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Glaucoma: Aetiology

The document discusses glaucoma, which refers to optic nerve damage caused by increased intraocular pressure. There are two main types: open-angle glaucoma, which accounts for about 70% of cases, and closed-angle glaucoma. Open-angle glaucoma is a neurodegenerative process where retinal ganglion cells slowly degenerate due to genetic factors and increased intraocular pressure deforming the lamina cribrosa. Closed-angle glaucoma is an ophthalmologic emergency where the iris bulges forward and seals off the trabecular meshwork, rapidly increasing intraocular pressure and causing permanent vision loss if not treated urgently. Treatment involves medications or surgery to reduce intraocular pressure in

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james corden
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226 views3 pages

Glaucoma: Aetiology

The document discusses glaucoma, which refers to optic nerve damage caused by increased intraocular pressure. There are two main types: open-angle glaucoma, which accounts for about 70% of cases, and closed-angle glaucoma. Open-angle glaucoma is a neurodegenerative process where retinal ganglion cells slowly degenerate due to genetic factors and increased intraocular pressure deforming the lamina cribrosa. Closed-angle glaucoma is an ophthalmologic emergency where the iris bulges forward and seals off the trabecular meshwork, rapidly increasing intraocular pressure and causing permanent vision loss if not treated urgently. Treatment involves medications or surgery to reduce intraocular pressure in

Uploaded by

james corden
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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1:MDS4013 Vik Johal

Glaucoma
Introduction
 Glaucoma refers to the Optic Nerve damage caused by a significant rise in Intraocular Pressure
 Raised intraocular pressure is caused by a blockage in Aqueous Humour trying to escape the eye
 Glaucoma is the 2nd leading cause of blindness in the world and can be classified into two main types:

o Open-Angle Glaucoma (~70%) o Closed-Angle Glaucoma

 Glaucoma frequently presents asymptomatically and may be identified on routine ophthalmic examination
o Intraocular pressure is most often elevated, however may be normal in some cases
 Optic Disc Cupping is Dx of Glaucoma  Irreversible Peripheral Vision Loss & Central Vision Loss (if
untreated)

Basic Anatomy & Physiology


 Vitreous Chamber Filled with Vitreous Humour
 Anterior Chamber [Cornea (Anterior Chamber) Iris] Both filled with Aqueous Humour
 Posterior Chamber [Lens (Posterior Chamber) Iris] providing nutrients to the cornea
 Ciliary Body produces aqueous humour which flows around the iris to the anterior chamber
o Drains via the Trabecular Meshwork (TBM) at the angle between Cornea & Iris  Canal of Schlemm
 From the canal of Schlemm it eventually enters the general circulation
 Normal Intraocular Pressure (10-21 mmHg) is generated by resistance to flow through the TBM

Open-Angle Glaucoma (OAG)


Aetiology
 A Neurodegenerative Process wherein Retinal Ganglion Cells (RGCs) slowly degenerate
 A number of genetic factors have been identified in OAG, for example:
o GLC1A Locus Mutation  Adult & Juvenile-Onset OAG
o Myocilin Mutations  Primary OAG

Pathophysiology
 The exact pathophysiology is unknown however the following is observed:
o ↑IOP  Faster RGC Degeneration
o Lamina Cribrosa Deformation/Stress
o RGC Axoplasmic Flow Compression
 Clinically, obstruction of fluid outflow via the TBM or Uveoscleral Outflow Routes is not seen, however:
o ↑Pressure Δ Across TBM: Stresses/deforms Lamina Cribrosa & RGCs  eventual destruction
o ↑IOP: RGC Axon Compression  Impaired Axonal Transport  RGC Apoptosis 2o ↓Trophic Factors
o Ischaemia: 2o to impaired retinal blood flow may contribute to cell death and eventual blindness

Optic Disc Cupping


 ↑IOP  ↑Cup-to-Disc Ratio & Loss of Peripheral Vision (assessed by Automated Visual Field Testing)
 In the centre of a normal Optic Disc is a small indent (Optic Cup), typically < ½ the size of the optic disc
o In ↑IOP, this indent becomes larger as the IOP puts pressure on that indent making it wider &
deeper
 AKA Optic Disc “Cupping” whereby an optic cup >0.5 the size of the optic disc is abnormal
 As cupping develops, disc vessels are displaced nasally  Nasal & Superior VF Loss then Temporal VF Loss
o As damage progresses, the disc pales (atrophies)
 Glaucomatous optic nerve damage affects the Anterior Visual Pathway up to the Optic Chiasm

OAG Risk Factors


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 Increasing Age  Ethnicity (Black)
 Family History of OAG  Myopia (Near-Sightedness)

OAG Presentation
 ↑IOP often Asymptomatic (long time) and Dx by routine optometry screening
 Peripheral Vision affected first which gradually closes  Tunnel Vision. OAG presents with gradual onset of:

o Fluctuating Pain o Blurred Vision


o Headaches o Halos around Lights (esp. at night)

Non-Contact Tonometry
 Most common machine for estimating IOP by opticians (less accurate but good for general screening)
 Involves shooting a puff of air shot at the cornea to measure the corneal response to it

Goldmann Applanation Tonometry


 Gold Standard IOP measurement where device mounted on a Slip Lamp in Contact with the Cornea
o Applies different pressures to the front of the cornea to get accurate IOP measurement

OAG Diagnosis
 Goldmann Applanation Tonometry: IOP Measurement
 Gonioscopy: Peripheral Ant. Chamber Configuration & Depth Assessment
 US Pachymetry: Central Corneal Thickness Measurement
 Slit-Lamp Fundoscopy: Optic Disc Cupping & Optic Nerve Health Assessment
 Visual Field Assessment: Peripheral Vision Loss Assessment

OAG Management Principles


 Aim to reduce IOP (Note: IOP control does stop visual field loss however does not reverse it)
 Start treatment when IOP >24 mmHg with close patient follow-up to assess response to treatment

Medical Management
 Prostaglandin Analogues: Rx Latanoprost Eyedrops
o ↑Uveoscleral Outflow
o Eyelash Growth
o Eyelid/Iris Pigmentation
 Beta Blockers: Rx Timolol Eyedrops
o ↓Aqueous Humour Production
o Cautionary Use in Asthma & HF
o Dry Eyes
o Corneal Anaesthesia
o ↓Exercise Tolerance
 Carbonic Anhydrase Inhibitors: Rx Dorzolamide Eyedrops
o ↓Aqueous Humour Production
 Alpha Adrenergic Agonists: Rx Brimonidine Eyedrops
o ↓Aqueous Fluid Production
o ↑Uveoscleral Outflow
 Miotics: Rx Pilocarpine Eyedrops
o ↑Uveoscleral Outflow
o Miosis
o ↓Acuity
o Brow Ache 2o to Ciliary Muscle Spasm
 Sympathomimetics: Rx Dipivefrine Eyedrops
o Cautionary use in Heart Disease, HTn & CAG
 Fixed-Dose Combination Drops: Rx Dorzolamide + Timolol
3:MDS4013 Vik Johal
Surgical Management: Trabeculectomy
 Channel created from the anterior chamber through the sclera to a location under the conjunctiva
o Aqueous humour drains through a bleb under the conjunctiva & reabsorbed into circulation

Acute Closed-Angle Glaucoma (ACG)


 Ophthalmologic Emergency requiring urgent treatment to prevent permanent loss of vision
 ACG is a group of diseases in which closure of the anterior-chamber angle (↑IOP) is either:
o Reversible (Appositional)
o Adhesional (Synechial)
 ACG occurs when the Iris bulges forward (Pupillary Block), sealing off the TBM from the anterior chamber
o Contact/Apposition of the Iris & Lens at pupillary margin ↑ resistance to flow of aqueous humour
 Preventing aqueous humour from being able to drain away  Sudden ↑IOP (>30 mmHg)
 IOP ↑ in the posterior chamber causing ↑ pressure behind the Iris
o With further worsening of the closure of the angle
 ↑IOP in CAG causes the pupil to become fixed and dilated with
subsequent axonal death

Primary Angle-Closure
 Occurs in patients with an anatomical predisposition

Secondary Angle-Closure
 Arises from pathological processes e.g., traumatic haemorrhage
pushing the posterior chamber forwards

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