Ophthalmology Flashcards
Where do orbital fractures usually occur?
Medial + inferior walls as thinner
- Orbital rim#: usually at sutures of bones
- Blowout#: partial herniation of orbital contents into ethmoid/maxillary sinus, usually blunt trauma, if blood goes into maxillary sinus is better than accumulating in eye as less chance of optic nerve compression from raised IOP
- Orbital floor #; usually blow from an object e.g. tennis ball, often a/w soft tissue injury, vertical diplopia, enophthlamos, infraorbital anaesthesia
What is the role + innervation of the extra-ocular muscles?
- Levator palpebrae superioris: superior tarsal part innervated by CNS (is activated in fight or flight so eyes go wide) and rest by CN III
- Superior rectus - elevation, some adduction + MR, CN III
- IR - depression, some adduction + LR, CN III
- MR - adduction, CN III
- LR - abduction, CN VI
- SO - angular, depression abduction + MR, CN IV
- IO - angular, elevation abduction LR CN III
How does a CN III palsy present and what are the causes?
- Complete: ptosis (unopposed orbiculares oculi as LPS inhibited), down and out position of eyes (+diplopia) and mydriasis (dilated pupil-sphincter pupillae-PNS fibres carried on the CN III)
- Partial: any of the features
- Pupil involvement indicates compression from outside as these fibres are carried peripherally
Painful palsy - indicates an intracranial event, non-painful indicates a medical cause like DM or HTN
Outline the structure of the eyeball
- Supplied by ophthalmic artery (from ICA)
- Fibrous layer (sclera [attachment of muscles] + cornea [central, refraction])
- Vascular layer: choroid, ciliary body iris (contains S+D pupillae muscles)
- Retina
- Lens between VH + pupil
- Vitreous humour behind lens
- Anterior + posterior chamber - contain aqueous humor
What is exophthalmos?
Eyeball protrudes - eyelids open more to accommodate - more sclera visible
E.g. in thyroid eye disease
What is the effect of RICP on the eye?
Raised CSF pressure in subarachnoid space - optic nerve surrounded by meninges so gets compressed - affects the veins and then the arteries
Outline the structure of the eyelids
- Skin and loose CT tissue (no fat-easily distended by oedema), glands (ciliary glands of Moll + sebaceous glands of Zeis)
- Orbicularis oculi: CN VII, closes eyelids + drains tears
- Tarsal plates: attachment for LPS, has the Meiobiam/tarsal glands which secret lipid to stop eyelids sticking
- Levator apparatus: LPS + superior tarsal muscle
- Conjunctiva: thin MM called palpebral conjunctiva, reflected onto sclera (bulbar conjunctiva)
Meiobiam cyst vs stye
- Meiobiam cyst/chalazion: blockage of the M gland which makes the oil layer of the tear film; deeper, last ~6m, treat with warm compress or in younger child may do surgery if interfering with vision due to risk of amblyopia or astigmatism
- Stye/hordeolum: acute infection of a gland of Moll/Zeiss/eyelash follicle, ducts of ciliary glands become obstructed causing a painful swelling in lid margin. M-topical fusidic acid
Outline the structure of the lacrimal glands
- Lacrimal gland in lacrimal fossa in supers-lateral part, goes through ducts and blinking spreads over cornea
- Lacrimal apparatus to drain: conjunctival sac - lacrimal lake at medial eye - lacrimal canals - lacrimal sac - nasolacrimal duct - inferior meatus of nasal cavity - nasopharynx - swallowed
What is epiphora?
Overflow of tears due to obstruction in the lacrimal system. Stagnant tears predispose to infection
What is in tears?
- Smooth surface for refraction, lubrication and antibacterial
- Surface lipid layer from Meiobian glands, middle aqueous layer from lacrimal gland + inner mucous layer from goblet cells
What is the cause of dry eyes?
Usually describing mild tear film instability due to blepharitis - focus on cause not artificial tears. True dry eyes can be v painful + threaten vision
- CF: burning, itch, blurred vision if in cornea, mucus strands
- Aqueous deficiency: Sjogren’s syndrome (primary or due to RA/SLE etc), lacrimal gland deficiencies (age, congenital, ablation, denervation), lacrimal duct obstruction e.g. erythema multiforme, reflex hypo secretion like CL wear/DM/CNVII damage, systemic drugs
- Evaporative: Meibomian oil deficiency, drugs, low blink rate, vit A deficiency, topical drugs, CL wear, ocular surface disease
What is the structure and function of the cornea?
Avascular structure in the centre to maintain transparency, protect the eyes (physical + corneal reflex) and refraction of incoming light - is the main refracting surface as first thing light enters
Innervated by CNV1
Layers: epithelium of non-keratinised stratified squamous epi (only layer that regenerates), Bowman’s membrane (acellular), collagenous stroma, descemet’s membrane (like a basement membrane) and endothelium (for hydration, simple squamous)
Infective keratitis?
Infection of the cornea due to disruption to the epithelial surface
RF: contact lenses, trauma, dry eyes, immunocompromise
CF: severe pain, peri-corneal vascularity + red eye, watery discharge/epiphora, reduced visual acuity (surface + tear film disrupted + oedema), photophobia, may have a mucho-purulent DC, corneal infiltrate (white deposit), hypopyon (pus behind cornea in AC), ‘cells’ (leucocytes) and ‘flare’ (protein) in AC due to leaking bv in iris
What is the sclera?
An opaque white tissue continuous with the cornea at the limbus, where the extra-ocular muscles are attached and the optic nerve enters
How is the intra-ocular pressure formed?
- Aqueous humour produced by ciliary processes of the ciliary body
- AH drained through the trabecular meshwork + canal of Schlemm
- Balance of production and drainage
What topical agents are used to lower IOP and how do they work?
- Beta blockers e.g. timolol - reduce production of aqueous humour by the ciliary body (beta stimulation causes production)
- Alpha agonists e.g. apraclonidine or brimonidine - reduce production of AH (as alpha agonists reduce production) + small increase in drainage
- Carbonic anhydrase inhibitors e.g. dorzolamide - reduce production of AH
- Parasympathomimetics [muscarinic agonist] e.g. pilocarpine - contract ciliary muscles to open trabecular meshwork so increase outflow of AH
What does the lens do?
Between the vitreous and the iris, function is to refract light (less power than cornea) + accommodation (changes its shape to vary amount it refracts - needed for near vision)
What is presbyopia?
Reduced ability of the lens to accommodation due to reduced elasticity + atrophy of the ciliary muscle
What is the uveal tract?
- Iris: divides eye into AC+PC and controls amount of light entering eye by varying pupil size
- Ciliary body: has ciliary muscle for accommodation and ciliary processes which make AH
- Choroid: covers the posterior part of the eye and separates the retina from the sclera, has a rich capillary bed and is involved in nutrient supply/waste removal to the retina
How does the pupil dilate and constrict?
- Mydriasis (dilation) in low light/SNS activation - dilator pupillae contracts
- Miosis (constriction) in bright light/PSNS carried on CN III
- Age also causes meiosis as dilator pupillae atrophies + sphincter pupillae fibroses
What is the anterior chamber?
Space between the cornea + iris that is filled with AH, supplies nutrients + oxygen to cornea
What is the vitreous?
Between he lens + retina and fills 2/3 volume of eye - holds retina in place + supports the lens
A water-based substance with collagen in
What is vitreal detachment?
Fluid fills the potential space between the vitreous and retina - vitreous detaches from retina
This can predispose to retinal detachment especially in parts where the V-R attachments are firmer
Describe the structure of the retina
- Outer pigmented epithelium, attached to Bruch’s membrane
- Neural retina: receives light and transforms into impulses which travel along axons in optic nerve to reach visual cortex.
- Early in embryology these fuse but can separate in retinal detachment as only really firmly attached at the optic nerve head
- Macula - central retina just lateral to the optic disc, yellowish colour. Depression (fovea) has a high concentration of photoreceptors so where high acuity vision is, supplied by central artery of retina
- Optic disc - where optic nerve enters, no photoreceptors
- Fundus - posterior part of retina
What is the blood supply to the retina?
- Inner 2/3 - central retinal artery, with branches as end-arteries. Retinal arteries overlie the veins so this is why in HTN you see AV nipping where they cross
- Macula - v dense capillary network
- Fovea - capillary free zone
- Outer 1/3 - from the choroid
What is retinal detachment?
Separation of the pigmented + neural retinal layers
CF: flashing lights, floaters, visual field defects (due to disrupted neural pathways)
What is retinal artery occlusion?
Obstruction to flow = in the artery p/w painless sudden loss of vision
Irreversible changes occur quickly
Outline the visual pathway
- Light goes in a straight line so light striking the temporal retina comes from the nasal visual field
- Temporal + nasal fibres merge at optic nerve and travel to optic chiasm
- At chiasm the nasal retinal fibres (from the temporal VF) decussate forming optic tracts
- Right optic tract has temporal retinal fibres from the right eye and nasal retinal fibres from the left eye - i.e. right optic tract as all the information from the left visual field
- Optic tract synapses at lateral geniculate nucleus
- Optic radiations arch through temporal lobe (inferior radiations) and parietal lobe (superior radiations) - inferior radiations carry info from superior visual field and vv
Why do injuries to the central cornea heal more slowly than those at the sides?
Stem cells are found peripherally in the cornea so regeneration takes longer for cells to move to the centre
What is the role of the tonometer?
Measures IOP by the force needed to flatten the corneal surface. Higher force=higher pressure
What drugs can affect pupil size?
- Mydriasis: tropicamide (anti-muscarinic), phenylephrine (sympathomimetic)
- Miosis: pilocarpine (muscarinic agonist)
What are the photoreceptor cells?
- Rods: sense contrast + motion rather than details, monochrome, useful in dark
- Cones: sense fine detail + colour vision
Highest concentration at the fovea (central part of the macula) for high acuity vision, absent at the optic disc (where the optic nerve enters)
How would you work out where a visual field defect arose from?
*Retinal lesions - monocular. Sudden onset in vascular/detachment, ARMD macular affected first with peripheries spared
*Pre-chiasmal: monocular, ipsilateral eye. Often affects acuity
*Chiasmal: bitemporal hemianopia
*Post-chiasmal: homonymous (matching) and image reversal means that right optic tract problem causes left visual field defect
-HH without macular sparing-main optic radiation
-Superior homonymous quadrantonopia - temporal radiation
-Inferior homonymous quadrantonopia - parietal radiation
“PITS-patietal inferior, temporal superior”. Tho in studies most quadranopias are from occipital lobe!
-Visual cortex - contralateral homonymous hemianopia with macular sparing
-Occipital lobe: if both cortical impairment (may still act like that have vision?), or just on one side a loss of visual perception from contralateral visual field
How is visual image projected?
Projected through lens onto retina upside down + laterally reversed
Information from each eye split at chasm:
- Medial fibres (temporal visual field) cross to opposite side
- Lateral fibres (nasal visual field) pass to ipsilateral optic tract
- This ensures info from both eyes about same part of VF passes to same part of visual cortex e.g. left half of VF in right optic tract
Differentials for painless loss of vision
- Cataract
- Open angle glaucoma
- Retinal detachment/PVD/vitreous haemorrhage
- CRV/CRA occlusion
- Diabetic retinopathy
- Posterior uveitis
- ARMD
- Optic nerve compression e.g. pituitary tumour
- Cerebral vascular disease e.g. amaurosis fugal, TIA, stroke
- Refractive error
- Corneal dystrophy
- Drugs - methanol, hydroxychloroquine, isoniazid, isotretinoin, tetracycline, ethambutol
Differentials for painful loss of vision
- Acute angle closure glaucoma
- GCA
- Optic neuritis
- Uveitis
- Scleritis
- Keratitis
- Shingles
- Orbital cellulitis
- Trauma
Differentials for the acute painful red eye
- Scleritis
- Uveitis
- Corneal abrasion
- Corneal ulcer
- Viral keratitis
- Acute angle closure glaucoma
- Endophthalmitis
- Foreign body
- Chemical injury
Differentials for the acute painless red eye
- Subconjunctival haemorrhage
- Episcleritis
- Conjunctivitis
- Dry eye
Scleritis
- CF: dull boring pain, headache, eye watering, painful movements, reduced VA (late), deep pink colour, tender, may have dilated superficial vessels
- Causes: rheumatological conditions (50%); may also be due to ocular surgery or infection
- Recurrent causes thinning
- M: treat the cause e.g. high dose steroids or Abx, all need urgent ophthalmology referral
Anterior uveitis
- CF: photophobia, red painful watering eye, VA often mildly reduced; hypopyon (pus), irregular pupil shape (due to posterior synechiae [iris attaching to lens capsule]), cloudy (cells in the AH + corneal oedema), injection around cornea, slit lamp may show flare + cells
- Causes: idiopathic young white males, systemic a/w HLA-B27 conditions (e.g. psoriatic arthritis, ankylosing spondylitis), IBD, sarcoidosis, Behcet’s disease, infections
- M: control inflammation, prevent visual loss + minimise long term comps (e.g.topical steroids + cytoplegics, may need immunosuppression or antimicrobials)
Corneal abrasion
A break in the corneal epithelium usually trauma e.g. gusts of wind or FB, common
- CF: v painful (exposed nerve endings), red watering eye, photophobia, blepharospasm (unable to open eye), FB sensation, VA may be mildly reduced if in visual axis. Stains with fluorescein drops + blue light
- Need to evert upper lid to check a FB isn’t lodged underneath
- M:
- Small: chloramphenicol ointment (reduce risk of bacteria + lubricant) + ocular lubricants + oral analgesic, avoid contact lenses until healed
- Large/VA affected refer
- Comps: microbial keratitis, recurrent erosions
Corneal ulcer
Emergency -can cause permanent scarring + significant LoV
- CF: v painful red eye photophobia, worsening VA, may see an epithelial defect + haziness
- Causes: usually an infected abrasion from extended contact lens wear, with respiratory pathogens or Pseudomonas (if tap water in CL) or acanthaemoeba from standing water. Haemophilus + Neisseria can penetrate without an initial insult
- M: if severe may need admission for Abx + mydriatic eye drops (e.g. every 30m)
Viral keratitis
- CF: pain, watering, photophobia, reduced VA, dendritic epithelial defect
- Causes: herpes simplex e.g. from cold sore or varicella zoster (may come with shingles w V1 distribution)
- M: refer to ophthalmology, topical antivirals
Acute angle closure glaucoma
Acutely raised IOP a/w physical obstruction in the AC
- CF: pain, headache, N+V, reduced VA, photophobia, hazy cornea, mid-dilated unreactive pupil
- M: lie flat on back to help open angle, IV/oral acetazolamide (reduce pressure), topical agents like BB (reduce AH production)/pilocarpine (constrict pupil to open angles), peripheral iridotomy (laser hole through iris to allow separate AH drainage route)
Endophthalmitis
Emergency!
- Causes: endogenous, from severe infection like endocarditis or exogenous e.g. after cataract surgery/intravitrela injection
- CF: severe pain, photophobia, rapidly progressive vision loss, hypopyon, injection, corneal oedema
- M: urgent ophthalmology, systemic + intravitreal Abx, biopsy vitreous for culture
Foreign body-low speed e.g. paint, dust, gravel
- CF: irritation, red/watering eye, FB sensation even after cleared, photophobia, minor visual changes if near visual axis, use fluoroscein to look for abrasions + evert upper eyelid - FB may have gone, be under upper eyelid, embedded in cornea/conjunctiva
- M: LA drops, remove FB with cotton bud, Abx drops for abrasions, lubricants to reduce FB sensation
Foreign body-high speed
More potential for damage like corneal lacerations or globe penetration
- CF: pain, watering, photophobia, VA changes, flashes + floaters (retinal), ferric FBs often leave an orange rust ring, corneal oedema
- Signs of penetrating: hyphaema (blood in AC), visible holes in iris/distortion, reduced IOP from AH leakage, ‘plugged’ wound from prolapses, fluorescein to look for leaks of AH
- M: emergency surgery, may do orbital XR/US if can’t see the FB. DO NOT PUT DROPS IN, plastic shield to minimise further trauma
Chemical injury
- Causes: accidental e.g. cleaning products, deliberate. Alkalis worse than acids as cause liquefactive necrosis so propagate deeper, acids coagulative necrosis so impede their own progress
- CF: severe eye pain, watering, reduced VA, skin blistering, corneal abrasion, blanching of the limbus (join between conjunctiva + cornea)
- White eye indicates v ischaemic eye and that the stem cells are dead-will need corneal graft
- Severity: alkali, duration of contact, corneal involvement, limbal involvement (where stem cells are), other injury like blunt trauma
- M: IRRIGATE (water, saline, Hartmann’s), test pH of the fluid, urgent r/v, topical anaesthetic, topical steroids to reduce inflammation + Abx to prevent infection + cytoplegics (e.g. cyclopentolate) paralyse iris to reduce pain, analgesia, acetazolamide if raised IOP
- Comps: conjunctival burns, limbal ischaemia, full thickness burns affecting retina etc, poor corneal healing, corneal opacification
Subconjunctival haemorhage
Common complaint that can cause FB sensation/grittiness
- Causes: trauma, sudden rise in intrathoracic pressure e.g. lifting, rubbing eye
- RF: HTN, anticoagulants/plts
- M: nothing, lubricants if feels gritty, adv will go in a few weeks (may go a faint yellow colour first); if secondary to trauma consider a FB or occult globe rupture
Episcleritis
- CF: feels uncomfortable but not frank pain, sectoral area of hyperaemia + dilated superficial vessels (moveable with a swab pressed gently on cornea), blanches with phenylephrine (vasoconstrictor)
- Usually no underlying cause but can be a/w autoimmune e.g. UC
- M: self limiting, analgesia + topical lubricants, sometimes topical steroids/NSAIDs
Conjunctivitis
Inflammation over the sclera (bulbar) + inner (tarsal) eyelids, usually b/l due to symmetrical pathologies (eye drops, allergy) or cross-infection. Common CF are general discomfort, watering, gritty, discharge, crusted eyes shut in morning, injection, chemises, debris
May be viral, bacterial, STI or allergic
Dry eye
B/L ocular irritation worsened with exposure e.g. to wind/excessive screen time
May be evaporative meaning that tears evaporate so eyes water in response e.g. blepharitis, or tear deficiency e.g. Sjogren’s syndrome
CF in blepharitis: irritated margins with capping, crusting + matted eyelashes, may also see chalazions
M of blepharitis: good lid hygiene, warm compresses with lid massage, ocular lubricants (thin in day, ointment at night), in severe causes occlusion of the puncta is used to reduce drainage + improve lubrication
Causes of tunnel vision
- Papilloedema
- Glacuoma
- Retinitis pigmentosa
- Choroidoretinitis
- Optic atrophy in tabes dorsalis
- Psychological
Causes of mydriasis
- Third nerve palsy
- Holmes-Adie pupil (usually u/l constriction of a pupil with slow accommodation + poor light reflex)
- Traumatic iridoplegia
- Phaeochromocytoma
- Congenitla
- Topical mydriatics-tropicamide, atropein
- Sympathomimetic drugs-amphetamines, cocaine
- Anticholinergic drugs-TCAs
What is RAPD and what causes it?
aka Marcus-Gunn pupil
detected by swinging light test - paradoxical dilation of affected pupil when light shines into it. usually first time constricts as normal then when swing it dilates (and normal pupil also dilates-consensual) - relative as compared to the other pupil
Due to a lesion to the retina or optic nerve
What is the normal pathway for the pupillary light reflex?
afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
What causes optic atrophy?
- Acquired: MS, chronic papilloedema, raised IOP, retinal damage e.g. ischaemia, toxins e.g. arsenic, nutritional deficiencies e.g. B1/2/6/12
- Congenital: Friedreich’s ataxia, mitochondrial disorders, DIDMOAD (Wolfram syndrome)
What does cupping of the optic disc mean and what causes it?
Neuro-retinal rim thins which causes the cup to disc ratio to be enlarged (cup > half the disc diameter); defined as enlarged when cup to disc ratio is >0.7 (suspect glaucoma)
Usual cause is glaucoma - death of optic nerve axons + glia, so the rim thins and the support structure goes so the cup part looks bigger
What actually is the cup vs the disc of the optic nerve?
- Cup: central portion of the disc, usually quite small compared to entire disc
- Disc: optic nerve head, mostly filled with axons, fibres grouped around it in a rim
Why should you never give steroids for an undiagnosed red eye?
If is on HSV keratitis will cause a geographic ulcer as you have impaired the immune response
What is the difference between herpes simplex and herpes zoster keratitis?
- HSV: primary periocular infection usually occurring in children, looks like a branching ulcer (like HZ) but has terminal bulbs (unlike HZ), cause a patchy iris defect
- Herpes zoster ophthalmicus: segmental iris defect, Hutchinson’s sign (rash on nose indicates in cornea, as both are supplied by the nasociliary branch of CNV1)
What’s the difference between scleritis and episcleritis?
- Scleritis: 50% have underlying cause e.g. RA. Vessels don’t blanch with phenylephrine, dull pink areas of inflammation, v painful, dull pinkish area may have overlying bright red vessels that aren’t moveable, sight-threatening, if recurs causes thinning of the area so choroid more exposed (so looks darker), diffuse + can have areas of necrosis
- Episcleritis: 30% a/w systemic conditions like UC. Dilated vessels are moveable and blanch with phenylephrine (a vasoconstrictor), not acutely painful may be sore/gritty, redness in sectors, usually self-limiting but may recur (but won’t cause thinning)
Viral conjunctivitis
- Adenovirus main pathogen
- V contagious -can cause epidemics
- 50% u/l
- CF: eye watering, coryzal sx, pre-auricular lymphadenopathy, corneal inflammation
- M: lubricants, cold compress, hygiene. Topical steroids if cornea involved. Adv may take weeks
- Herpes simplex type - usually UL, cutaneous vesicles on skin, burning/FB sensation, high risk of dendritic ulcer so give topical aciclovir
- Molluscum type - papule on lid margin, excise the lesions. Chronic course
Bacterial conjunctivitis
- Resp pathogens like S pneumonia and Haemophilus
- Usually b/l
- CF: extensive conjunctival injection + DC
- M: topical chloramphenicol drops/ointment or fusidic acid, hand washing, f/u if worsens or persists, not sharing towels, don’t use contact lenses during the infection
Chlamydial conjunctivitis
Typically u/l conjunctivitis with serous DC, PCR for diagnosis, needs systemic Abx (e.g. doxycycline) + refer to GUM, can cause scarring
Gonorrhoeal conjunctivitis
Severe swelling, hyper-purulent DC.
Refer to GUM – systemic Abx
Comps include corneal ulcer + scarring
Allergic conjunctivitis
Common, h/o atopy, occurs on exposure to allergen. Seasonal (S+S) or perennial (peak autumn) type, type I hypersensitivity a/w mast cells
- CF: itch, swelling of lids/conjunctiva, pink-red eyes, watering, stringy discharge, occ chemosis, coryzal sx.
- M: cold compress, topical or oral antihistamines, wash face after exposure, for more severe topical mast cell stabilisers (e.g. sodium cromoglicate-but they need longer time for therapeutic benefit for several weeks), lower allergen load, ocular lubricants (dilute allergen)
Thermal burns
- CF: keratopathy or burns to lids
- M: burins specialists, IV fluids if >10-15% of BSA affected, use non-adherent dressings, simple emmolients, irrigate with cool liquid, topical cytoplegics+lubricants, analgesia, steroids if oedema
- Comps: loss of lid tissue, lid cicatrization (fibrous tissue contraction), epiphora, conjunctival burns, limbal ischaemia
CF of orbital #
Periorbital bruising, oedema or haemorrhage
Surgical emphysema
Abnormal globe position
Abnormal pupil responses or RAPD
Subconjunctival haemorrhage
Dysmotility
Associated injuries to head, neck or teeth
Corneal foreign body
Usually metallic so rarely cause infection, microbes more likely in stone/ceramic/organic matter
- CF: photophobia, pain, injection, lacrimation, blurred vision, FB, rust ring, anterior uveitis
- M: only remove under slit lamp, give LA drops and topical Abx + NSAID
What is hyphaema?
Blood in anterior chamber - causes include blunt trauma, surgery and haematological disease
Usually apparent on slit lamp but if extensive may see with naked eye
Comps: corneal staining, red cell glaucoma
M: bed rest, globe protection, avoid aspirin/antiplt/NSAID, cytoplegic e.g. atropine, topical steroid
What is retrobulbar haemorrhage?
Compartment syndrome of the eye socket
- Causes-trauma, surgery
- CF: tight swollen eyelid, u/l fixed+dilated pupil, reduced eye movements, profound LoV. If no movement/pupil unreactive optic nerve must be v compressed - needs urgent lateral canthotomy + cantholysis (make hole at the side, not in the globe, to allow blood out)
What are the causes of orbital cellulitis?
- Causes: S pneumonia, S aureus, S progenies, H influenzae (less since HiB vaccine)
- RF: sinus disease, dental/facial infection, dacryocystitis, trauma, surgery to orbit/lacrimal/vitreoretinal, endogenous spread in immunocompromised pt
How does orbital cellulitis present and what is the management?
- CF: fever, malaise, periocular pain, inflamed lids, chemises, proptosis, painful restricted movements, diplopia, lagophthalmos, optic nerve dysfunction (reduced VA/RAPD/reduced colour)
- CT orbit sinus brain - may see sinus opacity, orbital infiltrate or abscess
- M:
What may cause orbital inflammation?
Orbital cellulitis, preseptal cellulitis, myositis, dacryoadenitis (lacrimal gland), thyroid eye disease, granulomatosis with polyangiitis, sarcoidosis
What cystic lesions may arise on the orbit?
- Dacryops: lacrimal duct cyst, painless blue-grey areas in superolateral fornix
- Dermoid cyst - may disturb orbit or cause recurrent inflammation, need excision
- Mucocele: blocked sinus opening so secretions cause a collection, need ENT to sort sinus out
What is the difference between orbital cellulitis + preseptal (periorbital) cellulitis?
- Preseptal: more limited disease, but in young children is serious because the orbital septum isn’t fully developed so it can spread to orbit. Causes fever pain + swollen lid, but eye movements + conjunctiva + optic nerve unaffected
- OC has proptosis, restricted eye movements, reduced A, RAPD
Name some common eyelid disorders
- Trichiasis (misdirected lashes) - causes irritation, can cause corneal changes so if severe may need lash removal/surgery
- Lash infestations with head lice or crab lice - causes itch, blepharitis, conjunctivitis
- Madarosis - partial/complete loss of lashes. Local causes e.g. chronic blepharitis or systemic e.g. alopecia/psoriasis/hypothyroidism
- Entropion - lid margin rolls inwards so lashes cause irritation + red eye, usually need surgery
- Ectropion - lid margin rolls out, lacrimal sac in wrong place so watery eye, more likely in CN VII palsy, usually surgery
- Blepharitis - inflammation of lid margins
Blepharitis
- Causes: Meibomian gland dysfunction, seborrhoea, S aureus infection (linked to many conditions inc preseptal cellulitis)
- CF: asymptomatic or itchy burning eyes, crusty scaly deposits on lashes, may see Meibomian glands plugged with secretions/evidence of chalazion
- M: lid hygiene to reduce bacteria + unblock MG, mechanical removal of debris from lid margins (e.g. cotton wool in cooled boiled water mixed with baby shampoo), topical chloramphenicol/fusidic acid, oral doxycycline if severe/suspect acne rosacea
- Artificial tears for sx relief
Common lid lumps and their management
- External hordeolum (stye): abscess in lash follicle in gland of Zeis (sebum) or Moll (sweat), usually Staph, M-warm compress and topical Abx only if there is conjunctivitis
- Internal hordeolum (stye): abscess within a MG, usually Staph tender lump, M-warm compress, oral Abx if cellulitis, chronic-incise, may leave a chalazion
- Chalazion (Meibomian cyst): commonest lump, chronic inflammation of a MG, a/w chronic blepharitis/rosacea/seborrheic dermatitis. Firm and painless. M-hot compress to drain, if symptomatic may remove or in children if obstructing vision (as blocks development so amblyopia risk)
- Cyst of Moll and Zeis: chronic cysts
- Xanthelasma: SC lipid deposits in medial area
- Molluscum contagiosum: pearly umbilicate nodules caused by poxvirus, may remove if causing issues
- Benign tumours like papillomas, seborrheic keratosis or capillary haemangiomas
- Malignant tumours like basal cell carcinoma (deffo remove if near eye as can be locally invasive + destructive), SCC (higher risk of mets)
Give some causes of acquired ptosis
- Involution: disinsertion of LPS a/w age + surgery, may cause high upper lid crease + compensatory brow lift. Can have surgery
- Neurogenic: CN III palsy (complete ptosis from los of LPS, usually down + out and sometimes dilated pupil if affected the PNS), Horner’s syndrome (partial ptosis, may also have meiosis + lower lid elevation + anhidrosis)
- Myasthenia gravis: fatiguable eyelid, consider when skin crease is normal
- Myopathy: b/l + symmetrical, restricted ocular movement
- Mechanical from masses or oedema
- Pseudoptosis: brown ptosis (frontalis dysfunction), dermatochalasis (upper eyelid skin hangs in folds in elderly pt), blepharochalasis (abnormal lid elastic tissue)
What causes a watery eye?
- Increased production: autonomic disturbance, drugs, chronic lid disease, local irritants, aberrant regeneration after CNVII palsy
- Lacrimal pump failure: lid laxity, orbiculares weakness, ectropion
- Reduced drainage: punctal obstruction like stenosis in the elderly, canalicular obstruction like idiopathic/from 5-FU, lacrimal sac obstruction from sarcoid/granuloma/papilloma, nasolacrimal duct obstruction eg. nasal #
Dacryocystitis
Inflammation of the lacrimal sac - causes painful lump at side of nose next to lower lid
Causes:
- Acute: causes tender erythematous lump inferior to medial canthus, need Abx to prevent abscess which can lead to fistula.
- Chronic: recurrent ipsilateral conjunctivitis, mucocele
M: oral Abx, watch for cellulitis, refer to ophthalmology as may have an underlying cause e.g. mucocele that needs surgery
Neonatal conjunctivitis
- Chlamydia trachomatis commonest cause . Check for otitis media + pneumonia, M-oral erythromycin. Onset ~2w after birth
- 30-50% accounted for by Staph, Strep Haemophilus, Pseudomonas. Topical therapy or oral in Pseudomonas
- Viral infections less common in neonate
- Gonorrhoea <1% nowadays. Onset within days, hyperacute injection + chemosis + lid oedema + severe purulent discharge, may have corneal ulceration + perforation. Need hourly saline lavage and IM/IV ceftriaxone.
Purulent/mucopurulent discharge, conjunctival injection, swelling; may have systemic signs
Why do you use oral erythromycin for neonatal Chlamydial conjunctivitis?
Topical not sufficient
and
if its in eyes its likely to also be in the respiratory tract
What is chemosis?
Conjunctival oedema
Vernal keratoconjunctivitis
Uncommon but serious, affects 5-15yo with atopic history usually, lasts 5-10y
- CF: itch, thick mucus, tarsal giant papillae, limbal papillae or white dots, keratitis. Causes corneal scarring
- M:
- Acute: intensive topical steroids + antihistamines
- Steroids spared where poss cos of cataract risk
- Chronic: topical mast cell stabiliser, cyclosporin, mucolytics e.g. acetylcysteine
- Surgical debridement may be needed
Atopic keratoconjunctivitis
Eczema of lids + staphylococcal lid disease –> keratitis, anterior blepharitis, limbal hyperaemia, chemosis
A/w keratoconus + cataract
Cicatricial conjunctivitis
Conjunctival inflammation a/w scarring, rare, sight-threatening
Causes include physical damage, infections like trachoma, oculocutaneous disorders such as bulllous pemphigoid or SLE, rosacea, Sjogren’s, IBD, graft vs host disease, drug-induced from anti-glaucoma meds
What are the causes of keratitis?
- Commonest - gram + like S aureus/epidermidis or S pneumoniae
- G negs like Pseudomonas (a/w CL), H influenza, N gonorrhoea
- Herpes simplex virus - cells lyse forming a dendritic ulcer, more likely in immunosuppression, virus lies dormant in CN V ganglion, M-aciclovir ointment
- Contact-lens related: not common but can cause infective corneal ulcers
- Blepharitis
RF for keratitis
Trauma causing abrasions, extended CL wear, poor hygiene e.g. rinsing in tap water- Acanthamoeba
How does keratitis present?
FB sensation, pain, photophobia, lacrimation, reduced vision, discharge, injection, white opacity
Comps: limbal + scleral extension, corneal perforation, endophthalmitis (rare unless certain things like fungi)
How do you manage keratitis?
- Send scrapes + contact lenses for MCS
- Topical Abx intensive sterilisation
- In healing phase add steroids + lubricants
- Stop CL wear, report to Yellow Card scheme if CL-associated
Herpes simplex keratitis
- Usually blepharitis but can spread to cornea using dendritic erosion (branching, terminal bulbs) + geographic ulcers in areas of de-epithelialisation
- Superficial punctate keratitis, pseudodendrites
- Need systemic antivirals, topical lubricants
Herpes zoster ophthalmicus
- Reactivation of VZV in area supplied by CNVa
- CF: viral prodrome, preherpetic neuralgia, rash (papules-vesicles-pustules-scabs), Hutchinson’s sign, cornea more vulnerable to bacteria + fungi
- M: oral antivirals, IV if severe/immunocomrpomised
- Comps: episcleritis, anterior uveitis, ptosis, post-herpetic neuralgia
Keratoconus
A common progressive cone-shaped bulge that affects vision leading to astigmatism + myopia. Mostly in younger people
RF: FH, allergic diseases causing chronic rubbing, CT disease causing abnormal corneal structure, Apert’s syndrome
CF: worse prognosis the earlier the onset, usually b/l but asymmetrical, irregular astigmatism with reduced VA, usually stabilises by mid-30s
Comps: rupture of Descemet’s membrane causing oedema, corneal scar
M: glasses/soft CL to correct vision, corneal cross-linking procedure, corneal transplant
Corneal dystrophy
- Endothelial e.g. Fuch’s corneal dystrophy. Gradual onset, blindness in 40-60s if don’t do a transplant
- Epithelial
- Stromal
What is a penetrating keratoplasty?
A corneal transplant - full or partial thickness
- Inds: keratoconus, corneal thinning, perforation, Fuch’s endothelial dystrophy
- Post-op need topical steroid + Abx for infection risk and rejection for minimum 2y but poss lifelong
What is a cataract?
An opacity in the lens that reduces its transparency
