11/14/24, 10\:49 AM Primary Open-Angle Glaucoma

Primary Open-Angle Glaucoma

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Key points ⚡
Succinct notes to superpower your revision
Glaucoma\: group of eye diseases causing progressive optic neuropathy, often with raised intraocular pressure (IOP).
Primary open-angle glaucoma (POAG)\: most common type, a
Aetiology\: increased resistance to aqueous humour out
cell death and visual loss.
Risk factors\: myopia, age >65, family history, African-Caribbean ethnicity, untreated ocular hypertension, cardiovascular
disease, type 2 diabetes.
Symptoms\: often asymptomatic; initially causes peripheral vision loss, progressing to central vision loss in advanced stages.
Clinical
Investigations\: Goldmann applanation tonometry (IOP), fundoscopy, visual
thickness measurement.
Diagnosis\: based on visual
thickness.
Management\: selective laser trabeculoplasty (SLT) for newly diagnosed patients, prostaglandin analogue eye drops (e.g.
latanoprost), beta-blockers, carbonic anhydrase inhibitors, parasympathomimetics, trabeculectomy surgery.
Complications\: irreversible vision loss, impact on quality of life, potential loss of driving licence if vision signi
a
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A comprehensive topic overview

Introduction

Glaucoma is a group of eye diseases which cause progressive optic neuropathy commonly associated with raised
intraocular pressure (IOP).
Glaucoma can be open angle or closed angle depending on the anatomical structure of the anterior chamber of the eye.
Primary open-angle glaucoma (POAG) is the most common type associated with an open anterior chamber angle of the
eye. POAG a
1
There are a few diacute angle-closure glaucoma (AACG) which is an
ophthalmic emergency. However, AACG is rare, and this article will concentrate on POAG.
You may also be interested in our OSCE guide to explaining a diagnosis of glaucoma

Aetiology

Anatomy

Aqueous humour is a clear
travels from the posterior chamber through the pupil into the anterior chamber.
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The aqueous humour then drains out of the anterior chamber through two independent pathways\:
The trabecular meshwork into the canal of Schlemm in the iridocorneal angle
The uveoscleral pathway
The constant cycle of production and drainage of aqueous humour helps maintain the eye in a normal pressured state of
12 - 21mmHg.
For more information on anatomy, see the Geeky Medics guide to eye anatomy.
Figure 1. Schematic diagram of the
human eye.

Pathophysiology

In POAG, even though the iridocorneal angle appears open, there is increased resistance to the out
humour through the trabecular meshwork into the canal of Schlemm.
This causes the IOP to rise, which if sustained will lead to retinal ganglion cell death causing permanent visual loss.
In POAG the loss of retinal ganglion cells and the nerve
before superior loss.
This pathophysiology diacute angle-closure
glaucoma.
Figure 2. Comparison of open and closed
angles in the eye.

Risk factors

Risk factors for POAG include\:
2
Myopia (short-sightedness)
Increased age particularly after 65 years
Family history
African-Caribbean ethnic origin
Untreated ocular hypertension (raised IOP)
Cardiovascular disease
Type two diabetes (this is a secondary glaucoma)

Clinical features

POAG is typically insidious in onset, following a slow and chronic course. It is usually adult onset and a

History

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Unfortunately, in most cases, patients will be asymptomatic and not aware of any visual disturbances.
Initially, POAG causes loss of peripheral vision, usually in the superior visual
regularly use our superior visual
stage of POAG.
3,4
It is important to check if there is any relevant family history of glaucoma. People with a family history of glaucoma are
entitled to free annual eye tests to screen for disease.
For more information, see the Geeky Medics guide to ophthalmic history taking.

Clinical examination

POAG is usually picked up through routine eye checks by an optician.
The eye will not appear red or painful, as there is no acute rise in IOP or in
Typical clinical
Increased IOP
Visual
Fundoscopy\: cupped optic discs

Investigations

Measuring intraocular pressure

The gold standard investigation to measure intraocular pressure is with a Goldmann applanation tonometer.
This device is mounted on a slit lamp and makes brief contact with the cornea after numbing with eye drops. It measures
the pressure needed to indent the cornea by a speci
Non-contact tonometry may also be used to estimate intraocular pressure by opticians. This involves shooting a small pu
of air at the cornea and measuring its rebound. Non-contact tonometry is less accurate but useful for general screening.

Optic nerve assessment

As glaucoma causes progressive optic neuropathy it is important to establish if there is any damage or changes to the
optic nerve.
Fundoscopy with pupil dilatation can be performed using a handheld ophthalmoscope, or a stereoscopic slit lamp can
be used for an improved view.
Optic disc examination is a direct marker of the disease progression. Damage is assessed by looking at the vertical optic
cup-to-disc ratio, which will increase in glaucoma. A normal ratio is less than 0.5 though disc asymmetry is important too.
Glaucoma is suggested by an increased ‘cupped’ appearance of the optic disc over time.
Glaucoma can also lead to primary optic nerve atrophy. This describes the death of nerve
gives the appearance of a pale optic disc.
Figure 3. Cup-to-disc ratios (normal vs
glaucoma)

Visual

Visual
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Peripheral vision is particularly important in detecting movement outside the area of focus and is a key factor in
determining eligibility for driving.
Other areas of the visual
Figure 4. Visual

Gonioscopy

and cornea.
Gonioscopy is the gold standard investigation for assessing the drainage angle of the anterior chamber between the iris
In POAG this will show the angle is open. The trabecular meshwork will be visible.

Diagnosis

POAG will usually be picked up by an optometrist during routine eye checks.
If suspected, they will normally be referred to a consultant ophthalmologist for con
NICE guidelines state to diagnose chronic open-angle glaucoma, the following tests should be o
5
Visual
Optic nerve assessment and fundus examination using stereoscopic slit lamp biomicroscopy, with pupil dilatation
IOP measurement using Goldmann applanation tonometry (slit lamp mounted)
Peripheral anterior chamber con
Central corneal thickness (CCT) measurement\: IOP measurement can be a
allowances must be made
It is also important to obtain an image of the optic nerve head at diagnosis to keep as a baseline before initiating
treatment.

Management

Treatment for suspected and con
The aim of treatment in POAG is to prevent the development and progression of optic nerve damage and preserve sight
as much as possible. Di
Treatment will usually be started in patients with an IOP >24mmHg.

Laser management

In 2022, NICE updated its guidance to recommend o
360° selective laser trabeculoplasty (SLT).
This involves using short pulses of low-energy light to target particular cells in the eye, triggering processes within the
eye to remove and rebuild a meshwork that will function e

Medical management

Medical management involves a variety of eye drop preparations that either reduce the production or increase the
out
6
First-line preparations include generic prostaglandin analogue (PGA) eye drops (e.g. latanoprost). Side e
latanoprost may include eyelash growth, eyelid pigmentation and iris pigmentation.
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Other pharmacological interventions include beta-blockers (e.g. timolol), carbonic anhydrase inhibitors (e.g.
acetazolamide) and parasympathomimetics (e.g. pilocarpine).

Surgical management

For patients with advanced open-angle glaucoma, surgery may be indicated.
Trabeculectomy surgery involves creating a channel in the sclera for aqueous humour to drain.
Glaucoma surgery is o
used during the initial stages of trabeculectomy to prevent excessive postoperative scarring and therefore reduce the risk
of failure.
Tiny plastic shunts can also be inserted if needed, to create a permanent drainage channel for the aqueous humour.

Complications

The main complication of untreated glaucoma is the irreversible loss of vision. It is important to seek early advice and
management to optimise vision as this can have a signi

Driving

Many patients when diagnosed with glaucoma worry about the possibility of losing their driving licence. However, if
diagnosed and treated early, many people are still able to keep their licence.
In the United Kingdom, the Driver and Vehicle Licensing Agency (DVLA) requires patients to inform them of a new
diagnosis of glaucoma if it a
responsibility.
7,8

References

NICE CKS. G l a u c o m a . March 2022. Available from\: [LINK]
Sheybani, A. P r i m a r y O p e n-A n g l e G l a u c o m a . December 2021. Available from\: [LINK]
National Eye Institute. April 2022. Available from\: [LINK]
Glaucoma UK. P r i m a r y O p e n A n g l e G l a u c o m a . Available from\: [LINK]
NICE. G l a u c o m a \: D i a g n o s i s a n d M a n a g e m e n t . January 2022. Available from\: [LINK]
NHS.uk G l a u c o m a . February 2021. Available from\: [LINK]
Sachdev, A., Tahhan, M., Sung, V.C.T. G l a u c o m a a n d d r i v i n g \: A r e w e d o c u m e n t i n g d r i v i n g s t a t u s a n d a d v i s i n g p a t i e n t s w i t h
g l a u c o m a a p p r o p r i a t e l y a b o u t t h e i r d r i v i n g? International Ophthalmology. 38, 419-423. February 2017. Available from\: [LINK]
Glaucoma UK. D r i v i n g w i t h g l a u c o m a . Available from\: [LINK]
Mayo Clinic. October 2020. Available from\: [LINK]

Image references

Figure 1. Wikipedia. Rhcastilhos and Jmarchn. S c h e m a t i c d i a g r a m o f t h e h u m a n e y e . Licence\: [CC BY-SA 3.0]
Figure 2. Moran CORE. A c u t e a n g l e c l o s u r e g l a u c o m a . Licence [CC BY-NC-ND 4.0]
Figure 3. Community Eye Health Journal. Adapted by Geeky Medics. License\: [CC BY-NC 2.0]
Figure 4. Community Eye Health Journal. License\: [CC BY-NC 4.0]

Reviewer

Dr Anne Gobbett
Speciality Doctor in Ophthalmology
Sunderland Eye In
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Related notes

Acute Angle-Closure Glaucoma
Age-related Macular Degeneration (ARMD)
Amblyopia
Ametropia
Anisocoria

Test yourself

Contents

Introduction
Aetiology
Risk factors
Clinical features
Investigations
Source\: geekymedics.com
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