Ophthalmology Flashcards
Layers of the retina
Neural - inner, contains photoreceptors
Pigmented - outer, continuous with whole inner surface of eye
Most eye surgery take place in which part of the eye?
Anterior chamber - 3mm depth
Ophthalmic artery arises from..
The internal carotid artery
Vascular supply to retina
Central artery of the retina, arises from ophthalmic artery
Flow of vitreous humor
Posterior chamber TO
Anterior chamber TO
Canal of Schlemm TO
Trabecular meshwork
Function of Levator Palpebrae Superioris
Elevates upper eyelid
Nerve supply to Levator Palpebrae Superioris
CN III
Extraocular muscles supplied by CN III
Medial, Superior and inferior recti
Inferior obliques
Extraocular muscles supplied by CN IV
Superior obliques
Extraocular muscles supplied by CN VI
Lateral recti
Deviation of the eye seen in CN III palsy
‘Down and out’
Lateral rectus pulls laterally, superior oblique pulls down
Movement of the eye caused by superior oblique
Down and in
Movement of the eye caused by inferior oblique
Up and in
Movement of the eye caused by inferior rectus
Down and out
Movement of the eye caused by superior rectus
Up and out
Edinger-Westphal nucleus connects which 2 cranial nerves
CN II and III.
CN II senses light, passes information onto CN III to cause bilateral pupillary constriction
Myopia
Short sighted, large eye
Hypermetropia
Long sighted, small eye
Astigmatism
Refractive power is different between the two eyes
Features of Mild Nonproliferative Diabetic Retinopathy
1 or more microaneurysms (dot haemorrhages)
Management of Mild Nonproliferative Diabetic Retinopathy
Observation only.
Optimise blood pressure and glycaemia.
Intravitreal anti VEGF +/- macular laser therapy if clinically significant macular oedema (CSMO)
Features of Moderate Nonproliferative Diabetic Retinopathy
Microaneurysms (dot haemorrhages
Blot haemorrhages
Hard exudates/lipid deposits
Cotton wool spots, Venous beading or looping & intraretinal microvascular abnormalities
Management of Moderate Nonproliferative Diabetic Retinopathy
Observation only.
Optimise blood pressure and glycaemia.
Intravitreal anti VEGF +/- macular laser therapy if clinically significant macular oedema (CSMO)
Features of severe Nonproliferative Diabetic Retinopathy
Dot and blot haemorrhages in 4 quadrants
Venous beading in at least 2 quadrants
Intraretinal microvascular abnormalities in 1 quadrants
+/- Cotton wool spots
Management of Severe Nonproliferative Diabetic Retinopathy
Panretinal photocoagulation
If Clinically Significant Macular oedema:
Intravitreal anti VEGF therapy +/- macular laser therapy +/- panretinal photocoagulation
Features of proliferative diabetic retinopathy
New vessels
+/- dot and blot haemorrhages
+/- venous beading
+/- cotton wool spots
Management of proliferative diabetic retinopathy
Urgent panretinal photocoagulation + intravitreal anti VEGF therapy +/- macular laser therapy
Vitrectomy if severe
Features of maculopathy
Any retinal abnormality in the macular area. Any changes in this area are potentially serious and can affect visual acuity.
Management of diabetic maculopathy
Anti VEGF for any clinically significant macular oedema
Cotton wool spots Vs Exudates
Cotton wool spots are areas of ischaemia - will obscure superficial vasculature
Exudates are areas of fluid leakage due to damaged pericytes - overlying vasculature is visible.
Referral guidelines for diabetic retinopathy
Proliferative - urgent referral
Severe NPDR - routine referral
Macular oedema - routine referral
Early NPDR can be managed in primary care.
Within 1 week of eye surgery, patient experiences:
↓ visual acuity
Eye ache
Eyelid oedema
Corneal oedema
Endophthalmitis
Management of endophthalmitis
Immediate referral to ophthalmology (within 24 hours)
‘Tap and inject’ - aqueous/vitreous sample sent for cultures, intravitreal injection of broad spectrum antibiotics
Internuclear ophthalmoplegia
On voluntary gaze to one side, there is impaired adduction of one eye with horizontal nystagmus of contralateral eye.
Blepharitis
Inflammation of eyelid margins due to Meibomian gland dysfunction
Meibomian Glands
Glands which secrete oil onto eye surface to prevent rapid evaporation of tear film.
Presentation of blepharitis
Bilateral, grittiness and discomfort of the eyes.
Eyes may be sticky in the mornings with red margins.
+/- Styes and chalazions
Management of blepharitis
Managed in primary care.
Softening of lid margin using hot compresses BD
Mechanical removal of debris using cotton wool buds, boiling water and baby shampoo
+/- Artificial tears (symptom relief)
Stye
Infection of eyelid glands
Hordeolum externum
Type of stye caused by staph infection of sebum or sweat glands
Hordeolum internum
Type of stye caused by infection of meibomian glands.
Presentation of Stye
H. externum - thin walled cyst on lid margin, containing clear fluid
H. internum - cyst on lid margin containing sebum
Management of a stye
Primary care management
Hot compress and analgesia
Chalazion
Cyst of meibomian gland
Presentation of Chalazion
Firm, painless lump on eyelid
Slowly enlarging
Management of a Chalazion
No referral required
Usually resolve spontaneously. Some require surgical drainage.
Entropion
In-turning of eyelids, causing eyelashes to abrade the eyeball.
Due to ageing, conjunctival scarring of spasm of orbicularis oculi
Presentation of entropion
Foreign body type sensation
Reflex watering
Increased risk of bacterial corneal infection and ulceration
Management of entropion
Routine referral for surgery
Botox may help with blepharospasm
Ectropion
Out-turning of eyelids
Due to ageing, facial nerve palsy, eyelid skin scarring, bulky eyelid tumours
Presentation of ectropion
Exposure of conjunctiva on lower eye lid
Inflammation and keratinisation of conjunctiva
Eye watering
Management of ectropion
Routine referral for surgery.
Surgery not required if CN VII palsy is considered to be reversible.
Herpes Zoster Ophthalmicus
Reactivation of VZV in the area supplied by the ophthalmic division of CN V.
Accounts for 10% of all cases of shingles.
Features of Herpes Zoster Ophthalmicus
Vesicular rash around the eye
Hutchinson’s sign - rash on tip or side of nose, indicating nasociliary involvement. Strong risk factor for eye involvement.
Management of Herpes Zoster Ophthalmicus
Oral aciclovir for 7-10 days, within 72 hours
Oral corticosteroids
Urgent ophthalmology review if ocular involvement (within 1-3 days)
Complications of Herpes Zoster Ophthalmicus
Ocular: conjunctiv/kerat/episcler/anterior uveitis
Ptosis
Post-herpetic neuralgia
Horner’s syndrome
Oculosympathetic paresis:
Miosis - anisocoria is more marked in the dark, since there is limited dilatation in the affected eye
Ptosis
Anhidrosis
PICA Syndrome
AKA Wallenberg or Lateral Medullary Syndrome
Results from blockage in Posterior Inferior Cerebellar Artery
Horner's syndrome (miosis, ptosis, anhidrosis) Vertigo and ataxia Hoarseness Sensory loss Dysphagia
Second order Horner’s syndrome is due to pathology affecting the…
Sympathetic trunk
e.g. Trauma or surgery, thoracic outlet, lung apex malignancy
Painful Horner’s should immediately be suspected as:
Carotid Artery Dissection (until proven otherwise!)
A patient presents with painful Horner’s syndrome. Which investigations are important to determine whether or not there is a Carotid Artery Dissection?
Neck MRI
MRI of cavernous sinus
Stage I Hypertensive Retinopathy
Arteriolar narrowing and tortuosity i.e. silver wiring
Stage II Hypertensive Retinopathy
Arteriolar narrowing and tortuosity i.e. silver wiring
Arteriovenous nipping
Stage III Hypertensive Retinopathy
Arteriolar narrowing and tortuosity i.e. silver wiring Arteriovenous nipping Cotton Wool Spots Retinal Haemorrhages Exudates
Stage IV Hypertensive Retinopathy
Arteriolar narrowing and tortuosity i.e. silver wiring Arteriovenous nipping Cotton Wool Spots Retinal Haemorrhages Exudates Papilloedema
Appearance of papilloedema on fundoscopy
Venous engorgement Blurring of optic disc margin Elevation of optic disc Loss of optic cup Paton’s lines - concentric/radial lines cascading from optic disc
Common Differentials for Papilloedema
Space occupying lesion: neoplastic or vascular Malignant hypertension Idiopathic intracranial hypertension Hydrocephalus Hypercapnia
Management of Hypertensive retinopathy
Optimise blood pressure control using conservative +/- pharmacological methods.
With good control, changes may regress.
Differentials for Painless, gradual visual loss
Macular Degeneration
Primary open angle glaucoma
Diabetic and hypertensive retinopathy
Cataracts
Differentials for Sudden, Painful visual loss
Optic Neuritis
Arteritic Anterior Ischaemic Optic Neuropathy
Acute Angle Closure Glaucoma
Differentials for Sudden, Painless visual loss
Retinal vein or artery occlusion
Non arteritic Ischaemic Optic Neuropathy
Exudative Macular Degeneration
Retinal Detachment
Vitreous haemorrhage
Risk factors for Age-related Macular Degeneration
Age > 55 years Smoking Family history Caucasian High cumulative UV exposure Female CVD
Features of age-related macular degeneration
Reduced visual acuity “blurred vision” (central vision affected first)
Distortion “Straight lines appear crooked/wavy”
Central scotomas
Dry age-related macular degeneration
Progressive atrophy of retina
Wet age-related macular degeneration
Leakage of exudate into macula due to new vessels
Wet or dry age-related macular degeneration has the worst prognosis?
Wet
Management of age-related macular degeneration
Urgent referral - within 1-3 days
Smoking cessation
Referral to low vision services
Anti-VEGF and steroid injections may be useful for wet AMD.
Pathology of Open Angle Glaucoma
Slow clogging of aqueous humor causing atrophy of optic disc from the outside in.
Presentation of open angle glaucoma
Gradual, painless visual loss (peripheral then central i.e. tunnel vision)
Nasal scotomas
Optic disc cupping and pallor
Pathology of acute angle closure glaucoma
Lens pushing against iris, blocking flow of aqueous humor