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
