Ophthalmology Flashcards
Borders of the orbit
Floor - maxilla, zygoma, palatine
Roof - frontal bone, lesser wing of sphenoid
Medial border - maxilla, lacrimal, ethmoid, sphenoid
Lateral border - zygomata and greater wing of sphenoid
Apex - optic foramen
Base - eyelid margins
Innervation of the extraocular muscles
CNIII: levator palpebrae superioris, superior rectus, inferior rectus, medial rectus, inferior oblique
CNIV: superior oblique
CNVI: lateral rectus
Components of the retina
Two cellular layers:
- Neural layer: innermost layer, consisting of photoceptors, located posteriorly and laterally
- Pigmented layer: outer layer, attached to the choroid and supports the neural layer, continues around the whole inner surface of the eye
Macula: centre of the retina. Yellow. Highly pigmented.
Contains a depression (fovea) which has a high conc of light detecting cells.
Optic disc: where the optic nerve enters the retina. Contains no light detecting cells. Blind spot.
Anterior chamber and posterior chamber
Anterior chamber is located between the cornea and iris, filled with aqueous humor
Posterior chamber is located between the iris and ciliary processes, filled with aqueous humor
Aqueous humor production and drainage
Clear plasma-like fluid that nourishes and protects the eye.
Produced constantly by the ciliary body in the posterior chamber, and diffuses into the anterior chamber and drains via the trabecular meshwork at the base of the cornea into the Schlemm canals and then in to the vascular system
Vasculature of the eye ball
Eyeball receives arterial blood from ophthalmic artery (branch of ICA)
Central artery of the retina is a branch of the ophthalmic artery, supplying the internal surface of the retina
Venous drainage via superior and inferior ophthalmic veins -> drains into cavernous sinus
Layers of the eyelid
Skin and subcut tissue
Orbicular oculi muscle (CNVII, closes the eyelid)
Tarsal plates (contains meibomian glands)
Levator apparatus: levator palpebrae superioris (CNIII, opens the eye lid), and superior tarsal muscle (Muller muscle, opens eyelid, innervated by sympathetic fibres)
Conjunctiva (palpebral part on the eyelid and bulbar part reflects onto the sclera)
Sensory innervation of the eyelid
Motor innervation of the eyelid
Upper eyelid - ophthlamic branch of trigeminal (CNV1)
Lower eyelid - maxillary branch of trigeminal (CNV2)
Motor:
CNIII opens the eyelid (levator palpebrae superioris)
CNVII closes the eyelid (orbicularis oculi)
Sympathetic fibres opens the eyelid (superior tarsal muscle)
Lacrimal apparatus: production and drainage
Lacrimal fluid is produced in the lacrimal gland (sits at the upper lateral corner of the eye)
Spreads over cornea
Accumulates in the lacrimal lace (medial canthus of the eye)
Then drains into lacrimal sac via a series of canals
Then down the nasolacrimal duct
Then empties into the inferior meatus of the nasal cavity
Innervation of the lacrimal system
Sensory: lacrimal nerve (branch of ophthalmic, CNV1)
Parasympathetic fibres stimulate lacrimal fluid secretion (preganglionic greater petrosal branch of CNVII, postganglionic maxillary nerve CNV2 and zygomatic nerve CNVII)
Sympathetic fibres inhibit lacrimal fluid secretion (originate from superior cervical ganglion)
Normal pupil size in light and in dark
Light: 2-4mm diameter
Dark: 4-8mm diameter
Accommodation reflex
Automatic constriction of pupil and convergence of eyes when suddenly moving gaze from a far object to a near object
Afferent= CNII Efferent= CNIII
Contraction of ciliary muscles loosens suspensory ligaments causing lens to become rounder and focuses on the near object
Presbyopia
Ageing causes lens to become denser and less elastic -> reduced accommodation capacity
Corrected with glasses or bifocals
Near light dissociation
- how to test
- what is it
- 2 conditions
Patient looks at distant target, shine light in both eyes and observe pupil constriction
Patient then looks at near object and observe constriction (without shining the light)
Near-light dissociation = patient has a better pupillary near reflex (accommodation) than a pupillary light reflex
Argyll-Robertson pupil (neurosyphilis) causes a pupillary response to accommodation but not to light
Holmes-Adie pupil slowly reacts to accommodation and poorly responds to light/if at all
Direct pupillary light reflex
Shine light into pupil 1 and observe constriction of pupil 1
Lack of constriction = CNII damage (afferent) or CNIII damage (efferent)
Consensual pupillary light reflex
Shine light into pupil 1 and observe constriction of pupil 2
Lack of pupil 2 constriction = CNII damage in pupil 1, CNIII damage in pupil 2, or damage in Edinger-Westphal nucleus in pupil 2
Swinging light test and relative afferent pupillary defect
- what does the swinging light test assess?
- what is the test?
- what happens in the test with RAPD?
Compares direct and consensual pupillary constriction of each eye to look for a difference in afferent conduction between them
Test: shine light into pupil 1, both eyes constrict -> shine the same light into pupil 2 and the degree of constriction should remain the same because the intensity of light is the same
RAPD= CNII damage or severe retinal disease.
RAPD in pupil 1: shine light into pupil 1, both pupils constrict because although there is optic nerve damage the light is still brighter than the surrounding environment. Move light to pupil 2 and both pupils remain constricted. When light moves back to pupil 1 both pupils will dilate because the light is perceived to be darker compared to when the light was in pupil 2.
RAPD in pupil 2: shine light into pupil 1, both pupils constrict. Then shine the same intensity light into pupil 2 -> the optic nerve won’t recognise that light as being as intense so the pupils will dilate in response to a perceived ‘darker’ environment.
Visual pathway
Light enters the left side of each eye -> light hits the retina on the right side of each eye. The left nasal optic nerve fibres cross at the optic chiasm to the join the right temporal optic nerve fibres, forming the right optic tract. They reach the right lateral geniculate nucleus where they separate into superior (parietal) and inferior (temporal) radiations. The radiations then reach the right side of the occipital lobe where the image is processed.
Light enters the right side of each eye and hits the retina on the left side of each eye (left temporal retina and right nasal retina). The right nasal optic fibres cross at the chiasm to meet the left temporal fibres, forming the left optic tract. The left optic tract travels to the left lateral geniculate nucleus. They then separate into superior and inferior radiations and terminate at the left occipital lobe.
What information does the superior optic radiation carry to the primary visual cortex?
What visual defect occurs when there is damage to the superior optic radiation?
Superior optic radiation travels through the parietal lobe and carries the information from the superior portion of the retina, which represents the inferior part of the visual field.
Damage to the left superior optic radiation causes a right inferior quadrantanopia
What information does the inferior optic radiation carry to the primary visual cortex?
What visual defect occurs when there is damage to the inferior optic radiation?
The inferior optic radiation travels through the temporal lobe (meyers loop) and carries information from the inferior portion of the retina which represents the superior visual field.
Damage to the left inferior optic radiation causes a right superior quadrantanopia
Causes of painless sudden visual loss
Vitreous haemorrhage CRVO CRAO WARMD Diabetic maculopathy Stroke Retinal detachment
Causes of painful sudden visual loss
Iritis Scleritis Keratitis AACG Optic neuritis Migraine Benign Intracranial HTN
Myopia vs. Hypermetropia vs. Astigmatism
Myopia: light from a distant object focuses in front of retina (long axial length with average cornea, or average axial length with high power cornea). Correct with biconcave lens.
Hypermetropia: light from distant object focuses beyond the retina (short axial length with average cornea, or lower power cornea with average axial length). Correct with biconvex lens.
Astigmatism: anatomical variation
Blepharitis
- what is it
- two types
Chronic, intermittent inflammation of the eyelid margins
Anterior blepharitis: inflamm of the base of the eyelashes. Caused by Staphylococci, may be associated with seborrhoeic dermatitis
Posterior blepharitis: inflamm of the meibomian glands. Associated with meibomian gland dysfunction and rosacea
Blepharitis features
Bilateral symptoms
Grittiness, discomfort, particularly around eyelid margins
Eyes may be stuck together in the morning
Eyelid margins may be red
Swollen eyelidds may be seen in Staphylococcal blepharitis
Styes and chalazions more common with blepharitis
Secodary conjunctivitis may occur
Function of the meibomian gland and consequences of meibomian gland dysfunction
Meibomian gland secretes oil on to the eye surface to prevent rapid evaporation of the tear film -> any problems with the gland causes drying of the eye, leading to irritation
Management of blepharitis
Softening and cleaning the lid margin using hot compresses twice a day
Mechanical removal of debris from lid margins
Artificial tears for symptomatic relief
If ineffective ->
Anterior = topical abx (chloramphenicol)
Posterior = oral abx (doxycycline)
Chalazion/ meibomian cyst
- what is it
- features
- management
- most common type of benign eyelid lump, due to an obstructed meibomian gland, leading to a granuloma within the tarsal plate
- Features: painless swelling in the posterior lamella, may discharge anteriorly or posteriorly, more common in patients with chronic blepharitis, seborrhoeic dermatitis, rosacea
Stye
- what is it
- different types
- features
- management
-Acute abscess within a lash follicle and its associated glands
- External stye: staph infection of the glands of Zeis (sebum) or glands of Moll (sweat)
- Internal stye: infection of the meibomian glands, may leave residual chalazion
-Features: tender lump with associated inflammation
-Management: hot compress, analgesia
Only consider topical abx if there is associated conjunctivitis
Entropion vs ectropion
Entropion: in-turning of the eyelid (usually lower eyelid)
Ectropion: out-turning of the eyelid (usually lower eyelid)
Causes of ptosis
Lid pulled down due to gravitational effect of mass/ scar
Defect in levator aponeurosis
Myopathy of levator muscle or NMJ (MG, myotonic dystrophy)
Innervational defect (Horners, CNIII palsy)
Blow out fracture pathophysiology (including trapdoor fracture in children)
Blunt trauma to the orbit -> the force of the blow is dissipated by a fracture of the orbital floor (maxillary bone) and/or medial wall (ethmoidal bone)
Maxillary bone fracture opens up into the maxillary sinus, causing blood to leak into the maxillary sinus
In children, the flexibility of the orbital floor causes the fracture maxillary bone to snap back, causing a trapdoor fracture. It traps the inferior rectus, leaving the eye stuck in a down and out position. Requires surgery.
Features of a blow out fracture
Periorbital bruising Periorbital oedema Subconjunctival haemorrhage Surgical emphysema Vertical diplopia due to mechanical restriction of upgaze Pain Enophthalmos Infraorbital anaesthesia due to nerve damage in the infraorbital canal
Investigations and management of blow out fracture
CT head is first line
If X-ray is done, a teardrop sign is seen (polypoid mass hanging from the floor into the maxillary sinus)
Air-fluid level in the maxillary sinus due to blood
Mx:
- Avoid blowing nose in case of orbital emphysema
- Nasal decongestants
- Prophylactic co-amoxiclab
- Surgery required if: enophthlamos, diplopia, inferior rectus entrapment, large fracture
LOOK OUT FOR RETROBULBAR HAEMORRHAGE (emergency)
Retrobulbar haemorrhage
- what is it
- when do you get it
- features
- management
Ophthalmic emergency
Risk with any direct trauma to the orbit, including surgery
It is effectively a compartment syndrome of the eye socket with risk of complete loss of vision within hours
Features: Tight swollen eyelid Unilateral fixed dilated pupil Reduced eye movements Profound vision loss
Must force eyelids open to check pupil reaction (optic nerve in check)
Management: urgent canthotomy and cantholysis
Orbital cellulitis features
Ophthalmic and medical emergency Fever, malaise, periocular pain Inflamed lids May have chemosis and proptosis Painful restricted eye movements Diplopia Lagophthalmos Optic nerve dysfunction (reduced VA, reduced colour vision, RAPD)
What is the orbital septum and what is its function
Thick piece of connective tissue, between the lids and the orbit, acting as a barrier to the spread of infection
Orbital cellulitis causative organisms
Streptococcus pneumoniae
Staphylococcus aureus
Streptococcus pyogenes
Haemophilus influenzae (commoner in children but reducing because of HiB vaccine)
Orbital cellulitis risk factors and complications
Risk factors: sinus disease (ethmoidal sinusitis), trauma (sepal perforation, retained FB), recent orbital surgery, immunocompromised
Ocular complications:
Exposure keratopathy, raised intraocular pressure, CRAO, CRVO, optic neuritis
Systemic complications:
Orbital and periorbital abscess, cavernous sinus thrombosis, meningitis, cerebral abscess
Orbital cellulitis investigations
Temperature
FBC
Blood culture
CT orbit/sinus/brain
Management of orbital cellulitis
Admit for IV cefuroxime
Monitor extent of skin inflam
Regular review of orbital and visual functions
ENT input to assess sinus drainage
Repeat CT if there is deterioration to exclude abscess formation
Preseptal cellulitis
- causative organisms
- at risk population
- risk factors
Causative organisms: Staphylococci and Streptococci
Common in children
Risk factors:
Infection of adjacent structures (dacrocystitis, styes)
Systemic infection (URTI)
Trauma (lacterations)
Preseptal cellulitis features
Fever, malaise
Painful, swollen lid/periorbital
Inflamed lids but with no proptosis (bulging of eye)
Normal eye movements, white conjunctiva, normal optic nerve function
Preseptal cellulitis investigations and management
Ix: clinical diagnosis. investigations are not usually necessary unless there is doubt about orbital or sinus involvement
Mx: daily review until resolution, oral antibiotics (flucloxacillin or co-amoxiclav)
Dacrocystitis
- what is it
- common organisms
- in what patients is it more common in
Infection of the lacrimal drainage sac
Usually due to Staph or Strep
Common in patients with partial or complete nasolacrimal duct obstruction
Features of dacrocystitis
-Red, very tender swelling at the medial canthus
-Worsening epiphoria (excessive lacrimation)
-May express pus from puncta on palpation
+/- Localised cellulitis
Investigations and management of dacrocystitis
Ix: clinical diagnosis, can send discharge to microbiology
Mx: urgent management to prevent spreading cellulitis
- High dose oral co-amoxiclav
- Analgesia
- Warm compress
- Gentle massaging
- Consider incision and drainage
- Surgical correction of nasolacrimal duct obstruction
- Referral to lacrimal clinic
Complications of dacrocystitis
Rarely becomes a severe cellulitis
Spontaneous or surgical drainage through the skin risks the formation of a fistula
Risk factors for cataracts
Smoking, alcohol, trauma, DM, long term corticosteroids, radiation, myotonic dystrophy, hypocalcaemia
Features of cataracts
Gradual onset monocular diplopia Gradual onset reduced vision Faded colour vision Glare (lights appear brighter than usual) Halos around lights
Investigations for cataracts
Defect in red reflex (cataracts prevents light from getting to the retina)
Ophthalmoscopy following pupil dilation (normal)
Slit lamp examination shows visible cataract
Types of cataract
Nuclear: most common, old age. Clouding of central lens.
Polar: localised, commonly inherited. Lies in visual axis
Subcapsular: common in steroid use. Opacity often focal of the posterior lens
Dot opacities: common in normal lenses, also seen in DM and myotonic dystrophy
Management of cataract
First line: stronger glasses/contact lenses, brighter lighting
Surgery is the only effective treatment - remove cloudy cataract and replace with artificial one
Complications of cataract surgery
Posterior capsule opacification
Retinal detachment
Posterior capsule rupture
Endophthalmitis
Allergic conjunctivitis features and management
Features:
Bilateral
Very itchy, conjunctival erythema, swelling, watery discharge
History of atopy (seasonal variation)
Mx:
avoid allergen
Topical or systemic antihistamines or mast cell stabilisers
Bacterial conjunctivitis features, causative organisms and management
Features:
Usually unilateral
Acute, red, gritty eyes with purulent discharge
Common organisms:
Staphylococcus epidermidis, Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae
Management:
Topical chloramphenicol abx or fusidic acid if pregnant
Viral conjunctivitis features, causative organisms, investigations, management, complications
Features:
Bilateral, acute watery discharge, periauricular lymph nodes, lid oedema
History of recent URTI
Highly infectious but usually self limiting
Common causes: adenovirus, molluscum contagiosum, HSV1
Ix: conjunctival swabs for PCR
Mx: cool compress, artificial tears, follow-up if condition worsens
If molluscum, remove the lesion
If Herpes give aciclovir
Complications: may develop secondary corneal involvement with blurring of vision -> rapid access eye clinic -> give topical steroids to treat it and prevent corneal scarring
Chlamydial conjunctivitis
- features
- systemic features
- ix
- mx
2-3weeks after infection
Usually unilateral, mucopurulent discharge, lid oedema, ptosis, follicles, non-tender lymphadenopathy, keratitis
May also have cervicitis and urethritis
Ix: conjunctival swabs for PCR, refer to GUM clinic
Mx: topical chloramphenicol, systemic treatment (azithromycin)
Alkali corneal burn
- why is alkali worse than acid burn?
- management
Emergency- rapid absorption and intraocular penetration of alkali, leading to both superficial and intraocular complications
More serious than acid burns as it continues to denature surface proteins and penetrate eyeball for hours
Mx: copious irrigation for prolonged period until pH normalises, if severe then on call team should be called and fornices should be swept with a glass rod following irrigation. Analgesia, topical abx, topical steroids, bandage contact lens
White eye in a history of severe burn is worse than red eye (white = ischaemia)
Risk factors for infective keratitis
Contact lenses Corneal trauma Corneal abrasions/ erosions Poor immune function history of autoimmune disease
Common causative bacteria and viruses for infection keratitis
Bacteria: pseudomonas aeruginosa, Stap aureus, Staph epidermidis, Strep pneumoniae, Haem influenzae, Moraxella catarrhalis
Viruses: Herpes simplex, Herpes zoster
Features of infective keratitis
Redness, severe pain, increased lacrimation, lid oedema, discharge, reduced visual acuity, photophobia, raised intraocular pressure
Dendritic ulcer = herpes simplex
Infective keratitis investigations and diagnosis
Corneal scraping for a microscope slide
Corneal scraping for cultures and sensitivity
FBC
HIV test
Diagnosis =
Presence of risk factors
Corneal infiltrate (oedema and opacification)
Corneal ulcer
Dendritis or geographical epithelial lesion (herpes)
Management of bacterial keratitis
- Topical quinolone
- Cytoplegics (atropine, cyclopentolate): paralyse the ciliary muscles, thus dilating the eye and preventing ciliary spasm (prevents pain and photophobia), and prevents posterior synechiae
- Simple analgesia
Management of herpetic keratitis
Topical aciclovir or trifluridine
Cycloplegics (relieves pain/photophobia, and prevents synechiae formation)
Simple analgesia
May require topical corticosteroids
Herpes zoster ophthalmicus
- where does the virus lie dormant?
- features
- Hutchinsons sign
Herpes zoster (DNA virus) lies dormant in the ophthalmic division of the trigeminal ganglion (varicella zoster lies dormant in the dorsal root ganglion)
Features:
Tingling over scalp and forehead
Vesicular rash around the eye and forehead that doesnt cross the midline
Hutchinson’s sign - rash/vesicles on the tip or side of the nose indicates nasociliary involvement and is a strong risk factor for ocular involvement
Herpes zoster ophthalmicus
- diagnosis
- management
- consequences
Clinical diagnosis
Management:
Oral antiviral treatment 7-10days
IV antivirals if severe or immunocomp
Topical corticosteroids for secondary inflam of the eye
Ocular involvement requires ophthalmology review
Consequences:
Conjunctivitis, keratitis, episcleritis, anterior uveitis
Ptosis
Post-herpetic neuralgia
