Opthalmology Flashcards
Hypopyon and hyphema, herpetic keratitis
Hypopyon - pus in anterior chamber of the eye
Hyphema - blood in anterior chamber of the eye
Herpetic keratitis - Form of keratitis caused by recurrent herpes simplex viral infection within the cornea
Amaurosis fugax and retinal detachment types
Amaurosis fugal - temporary loss of vision in one or both eyes due to lack of blood supply in the retina
Retinal detachment - neurosensory layer of the retina separates off from the underlying retinal pigment epithelium (RPE)
types:
- rhegmatogenous (most common) retinal tear leading to separation of retina from epithelium
- traction, fibrosis/fibrovascular proliferation leads to scar tissue pulling off the retina
- serous, accumulation of sub retinal fluid leads to retinal separation
visual field defects
central scotoma - blind in central vision of affected eye
monocular vision loss - loss of total vision in one eye
bitemporal hemianopia - loss of half visual feel in both eyes (outer half lost)
contralateral homonymous hemianopia - loss of half visual field in both eyes on the same side of visions (e.g. both eyes lose left half of vision)
contralateral superior/inferior quanrantopia - loss of a quarter of visual field in both eyes on the same side in each eye either superior quarter or inferior quarter
contralateral homonymous hemianopia with macular sparing - half visual field lost aside from the central portion where macula is located (macula sparing) in both eyes
Blepharitis
Background:
Chronic inflammatory condition affecting the margin of the eyelids
Anterior blepharitis - inflammation of the base of the eyelashes (anterior margin of the eyelid_
Posterior blepharitis - inflammation of the meibomian glands
Complications - chalazion, external stye (hordeolum), eyelash changes (loss, misdirection and depigmentation), eyelid thickening, ulceration and scarring (ectropion or entropion), contact lens intolerance, conjunctivitis, corneal inflammation (keratitis)
Pathology:
Meibomian glands are a set of glans running along the posterior eyelid margin that produce lipid secretion, providing the lipid layer of the tear film
Aetiology:
Can be associated with seborrheic dermatitis, eczema and acne rosacea
S. aureus is the most common bacterial pathogen
Mite infestation can occur if part of the normal flora on the eyelid
Anterior blepharitis - usually bacteria (staph) or seborrhoeic dermatitis causes
Posterior blepharitis - meibomian gland dysfunctions
Blepharitis presentation and investigations
Presentation:
Inflammation around the eyelid margins
Sticky discharge or crusty in the mornings
Irritation or foreign body sensation in eye
Madarosis (loss of eyelashes)
Chalazion - meibomian gland cyst
Marginal keratitis (corneal ulcer)
Burning, itching and/or crusting of eyelids
Symptoms worse in the mornings
Recurrent hordeolum
Contact lens intolerance
Investigation/diagnosis:
Clinical diagnosis based on history
Swabs for severe, recurrent or resistant symptoms
Blepharitis management and referrals
Conservative:
Eyelid hygiene - clean flannel or cotton bud with cleanser (johnson’s baby shampoo and warm water) to remove debris
Warm compresses - clean cloth or flannel soaked in kettle boiled cooled water, apply to closed eyelids for 5-10 minutes once or twice daily
Brief gentle eyelid massage after cleansing may improve expression of meibomian gland secretions inpatients with posterior blepharitis.
Consider replacing eye makeup
Continue eye hygiene even when asymptomatic as a preventative measure
Medical:
2nd line if conservative measures are ineffective
Anterior blepharitis - chloramphenicol ointment or drops and rubbed into margins
Posterior blepharitis - oral antibiotics doxycycline or tetracycline (CI pregnancy, lactation and <12 YO)
Eye drops: artificial tears to aid dry eyes
Referral:
Same day referral for pain and blurred vision (corneal disease), rapid onset visual loss, orbital or preseptal cellulitis or painful and/or red eye
Urgent or routine referral for eyelid asymmetry/deformity (malignancy), gradual deterioration of vision, underlying conditions (Sjogren’s or ocular pemphigoid), failure in primary care treatment or uncertain diagnosis.
Conjunctivitis
Background:
Inflammation of the conjunctiva due to allergic or immunological reactions, infection, mechanical irritation, neoplasia or contact with toxic substances
Types - allergic or infective
Can be acute (<4 weeks), chronic (>4 weeks) or recurrent
Complications - allergic type can cause vernal/atopic keratoconjunctivitis can cause thickening of eyelid, ptosis, scarring, corneal neovascularization, thinning, ulceration, infection and loss of vision. Bacterial type can cause epidemic keratoconjunctivitis, keratitis, corneal perforation, trachoma (scarring)
Pathology:
Conjunctiva is a thin, transparent mucous membrane lining the anterior part of the sclera (bulbar conjunctiva) and the under-surface of the eyelids
Inflammation of infection of the conjunctiva causes dilation of conjunctival vessels leading to hyperaemia and oedema of the conjunctiva which may be associated with discharge
Associated corneal involvement (keratoconjunctivitis) and eyelid involvement (blepharoconjunctivitis)
conjunctivitis causes and risk factors
Aetiology:
Allergic - IgG response to allergen, causing degranulation of mast cells triggering inflammatory cascade and histamine/prostaglandins release leading to ocular itching, blephara redness and swelling
Viral - most commonly adenovirus but can be herpes simplex, varicella zoster, molluscum contagiosum, EBV etc.
Bacterial - most commonly strep. Pneumoniae, staph. Aureus, moraxella catarrhalis and H. influenzae. Can include chlamydia trachomatis and N. gonorrhoeae
Ophthalmia neonatorum (ON) - chlamydia, gonorrhoea, haemophilus species, strep. Species etc. (non-sexually transmitted in 30-50% of cases)
Risk factors:
Dry eyes, eczema, rosacea can worsen allergic conjunctivitis symptoms
conjunctivitis presentation and investigations
Presentation: Erythema Foreign body sensation/burning/itching Lacrimation Discharge (watery - allergic or viral, purulent - bacterial) Blurred vision (occasional)
Investigation/diagnosis:
Clinical diagnosis - difficult to determine viral and bacterial infection
conjunctivitis management
Allergic - self limiting, reduce allergen exposure (sunglasses, washing hair before bed, avoid rubbing eyes, cold compresses), topical antihistamines (antazoline sulphate, ketotifen) +/- mast cell stabilisers (sodium cromoglicate)
Infections - may resolve within 5-7 days, warm compresses with boiled water/saline, avoid contacts
If contagious - avoid sharing towels, makeup etc. may need time off school or work
Bacterial - Deferred antibiotics for 72 hours - chloramphenicol drops (apply 1 drop 2 hourly for 2 days then 4 times daily for 5 days) or ointment (apply four times daily for 2 days then twice daily for 5 days)
2nd line fusidic acid eye drops BD for 7 days
Artificial tears/topical antihistamines for viral infections
Chalazion
Background:
AKA meibomian cyst
Sterile inflammatory granuloma caused by obstruction of the sebaceous glands
Complications - astigmatism and visual disturbance, infection (cellulitis)
Pathology:
Blocked meibomian gland resulting in extruded lipid secretions
Glands sit alongside the eyelid margin, producing lipid layer secretions of the tear film
Blockage of the duct causes enlargement and rupture, releasing accumulated lipid contents into the surrounding eyelid soft tissue
This triggers an inflammatory response against the lipid content (lipogranulomatous reaction) which subsides with time
Aetiology:
Blocked meibomian gland
Chalazion risk factors and presentation
Risk factors: Chronic blepharitis Seborrhoeic dermatitis Rosacea Pregnancy Diabetic Elevated serum cholesterol Chronic hordeola (styes)
Presentation: Swollen eyelid Inflammation Firm nodule, painless Fluctuant - may spontaneously drain
Chalazion investigations and management
Investigation/diagnosis:
Clinical diagnosis, chalazion are typically painless and bigger in size
Rule out signs of orbital cellulitis - RED FLAG
Management:
May resolve spontaneously within weeks or months
Warm compresses 10-15 minutes up to 5 times a day
Massage with clean hands/cotton bud in direction of the lashes to encourage discharge
Incision and curettage via ophthalmology referral for persistent, recurrent symptoms causing significant astigmatism or cosmetically unacceptable
2WW if diagnosis unclear and malignancy suspected
Pterygium
Background:
Benign triangular fibrovascular conjunctival growth
Pathology:
Theorised that pterygia develop as a result of UV exposure
Can encroach on cornea placing tension resulting in astigmatism and loss of vision sharpness
Aetiology:
Multifactorial - thought to be from UV exposure
Risk factors: Increased UV exposure Environment - desert, dry arid climate Increasing age Male gender
Pterygium presentation and investigations
Mild irritation Erythema Dryness Foreign body sensation Inflammation Bilateral asymmetrical growth
Investigation/diagnosis:
Clinical diagnosis
Pterygium management
Usually needs specialist referral
Revolves around UV protection: sunglasses (tinted), hat (brimmed)
Cold compresses may help periods of inflammation
Topical steroids (fluorometholone for one month)
NSAIDs
Artificial tears/lubricating ointments
Surgical excision if infringing on the middle cornea, threatening vision or if inflammation cannot be controlled
Orbital cellulitis
Background:
Infection involving the deep soft tissue surrounding the eyeball, located posterior to the orbital septum
Can be orbital and periorbital
More common in under 10 years old
Periorbital cellulitis - infection anterior to the orbital septum
Pathology:
Infection involving the deep soft tissue surrounding the eyeball, located posterior to the orbital septum
Aetiology:
Staph and strep organisms, Haemophilius species are typically the causatives
Often precipitated by acute sinusitis (especially ethmoid), trauma, dacryocystitis, preseptal cellulitis, dental abscesses
Periorbital precipitators - URTI, dacryocystitis, hordeolum, impetigo, trauma, recent eye surgery
Orbital cellulitis presentation
Periorbital - ptosis (eyelid retraction), fever, malaise, NO ocular involvement, may breach orbital rim Unilateral eyelid oedema Severely painful red eye Infection extends past the orbital margins into the maxilla Restricted eye movements Proptosis (eyeball protrusion) Pupillary defects Headaches, fever, malaise
Orbital cellulitis investigations and management
Investigation/diagnosis:
Clinical diagnosis
Bloods, cultures
CT/XR
Management: Same day admission - medical urgency Can rapidly progress to lid deterioration (presetal), loss of vision, cerebral complications (thrombosis, meningitis, central abscesses) Take blood cultures to confirm species Antibiotics determined by species
dacryoadenitis
Background:
Inflammation of the main or accessory lacrimal gland
Can be acute or chronic
Dacryocystitis - inflammation of the lacrimal tear sac
Pathology:
Lacrimal glands are a serious type exocrine glands that secrete lacrimal fluid onto the surfaces of the conjunctiva and cornea of the eye
Lacrimal fluid acts to clean, nourish and lubricate the eyes and forms tears when produced in excess
Aetiology:
Inflammation of the gland can be due to infectious or inflammatory sources but may be idiopathic
dacryoadenitis presentation
Symptoms may be unilateral or bilateral and include pain/tenderness in superolateral orbit
Erythema
Exudate (bacterial cause)
Swelling - temporal side of upper eyelid +/- ptosis
Upper eyelid may becomes S shaped due to enlargement of lacrimal gland
Conjunctival infection +/- chemosis (swelling of conjunctiva)
Regional LAP
Proptosis (eye protrusion)
Limited ocular motility and visual loss (rare)
Fever and malaise (infective causes)
dacryoadenitits investigations and management
Investigation/diagnosis:
Clinical diagnosis
CT head - enlarged lacrimal gland
ACUTE - Viral serology (EBV, adenovirus, mumps, herpes simplex, herpes zoster)
ACUTE - Swabs - staph. Aureus, strep pneumoniae, TB, gram -ve rods
Chronic - sjogren syndrome, sarcoidosis, crohn’s disease, granulomatosis with polyangiitis and thyroid disease
Bloods - FBC, ESR, CRP, ANA and autoantibodies, TFTs, IgG4
Management:
Viral - self-limiting resolves within 4-6 weeks, warm compresses and symptomatic Mx of NSAIDs, antihistamines is helpful
Bacterial - antibiotics, incision and drainage (abscess)
Inflammatory causes - steroids, manage underlying causes as may become chronic relapsing remitting pattern
Surgery for severe or recurrent cases - biopsy of lacrimal gland for diagnostic value.
Corneal abrasion
Background:
Recurrent corneal erosion syndrome - if presenting recurrently with corneal abrasion, can occur many months or years after initial corneal abrasion
Pathology:
Scratch on the cornea of the eye
Recurrent corneal erosion syndrome - initial scratch damages the cornea and does not heal completely, forming a blister. The blister sticks to the underside of the eyelid (usually whilst sleeping, dry eyes or dusty environments). When the eye opens the blister may pop or tear causing the damage to reappear.
Aetiology:
Fingernails, hairbrushes, dust particles, grit, accidental traumas
Corneal abrasion presentation and investigation
Presentation:
Foreign body sensation/foreign body still present
Painful eye
Red eye
Watery
Photophobia
Recurrent corneal erosion syndrome - watery eye, painful, worse in the morning, photosensitivity, vision blurring
Investigation/diagnosis:
Eye examination; Snellens chart, appearance, movements, visual fields, PEARL size, fluorescein staining, slit lamp (abrasions), flip the eyelid!!
Pupil, equal and reactive to light = PEARL
Corneal abrasion management
Topical anaesthetic drops (tetracaine, oxybuprocaine) interfere with Na ions entering nerve cells, reducing impulse generation and pain perception. WARN patient that it may sting on application and to let you know when the stinging stops. Usually wears off within 20 minutes - NOT prescribed as pain relief ONLY prescribed for eye examination as can slow corneal healing.
Usually heals on its own, pain settles over 24-48 hours, take simple painkillers as needed
Eye can feel gritty for several weeks
Risk of eye infection - give chloramphenicol eye ointment QDS for 5 days (pull down lower eyelid and apply 1cm strip, blink to spread medication)
Eye patch IF necessary for several hours
Sunglasses might help photophobia and avoid touching/rubbing the eye
AVOID contact lenses
Lubricant eye drops PRN.
Recurrent corneal erosion syndrome - treat as corneal abrasion but with long term eye lubricant use (eye drops and ointments) regular use at night, artificial tears throughout the day to provide a barrier between the lid and cornea preventing blister tearing/sticking. Continue for several months even once asymptomatic
Foreign body in eye
Pathology:
Foreign object becomes lodged under the eyelids or in the eye
Rust rings - may form around foreign bodies that contain iron, typically those that are metallic. Salt in tears interacts with the Fe forming rust in the eye. The reaction begins within 2-4 hours of the foreign body embedding into the eye. Complete rust ring formation can be after 8 hours. The ring may persist even after foreign body removal, staining the cornea. Residual rust can also migrate to the surface within 24 hours usually.
Aetiology:
Fingernails, hairbrushes, dust particles, grit, accidental traumas, metals etc.
Foreign body in eye presentation and investigation
Foreign body sensation/foreign body still present Painful eye Red eye Watery Photophobia Rust rings
Investigation/diagnosis:
Eye examination using topical anaesthetic (EVERT EYELID) - Snellens chart, appearance, movements, visual fields, PEARL size, fluorescein staining, slit lamp (abrasions), flip the eyelid!!
Pupil, equal and reactive to light = PEARL
Foreign body in eye management and referrals
Management:
Topical anaesthetic drops (tetracaine, oxybuprocaine) interfere with Na ions entering nerve cells, reducing impulse generation and pain perception. WARN patient that it may sting on application and to let you know when the stinging stops. Usually wears off within 20 minutes - NOT prescribed as pain relief ONLY prescribed for eye examination as can slow corneal healing.
Once confirmed, moisten a cotton bud with saline drops and gently remove the foreign body with a cotton bud, sweeping from the conceal surface
Only use a needle to remove if you have been trained and have appropriate magnification
If unable to remove, apply eye patch and refer to ophthalmologist for removal
It is likely you may cause corneal abrasion via removal techniques if the object is difficult to remove
Referrals:
Unable to remove foreign body
Rust rings present
Visual acuity or fields are affected (blurred vision or blind spots)
Pupil concerns - unequal or unreactive to light
Bleeding from eye or around eye
Clear or bloody fluid coming from the eyeball
Keratitis
Background:
Can be infectious or not
Common condition, more frequent in those wearing contact lenses
Bacterial keratitis is the most common form.
Pathology:
Inflammation of the cornea
Aetiology:
Noninfectious - eye injury, contact lenses, foreign body in eye, swimming with contact lenses
Bacteria - pseudomonas aeruginosa and staph. Aureus are the most common causes, usually in people who improperly use contact lenses
Fungi - fungal keratitis caused by aspergillus candida or fusarium, usually in people who improperly use contact lenses or from outdoor exposure
Parasites - acanthamoeba in those with contacts (swimming lakes, wooded areas)
Viral - herpes simplex virus, often progresses to keratitis from conjunctivitis
Risk factors:
Contact lenses
Keratitis presentation
Red eye Pain and irritation Blurry or vision changes Photophobia Difficulty opening the eye Discharge +/- hypopyon (leukocyte collection at bottom of anterior chamber in severe cases) Round corneal infiltrate or ulceration Excessive tearing
acanthamoeba keratitis
bacterial keratitis
keratitis investigation and management
Investigation/diagnosis:
Scrape or test for underling culture
Eye examination: Snellens chart, appearance, movements, visual fields, PEARL size, fluorescein staining, slit lamp (abrasions), flip the eyelid!!
Pupil, equal and reactive to light = PEARL
Management:
Urgent referral to ophthalmology
Can lead to corneal ulcers and destruction of the stroma leading to perforation
Treat cause - antibiotics/antifungals/antivirals etc.
Severe cases - corneal transplant
Glaucoma background and types
Background:
Eye disorder leading to progressive damage of the optic nerve, loss of nerve tissue resulting in vision loss
Most common form is primary open angle glaucoma
Acute angle closure glaucoma - rare medical emergency, can cause vision loss within 24 hours, affects 1 in 1000 people in their lifetime. Can be acute or chronic.
Types:
Primary open angle glaucoma (chronic simple glaucoma)
Acute angle closure glaucoma
Secondary glaucoma
Congenital glaucoma - rare but usually present at birth or develops shortly after. Caused by eye abnormality
glaucoma pathology and cause
Pathology:
Primary open angle glaucoma - fluid pressure inside the eye increases, due to increased resistance through the trabecular meshwork in the eye, increasing pressure may cause damage to the optic nerve and causes a loss in nerve fibres
Normal intraocular pressure is 10-21mmHg
Advanced glaucoma leads to blindness
Acute angle closure glaucoma - with age the lens becomes larger, pushing the iris forward and narrowing the space between the iris and cornea. As this angle narrows the fluid from the eye is blocked from the drainage system. This suddenly increases the intraocular pressure. Although the attack often only affects one eye, the other may be at risk as well.
Aetiology:
Secondary glaucoma - result of eye injury or underlying conditions such as uveitis
Acute angle closure glaucoma - narrow drainage angle
glaucoma risk factors
Acute angle glaucoma - more common in those >40 YO often between 60-70 YOs. long sighted, women, southeast asian and inuit people. More likely to come on whilst pupils are dilated. Medications like eye drops, SSRIs, TCAs, ipratropium topiramate and ranitidine cause pupil dilation.
primary glaucoma: Family history (up to 10 fold) Age 60+ African and hispanic people Thin corneas Myopia (short sighted) Increased ocular pressure >21mmHg Possibly HTN/diabetes
Glaucoma presentation
Primary open angle glaucoma - develops slowly, asymptomatically until significant vision loss is reached, usually loss of peripheral vision (tunnel vision) and eventual loss of central vision
Subacute or intermittent Acute closed angle glaucoma - intermittent attacks of burning, haloes without pain, attack may end when going into brighter rooms due to pupil constriction pulling the iris away from drainage channels. Attacks can last a few hours then symptoms improve. With each attack vision may be damaged further.
Acute angle closure glaucoma - blurred vision, haloes, coloured rings around lights, severe sudden pain in one eye, can radiate to severe headache, red eye, nausea and vomiting, generally unwell, hazy cornea, worsening symptoms. Hard eyeball Fixed pupil Dilated pupil Hazy cornea Circumcorneal erythema
Glaucoma investigations
Eye vision screening, routine or due to visual disturbance, visual fields test
Fundoscopy - optic disc cupping, optic nerve health
Ocular pressure estimate (non-contact tonometry, uses puff of air to measure corneal response)
Goldmann applanation tonometry - gold standard for measuring ocular pressure. Device applies pressure to the cornea to determine intraocular pressure
Blowout fracture
Background:
Characterised by double vision, sunken ocular globes, loss of sensation of the cheek and upper gums due to infraorbital nerve injury
Two broad categories of blowout fractures - open door (large, displaced and comminuted) and trapdoor (linear, hinged and minimally displaced)
Trapdoor fracture - Seen in children and young adults due to elasticity of the orbital floor. Fractures may be subtle and are associated with high risk of tissue entrapment
The floor of the orbit is the most common portion to sustain fracture
Pathology:
The orbit holds the eye in place and protects the eyeball
Following trauma, the muscles, fat and connective tissue can be bruised and displaced. If enough volume is lost from the orbit, the eye sinks back into the orbit (enophthalmos) causing cosmetic and functional concern
If eye muscles are impacted by fracture then eye motility and possibly double vision is affected
Children <7 years have thinner bones and have not fully developed the maxillary sinus, making them more likely to break the orbital bone as the floor bone.
Trapdoor fracture - fracture of the orbital floor where the inferiorly displaced blowout fracture recoils back to its original position and potentially entraps contents of the orbit.
Aetiology:
Trauma to the eye/orbital region
Risk factors:
Children <7 YOs
blowout fracture presentation and investigation
Presentation:
Most commonly bruising, tenderness and swelling around the eye
Diplopia
Cheek numbness, nose or teeth
Disruption of smooth contour of orbital floor on palpation
Reduced eye motility especially up and downward movements
Air under skin around the eye
Trapdoor fracture - pain with eye movements, N+V, diplopia
Investigation/diagnosis:
Eye examination - Snellens chart, appearance, movements, visual fields, PEARL size, fluorescein staining, slit lamp (abrasions), flip the eyelid!!
Pupil, equal and reactive to light = PEARL
blowout fracture management
All patients need a follow up with ophthalmology within 1 week of fracture
Advice to avoid blowing nose, can use nasal decongestants to prevent orbital emphysema.
Most fractures heal spontaneously without significant consequence
Surgery indicated if there is enophthalmos >2mm on imaging, diplopia on primary or inferior gaze, entrapment of extraocular muscles or fracture involving >50% of the orbital floor. Surgery is rarely performed immediately, can be safely postponed for up to 2 weeks if needed for swelling to subside. Usually provides permanent cure but sometimes provides only partial relief from diplopia or sunken eye.
Glaucoma management
Management:
Treatment usually started if pressure is >24mmHg
Eye drops to reduce intraocular pressure - topical prostaglandin analogue to increase aqueous outflow e.g. latanoprost or topical B blocker reducing aqueous secretion e.g. timolol
Laser - stimulate biochemical change to improve outflow of fluid form the eye
Surgery - trabeculectomy (channel ‘bleb’ is created from which fluid drains from the eye)
Acute angle closure glaucoma
Emergency referral to ophthalmology, do NOT cover with eyepatch or leave in darkened room, this dilates pupil and worsens symptoms,
NICE first line - lie patient flat, head NOT supported by pillows as may relieve pressure
Pilocarpine eye drops constricting pupils helping fluid drainage
Acetazolamide orally 500mg, analgesia and antiemetic if needed
Beta blocker and steroids to reduce fluid production and inflammation (timolol)
Mannitol IV to reduce fluids.
Once attack has ceases - preventative measures such as laser (peripheral iridotomy) to assist drainage or surgery (surgical iridectomy), often done for both eyes not just the symptomatic one
Sometimes eye drops are needed longer term for intraocular pressure control
corneal arcus
Grey thickened film across the lens is NOT a cataract - it is the corneal arcus and is not usually a cause for concern
Formed from cholesterol deposits building up during ageing leading to the grey ish ring presentation around the iris
Typically related to the slowdown in lipid metabolism as the patient ages, however, if presenting before age 40 could indicate more sinister pathology.
Can indicate atherosclerosis, high cholesterol, hypertension and other conditions if in those under age 40
The condition itself is not harmful to vision or eye health but it is wise to get blood tests screening for cholesterol, LFTs, U+Es, and measure blood pressure
cataracts and risk factors
Background:
Gradual progressive clouding and thickening of the lens of the eye
Major cause of treatable blindness worldwide
Usually an age related condition common in >65 YO most common in women
Rarely it can be congenital (juvenile cataract)
Cataracts can obscure other pathologies such as AMD or glaucoma
Pathology:
Eye lens is made mostly of water and protein fibres
Clouding of vision occurs when lens proteins (crystallins) clump together, resulting in poor light refraction and therefore worsening sight
Aetiology:
Clumping of the crystallin proteins within the optic lens
Risk factors: Smoking Alcohol consumption Diabetes Steroid treatment UV exposure Poor nutrition and socio-economic status
cataracts presentation and investigations
Build up of brown-yellow pigment (lens proteins)
Grey cloudy appearance on the PUPIL (NOT the iris)
Decreased visual acuity - blurred vision
Gradual painless loss of vision (rapid with diabetic cataracts)
Difficulty reading
Failure to recognise faces
Problems watching TV
Reduction in colour intensity
Diplopia in one eye (advanced)
Starbursts around lights, especially at night time
Investigation/diagnosis:
Eye examination - visual acuity, colour vision
Loss of red reflex
CN II exam
cataracts management and referrals
Ophthalmology referral for surgery based on level of visual impairment, how it affects their life, willingness to have surgery, comorbidity which may benefit from surgery, diabetic retinopathy, diplopia, change in colour perception or where complications (secondary glaucoma or uveitis) is likely.
Faster referral - diabetics, colour vision damage
Surgery is an intraocular lens implant (IOL) by LA/GA and is the only effective management, has low morbidity and mortality with high success rates
One rare but serious complication of surgery is endophthalmitis - inflammation of the inner eye usually from infection, can lead to loss of vision or the eye itself. Treated with intravitreal antibiotics injected into the eye.
Urgent referrals:
Suspected AMD, particularly with vision distortion or rapid changes (diabetic retinopathy)
Sinister pathology is suspected
Vision loss is bilateral
Pain or erythema in eye or additional visual symptoms e.g. flashes
Rapid visual deterioration, progressive or new deterioration
Mononuclear patients or those who already have poor vision in one eye. Any vision loss in the ‘good’ eye requires urgent assessment
congenital cataracts
Background:
Onset <6 months
Juvenile cataracts
Has a risk of amblyopia (lazy eye)
Pathology:
Eye lens is made mostly of water and protein fibres
Clouding of vision occurs when lens proteins (crystallins) clump together, resulting in poor light refraction and therefore worsening sight
Aetiology: Congenital infections (TORCH)
congenital cataracts presentation, investigation and management
Presentation:
Irregular/partially absent red reflex detected in initial screening (when shining light onto pupils they usually turn red but instead turn white/grey)
Presence of leukocoria or white reflex in light or photos
Investigation/diagnosis:
Eye examination - CN II
Screen for TORCH syndrome (congenital infections) - toxoplasmosis, other agents (syphilis, parvovirus, varicella zoster, zika virus), rubella, cytomegalovirus, herpes simplex
Red reflex screening in neonates
Management:
Urgent referral within 4 weeks to ophthalmologist
strabismus
Background:
Abnormality of the coordinated movement of both eyes
Congenital - onset <6 months of age or acquired from >6 months of age
Exotropia - divergent squint, one eye turned out
Esotropia - convergent squint, one eye turned in
Hypertropia - upward turn
Hypotropia - downward turn
Paralytic squint - paralysis of CN III, IV and VI, direction of gaze does affect the size of the squint or presence of the squint.
Non-paralytic squint - other cause, size of deviation does not vary with direction of gaze, usually congenital
Convergent squint (esotropia) is most common in children, they have a risk of strabismic amblyopia from the brain suppressing deviated images and leading to the visual pathway not developing normally
Divergent squint is more common in older children and has less risk of amblyopia
Heteropia or manifest squint - slight tendency for gaze to deviate particularly when gazing in the distance or daydreaming. This is usually normal as perfect gaze alignment (orthophoria) is unusual
Squint can be intermittent of persistent, most intermittent squints are accommodative in origin
Pathology:
For single vision, fine coordination of both eye movements is needed (CN III, IV and VI)
Misalignment of the eyes results in the retinal image not in corresponding areas of both eyes which can cause diplopia (adults) and amblyopia (children)
strabismus cause, risk factors and presentation
Aetiology:
Palsy/dysfunction in cranial nerves CN III, IV and/or VI
Sometimes can be caused by disorder to the external ocular muscles
Manifest squint - muscle strength inadequate to maintain alignment, stimulus to maintain alignment is weak (blurred vision) or problems with neurological pathways
Risk factors:
Disorders affecting the brain such as Down’s syndrome, hydrocephalus, space-occupying lesions, stroke, graves disease
Trauma
Presentation:
Reduced visual acuity
Diplopia
Asthenopia (eye strain, fatigue or pain) particularly in the afternoon or end of the day
Low school performance or issues
Walking difficulties
Manifest squint - one eye covered and movement of uncovered eye takes up fixation
Latent squint (phoria) - one eye covered, no squint in the other eye, then covering is removed and there is movement of the previously covered eye
abnormal red reflex - light shone into eye
strabismus investigation and management
Screening tests - corneal reflection (light reflex test; should fall centrally and symmetrically on each cornea, will be asymmetrical with squint), ocular alignment test
Cover test
Cover-uncover test
Management: 3Os
Optical - diagnosis and treatment (spectacles) or refractory erros (reduce risk of anisometropic amblyopia)
Othoptic - patching the good eye encouraging use of the squint eye
Operations - resection and recession of rectus muscles to correct alignment
Age related macular degeneration
Background:
Age-related macular degeneration is one of the most common causes of blindness in the UK
Can be wet (10%) or dry (90%) macular degeneration
Wet AMD progresses more rapidly and carries a worse prognosis and often progresses to bilateral disease
Pathology:
The macula is located in the retina in the centre at the back of the eye globe. It contains a concentrated area of rods and cones called the fovea which is vital for central vision.
It is made of four layers, the choroid (contains blood vessels), Bruch’s membrane, retinal pigment epithelium and then photoreceptors
Degeneration and defective changes in the macula cause atrophy of the retinal pigment epithelium
WET AMD - aberrant vessels grow from choroid into the neuro-sensory retina and leak, causing oedema and rapid loss of vision.
DRY AMD - Drusen and degenerative changes at the macular (small yellow deposits of fatty proteins accumulating in the retina)
risk factors for AMD and presentation
>50 YO Family history Smoking Caucasian Diet high in saturated fats (meats, butter, cheese) Overweight HTN
Presentation:
Deteriorating central vision (loss of central fields) - scotoma (central patch of vision loss)
Ophthalmoscopy - pigment, drusen +/- bleeding at the macula
DRY AMD - Drusen and degenerative changes at the macular (small yellow deposits of fatty proteins accumulating in the retina)
WET AMD - aberrant vessels grow from choroid into the neuro-sensory retina and leak, progresses rapidly
Amsler grid - blurry, wavy lines, dim areas
Atrophy of the retinal pigment epithelium
AMD investigations and management
Investigation/diagnosis:
Optical coherence tomography - scans retina and macula
Slit lamp biomicroscopic fundus exam - specialist exam
Ophthalmoscopy
Fluorescein angiography - blood supply, oedema and neurovascularisatoin
Visual exam using Amsler grid, snellen chart
Management:
Smoking cessation, vitamin supplements (C, E, Zinc) can slow progression
Diet rich in green vegetables and fruits
Wet AMD - anti-VEGF intravitreal injections (ranibizumab, bevacizumab, pegaptanib) once monthly
Laser photocoagulation
intravitreal steroid injections
Ectropion of the eyelid
Background:
Can be with increasing age or cicatricial (trauma)
Common in older adults, generally affecting the lower eyelid only but can affect the entire length of the eyelid if severe, usually only one segment sags away from the eye
Pathology:
Lower eyelid turned out due to natural loss of muscle tones and orbital fat in older age
Excessive tearing can occur due to lack of proper drainage and tears may pool/overflow the eyelid constantly
Sensitivity to light may occur due to the surface of the cornea being irritated
Secondary infection due to the exposed conjunctiva can lead to keratitis
Aetiology:
Natural loss of muscle tone with age
Risk factors:
Increasing age
ectropion (eye) presentation, Ix and Mx
Presentation:
Usually lower eyelid section or entire eyelid pulling downwards away from the eye, turning out to expose inner eyelid margins
Watery or teary eyes
Excessive dryness - gritty, sandy
Irritating - stagnant tears or dryness causing irritation, burning and redness
Sensitivity to light
Infection or keratitis
Investigation/diagnosis:
Clinical diagnosis
Eye exam
Management: Artificial tears Lubricating eye ointments Treating secondary infections Surgical correction PRN
Entropion (eye) and presentation
Pathology:
Eyelid turned inward, generally only the lower eyelid due to atrophic changes in the affected eyelid
Exacerbated often by the inturning of eyelashes causing conjunctiva and corneal irritation
Aetiology:
Atrophic changes in lower lid retractors due to trachoma infection (common in africa, asia)
Congenital
Risk factors:
Family history
Living in africa or asia
Presentation:
Lower eyelid usually turned inwards, eyelashes inverted
Reported irritation of the eye, redness, pain
Foreign body sensation
Corneal damage
Entropion (eye) investigation and management
Investigation/diagnosis:
Clinical diagnosis
Eye exam
Management:
Artificial tears
Lubricating eye ointments to relieve irritation
Surgery to correct eyelid - if left untreated can cause damage to the cornea, eye infections and vision loss
retinal vein occlusion
Pathology:
The central retinal vein runs through the optic nerve and drains blood from the retina, there are four branches that converge to form the central retinal vein, blockage in one can cause problems in one area whereas blockage in the central vein causes drainage problems in the whole eyeball.
Occlusion leads to venous stasis - increased viscosity, fluid and blood stagnate and leak from blood vessels into the retina tissue
This forces the layers of the retina apart (serous retinal detachment) and affects the retinas ability to respond to light
Aetiology:
Thrombosis or external pressure on the retinal vein causing vessel occlusion
External pressure due to hypertensive or sclerotic changes in the central retinal artery in the optic nerve head
Occlusion of the central retinal vein at its exit from the eye by raised intraocular pressure (e.g. chronic glaucoma)
retinal vein occlusion RFS and presentation
Risk factors: >60 YOs HTN Hypercholesterolaemia Raised eye pressure (glaucoma) Diabetes Smoking Thrombophilic disorders
Presentation:
Leaking, swollen vessels, bleeding seen on fundoscopy
Reduced vision in affected eye
Unilateral painless loss of vision (unless complicated by glaucoma)
May be asymptomatic if blockage is small
retinal vein occlusion Ix and Mx
Investigation/diagnosis:
Fundoscopy - flame and blot haemorrhages, optic disc oedema, macula oedema
Bloods - FBC (LEUKAEMIA), ESR, serum glucose
Blood pressure
Eye exam - visual acuity
Management:
It is not possible to treat or remove occlusions in retinal veins, management focussed on minimising damage, reduce risk of further occlusion and treating complications
anti-VEGF intraorbital injections stops abnormal blood vessels growing then leaking and bleeding into retina
Steroids intraorbital injections (often repeated regularly)
Panretinal photocoagulation PRP laser treatment sometimes used to branch retinal vein occlusions and can be helpful to central vision
retinal artery occlusion
Background:
Ophthalmic emergency
Occurs to 1 in 100,000 a year
Pathology:
Blockage of the blood flow through the central retinal artery which supplies blood to the retina
Branch of the ophthalmic artery from the internal carotid
Aetiology:
Embolism/atherosclerosis is the most common cause
Ophthalmic causes include severely raised intraocular pressure
GCA - vasculitis affects the ophthalmic or central retinal artery reducing blood flow
retinal artery occlusion RFs and presentation
Risk factors: Increasing age Family history Smoking Alcohol intake Diabetes HTN Poor diet Inactivity Obesity GCA
Presentation:
Sudden, painless loss of vision
Usually unilateral
Relative afferent pupillary defect - pupil constricts more when light is shone into the other eye in comparison to when light is shone into the affected eye directly, as ischaemia means it does not detect the input as well
Fundoscopy reveals a pale retina with attenuation of vessels and a cherry red spot
retinal artery occlusion Ix and Mx
Investigation/diagnosis: Fundoscopy Clinical diagnosis Eye examination Bloods - ESR if GCA indicated Temporal artery biopsy if GCA indicated
Management:
Emergency hospitalisation for specialist management
Ocular massage
Remove fluid from anterior chamber to reduce intraocular pressure
Inhaling carbogen to dilate artery
Sublingual isosorbide dinitrate
Long term - manage reversible risk factors and secondary prevention of CVD
retinal detachment
Background:
Ophthalmic emergency
Pathology:
Separation of the neurosensory layer of the retina from the choroid layer, causing traction of the retina and potentially leading to retinal tearing
Aetiology:
Retinal tear allowing vitreous fluid to fill the space most commonly (rhegmatogenous)
Fibrosis and proliferation leading to scar tissue pulling the retina off (traction)
Accumulation of subretinal fluid leading to retinal detachment (serous)
Risk factors: Increased age Myopia - severe nearsightedness Proliferative diabetic retinopathy Severe HTN Family history Previous cataract surgery Ocular trauma
retinal detachment presentation Ix and Mx
Sudden onset of floaters and flashes in vision
Loss of vision (PAINLESS)
Blurred and distorted vision
Fundoscopy can show fluid under the retina, tear in retina or lines of detachment
Investigations/diagnosis:
Eye examination - visual acuity, visual field tests
Fundoscopy
Management:
Same day referral to specialist, urgency dependent on clinical suspicion, changes in visual acuity, visual field loss or fundoscopy findings
Cryotherapy or laser photocoagulation to achieve permanent adhesion between the retina and RPE.
This prevents recurrence of fluid in 95% of cases and stops retinal detachment progression
optic neuritis and presentation
Pathology:
Inflammation of the optic nerve, in patients with MS often presents with acute demyelinating optic neuritis (ADON)
Aetiology/risk factors: MS - acute demyelinating optic neuritis (ADON) Diabetes Vitamin deficiency (B12) Syphilis
Presentation:
Sudden painless loss of vision, varying severity over hours or days
Eye pain, around the eye particularly with movement
Impaired colour vision - Dyschromatopsia - reds appear less red, ‘red desaturation’
Uhthoff’s phenomenon - transient worsening of vision with increased body temperature
optic neuritis Ix and Mx
Investigation/diagnosis:
MRI of brain and orbit
Bloods - autoantibodies, HbA1c, syphilis serology, U+Es, vitamin B12, intrinsic factor
Management:
Refer to ophthalmologist or neurologist (asses risk of developing MS - look for demyelination)
Recovery usually over 2-6 weeks however 38-50% of ADON develop MS within the next 15 years
High dose methylprednisolone for 72 hours, then 1mg/kg daily for the next 11 days which may briefly delay onset of MS
optic atrophy
Background:
A syndrome or sign of a potentially more serious condition
Pathology:
Loss of axons and shrinkage of myelin leading to widening of the optic cup
Aetiology/Risk factors:
Increased intraocular pressure (glaucoma)
Chronic papilloedema
Ischaemia (retinal artery occlusion, GCA)
Toxins (tobacco, methanol, lead, arsenic, quinine, carbon bisulfide)
MS
Syphilis
External pressure on optic nerve (tumours, pagets disease of bone)
optic atrophy presentation, Ix and Mx
Presentation:
Gradual loss of vision
Pale optic disc
Widening of optic cup
Investigation/diagnosis:
Eye examination
Fundoscopy
Bloods - autoantibodies, syphilis screening, inflammatory markers
Review of medications and substances (smoking, alcohol, occupational exposure)
Management:
Treat underlying condition
Optic atrophy related to optic neuritis may be limited using steroids
Complication - visual loss
Prognosis - irreversible condition, treatment aimed at limiting progression
diabetic retinopathy
Background:
Diabetes is the most common cause of blindness in people under 65 YOs
Blood vessels in the retina are damaged by prolonged exposure to hyperglycemia causing progressive deterioration in the health of the retina
Nonproliferative - background/preproliferative retinopathy - does not include neovascularization
Proliferative type - includes neovascularization
Diabetic maculopathy is a separate condition and can coexist
Pathology:
Hyperglycemia leads to damage to the retinal small vessels and endothelial cells.
Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages and the formation of hard exudates
Hard exudates are yellow/white deposits of lipids in the retina
Damage to blood vessel walls leads to microaneurysms and venous beading (where the walls of the veins are no longer straight and parallel - look like string of beads/sausages).
Microaneurysms are where weakness in the wall causes small bulges.
Damage to nerve fibres in the retina causes fluffy white patches to form on the retina called cotton wool spots
Intraretinal microvascular abnormalities (IMRA) - dilated and tortuous capillaries in the retina act as a shunt between arterial and venous vessels
Neovascularization - growth factors released in the retina causing development of new blood vessels
Aetiology:
Insulin resistance or lack of production (type I or II diabetes)
diabetic retinopathy presentation
Nonproliferative - background/preproliferative retinopathy - mild (microaneurysms), moderate (microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous bleeding), severe (blot haemorrhages + microaneurysms in 4 quadrants, venous beating in 2 quadrants, intraretinal microvascular abnormality in any quadrant)
Proliferative type - neovascularization and vitreous haemorrhages
Diabetic maculopathy - macular oedema and ischaemic maculopathy, hard exudates (waxy yellow lesions with distinct margins arranged in clumps or rings)
Complications - retinal detachment, vitreous haemorrhage, rubeosis iridis (new blood vessel formation in the iris), optic neuropathy, cataracts
diabetic retinopathy investigation and management
Investigation/diagnosis:
Eye examination
Fundoscopy
Management:
Laser photocoagulation
anti-VEGF intravitreal injections (ranibizumab and bevacizumab)
Vitreoretinal surgery (keyhole surgery on eye) for severe disease
Hypertensive retinopathy
Background:
Damage to small blood vessels in the retina relating to systemic HTN
Pathology:
Increased blood pressure chronic or acute leads to increased intraocular pressure >21mmHg causing damage to the retinal blood vessels leading to leaking of vessels and oedema
Aetiology:
Chronic HTN
Malignant HTN
Risk factors:
HTN
Hypertensive retinopathy presentation
Grade 1 - changes of early HTN retinopathy are subtle with generalised arteriolar narrowing
Grade 2 - development of areas of focal narrowing, compression of venules at sites of arteriovenous crossing (AV nipping/AV nicking)
Grade 3 - development of features similar to those of diabetic retinopathy, retinal haemorrhages, hard exudates, cotton wool spots
Grade 4 - all features of grade 3 + optic disc swelling, headache, eye pain, reduced visual acuity, FND
Silver wiring or copper wiring - walls of the arterioles become thickened and sclerosed causing twisting and coiling of arteries
Arteriovenous nipping -
arterioles cause compression of veins where they cross. This is due to sclerosis and hardening of the arterioles and sclerosis
Cotton wool spots - ischaemia and infarction in the retina causing nerve fibre damage
Hard exudates - damaged blood vessels leaking lipids into the retina
hypertensive retinopathy investigation and management
Investigation/diagnosis: Eye exam Blood pressure Fundoscopy Keith-Wagener classification (grade 1-4)
Management:
Focused on controlling blood pressure and reversible risk factors (smoking cessation, lipid levels, exercise and diet, alcohol reduction)
Papilloedema/optic nerve swelling
Background:
Optic disc swelling is a general term usually referring to papilloedema secondary to raised intracranial pressures.
Pathology:
Depends on underlying cause
Aetiology/Risk factors: Intracranial space-occupying lesions (tumours) Sinus thrombosis Hydrocephalus Meningitis or encephalitis Optic neuritis (MS) Malignant HTN Uveitis
Papilloedema/optic disc swelling presentation and investigations
Optic disc margins are blurred
Small haemorrhages may be present
Signs of underlying pathology
Investigation/diagnosis:
Eye examination
Vitals - BP, temperature, neck stiffness,
Bloods - CRP, ESR, viral serology, cultures, G+S
History for clinical diagnosis/red flags (headaches, neck stiffness etc.)
CT/MRI scan
papilloedema/optic nerve swelling management
Find and treat underlying cause
tumours surgery/chemotherapy etc.
Raised intracranial pressure:
Early involvement of neurosurgeon or neurologist
Elevate head of bed to 30 degrees
Correct hypotension with fluid resus (3% hypertonic saline to increase blood osmolality encouraging water movement into blood away from intracranial compartments)
Hyperventilation inducing to lower ICP (induces hypocapnic vasoconstriction; causes PaCO2 decrease, leading to arterial vasoconstriction thus lowering cerebral blood flow, blood volume and ICP)
Mannitol (might induce hypovolaemia; monitor serum osmolarity) or dexamethasone to reduce ICP (with tumours must discuss with senior before giving these)
Avoid pyrexia, manage seizures (increases ICP)
CSF drainage with intraventricular catheter and monitor ICP
Analgesia and sedation - usually IV propofol, etomidate r midazolam with morphine/alfentanil
Neuromuscular blockade to avoid further ICP increase from intrathoracic pressure increases
retinoblastoma
Background:
Embryonal tumour of the retina
Most common malignancy of the eye in children
Onset is gradual between third month of pregnancy and 5 years of age
Patients with bilateral disease are presumed to have the heritable form even though only 25% of patients have an affected parent
60% of patients have non-heritable form, normal life expectancy once eye cancer is cured.
Hereditary form is associated with increased risk of non-ocular cancers particular Ewing’s sarcoma, olfactory neuroblastoma and osteosarcoma
Increased risk of soft tissue and bone sarcomas persists for decades after retinoblastoma diagnosis
Pathology:
Cancer develops from cells with cancer-predisposing variants of Rb1 gene on chromosome 13 (recessive mutation)
Aetiology:
40% cases are hereditary mutations on chromosome 13 on the b1 gene
retinoblastoma presentation and investigations
Presentation:
Abnormal pupil appearance - leukocoria (white pupillary reflex to light)
Vision deterioration, red and irritated eye
Faltered growth or delayed development
Squint/strabismus
Heritable disease - usually present before 12 months of age
Nystagmus
Family history
Asymmetrical red eye reflex
Eye enlargement
Investigation/diagnosis:
Eye examination
Red reflex test by ophthalmoscope
Genetic testing
Bi-dimensional ocular USS and MRI (preferred over CT to avoid radiation exposure)
Staging - groups A-E depending on tumour size and invasion
Retinoblastoma management
Referral urgently (2WW) for those with leukocoria, new squint or change in visual acuity, family history of retinoblastoma
Royal london hospital and birmingham children’s hospital are UK centres for ophthalmology
Photocoagulation for small tumours
Cryotherapy
Transpupillary thermotherapy
Plaque radiotherapy
Systemic chemotherapy, Periocular chemotherapy, ophthalmic artery chemotherapy
External beam radiotherapy
Enucleation as a last resort to prevent spreading
Regular follow up needed depending on the case and specialist centre for several years after management - MRI screening every 6 months for 5 years (heritable disease)
Those with known Rb1 gene should be screened every 3-4 weeks until 6 months of age then less frequently until age 3, clinical examination every 3-6 months until age 7 and eventually biennial for life
Thyroid eye disease
Background:
AKA Graves’ orbitopathy
Inflammation of the eye muscles, eyelids, tear glands, fatty tissue causing the eye to become uncomfortable, swollen, red and pushed forward (bulging)
Around ¼ of people with Graves’ disease will develop thyroid eye disease
Pathology:
Autoimmune condition causing attack on surrounding eye tissue leading to inflammation around and behind the eye
In most patients these autoantibodies also attack the thyroid gland causing Graves’ disease
Aetiology:
Autoimmune condition
Risk factors:
Graves’ disease
Smoking - double risk increase for those with Graves’ disease
Thyroid eye disease presentation
Eyes are protruding forward
Red, swollen eyes
Reportedly uncomfortable eyes, feeling of foreign bodies or gritty
Photophobia
New bags under eyes
Pain in or behind the eye especially when moving eyes
Difficulty moving eyes
Rare - vision changes (diplopia or reduced vision)
Investigation/diagnosis:
Bloods - autoantibodies, TFTs, U+Es
Thyroid examination
eye examination
thyroid eye disease management
Smoking cessation
Liquid tears and eye lubricant drops for symptoms
Symptoms tend to worsen for the first 6-12 months but then stabilize
If symptoms are severe then steroid or immunosuppressive intraocular injections can be given
Control hyperthyroidism
6 month course of selenium supplements 100mcg BD (mild cases) can but OTC
Decompression surgery, eye muscle or eyelid surgery for extreme cases with pressure on the optic nerve or visual disturbances
Prisms on spectacles can help diplopia for those not eligible for surgery
Horner’s syndrome
Background:
Rare condition resulting from disruption of the sympathetic nerves supplying the eye
Triad of ptosis, miosis and hemifacial anhidrosis
Congenital horner syndrome is associated with heterochromia (different colour iris on affected side)
Pathology:
Depends on underlying cause
Sympathetic nerves arise from the spinal cord in the thorax (preganglionic) and enter into the sympathetic ganglion at the base of the neck and exit as post ganglionic nerves which travel into the head, running alongside the internal carotid artery
Aetiology:
Central lesions - 4Ss: Stroke, multiple Sclerosis, Swelling/tumours, Syringomyelia (cyst in the spinal cord)
Preganglionic lesions - 4Ts: Tumour (pancoast tumour), Trauma, Thyroidectomy, Top rib (cervical rib misplaced)
Postganglionic lesion - 4Cs: Carotid aneurysm, Carotid artery dissection, Cavernous sinus thrombosis, Cluster headache
Horner syndrome presentation, investigation and management
Presentation: Ptosis Miosis Hemifacial anhidrosis Enophthalmos (sunken eye)
Investigation/diagnosis:
CXR
CT/MRI of head
Cocaine eye drops (stops noradrenaline reuptake at NMJ) - normally cause pupil dilation, but will NOT in horner syndrome (apraclonidine alternative)
Management:
Diagnosis and management of underlying condition
third nerve palsy
Pathology:
CN III, oculomotor nerve supplies all extraocular muscles aside from the lateral rectus and superior oblique and it supplies the levator palpebrae superioris muscle, responsible for lifting the eyelid
When there is a palsy or lesion in CN III the muscles stop receiving signals from the nerve, causing the eye to turn outwards and downwards as only the lateral rectus and superior oblique are still functioning without resistance from other muscles. It also causes ptosis from lack of palpebrae superioris muscle action
CN III also contains parasympathetic fibres innervating the sphincter muscles of the iris therefore palsy causes fixed dilated pupils as well.
Aetiology: Cavernous sinus thrombosis Posterior communicating artery aneurysm Idiopathic Tumour Raised intracranial pressure Sparing of the pupil suggests microvascular cause - diabetes, HTN or ischaemia
third nerve palsy presentation, Ix and Mx
Presentation:
Ptosis
Dilated, non-reactive pupil
Divergent strabismus in the AFFECTED eye causing DOWN and OUT positioning
Investigation/diagnosis: Eye examination - movements limited Bloods - tumour markers, FBC, iron studies, HbA1C Blood pressure CT/MRI - thrombosis or aneurysm, tumours
Management:
Identify underlying cause and manage appropriately
Most CN III palsies caused by vascular conditions like diabetes may recover completely
Maximum improvement usually occurs during the first 6 months after onset but can occur up to 18 months after onset
Congenital third nerve palsy is unlikely to resolve spontaneously
Holme-adie
Background:
Benign condition
Unilateral dilated pupil that is sluggish to react to light, has slow dilation of the pupil following constriction.
Holmes-adie syndrome is where the holmes-adie pupils are present with absent ankle and knee reflexes
Most common in younger women 30-40 YOs
Pathology:
Damage to the postganglionic parasympathetic fibres
Holme-adie syndrome also involves autonomic nerve dysfunction
Aetiology:
Unknown but may be viral
Holme-adie presentation, Ix and Mx
Presentation:
Unilateral dilated pupil that is sluggish to react to light, has slow dilation of the pupil following constriction.
Absent ankle and knee reflexes
80% unilateral pupil abnormality
Pupil constricted for prolonged amount of time (tonic pupil)
Over months-years pupil size diminishes eventually becoming mitotic
Investigation/diagnosis:
Eye examination - light, accommodation, visual fields, eye movements
Management:
Corrective spectacles can be prescribed and no other treatment is usually needed
Infants <1 YO refer to paediatric neurologist to rule out familial dystonias
Argyll-robertson pupil
Specific finding on neurosyphilis. A constricted pupil that accommodates when focussing on near objects but does NOT react to light.
Often irregular shaped, commonly called prostitutes pupil
Hyphema
Pathology:
Collection of blood pooling inside the anterior chamber of the eye
May cover the iris and pupil, blocking vision partially or completely
Vision problems can become permanent if not treated
Aetiology: Trauma to eye Increased intraocular pressure Sickle cell anaemia Hemophilia Cancer Abnormal vessels on iris Herpes zoster infection
hyphema presentation, Ix and Mx
Presentation: Painful eye Visual impairment Visible blood in anterior chamber Photophobia Blurry, clouded or blocked vision
Investigation/diagnosis: Eye examination Fundoscopy Eye pressure (tonometer) Slit lamp examination CT scan if orbital fracture suspected
Management:
Mild - self resolving in around one week, take OTC pain medication AVOID aspirin (can increase bleeding risk)
Steroid eye drops to limit inflammation
Dilating drops to ease pain and encourage drainage
Patch over affected eye - encourage dilation
Bed rest, head elevated to 40 degrees when sleeping
Daily eye pressure monitoring
Myasthenia gravis and LEMS eye disorder
Background:
Myasthenia gravis - autoimmune condition
lambert-Eaton myasthenic syndrome (LEMS) - rare autoimmune condition
Eye muscle weakness is uncommon in LEMS but more common in myasthenia gravis
They are separate autoimmune conditions both where damage to the NMJ occurs and can present slightly similarly
Pathology:
Autoantibodies attack the NMJ, affecting communication between nerve and muscle cells
Causes muscle weakening over time as they receive less and less stimuli
Predominantly affects voluntary muscles but involuntary muscles such as eye responses can also be affected
Aetiology:
Autoimmune disease
Myasthenia gravis and LEMS eye disorder presentation, Ix and Mx
Presentation: History of LEMS - limb weakness especially with voluntary muscle use Ptosis Diplopia Reduced vision Dry eyes Abnormal eye movements Strabismus Pupillary dysfunction Blurry vision causing headaches
Investigation/diagnosis:
Eye examination
Clinical diagnosis
Management:
Lubricating eye drops/ointments
Corrective spectacles for squints or pupillary dysfunctions
Treatment of autoimmune conditions.
Cranial nerve III overview
CN III - oculomotor nerve
Responsible for all extraocular muscles of the eye aside from lateral rectus and superior oblique muscles
Also has parasympathetic fibres to ciliary and pupillary sphincter muscles, controlling accommodation reflex
Dysfunction: unable to move eye up/down/side to side (DYSCONJUGATE GAZE); ptosis uni or bilateral; loss of accommodation reflex
Cranial nerve IV overview
CN IV - trochlear nerve
Responsible for superior oblique extraocular muscle
Dysfunction: loss of downward and inner eye movement (DYSCONJUGATE GAZE)
(same tests as III oculomotor)
Cranial nerve VI overview
CN VI - abducens nerve
Responsible for lateral rectus extraocular muscle
Dysfunction: loss of lateral outward eye movement (DYSCONJUGATE GAZE)
