glaucoma rcsi
DESCRIPTION
RCSITRANSCRIPT
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