Ophthalmology Flashcards
Acute Angle-Closure Glaucoma (ACCG) Definition
Optic neuropathy due to increase in intraocular pressure (IOP) secondary to an impairment of aqueous outflow.
Pathophysiology of AACG
- Iris bulges forward and seals off the trabecular mesh work from the anterior chamber
- Prevents aqueous humour from draining
- Continual increase in intraocular pressure
- Pressure builds in the posterior chamber
- Iris is pushed forward exacerbating the angle closure
Medications precipitating AACG
- Adrenergic medications (noradrenaline)
- Anticholinergics (oxybutynin, solifenacin)
- TCA (amitriptyline) > has anticholinergic effects
Risk Factors for AACG
- Hypermetropia
- Pupillary dilatation
- Lens growth associated with increasing age
- Family history
- Female
- Chinese and East Asian
Features of AACG
- severe pain: may be ocular or headache
- decreased visual acuity
- symptoms worse with mydriasis (e.g. watching TV in a dark room)
- hard, red-eye
- haloes around lights
- semi-dilated non-reacting pupil
- corneal oedema results in dull or hazy cornea
- systemic upset may be seen, such as nausea and vomiting and even abdominal pain
Investigations for AACG
- Slit lamp examination
- Gonioscopy
- Tonometry
- Automatic static perimetry
AACG: What is slit lamp examination and how will AACG be identified
- To look at anterior chamber length and size of phakic lens
- Results
- shallow anterior chamber
- signs of glaucoma → corneal oedema, lens changes, corneal endothelial loss
AACG: What is Gonioscopy and what how can you identify AACG
- Oscopy = looking + Gonio = angle → looking at the angle
- Special lens for the slit lamp allowing visualisation of angle
- Examines the anterior chamber angle
- Trabecular meshwork is not visible in angle closure because the peripheral iris is in contact with it
AACG: How does tonometry show AACG
Elevated IOP
AACG: What does Automatic Static Perimetry do
Identifies the presence and amount of visual field loss
Differentials for AACG
- Open-angle glaucoma (primary and secondary)
- Clinically indistinguishable from chronic ACG
- Gonioscopy shows open angle
- Optic neuropathies (eg. compressive)
- Visual field defects different
- IOP normal
- Trauma
- IOP usually normal
- Anterior chamber depth usually normal
What does AACG look like on examination
- Red eye
- Hazy cornea
- Decreased visual acuity
- Mid-dilated pupil
- Fixed-size pupil
- Hard eyeball on gentle palpation
Primary management of AACG
- Immediate referral to ophthalmology
- Lie on back without pillow
- Pilocarpine eye drops > topical ophthalmic cholinergic agonist (miotic agent)
- Acetazolamide > carbonic anhydrase inhibitor (reduces aqueous humour formation)
Specialist management of AACG
-
Carbonic anhydrase inhibitors +/ topical beta-blocker +/ topical alpha-2 agonist
-
Dorzolamide or Brinzolamide → topical / Acetazolamide → oral/IV
Reduces aqueous humour formation, topical>systemic
+/ -
Timolol → topical, decreases aqueous humour production
+/ - Brimonidine → topical, dual mechanism: decreases aqueous humour production and increases uveoscleral outflow
-
Dorzolamide or Brinzolamide → topical / Acetazolamide → oral/IV
- Ophthalmic cholinergic agonist
- Pilocarpine
- Typically alongside 1
- Hyperosmotic agents
- Mannitol
- If failure of initial medical treatment or IOP >50mmHg
Surgical management of AACG
Laser peripheral iridotomy
- Definitive
- Done when AACG acute attack settled
- Creates tiny hole in peripheral iris → aqueous humour flows directly from posterior to anterior chamber → relieves pressure and opens pathway for aqueous humour to drain
