Ophthalmology Flashcards
Features of acute angle closure glaucoma
Severe pain, may have headache
Decreased visual acuity
Symptoms worse with pupil dilation (watching tv in a dark room)
Firm, red eye
Haloes around lights
Semi dilated non reacting pupil
Dull or hazy cornea
Systemic upset- nausea and vomiting, abdominal pain
Investigations for acute closure glaucoma
Refer to ophthalmology
Check visual fields, acuity, eye movements, cranial nerves
Slit lamp examination (without dilation)
Check intraocular pressure with Goldman Tonometry
Management of acute closure glaucoma
Refer to ophthalmology
Combination of eye drops- pilocarpine, beta blocker (timolol), alpha agonist (apraclonidine)
Intravenous acetazolamide
Surgery- laser peripheral iridotomy (do in other eye prophylacticaly)
NB- if in community, lie patient down, give pilocarpine eye drops, antiemetic/analgesic, and oral acetazolamide
Risks for ARMD
Advancing age
Smoking
FH
HTN, dyslipidaemia, DM
Dry macular degeneration
90% cases
Characterised by drusen
Wet macular degeneration
10%
Choroidal neovascularisation
Worst prognosis
Features of ARMD
Subacute onset
Reduced visual acuity (near field objects)
Central vision loss
Worse vision at night
Perception of flicking lights
Straight lines become wavy
On exam;
Distorted line perception on Amsler grid
Drusen (dry)
Fluid leak/haemorrhage (wet)
Macula depogmentation (both)
Investigations for ARMD
Visual acuity, fields, eye movements, cranial nerves
Fundoscopy
Slit lamp microscopy
Fluorescin angiography
OCT- retinal layers
Treatment of ARMD
Refer to ophthalmology, advice on driving
Dry- avoid smoking, control BP, healthy lifestyle, visual aids, social support groups, high dose vitamins and minerals eg. vitamin C, zinc, beta carotene can reduce rate of visual loss
Wet- same stuff, but Anti VEGF injections, then laser therapy 2nd (laser neovascularisation)
Allergic conjunctivitis
May be seen alone or in context of hay fever
Bilateral symptoms
Conjunctival erythema and swelling (chemo sis)
Itch
History of atopy
Management- Topical or systemic antihistamines, then mast cell stabilisers eg. Sodium cromoglicate
Features of anterior uveitis
Acute onset
Ocular pain (may increase with use)
Pupil may be small and fixed, or abnormally shaped
Intense photophobia
Blurred vision
Red eye
Lacrimation
Ciliary flush (red ring)
Hypopyon (visible fluid level)
Visual acuity normal- gradually gets worse
Conditions associated with anterior uveitis
Ankylosing spondylitis
Reactive arthritis
IBD (UC, Crohns)
Beckets disease
Sarcoidosis
Management of anterior uveitis
Urgent referral to ophthalmology
Pupil dilation
Steroid eye drops
Argyll Robertson pupil
Small, irregular pupils
No response to light, but there is accommodation
Causes- DM, syphyllis
Blepharitis
Inflammation of eyelid margin
Due to memobian gland dysfunction, seborrhoeic dermatitis/staph infection
Features of blepharitis
Bilateral
Grittiness
Sticky eyes in morning
Red eyelid margins
Styes and chalazions are more common
May get secondary conjunctivitis
Management of blepharitis
Hot compress twice a day
Lid hygiene- clear debris away with cotton wool buds dipped in boiling water
Artificial tears
Causes of blurred vision
Refractive error (most common)
Cataracts
Retinal detachment
ARMD
Acute angle closure glaucoma
Optic neuritis
Amaurosis fugax
Investigations for blurred vision
Visual acuity (logMAR chart- pinhole occluders (if it improves- due to refractive error), fields, cranial nerves, eye movements
Fundoscopy
Causes of cataracts
Advancing age
Smoking
Increased alcohol
Trauma
DM
long term corticosteroids
Radiation exposure
Hypocalcaemia
Steroids and intraocular pressure
Steroids (whether topical or systemic), can increase intraocular pressure and cause glaucoma
Tell patients who recently start steroids to have an eye test in 3 weeks
Features of cataracts
Reduced vision
Faded colour vision (things becoming more brown or yellow), colours not as sharp
Glare- lights appear brighter than usual
Starbursts around lights
Defect in the red reflex
Investigations for cataracts
Visual fields, acuity, eye movements, cranial nerves
Ophthalmoscopy (normal)
Slit lamp examination- visible cataract
Management of cataracts
Non surgical- stronger glasses, use brighter lights
Surgery- remove cloudy lens and implant an artificial one (referral to surgery depends upon whether visual impairment is present, the impact on quality of life, and patient choice)
Referral to ophthalmology regarding corneal foreign body
Penetrating eye injury due to sharp or high velocity object
Significant trauma
Chemical injury (irrigate first)
Organic material foreign body (seeds, twig, soil- infection)
Center of cornea
Red flags- severe pain, irregular dilated or non reactive pupils, reduced visual acuity
Pathophysiology of diabetic retinopathy
Hyperglycaemia damages the endothelial cells in retinal vessels
Increased vascular permeability causes leakage from vessels
Blot haemorrhages, hard exudates
Non proliferative diabetic retinopathy
Micro aneurysm, blot haemorrhages, hard exudates, Colton wool,spots, venous beading, intra retinal micro vascular abnormalities
Question to always ask in an ophthalmology history
DIABETES, well controlled, compliant with meds etc.
ALWAYS CHECK BM during investigations for an eye history
NB- this isn’t a condition that can be easily elucidated from the history
Proliferative diabetic retinopathy
Neovascularisation
Vitreous haemorrhage
Diabetic maculopathy
Macular oedema
Ischaemic maculopathy
Complications of diabetic retinopathy
Retinal detachment
Vitreous haemorrhage
Rebeosis iridis (new blood vessels in iris)
Optic neuropathy
Cataracts
Management of diabetic retinopathy
Lifestyle measures (as usual)/ glycaemic control (ask if they need support with this)
Laser photocoagulation
Anti VEGF injections
Vitreoretinal surgery
Features of episcleritis
Red eye
Classically not painful (in comparison to scleritis)
Watering and mild photophobia
Injected vessels are mobile when gentle pressure is applied to the sclera (in scleritis, the vessels don’t move)
If phenylepinephrine makes it’s better- confirms epislceritis
50% bilateral
Conservative management
Artificial tears
Herpes simplex keratitis
Commonly presents with a dendritic corneal ulcer
Red, painful eye
Photophobia
Watery eye
Decreased visual acuity
Fluorescin staining- ulcer
Management of herpes simplex keratitis
Immediate referral to ophthalmologist
Topical aciclovir
Herpes zoster ophthalmicus
Reactivation of varicella zoster in the area supplied by the ophthalmic division of the trigeminal nerve
Vesicular rash around eye
Hutchinson’s sign- rash on tip or side of nose (nasociliary involvement)
Management of herpes zoster ophthalmicus
Oral aciclovir for 7-10 days, within 3 days
May need topical corticosteroids
Same day ophthalmology referral if Hutchinson’s sign is present (rash on tip of nose)
NB- different to herpes keratitis
Holmes adie pupil
Benign
Mostly seen in women
Unilateral
Dilated pupil, when constricted, remains that way for a long time, slowly reacts to accommodation, very poorly to light
Causes of Horner’s syndrome
Central lesions
Anhidrosis of the face, arm and trunk
Stroke
Syringomyelia
Sclerosis (Multiple)
SOL
Encephalitis
Pre-ganglionic lesions
Anhidrosis of the face
Tumour (Pancoast)
Thyroidectomy
Trauma
Cervical rib
Post-ganglionic lesions
No anhidrosis
Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache
NB- STC
Fundoscopy features of hypertensive retinopathy
Silver or copper wiring
Arteriovenous nipping
Cotton wool spots (infarcted retina/damaged nerve fibres)
Hard exudates (lipids leak into retina)
Retinal haemorrhages
Papilloedema (ischameia to optic nerve resulting in optic nerve oedema/swelling)
Keith-Wagener classification
1- silver wires, 2- nipping, 3- cotton wool and haemorrhage, 4- papilloedema
Management- lifetsyle eg. smoking, exercise, diet
Comply with anti BP, control other factors like lipids and DM
Bacterial conjunctivitis
Sore eye
Sticky eye (stuck together in morning)
Purulent discharge
Usually unilateral
NB- conjunctivitis does not cause pain, photophobia or reduced visual acuity (vision may be blurry when the eye is covered with discharge)
Viral conjunctivitis
Sore, red eye
Serous discharge
Recent URTI
Periauricular lymph nodes
Usually bilateral
Management of infective con
Normally self limiting and settles within 1-2 weeks
Don’t wear contacts, eye hygiene (cotton wool), don’t share towels, don’t keep rubbing eye
Chloramphenicol drops (ABX), topical fusidic acid (pregnant women)
Causes of keratitis
NB- keratitis is inflammation of the cornea
Bacterial- staph, pseudomonas (contact lens wearers)
Fungal
Amoebic (acanthamoebic keratitis- exposure to soil or contaminated water)
Parasitic- onchocercal keratitis
Viral- herpes simplex
Contact lens acute red eye (CLARE)
Exposure keratitis- inadequate eyelid cover
Clinical features of keratitis
Red eye, pain
Photophobia
Gritty sensation
Hypopyon may be seen
Reduced visual acuity
Watery eye
Investigations for keratitis
Visual acuity, fields, eye movements, cranial nerves
Fundoscopy
Slit lamp examination
Swabs (bacteria, viruses, chlamydia) and corneal scrapings for PCR (virus) and acanthamoeba
Management of keratitis
Refer to ophthalmology
Stop using contacts until symptoms resolve
Topical antibiotics or bacterial (chloramphenicol), oral aciclovir if viral
Pain relief (cyclopentolate (cycloplegic))
Causes of optic neuritis
MS
DM
Syphyllis
Features of optic neuritis
Unilateral decrease in visual acuity over hours to days
Poor discrimination of colours (red desaturation)
Pain worse on eye movement
RAPD
Central scotoma
NB- fundoscopy may be normal (or may show blurring of the optic disc, if it is involved)
Management of optic neuritis
High dose steroids
Recovery usually takes 4-6 weeks
What is orbital cellulitis
Infection affecting the fat and muscles posterior to the orbital septum within orbit (but not involving the globe)
Risks factors for orbital cellulitis
Childhood
Previous sinus infection
Recent insect bite near eye
Ear of facial infection
Presentation of orbital cellulitis
Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Painful eye movements (ophthalmolplegia)l Diplopia
Eyelid oedema and ptosis
Nausea and vomiting
Drowsiness
Fever
Difficulty perceiving colour
Orbital cellulitis vs pre septal (peri orbital) cellulitis
Reduced visual acuity, proptosis, ophthalmoplegia not seen in preseptal cellulitis
Investigations for orbital cellulitis
Ophthalmology review- visual fields, acuity, eye movements, pupils, cranial nerves, eye swab
Bloods- culture, FBC UE LFT CRP
Head CT with contrast (inflammation of orbital tissue, sinusitis)
NB- admit to hospital for IV ABX (cellulitis near the eyes or nose- co-amoxiclav (amoxicillin and clavulanic acid))
Features of papilloedema on fundoscopy
Almost always bilateral
Venous engorgement
Blurring of optic disc margin
Elevation of optic disc
Loss of optic cup
Patons lines
NB- When looking for elevation of the optic disc, look at the way the retinal vessels flow across the disc. Vessels are able to flow straight across a flat surface, whereas they will curve over a raised disc.
Causes of papilloedema
SOL- neoplastic, vascular
Malignant hypertension
Idiopathic intracranial hypertension
Hydrocephalus
Hypercapnia
Hyperparathyroidism
Hypocalcaemia
Vitamin A toxicity
Posterior vitreous detachment
Separation of vitreous membrane from retina
Common, doesn’t cause pain or loss of vision
But, it can lead to tears and detachment of retina
Risk factors for PVD
Older age
Near sighted people
Symptoms of PVD
Sudden appearance of floaters
Flashes of light in vision
Blurred vision
Cobwebs across vision
Appearance of dark curtain descending (Also retinal detachment)
Weiss ring on Ophthalmoscopy
Investigations for PVD
Refer to ophthalmology
Visual acuity, fields, eye movements, cranial nerves
Fundoscopy
Slit lamp
NB- no treatment if no retinal tears or retinal detachment
Preseptal cellulitis
Infection of soft tissue around the eye eg. Eyelids, skin, soft tissue, but not the contents of the orbital cavity
Infection spreads from nearby sites eg. Breaks in skin, sinusitis, URTI (common in children)
Usually staph aureus, staph epidermidis, strep etc.
Symptoms of preseptal cellulitis
Red swollen painful eye of acute onset
Fever
Erythema and oedema or eyelids
Partial or complete ptosis
If orbital signs- visual disturbance, restricted eye movements, then it’s orbital cellutlitis
Investigations for preseptal cellulitis
Same as orbital cellulitis
Management of preseptal cellulitis
Refer to ophthalmology
Oral antibiotics (co amoxiclav)
Children may require admission for observation
Primary open angle glaucoma
Trabecular network offers increased resistance to drainage of aqueous humour (close angle- the iris has moved forward and sealed off the trabecular network)
Risk factors for open angle glaucoma
Older age
Genetics
Black patients
Myopia
HTN
DM
Corticosteroids
Features of open angle glaucoma
Peripheral visual field loss (nasal scotomas progressing to tunnel vision)
Decreased visual acuity
Optic disc cupping
Haloes around lights
Headaches, impaired adaption to darkness
Optic disc cupping (cup to disc ratio greater than 0.7, normally 0.4-0.7)
Optic disc pallor (atrophy)
Bayoneting of vessels
Cup notching
Disc haemorrhages
Investigations for open angle glaucoma
Ophthalmology referral
Visual fields, acuity, eye movements, cranial nerves
Fundosocpy WITHOUT DILATION (don’t dilated pupils with increased IOP)
Slit lamp examination with pupil dilation
Tonometry to measure IOP
Gonioscopy (measure chamber configuration and depth)
RAPD/Marcus Gunn Pupil
Found by swinging light test
Caused by lesion anterior to chiasm
Caused by retinal detachment and optic neuritis (MS)
Risk factors for retinal detachment
Age
Previous cataract surgery
Myopia
Ear trauma
FH
Previous history of the condition
Retinitis pigmentosa
Night blindness
Tunnel vision
Fundiscopy- pigmented peripheral retina
Alport syndrome
Ocular manifestations of RA
Keratoconjunctivitis Sicca (most common)
Episcleritis (erythema)
Scleritis (erythema and pain)
Corneal ulceration
Keratitis
Iatrogenic;
Steroid induced cataract s
Chloroquinine retinopathy
Features of scleritis
Red eye
Painful
Watering and photophobia
Gradual decrease in vision
Causes of sudden loss of vision
Ischaemic/vascular (amaurosis fugax)- thrombosis, embolism, temporal arteritis etc.
vitreous haemorrhage
Retinal detachment
Retinal migraine
Posterior vitreous detachment
Flashes of light (photopsia) in peripheral field of vision
Floaters (temporal)
Retinal detachment
Dense shadow that peripherally progresses towards central vision
Veil or curtain over filed of vision
Flashing lights
Spider Webs
Straight lines appear curved
Central vision loss
GREY RETINA ON FUNDOSCOPY
Vitreous haemorrhage
Large bleeds cause sudden painless visual loss
Numerous dark spots and floaters (days preceding)
Red hue in vision
Signs;
Decreased visual acuity
Visual field defect
NB- predisposed by blood thinning agents, diabetes, and trauma
Causes of tunnel vision
Paipilloedema
Glaucoma
Retinitis pigmentosa
Most common cause of sudden painless loss of vision
Vitreous haemorrhage
Causes of vitreous haemorrhage
Proliferative diabetic retinopathy
Posterior vitreous detachment
Ocular trauma (children and young adults)
Investigations for retinal tears, PVD, vitreous haemorrhage
Referral to ophthalmology
Visual fields, acuity, eye movements, cranial nerves
Fundoscopy (dilated)
Slit lamp examination (red blood cells in anterior vitreous for haemorrhage)
OCT
NB- below are for vitreous haemorrhage
Fluorescin angiography (neovascularisation)
Obrital CT (if open globe injury)
Management of open angle glaucoma
Supportive- reading aids, support groups, home adoptions etc.
First line- prostaglandin analogue eye drop
Second line- beta blocker, carbonic anhydrase inhibitor, sympathomimetic eye drops
Surgery- trabeculectomy
NB- if FH, screening from 40
NB- reassessment important to exclude progression and visual field loss, do frequently
Strabismus
A squint. The eyes are misaligned and this causes double vision
Amblyopia
A lazy eye
This happens when a squint isn’t corrected in childhood- it’s signals are cut off and it becomes less functional
Causes of squint
Idiopathic
Hydrocephalus
Cerebral palsy
SOL (retinoblastoma)
Trauma
Corneal reflections / Hirschbergs tests
When a light is shone at the eyes there should be equal and symmetrical corneal reflections
A squint will show an abnormality in alignment on one side
Investigations for a squint
Same as usual
Management of strabismus
Refer to ophthalmology
Occlusive patch over good eye (make weaker eye work)- after referral
Funduscopy dry AMD
Drusen
Retinal hypopigmentation
Fundoscopy Wet ARMD
Retinal discolouration
Retinal haemorrhages
Intraocular pressure and pupil dilation
Don’t dilate pupils if increased IOP eg. Glaucoma
Management of open angle glaucoma
Refer to ophthalmology, lifestyle stuff, driving
Medical- eye drops
Surgical- trabeculectomy
Myopia (near sightedness)
Clear near vision, far vision unclear
Hyperopia (far sightedness)
Far vision clear, near vision unclear eg. Reading
Astigmatism
Abnormal curvature of cornea
Unclear vision at all distances
Risks for acute angle closure glaucoma
Increased age, females, FH, south Asian origin, medications eg. Noradrenaline, oxybutinin, TCA eg. Amitriptyline
Causes of CRAO
Embolism- carotid artery sclerosis, emboli from atria (AF),
Thrombosis of retinal vessels (atherosclerosis)
Vasculitis (GCA)
Causes of CRVO
HTN, DM
Hypercoaguable (polycythaemia Vera, sickle cell disease, OCP, laukaemia)
Features of CRAO
Sudden painless loss of vision
RAPD
Features of CRVO
Sudden painless loss of vision
NO RAPD
Fundoscopy CRAO
Pale retina
Cherry red spot (fovea- choroid underneath)
Fundoscopy CRVO
Flame and blot haemorrhages
Optic disc oedema
Macula oedema
Investigations for retinal vessels occlusion
Bedside- fundoscopy and all other eye tests
Bloods- FBC (leukaemia), exclude diabetes, ESR (inflammatory disorder eg. GCA), autoimmune profile (SLE (vein), vasculitis (artery))
Imaging and specialist tests
CRAO- carotid Doppler, echocardiogram, temporal arteritis tests
Management of CRAO
Treat reversible risk factors and secondary prevention of CVD
NB- intravenous tissue-type plasminogen activator (tPA) may be an option in some patients
Management of CRVO
Refer to ophthalmology
Laser photocoagulation
Intravitreal steroids
Anti VEGF injections
What is amaurosis fugax
Sudden painless loss of vision that lasts seconds to minutes and is followed by spontaneous recovery (transient occlusion caused by microemboli, not permanent, so not a CRAO)
Causes of amaurosis fugax
Atherosclerosis, carotid artery stenosis, cardiac thrombi
Vasculitides eg. GCA, polyarteritis nodosa
Management of amaurosis fugax
Same day ophthalmology review
Bedside- visual acuity, fields, fundoscopy, eye movements, cranial nerves
Check temporal Artery for tenderness
Bloods- FBC UE KFT lipids BM glucose ESR CRP
Imaging and specialist- Carotid Doppler ultrasound
Posterior vitreous detachment
Detachment of the vitreous from the lining of the retina
Features of endophthalmitis
Severe, deep seated ocular pain
Acute loss of vision
Features of sepsis
Floaters
NB- usually after eye surgery
On examination;
Conjunctival hyperaemia and chemosis
Hazy cornea
Hypopyon
RAPD
Decreased visual acuity
Investigations for endophthalmitis
Same as for cellulitis
Which muscles does CN III innervate
Medial rectus
Superior rectus
Inferior rectus
Inferior oblique
LPS
Which muscle does CN IV innervate
Superior oblique
Which muscle does CN VI innervate
Lateral rectus
CN III palsy at rest
Ptosis
Dilated pupil
Down and eye position
CN III palsy on examination
Inability to adduct eye
Inability to gaze upwards
Inability to gaze downwards
CN IV palsy at rest
Tilted head
Hypertropia (eye high up)
CN IV palsy on examination
Limited depression of adduction
CN VI palsy at rest
Eye turns inwards
CN VI palsy on examination
Can’t abduct eye
Third nerve palsy with sparing of the pupil causes
Diabetes
HTN
Ischaemic
Third nerve palsy without sparing of the pupil causes
Idiopathic
Tumour
Trauma
Cavernous sinus thrombosis
PCAA (pupil dilated, often associated pain)
Raised ICP
MS
Investigations for an eye cranial nerve palsy
Observations, diabetes check, full ophthalmic examination
HBA1c, CRP, lipids, FBC UE LFT
MRI head may need MRI angiography if pupil is involved
Features of orbital floor fracture
Unilateral periorbital pain, oedema, echymosis
Enophthalmos
Orbital rim step off
Diplopia
Restricted eye movements
Infraorbital paraesthesia
NB- CT head, but rule out brain or spinal cord injury first (severe impact to head)
Features of retinoblastoma
Leukocoria
Strabismus
Painful, red eye
Loss of vision
Retinal detachment
Management of retinoblastoma
Cryotherapy, photocoagulation, brachytherapy if low risk
Chemotherapy
Surgery (enucleation)
Features of congenital cataracts
Leukocoria
Strabismus
Nystagmus
Delay in motor skills
Associations with congenital cataracts
Hereditary congenital cataracts
TORCH infections eg. Rubella
Tetany
Trisomy
Alport syndrome
Causes of Leukocoria
Retinoblastoma until proven otherwise in children
Congenital cataracts
Retinopathy of prematurity
Retinal detachment
Coats disease
Management of non urgent diplooia (CN palsy)
Refer to optometry
Can have eye patch, or if they wear spectacles a prism can be attached to glasses
Surgery can be preformed as a last resort to realign eyes
Steroids and eye disease
Steroids can cause cataracts and increase intraocular pressure, causing glaucoma
NB- people on steroids, tell them to go to optician after 3 weeks to have eye pressure measured
Non medical support for ARMD
Magnification, enlargement of print, contrast enhancement, use of other senses, low vision clinic, support groups, patient education, sensory teams
Sudden visual loss in one eye
Optic neuritis
CRAO (CRVO)
AACG
Retinal detachment
Wet macular degeneration
Vitreous haemorrhage
Side effects of prostaglandin analogues
increased eyelash length, iris pigmentation and periocular pigmentation
Causes of bitemporal hemianopia
Lesion of optic chiasm
Upper quadrant more than lower- pituitary tumour
Lower quadrant more than upper- craniopharyngioma
What is optic neuropathy
A lesion of the optic nerve
reduced acuity in the affected eye
a scotoma (usually central)
impaired colour vision
an afferent pupillary defect
optic atrophy – pale disc
Causes of optic neuropathy
Inflammatory (optic neuritis), e.g. demyelination, sarcoidosis, vasculitis
Optic nerve trauma or compression, e.g. glioma, meningioma, aneurysm, bone disorders affecting orbit
Toxic, e.g. tobacco/alcohol, ethambutol, methyl alcohol, quinine, hydroxy chloroquine, radiation
Ischaemic optic neuropathy, e.g. giant cell arteritis
Nutritional deficiency, e.g. vitamins B1 and B12
Infection, e.g. orbital cellulitis, syphilis, tuberculosis
Papilloedema
Prostaglandin analogue
Latanoprost
Increases uveoscleral outflow
SE- brown iris, increased eyelash length
NB- first line treatment in patients with heart block
Beta-blockers
Timolol
Reduces aqueous production
SE- avoid in asthma/ heart block
Sympathomimetics/Alpha agonists
Brimonidine
Reduces aqueous production and increases outflow
SE- hyperaemia, and avoid with TCA’s/MAOI’s
Miotics/ Muscarinic receptor agonists
Pilocarpine
Increases uveoscleral outflow
SE- constricted pupil, headache, blurred vision
Causes of an abnormal pupil shape
Anterior uveitis
Acute angle closure glaucoma-vertical oval.
Rubeosis iridis
Coloboma- can cause a hole in the iris
Tadpole pupil- usually temporary and associated with migraines.
Causes of mydriasis (dilated pupil)
Third nerve palsy
Holmes-Adie syndrome
Raised intracranial pressure
Congenital
Trauma
Stimulants such as cocaine
Anticholinergics
Causes of miosis (constricted pupil)
Horners syndrome (cocaine eye drops have no effect)
Cluster headaches
Argyll-Robertson pupil (in neurosyphilis)
Opiates
Nicotine
Pilocarpine
Difference between Horner syndrome and 3rd nerve palsy
Both- ptosis
Horner- anhidrosis, constricted pupil (miosis)
(Surgical) 3rd nerve palsy- strabismus (down and out eye), dilated pupil (mydriasis)
Stye
A tender red lump along the eyelid that may contain pus (infected glands of Zeis or Moll)
Hot compresses and analgesia. Consider topical antibiotics (i.e. chloramphenicol) if it is associated with conjunctivitis or persistent.
Cholazion
Infected memobian glands (memobian cyst) It presents with a swelling in the eyelid that is typically not tender. It can be tender and red.
Hot compress and analgesia. Consider topic antibiotics (i.e. chloramphenicol) if acutely inflamed. Rarely, surgical drainage needed.
Essential treatment needed for eyelid dysfunction eg. Bell’s palsy, ectropion, entropion etc.
Lubricating eye drops (can develop exposure keratitis)- Bell’s palsy: tape eyelid shut
Trichiasis
Inward growth of the eyelashes (entropion- eyelid moves inwards, not the eyelash growth itself)
Corneal abrasion
Corneal abrasions are scratches or damage to the cornea. They are a cause of red, painful eye. There are some common causes:
Contact lenses
Foreign bodies
Finger nails
Eyelashes
Entropion (inward turning eyelid)
Features of a corneal abrasion
History of contact lenses or foreign body
Painful red eye
Foreign body sensation
Watering eye
Blurring vision
Photophobia
A fluorescein stain (not angiography) is used to diagnose corneal abrasions
Management of a corneal abrasion
Simple analgesia (e.g. paracetamol)
Lubricating eye drops can improve symptoms
Antibiotic eye drops (i.e. chloramphenicol)
Bring the patient back after 1 week to check it has healed
Cyclopentolate eye drops dilate the pupil and improve significant symptoms, particularly photophobia.
Subconjunctival haemorrhage
When small blood vessels within the conjunctiva rupture and release blood into the space between the sclera and the conjunctiva
They often appear after episodes of strenuous activity such as heavy coughing, weight lifting or straining when constipated (or trauma)
Causes of a subconjunctival haemorrhage
Idiopathic
Hypertension
Bleeding disorders (e.g thrombocytopenia)
Whooping cough
Medications (warfarin, NOACs, antiplatelets)
Non-accidental injury
Trauma
Causes of a subconjunctival haemorrhage
Idiopathic
Hypertension
Bleeding disorders (e.g thrombocytopenia)
Whooping cough
Medications (warfarin, NOACs, antiplatelets)
Non-accidental injury
Horner’s syndrome features
miosis + ptosis + enophthalmos +/- anhydrosis
PVD vs retinal detachment
Although this can cause flashes and floaters, PVD can be thought of as the preceding events leading to retinal detachment. The retina can be thought of as being tugged on, leading to the flashes and floaters until it eventually detaches, causing progressive visual loss peripherally inwards to the centre. Given that this patient has had this progressive visual loss, retinal detachment has occurred.
Quadrantinopias
PITS refers to which part of the visual field is affected: parietal-inferior visual field / temporal-superior visual field. However, the optic radiations are ‘opposite’ to the visual fields!
NB- PITS lesions are usually caused by an MCA infarction (however, the branch that supplies the area is opposite too eg. inferior quadrantopias (parietal region) are due to superior branch occlusion etc.))
