Glaucoma

Original article by Khadija Janoowala | Last updated on 19/5/2014
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Introduction 

Definition – gradual death of the optic nerve often associated with high intraocular pressure
 
High intraocular pressure is usually due to aqueous humour production and drainage imbalance
 

The Aqueous pathway

Aqueous humour – is a fluid produced by the ciliary body which helps to maintain the shape of the eye and nourishes the avascular lens and cornea.
The fluid fills both the anterior and posterior chamber and is drained out of the eye via the
irido-corneal angle in the anterior chamber. The aqueous humour filters back into the blood and circulation through the trabecular meshwork into the canal of Schlemm.
Pressure is therefore maintained by a balance between aqueous production and egress.
 
There are two main types of glaucoma
 

Open Angle Glaucoma

  • Most common type
  • Most patients >40 years old
 

Major risk factors

  • Family history
  • Age
  • Race- African Americans
  • Thin corneas
  • Large vertical nerve cupping
  • High eye pressure
 

Mechanism

  • Degeneration / clogging of the trabecular meshwork results in aqueous build up and chronically elevated eye pressure.
  • The prolonged high pressure has been proposed to lead to optic nerve atrophy by;
    • stretching
    • vascular compromise
    • alteration of glutamate transmitter pathways
  • Progressive destruction of optic nerve results in gradual vision loss
  • Because the vision loss occurs gradually patient don’t realise they have the disease until it is far advanced.
 

Presentation

Usually there are three main examination findings
Elevated eye pressure (Normal pressure - 10-22mmHg)
  • Measured with tonometer
    • how much force it takes to flatten a 3mm diameter of cornea
    • Pressure affected by corneal thickness
    • Thin cornea = pressure reading lower than actual value
    • Thick cornea = pressure reading higher than actual value
  • Fluctuate throughout the day – typically highest in the morning
  • NB – ‘normal pressure’ DOES NOT rule out glaucoma and ‘high pressure’ does not always indicate glaucoma
 

Optic disc changes

Seen on ophthalmoscopy
Optic disc (normal indentation or cup which is less than 1/3rd of disc diameter)

  • increased cupping
    • fewer nerves course through optic disc
    • Cup: disk ratio > 0.4-0.7
  • vertical thinning and notching of neural rim
    • Neural rim= space between inner cup and surrounding disc
    • Normal neural rim follows the “ISNT” rule
  • Haemorrhage at disc
  • Disc vessels displaced nasally
  • Optic atrophy – optic disc becomes pale as damage progresses 

“ISNT RULE”

  • Inferior rim                         Thickest
  • Superior rim                                                     
  • Nasal rim
  • Temporal rim                     Thinnest

NB - In glaucoma the ISNT rule is lost                                

 
 

Visual loss

  • Occurs in characteristic pattern…
  • Central vision typically SPARED e.g. late stage patients may have 20/20 central vision but peripheral blindness
 

Treatment

It is only possible to treat the risk factors i.e. lower the intraocular pressure to 20mmHG or lower
Medical
  • Topical β-blockers – decrease aqueous production at ciliary body
  • Prostaglandin analogues – increase aqueous humour outflow
  • Others – topical carbonic anhydrase inhibitors, alpha agonists
 

Surgical

  • Trabeculectomy – creation of tract between anterior chamber to space under the conjunctiva. Apply antimetabolites like mitomycin C to avoid re-closure by scar formation
  • Plastic tube shunt insertion into anterior chamber
  • Laser procedure 
    • Argon laser trabeculoplasty used to burn portions of trabecular meshwork which increases outflow.
    • Laser can also be used to burn portions of ciliary body to decrease aqueous production.
 
 

ACUTE GLAUCOMA (aka Closed – angle glaucoma

MEDICAL EMERGENCY!

Mechanism

Pupillary block
  • lens pushes up against the back of iris blocking flow of aqueous humour through the pupil
  • this resistance to aqueous flow produces a pressure-gradient across the iris
  • iris and lens are forced to move anteriorly
  • forward movement closes the irido-corneal angle and blocks the trabecular meshwork
  • this causes build up of the aqueous fluid = RAPID RISE in eye pressure
  • increased pressure damages the retina due to stretching and decreased blood supply
Closure of outflow angle in
  • hyperopic eyes which have naturally shallow anterior chambers
  • when the pupil dilates the iris gets thicker and the irido-corneal angle becomes smaller and is more likely to close spontaneously
  • medications that cause pupil dilatation – antihistamines and medications for colds
 

Presentation

  • Extremely red and painful eye often associated with nausea and vomiting
  • Patient may describe ‘halo around lights’
    • this is due to swelling of the cornea as water is pushed into    
    • the cornea stroma by the high pressure
 

On examination

  • sluggish and dilated pupil
  • high pressure > 60 mmHg
  • eye feels rock hard
 

Treatment          

  • Decrease eye pressure QUICKLY – many treatments at once
    • Topical B blockers (Timolol) – decrease aqueous production
    • Carbonic anhydrase inhibitor – decreases aqueous production
    • Osmotic agents (oral glycerin + IV mannitol)
    • Miotic (pilocarpine) - constrict pupil to open outflow angle
  • Ultimately need Surgical treatment
    • High intensity laser treatment – burn hole through the iris to create communication between the anterior and posterior chambers. This relieves the pressure gradient across the iris and moves it back to its normal position. The trabeuclar meshwork is re-opened and the aqueous fluid can drain out.
    • It is typically done on both eyes.