orbital cellulitis)
- Ear or facial infection
Presentation
- Redness and swelling around the eye
- Severe ocular pain
- Visual disturbance
- Proptosis
- Ophthalmoplegia/pain with eye movements
- Eyelid oedema and ptosis
- Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
Differentiating orbital from preseptal cellulitis
Reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis
Investigations
- Full blood count – WBC elevated, raised inflammatory markers.
- Clinical examination involving complete ophthalmological assessment – Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema.
- CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis.
- Blood culture and microbiological swab to determine the organism. Most common bacterial causes – Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
Management
admission to hospital for IV antibiotic
Complications
- Blindness due to optic N pressure
- Local extension –> meningitis and cavernous sinus thrombosis
Levator palpebrae superioris supply
Oculomotor but also sympathetic fibres
What is lateral medullary syndrome
aka Wallenberg
Occlusion of inferior cerebellar artery (supplies lateral part of medulla)
Presentation
1) Acute syncope
2) Ipsilareral
- Ataxia
- Nystagmus
- Dysphagia
- Loss of pain and temperature sensation in face
3) Contralateral
- Loss of pain and temperature sensation in limbs/trunk
What is Holmes Adie pupil
Features
Investigation
Cause
Syndrome features
Features
- Young F sudden blurring of near vision
- Initially unilateral and then bilateral pupil dilation (dilated has no response to light and sluggish to accommodation)
- A “tonic” pupil
Ix
- Iris shows wormy movements on slit lamp exam
Cause
- Damage to post ganglionic parasympathetic fibres
- Idiopathic: May have viral origin
Holmes adie syndrome
Tonic pupil + absent knee/ankle jerks and reduced BP
Argyll Robertson pupil
Features
- Small, irregular pupils
- Accommodate but doesn’t react to light
- Atrophied and depigmented iris
Cause
- DM
- Quaternary syphilis
Scleritis
Define
Presentation
Cause
Management
Vasculitis of the sclera
Presentation
- Generalised scleral inflammation - VESSELS DON’T MOVE OVER SCLERA
- Severe pain, worse on eye movement
- Conjunctival oedema
Causes
- SLE
- RA
- Vasculitis
- Wegener’s
Management
- Refere to specialist
- Most need corticosteroids or immunosuppressants
Hyphema
Risk
Management
Hyphema (blood in the anterior chamber of the eye) - especially in the context of trauma warrants urgent referral to an ophthalmic specialist for assessment and management.
The main risk to sight comes from raised intraocular pressure which can develop due to the blockage of the angle and trabecular meshwork with erythrocytes.
i.e. GLAUCOMA RISK
Strict bed rest is required as excessive movement can redisperse blood that had previously settled; therefore high-risk cases are often admitted. Even isolated hyphema will require daily ophthalmic review and pressure checks initially as an outpatient
Herpes zoster ophthalmicus
Features
Management
Complications
Herpes zoster ophthalmicus (HZO) describes the reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles.
Features
vesicular rash around the eye, which may or may not involve the actual eye itself
Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement
Management
oral antiviral treatment for 7-10 days
ideally started within 72 hours
intravenous antivirals may be given for very severe infection or if the patient is immunocompromised
topical antiviral treatment is not given in HZO
topical corticosteroids may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review
Complications
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia
