Glaucoma

GLAUCOMA

Glaucoma is a group of disorders in which there is damage to the optic nerve due

mainly to the effect of raised intraocular pressure

GLAUCOMA

• Most types of glaucoma can be controlled but rarely cured

• Poor control of glaucoma leads to blindness

Glaucoma

Intraocular pressure depends on the balance between the production of aqueous and it’s drainage

Aqueous is produced in the ciliary bodyIt flows from the posterior chamber through the

pupil into the anterior chamberAqueous is removed from the eye via the

trabecular meshwork in the anterior chamber angle

Glaucoma

• Glaucoma is a form of optic neuropathy• There is damage to the axons of the retinal

ganglion cells at the lamina cribosa or optic nerve head

• This leads to changes at the optic disc – cupping and visual field loss

• Optic disc cupping may be asymetrical

Visual Fields

• Glaucoma results in loss of visual field, and visual acuity is only affected in the end-stage of uncontrolled disease

• Diagnosis and/or progression of glaucoma is typically assessed using static perimetry, such as the Humphrey Visual Field Analyser

Humphrey visual fields

Normal visual field right eyeSuperior arcuate field loss in the left eye due to glaucoma

Humphrey visual fieldsGlaucomatous field lossMarkedly restricted peripheral fields- tunnel vision- left eye worse than right

Left eye normal. Right- marked superior arcuate and lesser inferior arcuate field loss

Optic disc cuppingThe optic nerve head (ONH), also known as the optic disc, is

made up of a pink neuroretinal rim and of a central pale optic cup

The neuroretinal rim is made up of nerve fibres derived from the nerve fibre layer of the retina, whereas the optic cup is that part of the ONH which does not contain nerve fibres

In glaucoma, there is loss of nerve fibres, and therefore the optic cup enlarges and the neuroretinal rim becomes thinner, and this is known as pathological optic nerve cupping or glaucomatous optic neuropathy

Some people have a large optic cup, but in the presence of a healthy neuroretinal rim, and this is known as physiological cupping

Look at optic discs with a direct ophthalmoscopeNormal disc on left and cupped disc on right

Note increased area of pallor and the bending of the blood vessels at the disc margin in the cupped disc.

Examination of the glaucoma patient

• Visual acuity• Visual fields – confrontation testing with

finger counting in four quadrants of each eye,(not very useful, Humphrey visual fields much better)

• Pupilary reactions – relative afferent pupilary defect with marked optic nerve damage

Examination of the glaucoma patient

• Examination with light source looking at anterior chamber depth

• Shine a light across the eye from the lateral side

normal eye -- both sides of iris illuminated shallow anterior chamber--

nasal side of iris not illuminated

Anterior chamber depthNormal – note light illuminating both sides of iris

Shallow – nasal side of iris is in darkness

Measurement of intraocular pressure (IOP)

• Normal IOP is 10-20mm Hg• It is usually measured with Applanation

tonometry• Opticians often use puff tonometry• Digital tonometry (using fingers to gauge

fluctuation) can only tell if pressures are very high

Goldman tonometerLocal anaesthetic plus fluorescein drops are instilled in the eyes.The tonometer prism touches the corneaThe dial is turned until the two green semi circles just touch.Intra ocular pressure is then read measured in mmHg, Patients must be warned not to rub their eyes for 15 to 20 minutes after drops are instilled

Primary open angle glaucoma (POAG) risk factors

• Raised intraocular pressure• Affects 1 in 200 people over 40 years of age,

and 1 in 10 over 80 years of age• More common and more severe in African

and Caribbean ancestry • A primary family member with a history of

POAG is associated with increased risk of the condition

Primary open angle glaucoma - symptoms

• It is a “silent” disease, and is therefore often diagnosed quite late

• Visual acuity may only be lost at the end stage of the disease whereas visual field has already gradually been lost throughout the disease process

• Treatment is aimed at stopping any further damage to the optic nerve – previous damage cannot be reversed

Primary open angle glaucoma-treatmentTreatment is to lower intraocular pressure

• Medical management by use of one or more anti-glaucoma medications, – Topical anti-glaucoma preparations• Prostaglandin analogues ( increase outflow, of

aqueous)• Beta-blockers (reduce production of aqueous)• Alpha2-agonists (enhance outflow of aqueous)• Carbonic anhydrase inhibitors (reduce production of

aqueous)• Miotics/Parasympathomimetic agents (enhance

outflow of aqueous)– Oral anti-glaucoma preparations• Carbonic anhydrase inhibitors (for short-term use only)

Surgical management of POAG

Trabeculectomy Reserved for a minority of cases where the

condition progresses in spite of maximal tolerable topical therapy

Selective laser trabeculoplasty SLT

Both above procedures increase outflow of acquous

TrabeculectomyNote 1.cystic drainage bleb under upper lid2.Peripheral iridectomy at 11oclock

Acute angle closure glaucoma

SymptomsOcular pain, often severeRed eyeBlurred visionHaloes around lightsNausea/vomiting

Acute angle closure glaucoma

SignsDilated fixed pupilNarrow anterior chamber angleHazy cornea due to oedemaHard eyePupillary block

Acute angle closure glauucoma

Red eye

Hazy oedematous cornea

Semi dilated pupil

Acute angle closure glaucoma

Patients with angle closure glaucoma need urgent referral to an eye unit for treatment

If treatment is not started early permanent loss of vision can ensue