acute glaucoma Flashcards
drainage of aqueous humor
- Aqueous humor is produced by the ciliary
body in the posterior chamber of the eye
►It diffuses from the posterior chamber,
through the pupil, and into the anterior
chamber
►From the anterior chamber, the fluid is
drained into the vascular system via the
trabecular meshwork and Schlemm canal
contained within the angle
what is glaucoma
Glaucoma is a group of conditions with characteristic optic nerve head changes associated with corresponding visual field defects, with or without raised intra ocular pressure
How does glaucoma affect vision?
- Glaucoma is the main cause of irreversible blindness in the world.
- Damage to the optic nerve affects the peripheral vision initially and then gradually causes total sight loss if left untreated.
what is normal IOP
Normal range is quoted as 10 to 21 mmHg with a mean of 16mmHg
gold standard test to measure IOP
Goldmann Applanation Tonometry (GAT)
medical ways to reduce IOP
Beta blockers e.g. Timolol Miotics: e.g. Pilocarpine Prostaglandin Analogues e.g. Xalatan or Lumigan Alpha Adrenergics: e.g. Alphagan CAI e.g. Azopt
aetiology of acute angle closure
- peripheral iris blocking the outflow of aqueous humour
narrow irido-corneal angle
- Relatively anterior location of iris-lens diaphragm (plateau iris)
- Shallow anterior chamber
- Floppy iris
predisposing factors of acute angle closure
Predisposing factors
- Age average 60 years - lens growth ass with age
- F:M 4:1 (as shallower anterior chamber)
- 1/1000 Caucasians, 1/100 Asians
- Hypermetropia - long sightedness
- FHx
- pupillary dilatation
symptoms of acute angle closure
- sudden onset of a painful red eye
- headache
- nausea and vomiting
- decreased vision
- coloured haloes around lights (corneal oedema)
- Photophobia
- fixed or sluggish, semi dilated, irregular, oval shaped pupil
- hard and tender to palpate
signs of acute angle closure
- semi-dilated non reactive pupil
- loss or red reflex
- ciliary injection
- corneal oedema
- shallow Anterior chamber
Flare in AC
raised IOP
tense on palpation
Post trabeculectomy complications
Iritis
Blebitis
Sudden increase or sudden decrease in IOPs
treatment for acute angle closure
Medical: to lower the pressure IOP beta blockers Topical steroid Iopidine pilocarpine Iv acetazolamide Surgical: Laser iridotomy (curative in most cases) Prophylactic to other eye
symptoms of open angle glaucoma
develops painlessly and insidiously over time
characterised by a slow rise in intraocular pressure: symptomless for a long period
typically present following an ocular pressure measurement during a routine examination by an optometrist
- peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
- decreased visual acuity
- optic disc cupping
screening in open angle glaucoma
cupping of the optic disc
visual field loss particularly peripheral field
if there is a hereditary risk for glaucoma what should one do
screening from 40 years and onward
pathophysiology of open angle glaucoma
trabecular meshwork is not working
creased resistance to aqueous outflow, causing increased IOP
risk factors for open angle galucoma
- genetics: first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease
- black patients
- myopia
- hypertension
- diabetes mellitus
- corticosteroids
fundoscopy of signs of primary open angle glaucoma
- Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
- Optic disc pallor - indicating optic atrophy
- Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
- Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
Ix for open angle galucoma
- automated perimetry to assess visual field
- slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline
- applanation tonometry to measure IOP
- central corneal thickness measurement
- gonioscopy to assess peripheral anterior chamber configuration and depth
- Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy
treatment for primary open angle glaucoma
first line: prostaglandin analogue (PGA) eyedrop
second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
if more advanced: surgery or laser treatment can be tried
example of prostaglandin analogues
lantantoprost
MOA of prostaglandin analogues
adverse effects
Increases uveoscleral outflow
once daily
brown pigmentation of the iris
increased eyelash length
periocular pigmentation
example of beta blockers used for glaucoma
MOA
CI
timolol
betaxolol
reduces aqueous production
Should be avoided in asthmatics and patients with heart block
examples of sympathomimetics
MOA
brimonidine
alpha 2 adrenoreceptor agonist
Reduces aqueous production and increases outflow
Avoid if taking MAOI or tricyclic antidepressants
Adverse effects include hyperaemia
example of carbonic anhydrase inhibitors
dorzolamide
Reduces aqueous production
examples of mitoics
MOA
SEs
pilocarpine
a muscarinic receptor agonist
Increases uveoscleral outflow
Adverse effects included a constricted pupil, headache and blurred vision
what is goniotomy
surgery for congenital glaucoma
signs of open angle glaucoma
increased intraocular pressure
visual field defect
pathological cupping of the optic disc1
case findings of open glaucoma
- optic nerve head damage visible under the slit lamp
- visual field defect
- IOP > 24 mmHg as measured by Goldmann-type applanation tonometry
- if suspected full investigations are performed
