Ophthal Flashcards
Types of conjunctivitis
Bacterial
Viral
Allergic
Conjunctivitis presentation
Unilateral or bilateral Red eyes Bloodshot Itchy or gritty sensation Discharge from the eye
Does not cause pain
How does bacterial conjunctivitis usually present
A purulent discharge and an inflamed conjunctiva. It is typically worse in the morning when the eyes may be stuck together. It usually starts in one eye and then can spread to the other. It is highly contagious.
How does viral conjunctivitis usually present
Is common and usually presents with a clear discharge. It is often associated with other symptoms of a viral infection such as dry cough, sore throat and blocked nose. You may find tender preauricular lymph nodes (in front of the ears). It is also contagious.
Management of conjunctivitis
usually resolves without treatment after 1-2 weeks.
Advise on good hygiene to avoid spreading (e.g. avoid sharing towels or rubbing eyes and regularly washing hands) and avoiding the use of contact lenses. Cleaning the eyes with cooled boiled water and cotton wool can help clear the discharge.
If bacterial conjunctivitis is suspected then antibiotic eye drops can be considered, however bear in mind it will often get better without treatment. Chloramphenicol and fuscidic acid eye drops are both options.
Why is it important to refer patients under 1 month with conjunctivitis
Neonatal conjunctivitis can be associated gonococcal infection and can cause loss of sight and more severe complications such as pneumonia
Management of allergic conjunctivitis
Antihistamines (oral or topical) can be used to reduce symptoms.
Topical mast-cell stabilisers can be used in patients with chronic seasonal symptoms. They work by preventing mast cells releasing histamine. These require use for several weeks before showing any benefit.
Lesion location in left homonymous hemianopia
Visual field defect to the left –> lesion of the right optic tract
Congruous vs incongruous visual defects
A congruous visual field defect is identical between the two eyes, whereas an incongruous defect differs in appearance between the eyes.
Congruous defects are complete whereas incongruous defects are incomplete
Which lesions cause incongruous visual defects
Optic tract lesions
Which lesions cause congruous defects
Optic radiation lesion or occipital cortex
Which lesions cause homonymous hemianopia
incongruous defects: lesion of optic tract
congruous defects: lesion of optic radiation or occipital cortex
macula sparing: lesion of occipital cortex
Which lesions cause superior homonymous quadrantanopias
superior: lesion of the inferior optic radiations in the temporal lobe (Meyer’s loop)
mnemonic = PITS (Parietal-Inferior, Temporal-Superior)
Which lesions cause inferior homonymous quadrantanopias
inferior: lesion of the superior optic radiations in the parietal lobe
mnemonic = PITS (Parietal-Inferior, Temporal-Superior)
Which lesions cause bitemporal hemianopia
lesion of optic chiasm
upper quadrant defect >
lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
What is glaucoma
Refers to the optic nerve damage that is caused by a significant rise in intraocular pressure.
The raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.
What is aqueous humour produced by
Ciliary body
Normal intraocular pressure
10-21 mmHg
The pressure is created by the resistance to flow through the trabecular meshwork into the canal of scheme
Pathophys of open-angle glaucoma
There is a gradual increase in resistance through the trabecular meshwork.
This makes it more difficult for aqueous humour to flow through the meshwork and exit the eye.
Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma.
Pathophys of acute angle-closure glaucoma
The iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away.
This leads to a continual build-up of pressure. This is an ophthalmology emergency.
Effect of increased intraocular pressure on the optic disc
Increased pressure in the eye causes cupping of the optic disc. In the centre of a normal optic disc is the optic cup.
This is a small indent in the optic disc. It is usually less than half the size of the optic disc.
When there is raised intraocular pressure, this indent becomes larger as the pressure in the eye puts pressure on that indent making it wider and deeper.
Abnormal optic cup size
An optic cup greater than 0.5 the size of the optic disc is abnormal.
Risk factors for open-angle glaucoma
Increasing age
Family history
Black ethnic origin
Nearsightedness (myopia)
Presentation of open-angle glaucoma
Asymptomatic
Peripheral vision affected first until it closes in to result in tunnel vision
Gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time
Diagnosis of open-angle glaucoma
Goldmann applanation tonometry can be used to check the intraocular pressure.
Fundoscopy assessment to check for optic disc cupping and optic nerve health.
Visual field assessment to check for peripheral vision loss.
When is treatment for open-angle glaucoma usually started
Treatment is usually started at an intraocular pressure of 24 mmHg or above. Patients are followed up closely to assess the response to treatment.
1st line mx for open-angle glaucoma
Prostaglandin analogue eye drops (e.g. latanoprost) are first line. These increase uveoscleral outflow.
Notable side effects of prostaglandin analogue eye drops
Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning).
Other options of management of open-angle glaucoma
Beta-blockers (e.g. timolol) reduce the production of aqueous humour
Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour
Sympathomimetics (e.g. brimonidine) reduce the production of aqueous fluid and increase uveoscleral outflow
Surgical intervention for glaucoma
Trabeculectomy surgery may be required where eye drops are ineffective.
This involves creating a new channel from the anterior chamber, through the sclera to a location under the conjunctiva.
It causes a “bleb” under the conjunctiva where the aqueous humour drains.
It is then reabsorbed from this bleb into the general circulation.
Risk factors for acute angle-closure glaucoma
Increasing age
Females are affected around 4 times more often than males
Family history
Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic origin.
Shallow anterior chamber
Medications which can precipitate acute angle-closure glaucoma
Adrenergic medications such as noradrenalin
Anticholinergic medications such as oxybutynin and solifenacin
Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects
Presentation of acute angle-closure glaucoma
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting
Examination findings in acute angle closure glaucoma
Red-eye Teary Hazy cornea Decreased visual acuity Dilatation of the affected pupil Fixed pupil size Firm eyeball on palpation
Initial management of acute angle closure glaucoma
same-day assessment by an ophthalmologist
Lie patient on their back without a pillow
Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
Give acetazolamide 500 mg orally
Given analgesia and an antiemetic if required
How does pilocarpine work
Pilocarpine acts on the muscarinic receptors in the sphincter muscles in the iris and causes constriction of the pupil.
Therefore it is a miotic agent. It also causes ciliary muscle contraction. These two effects cause the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork to open up.
How does acetazolamide work
Acetazolamide is a carbonic anhydrase inhibitor. This reduces the production of aqueous humour.
Secondary care management of acute angle-closure glaucoma
Pilocarpine Acetazolamide (oral or IV) Hyperosmotic agents such as glycerol or mannitol Timolol Dorzolamide Brimonidine
Purpose of hyper osmotic agents in acute angle closure glaucoma
Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in the eye
Use of beta-blockers in acute angle closure glaucoma
Beta-blockers reduce production of aqueous humour
Use of brimodine in acute angle closure glaucoma
Brimonidine is a sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow
Definitive treatment for acute angle-closure glaucoma
Laser iridotomy - involves using a laser to make a hole in the iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber. The relieves pressure that was pushing the iris against the cornea and allows the humour the drain.
What is posterior vitreous detachment
Posterior vitreous detachment is the separation of the vitreous membrane from the retina.
This occurs due to natural changes to the vitreous fluid of the eye with ageing.
Risk factors for posterior vitreous detachment
As people age, the vitreous fluid in the eye becomes less viscous, and thus, does not hold its shape as well. Therefore, it pulls the vitreous membrane away from the retina towards the centre of the eye.
Highly myopic (near-sighted) patients are also at increased risk of developing posterior vitreous detachment earlier in life. This is because the myopic eye has a longer axial length than an emmetropic eye.
Symptoms of posterior vitreous detachment
The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)
Signs of posterior vitreous detachment
Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).
IX for suspected vitreous detachment
All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.
Mx of posterior vitreous detachment
Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.
What is retinal detachment
Retinal detachment occurs when the neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium.
It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected.
Risk factors for retinal detachment
Age
Previous surgery for cataracts (accelerates posterior vitreous detachment)
Myopia
Eye trauma (consider boxing)
Family history
Previous history of retinal break/detachment in either eye
Symptoms of retinal detachment
New onset floaters or flashes, as these indicate pigment cells entering the vitreous space or traction on the retina respectively.
Sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery should also raise suspicion of detachment.
If the macula is involved, central visual acuity and visual outcomes become much worse.
Examination findings in retinal detachment
Peripheral visual fields may be reduced, and central acuity may be reduced to hand movements if the macula is detached.
Relative afferent pupillary defect if the optic nerve is involved.
On fundoscopy, the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms. If the break is small, however, it may appear normal.
Management of retinal tears
Management of retinal tears aims to create adhesions between the retina and the choroid to prevent detachment. This can be done using:
Laser therapy
Cryotherapy
Surgical options for retinal detachment
Vitrectomy involves removing the relevant parts of the vitreous body and replacing it with oil or gas.
Scleral buckling involves using a silicone “buckle” to put pressure on the outside of the eye (the sclera) so that the outer eye indents to bring the choroid inwards and into contact with the detached retina.
Pneumatic retinopexy involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble creates pressure that flattens the retina against the choroid and close the detachment.
What is anterior uveitis
inflammation in the anterior part of the uvea. The uvea involves the iris, ciliary body and choroid
Conditions associated with acute anterior uveitis
HLA B27 related conditions:
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis
Conditions associated with chronic anterior uveitis
Sarcoidosis Syphilis Lyme disease Tuberculosis Herpes virus
Acute anterior uveitis presentation
Unilateral Dull,aching,painful red eye Ciliary flush Miosis Photophobia Floaters and flashes
Tear production acute anterior uveitis
Increased
What is a hypoyon
Collection of white blood cells in the anterior chamber, seen as a yellowish fluid collection settled in front of the lower iris, with a fluid level. seen in acute anterior uveitis
Mx of acute anterior uveitis
Steroids
Cylopegic-mydriatic meds(atropine)
Immunsuppressants(DMARDS)
Laser therapy
Conditions associated with episcleritis
Rheumatoid arthritis
IBD
Presentation of episcleritis
Mild pain(no pain typically) Segmental redness(patch) Foreign body sensation Dilated episcleral vessels Watering of eye
Mx of episcleritis
Self-limiting - recovery in 1-4 weeks
Lubricating eye drops
Analgesia
Cold compress
Complications of scleritis
Necrotising scleritis
Perforation of sclera
Systemic conditions associated with scleritis
RA
SLE
IBD
Sarcoidosis
Presentation of scleritis
Severe pain Pain with eye movement Photophobia Eye watering Reduced visual acuity Abnormal pupil reaction to light
Mx of scleritis
Same day assessment by ophthalmologist
Consider underlying systemic condition
NSAIDS
Steroids
Immunosuppression
What is keratitis
Inflammation of the cornea
Most common cause of keratitis
Herpes simplex infection
Other causes of keratitis
Bacterial infection - pseudomonas or staph
Fungal - Candida
Contact lens acute red eye(CLARE)
Complications of herpes keratitis
Can lead to stromal keratitis(inflammation of layer between epithelium and endothelium) –> stromal necrosis, vascularisation and scarring and can lead to corneal blindness
Presentation of herpes keratitis
Painful red eye Photophobia Vesicles around the eye Foreign body sensation Watering eye Reduced visual acuity
Diagnosis of herpes keratitis
Staining with fluorescein will show a dendritic corneal ulcer
Slit-lamp examination
Corneal swabs/scrapings
Mx of herpes keratitis
Aciclovir (topical or oral)
Ganciclovir eye gel
Topical steroids may be used alongside antivirals to treat stromal keratitis
Corneal transplant if scarring caused by stromal keratitis
