leading cause of preventable blindness in NZ

• group of pregoressive conditions

  • damage to the optic nerve and a reduction in visual field

• all forms of glaucoma can lead to irreversible los sof vision

• chronic glaucoma = asymptomatic until advanced

• increased risk:

  • >45

  • family history of glaucoma

• treatment is not curative;

  • does slow progressive visual loss

• raised intraocular pressure (>21mmHg) no longer defining characteristic of glaucoma

  • 1/3 >55yo had IOP \<21

optic neuropathy for which ocular hypertension is most important risk factor

• reducing IOP only pharmacological strategy for slowing progression

  • including with IOP normal levels

• pathophysiology:

  • ganglion cell axons damaged at optic nerve head

    • most ant. section visible

    • characteristic cupped appearance

  • typical patttern of visual field loss

    • arcuate scotoma

      • sparing of the centre - vignette (black)

Open-angle glaucoma

• trabecular meshwork becomes blocked over time or tissues around it harden

  • preventing drainage of aqueous humour from anterior chamber of eye

Primary open-angle glaucoma

• most common form of glaucoma

• 90% in developed countries

• if normal pressure = “normal tension glaucoma”

Secondary open-angle glaucoma

• most often caused by pseudoexfoliation syndrome

  • deposition of flaky, white protein fibres within the anterior segment of the eye

    • resulting in trabecular meshwork becoming blocked

• genetic component

• also

  • UV light

  • oxidative stress

  • infection and inflammation

• common with increasing age

  • \~25% of people >60yo

• Eye trauma can cause neovascular open-angle glaucoma

  • blunt or penetrating

    • immediately -> years later

• Corticosteroids

  • oral, nasal, ocular routes

  • raise IOP

  • most common cuase of medicine-induced glaucoma

Angle-closure glaucoma

medical emergency - disucss immediately

• usually treated by laser iridotomy once IOP and any inflammation have been stabilised

• rare

  • narrow ocular drainage angle

  • thicker lens

  • thinner iris

• IOP can be incincrease 70mmHg

  • permanent damage to ganglion cells in days - weeks

• common causes

  • often occur when watching TV in dim lighting

  • during periods of acute stress or excitement

  • adverse effect of atropine following surgery

• common symptoms

  • intense deep eye pain

  • blurred vision

  • headache

  • nausea

  • vomiting

• signs

  • ciliary injection

  • fixed mid-dilated pupil

  • hazy cornea

  • decrease visual acuity

• uncommonly in both eyes

• increase risk of developing same in other eye in future

Intermittent angle-closure glaucoma

• series of minor acute angle-closure episodes

  • angle of drainage becoming partially or intermittently blocked

Chronic angle-closure glaucoma

• drainage meshwork occluded by iris synechiae

  • gradually without acute symptoms

  • minimic priamry open-angle claucoma

Risk factors

• increased IOP - most significant rsk factor

• 10% with ocular HTN devlop open angle glaucoma within 5yrs

• risk reduced by intervention

• Advanced age

• family hisotry

• myopia requring optical correction

  • stronger myopia

  • higher likelihood patient will develop glaucoma

• diabetes

  • twice risk

• African decent

• use of corticosteroid

  • increase expression of myocilin gene

  • long-term corticosteroid (>10mg prednisone) for periods of >2mo should be considered for referral to an Optometrist or Opthalmologist for eye assessment

Diagnosis

• primarily by optomotrist/opthalmologist

• opthalmoscopy = limited role

  • 2 dimensions

  • increase cup to disk ratio (verticla ratio >0.6)

  • thinning and/or notching of neuroretinal rim

  • flame-shaped disk haemorrhage

• ideally aged >45yo have full eye assessment

• if at risk or suspected = refer optomotrist

Management

• reducing IOP = focus

• iniital drop in IOP may occur within minute - hours of medicine administration

• step wise:

  • Prostaglandin analogues - increase uveoscleral outflow

    • first choice

    • once dialy (evening)

  • beta-blockers - reduce production of aquesous huymour

  • sympathomimetics (a2 agonists) dec aquous humour produciton and increase uveoscleral outflow

  • Carbonic anhydrase inhibitors - decrease production of aqueous humour

  • cholinrgics - miotics - increase trabecular outflow

• Double DOT

  • digital occulsion of tear duct and don’t open technique

  • preferred method

  • maximises efficacy and reduces systemic absorption by up to 70%

  • drop placed in eye with head horizontal

    • immediately after

      • eye closed

      • forefinger placed in corner of eye

        • (against nose)

        • for at least 2 minutes

    • sit or lie in supine position = easier for elderly periods

    • 5minutes between differnet medications

• soft contact lesn removed = can absorb components of solution

• eye -> nasolacrimal duct into nose

• readily/rapid absoption

  • without first pass metabolism

• topical beta blockers will produce some degree of systemic blockade

• consider acetozolamide

  • CI in severe heart failure

• betablockers

  • systemic absoprtion

  • asthma

  • hypo awareness

  • decrease awareness of hyperthyroidism

Monitoring long term

• 3-12 mo by opthalmologist

• ensure persisting with treatment

• confirm patient using Double DOT method

• Review any new diagnoses or treatments that may interact with glaucoma treatmnet

• confirm attending f/u

• ensure patient disucssed with family