Flashcards in Glaucoma Deck (25)
What are glaucomas, which ways can they be classified, and what are the three common shared features?
Glaucomas are a mixed group of disorders that can be classified into:
1. Primary vs secondary
2. Open versus closed
3. Congenital vs acquired
Three shared features include:
1. Optic disc cupping
2. Visual field loss
3. Raised intraocular pressure (usually)
What constitutes ocular hypertension (concept)?
Raised intraocular pressure without optic disc damage and visual field loss.
What is glaucoma called when it occurs in the absence of high pressure?
Low, or normal, tension glaucoma.
What is the most common type of glaucoma?
Acquired primary open angle glaucoma (POAG) accounts for one third of total glaucomas.
Affects 1% of those aged over 40, and 10% over 80.
Untreated, is usually a progressive disease.
General pathogenesis of POA glaucoma?
The trabecular meshwork in the angle between the cornea and the iris undergoes morphological changes over time (cause unknown). This impairs aqueous humour drainage and leads to increased IOP.
This is transmitted to the optic disc where nerve fibre damage occurs.
However, elevated pressure is not the sole cause of damage (given the existence of ocular hypertension and low tension glaucoma). It is likely that impairment of the optic nerve blood supply or aspects of the optic nerve head structure are important.
Name five risk factors for POA glaucoma.
1. Genetic: more common in first-degree relatives
2. Increasing age
3. Diabetes mellitus
5. Black ethnicity
What are the three chief signs of POAG and when do they occur?
1. Raised IOP
2. Optic disc cupping
3. Peripheral visual field loss
No symptoms until it is so advanced that central vision is threatened. No headache, eye ache, or loss of VA.
So, detection is either late or through chance, or on examination of at risk individuals.
What is the most reliable and accurate measurement of IOP?
Performed at a slit lamp, using a corneal applanating prism after instillation of anaesthetic and fluorescein drops.
Other methods include Ax of corneal resistance to a calibrated puff of air, and an electronic applicator. Digital assessment is not accurate.
Describe the normal optic disc (which has to be examined when assessing for glaucoma).
The normal optic disc contains:
1. Neuroretinal rim (nerve fibres), which is pink owing to vascular perfusion.
2. Optic disc cup (area without nerve fibres), which is white
3. Blood vessels
Describe the damage to the optic disc in POAG.
As nerve fibres are damaged and lost, the proportion of pink neuroretinal rim diminishes, the rim becomes pale and the cup enlarges.
This is expressed as the cup:disc ratio, which is assessed by comparing the vertical diameter of the optic disc with the vertical diameter of the cup.
A cup:disc ratio of 0.6 is highly suggestive of glaucoma.
Asymmetry between the eyes of 0.2 is also significant.
An increasing cup:disc ratio is indicative of progressive disease but is difficult to detect.
What is the classic visual field defect of POAG?
Arcuate scotoma (see p. 40).
Confrontational testing is unlikely to reveal an abnormality.
Perimeters (increasingly computer-based) can identify subtle visual field loss and are therefore routinely used in detection and follow-up of glaucoma.
Management of POAG?
Only Rx thought to help is lowering of IOP.
1. Through suppression of aqueous humour formation (drops and tablets - beta blockers, carbonic anhydrase inhibitors, alpha2 agonists, destruction of ciliary body).
2. Through increase in aqueous outflow (drops - pilocarpine, prostaglandin analogues (latanoprost); laser trabeculoplasty (drains into allows drainage into subconjunctival space) and drainage surgery).
What is pilocarpine?
A cholinergic drug which enhances outflow through the trabecular network.
However, it also constricts the pupil, which may cause disabling reduction in vision in patients with cataract.
In young people, it impairs accommodation.
How does latanoprost work in POAG?
A prostaglandin analogue.
It increases outflow through pathways other than the trabecular meshwork (where pilocarpine works) - the uveoscleral route.
Name four side effects of systemic acetazolamide.
A powerful systemic carbonic anhydrase inhibitor, but long-term treatment rarely possible due to:
3. Gastrointestinal upset
4. Renal calculi
Is (argon) laser trabeculoplasty effective?
The effect (lower IOP) is not permanent, and repeat treatment os not effective.
Pathogenesis of angle closure glaucoma?
The anatomy of the eyes predisposes it to failure of aqueous humour to pass through the pupil ('pupil block') and to crowding of the anterior chamber angle, preventing aqueous access to the trabecular meshwork.
The IOP rise is acute. The attack may resolve spontaneously, but if it becomes established, visual loss is severe and often permanent. More common in hyperopia/hypermetropia.
Name 7 features of angle closure glaucoma (where three features are lumped together as one, plus 6 others).
1. Pain, nausea & vomiting
2. Loss of vision (due to corneal oedema)
4. Red eye (usually unilateral)
5. Cloudy cornea (due to corneal oedema)
6. Oval, non-reactive pupil (due to iris ischaemia)
7. Loss of red reflex (due to corneal oedema)
How is clinical presentation of angle closure glaucoma different to other glaucomas?
Usually acute onset, presenting with pain and loss of vision.
Preceding history of intermittent pain, blurring and haloes.
What is the key to correct Mx of angle closure glaucoma?
Making the diagnosis.
No other cause of red eye leads to such pain and loss of vision, along with corneal haze and pupillary abnormality.
What are the main ways in which angle closure glaucoma is treated?
1. Elevated IOP: beta blockers and acetazolamide (aqueous suppressants)
2. Pupil block: reversed by pilocarpine
Once acute attack resolved, treatment to prevent recurrence and prevent involvement of the at-risk fellow eye must be undertaken: prophylactic laser iridotomy allows aqueous humour to pass from the posterior into the anterior chamber, by-passing the pupil.
It is common for IOP to remain moderately elevated and for pt to require lifelong medical treatment.
Is secondary glaucoma open or closed angle?
It can be either.
Name 7 causes of secondary glaucoma.
1. Inflammation (chronic uveitis in particular)
2. Pseudoexfoliation (abnormal proteins deposit in meshwork)
3. Pigment dispersion (iris pigment deposits in meshwork)
4. Aphakia (cause unknown)
5. Lens abnormalities
6. Iris neovascularisation (secondary to ocular/retinal ischaemia, such as occurs in diabetic retinopathy and retinal vein occlusion)
7. Steroid therapy (usually topical)
Management of secondary glaucoma?
Treat the cause.
eg. Inflammation with steroids, retinal ischaemia with photocoagulation, lens-induced glaucoma by cataract removal.
Thereafter, the sequence of medical treatment followed by surgical treatment (as for POAG) is pursued, with added extras along the way.