Primary Open-angle Glaucoma

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Chronic Open-angle Glaucoma written for patients

Glaucoma refers to a group of eye conditions that lead to damage to the optic nerve head with progressive loss of retinal ganglion cells and their axons. This leads to a progressive loss of visual field. There are typical optic nerve changes on slit-lamp examination. Glaucoma is usually associated with an intraocular pressure (IOP) above the normal range. However:

  • 20-52% (this varies between populations) of patients with glaucoma have IOP within the normal range. Patients with normal IOP who develop the characteristic changes associated with open-angle glaucoma are said to have low tension or normal pressure glaucoma.
  • Many patients have raised IOP for years without developing the changes of glaucoma. This condition is referred to as ocular hypertension.

Prior to 1978, glaucoma was defined as IOP above 21 mm Hg in an eye (the normal range is considered to be 10-21 mm Hg with 14 being the average). More recently glaucoma has been understood as an abnormal physiology in the optic nerve head that interacts with the IOP, with the degree and rate of damage relating to both factors. [1] 

Types of glaucoma

There are several glaucoma subtypes, although all are considered optic neuropathies.

  • Glaucoma may be primary or secondary to other conditions.
  • Glaucoma may be open-angle or closed-angle.
  • Glaucoma may be acute, acute-on-chronic, intermittent or chronic.
  • The end stage of glaucoma is referred to as absolute glaucoma. There is no functioning vision, the pupillary reflex is lost and the eye has a stony appearance. The condition is very painful .

Other separate articles that you may find relevant are Glaucoma and Ocular Hypertension, Angle-closure Glaucoma and Congenital Primary Glaucoma.

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Simple (primary) open-angle glaucoma (POAG) is a progressive, chronic condition characterised by:

  • Adult onset.
  • IOP at some point greater than 21 mm Hg (normal range: about 10-21 mm Hg).
  • An open iridocorneal angle (between the iris and the cornea, where the aqueous flows out).
  • Glaucomatous optic neuropathy.
  • Visual field loss compatible with nerve fibre damage.
  • Absence of an underlying cause.
  • It is usually bilateral.

The primary problem in glaucoma is disease of the optic nerve. The pathophysiology is not fully understood but there is a progressive loss of retinal ganglion cells and their axons. In its early stages it affects peripheral visual field only but as it advances it affects central vision and results in loss of visual acuity, which can lead to severe sight impairment and complete loss of vision.

For most types of glaucoma, optic neuropathy is associated with a raised IOP. This has given rise to the hypothesis of retinal ganglion apoptosis, whose rate is influenced by the hydrostatic pressure on the optic nerve head and by compromise of the local microvasculature. The resulting optic neuropathy gives rise to the characteristic optic disc changes and visual field loss.

In open-angle glaucoma, flow is reduced through the trabecular meshwork (whose role is absorbing aqueous humour). This is a chronic degenerative obstruction which occurs painlessly.

The IOP is not always raised: in normal-tension glaucoma (NTG), IOP is in the normal range, which has led to other theories, including vascular perfusion problems or an autoimmune component. Others have postulated that the optic nerve head is particularly sensitive in these patients, with damage occurring at much lower IOPs than in normal individuals. This could explain why these patients benefit from IOP-lowering medication.[2] 

  • This is the most common form of glaucoma.
  • Approximately 1-2% of the population aged over 40 are affected but about half are unaware of this.
  • Prevalence increases with age, affecting about 10% of people aged over 70.
  • It is responsible for 10-12% of all cases of registrations for severe visual impairment in the UK. 
  • Age - the incidence increases with age, most commonly presenting after the age of 65 (and rarely before the age of 40).
  • Family history - there is a clear inherited component in many individuals (IOP, aqueous outflow facilities and disc size are inherited characteristics). However, it is thought that there is incomplete penetrance and variable expressivity of the genes involved. There are also several factors thought to contribute to the inheritance and therefore the risk to relatives is currently only an estimate: 4% to children and 10% to siblings of an affected individual.
  • Race - it is three to four times more common in Afro-Caribbean people in whom it tends to present earlier and is more severe.
  • Ocular hypertension - this is a major risk factor for the development of glaucoma with about 9% of patients developing glaucoma over five years if left untreated.[3]
  • Other factors - myopia (short-sightedness) and retinal disease (eg, central retinal vein occlusion, retinal detachment and retinitis pigmentosa) can predispose individuals to POAG. Diabetes and systemic hypertension (and possibly also systolic hypotension may also contribute to risk.

Unfortunately, in the vast majority of cases, patients are asymptomatic. Because initial vsual loss is to peripheral vision and the field of vision is covered by the other eye, patients do not notice visual loss until severe and permanent damage has occurred, often impacting on central (foveal) vision. By then, up to 90% of the optic nerve fibres may have been irreversibly damaged.[3]

Open-angle glaucoma may be detected on checking the IOPs and visual fields of those with affected relatives. Suspicion may arise during the course of a routine eye check by an optician or GP, where abnormal discs, IOPs or visual fields may be noted.

An ophthalmologist will examine the eye thoroughly for evidence of glaucoma, comorbidity or an alternative diagnosis to the apparent findings. The details of a glaucoma assessment can be summarised as:

  • Gonioscopy - a technique used to measure the angle between the cornea and the iris to assess whether the glaucoma is open-angle or closed-angle.
  • Corneal thickness - this influences the IOP reading. If it is thicker than usual, it will take greater force to indent the cornea and an erroneously high reading will be obtained.
  • Tonometry - this is the objective measurement of IOP, usually based on the assessment of resistance of the cornea to indent. The normal range is considered to be 10 mm Hg-21 mm Hg.
  • Optic disc examination - this is a direct marker of disease progression. Optic disc damage is assessed by looking at the cup:disc ratio: normal is 0.3, although it can be up to 0.7 in some normal people:
    • Glaucoma is suggested by an increase in cupping with time, rather than by cupping alone. Marked but stable cupping may be hereditary.
    • The intra-observer variability in optic disc evaluation has been reduced by use of ocular coherence tomography (OCT), which produces excellent visual records and provides quantification of exact cup:disc ratio and areas of neuroretinal thinning.
  • Visual fields - assessment requires the co-operation of the patient and can also be affected by fatigue, spectacle frames, miosis and media opacities. See also the separate Visual Field Defects article.

National Institute for Health and Care Excellence (NICE) guidance (2009) states that at diagnosis all people with chronic open-angle glaucoma (COAG), suspected COAG or ocular hypertension (OHT) should have:[3] 

  • Goldmann tonometry for IOP measurement.
  • Corneal thickness measurement.
  • Gonioscopy (anterior chamber configuration and depth).
  • Perimetry (visual field measurements).
  • Slit-lamp assessment of the optic nerve and fundus (pupil dilated).

NICE also states that at each visit the following should be available:

  • Records of all previous tests.
  • Records of past medical history.
  • Current medication list (systemic and topical).
  • Glaucoma medication record.
  • Allergies and intolerances.

Scottish Intercollegiate Guidelines Network (SIGN) guidance (2015) offers guidance for referral to secondary care services:

  • Irrespective of IOP, patients with one or more of the following findings should be referred to secondary eye care services:
    • Optic disc signs consistent with glaucoma in either eye.
    • A reproducible visual field defect consistent with glaucoma in either eye
    • Risk of angle closure (occludable angle) - using Van Herick technique, if the peripheral anterior chamber width is one quarter or less of the corneal thickness - using gonioscopy, if ≥270° of the posterior pigmented trabecular meshwork is not visible.
    • Patients who have OCT with IOP >25 mm Hg may be considered for referral to secondary eye care services irrespective of central corneal thickness.
    • Patients who have OCT with IOP <26 mm Hg and central corneal thickness <555 micrometres should be referred to secondary eye care services if they are aged ≤65.
    • Patients who have OCT with IOP <26 mm Hg and central corneal thickness ≥555 micrometres may be monitored in the community.

These referral guidelines apply to opticians who are equipped to monitor IOP and perimetry. GPs, unless they have a secondary speciality on ophthalmology, are unlikely to manage these patients alone.[3] 

Several grading systems exist including:

  • The Brusini Staging System.[5] 
  • The Hodapp-Parrish-Anderson Grading Scale.[6] 
  • The Disk Damage Likelihood Scale.[7] 
  • The Glaucomatous Optic Nerve Head Classification.[8] 

All classify the disease according to features, such as changes to the optic disk, visual field deficit. Broadly glaucoma can be clinically classified as:

  • Mild - early visual field defects.
  • Moderate - presence of an arcuate scotoma ('n'-shaped visual field loss arching over the central visual field) and thinning of neuroretinal rim (cupping).
  • Severe - extensive visual field loss and marked thinning of the neuroretinal rim.
  • End-stage - only a small residual visual field remains. There may be very little neuroretinal rim remaining (cup:disc ratio would be in the region of 0.9-1.0).

There are variations across the NHS in management of this condition, reflecting conflicting literature and scattered reports. NICE guidelines (2009) and SIGN (2015) guidance attempt to offer clear recommendations on testing, diagnosis, monitoring and treatment.

Treatment aims[3][4] 

Treatment is not necessarily started immediately on simple detection of an elevated IOP. Given the potential for variation of findings from one assessment to the next, the patient should be assessed on several occasions unless the findings are unequivocal - the diagnosis is significant and treatment is usually lifelong. Apparent disc cupping is considered in conjunction with visual fields and IOP. In some patients, the disease is obvious and advanced, in which case treatment should start promptly.

  • Once a diagnosis and decision to treat have been made, a target IOP is set according to the degree of damage: this is the pressure below which further damage is considered unlikely. This is usually in the region of a 30% drop of IOP. It differs between patients and may be different in each eye.
  • Regular monitoring to assess IOP, the optic disc and the visual fields. Some areas have schemes whereby trained opticians carry out all the monitoring.
  • Patient education is essential, as this is a largely asymptomatic condition until it is very advanced and medication compliance is often poor.[3] Patients need to understand the irreversible nature of the disease, how to take drops correctly and their potential side-effects. They also need to be advised of the risk to other family members.

Medical therapy[3][9] 

This is the first-line and only treatment for many patients. There is no single drug that stands out above others as the optimal treatment of glaucoma.[11] 

Drugs that reduce IOP by different mechanisms are available for managing OHT and glaucoma. A topical beta-blocker or a prostaglandin analogue is usually the drug of first choice for the treatment of OHT.

Traditionally, beta-blockers were the preferred first option but, since about 2000, prostaglandin analogues have been favoured, as they are as efficient with fewer side-effects.[12] A prostaglandin analogue should be used to manage patients with early or moderate POAG.

It may be necessary to combine these drugs or add others (eg, sympathomimetics, carbonic anhydrase inhibitors, or miotics) to control IOP. Generally, drugs are initiated one at a time. Treatment may be to one or both eyes.

For urgent reduction of IOP and before surgery, mannitol 20% (up to 500 ml) is given by slow intravenous infusion until the IOP has been satisfactorily reduced. Acetazolamide by intravenous injection can also be used for the emergency management of raised IOP.[13] 

  • Prostaglandin analogues:
    • Action: increase aqueous outflow via the uveoscleral route.
    • Contra-indications: active uveitis, pregnancy and breast-feeding.
    • Caution: brittle or severe asthma, aphakia (patient with no lens), pseudophakia (patient with artificial lens); do not take within five minutes of using thiomersal-containing preparations.
    • Common ocular side-effects: change in eye colour: brown pigmentation, thickening and lengthening of eye lashes; more rarely: uveitis, ocular pruritus, photophobia and keratitis.
    • Systemic side-effects: rarely - hypotension, bradycardia.
  • Beta-blockers:
    • Action: reduce aqueous secretion by inhibiting beta-adrenoceptors on the ciliary body.
    • Contra-indications: bradycardia, heart block, uncontrolled heart failure, asthma and history of chronic obstructive pulmonary disease (COPD).
    • Caution: depression, myasthenia gravis, possible interactions with other medication such as verapamil.
    • Common ocular side-effects: irritation, erythema, dry eyes, blepharo-conjunctivitis and allergy anaphylactic reaction possible.
    • Common systemic side-effects: bronchospasm, bradycardia, exacerbation of heart failure, nightmares.
  • Carbonic anhydrase inhibitors:
    • Action: reduce aqueous secretion by ciliary body. Weak systemic diuresis when given orally.
    • Contra-indications: renal impairment, metabolite imbalance, severe hepatic impairment, sulfonamide sensitivity (acetazolamide), breast-feeding.
    • Caution: elderly, hepatic impairment, history of renal calculi, history of intraocular surgery, pregnancy and breast-feeding. Extravasation at infusion site of intravenous acetazolamide can cause necrosis.
    • Ocular side-effects: localised discomfort, lacrimation, topical allergy; more rarely: superficial punctate keratitis, uveitis, transient myopia.
    • Systemic side-effects: (particularly with systemic administration), taste disturbance, nausea/vomiting, headache, dizziness, fatigue, paraesthesia and sulfonamide-related side-effects.
  • Sympathomimetics:
    • Action: reduce aqueous secretion and increase outflow through trabecular meshwork.
    • Contra-indications: angle-closure glaucoma (due to mydriatic effects), patients currently taking monoamine-oxidase inhibitors (possibility of hypertensive crisis).
    • Caution: hypertension, heart disease.
    • Common ocular side-effects: mydriasis, dry eye, severe smarting and redness of the eye.
    • Common systemic side-effects: lethargy, hypotension.
  • Miotics:
    • Action: open up the drainage channels in the trabecular meshwork by ciliary muscle contraction.
    • Contra-indications: situations where pupillary constriction is undesirable (such as uveitis), presence of retinal holes.
    • Caution: darkly pigmented irides require higher concentrations but overdosage must be avoided, patients with retinal disease (especially previous detachment), cardiac disease, hypertension, asthma, peptic ulceration, urinary tract obstruction and Parkinson's disease.
    • Ocular side-effects: miosis - this can cause blurred vision which can affect driving and other skilled tasks, especially in the presence of a cataract. Accommodative spasm with brow ache (often causing intolerance in patients over 40), localised discomfort, pupillary block.
    • Systemic side-effects: sweating, bradycardia, gastrointestinal disturbance.

Laser and surgical treatments should be considered after unsuccessful trials with two different pharmacological treatments. However, before this, it is important to ascertain that the patient is actually managing to get the drops in.[3] 

Laser therapy

  • Argon laser trabeculoplasty (ALT) - lasering to the trabecular meshwork in the iridocorneal angle, so enhancing aqueous outflow. It has the benefit of reducing (or stopping) the need for drops whilst not having the complications of surgery.[14] 
  • Selective laser trabeculoplasty (SLT) - uses a laser at very low intensity, treating specific areas and leaving parts of the trabecular meshwork intact. It therefore, unlike ALT, preserves the trabecular meshwork architecture and can be repeated. It may be an alternative for those who have been treated unsuccessfully with medication and ALT. There is some evidence that it is slightly more effective than ALT.[15][16] 
  • Cyclodiode laser trabeculoplasty - similar principle as above, using a higher laser power.This is often used in refractory cases and for relief of pain in end-stage glaucoma.[17] 
  • Nd:YAG laser iridotomy - usually reserved for angle-closure glaucoma, a small hole is made in the iris in patients with angle-closure glaucoma, to enhance aqueous outflow.
  • Diode laser cycloablation - part of the secretory component of the ciliary body is destroyed, so reducing aqueous secretion. This is used in intractable end-stage glaucoma.

Surgical therapy

A Cochrane review found that primary surgery lowers IOP more than primary medication but is associated with more eye discomfort. One trial suggested that visual field restriction at five years is not significantly different whether initial treatment is medication or trabeculectomy.[10] However, the Cochrane review did not include recent trials that evaluated currently available drugs for glaucoma or modern surgical methods.

  • Trabeculectomy. This procedure creates a fistula between the anterior chamber of the eye and the sub-Tenon space (immediately around the globe), so allowing aqueous outflow. Adjunctive antimetabolites such as 5-fluorouracil and mitomycin C may be used to prevent scarring over of the fistula. A deep sclerectomy is a variation of this procedure.[3]
  • Artificial shunts in the form of plastic devices connecting the anterior chamber to the sub-Tenon space can be inserted but are associated with many postoperative complications.
  • New techniques and devices are being developed to minimise the complications of laser and surgical treatment. Examples include:
    • Canaloplasty whereby Schlemm's canal is artificially widened with a temporary tube and viscoelastic. Canaloplasty is not currently recommended by NICE.[18]
    • Trabecular stent bypass microsurgery aims to reduce IOP by creating a bypass channel between the anterior chamber and Schlemm's canal to improve drainage. NICE states that, although there is evidence of short-term efficacy, this is based only on a small number of patients.[19] 
    • Trabeculotomy ab interno for open-angle glaucoma aims to reduce IOP by removing a portion of the trabecular meshwork to improve drainage. It avoids creation of the subconjunctival bleb associated with traditional trabeculectomy. NICE states that the current evidence on the safety and efficacy of trabeculotomy ab interno for open-angle glaucoma is adequate to support the use of this procedure.[20] 

If there is ongoing disease progression after surgery, the options will be to go back on to medical treatment, to consider further surgical intervention or to try laser treatment.[3]

A visual field defect counts as a 'relevant disability' (as opposed to the 'absolute disability' of a reduced visual acuity) in law. There are certain criteria set out and assessed by the Driver and Vehicle Licensing Agency (DVLA).[21] 

The onus is on the patient to inform the DVLA (and it is important to document that you have advised them of this). It is the DVLA (and approved opticians) who will assess the visual fields and decide whether a patient can continue to drive. If you are concerned that the patient should not drive and has not told the DVLA (despite your clear advice to do so), it may be appropriate to inform the DVLA medical advisors. You will be breaching confidentiality in the public interest. If doing so you should inform the patient of your intentions and are best advised to liaise with your defence union to make sure that you have exhausted all other options and that in doing so your action is proportionate and defensible.

  • Treatment side-effects - see 'Medical Therapy', above.
  • Non-compliance - patient education and clear explanation of the risks, together with clear instructions on how to take medication will reduce non-compliance.
  • Steroid responsiveness - topical (to the eye) steroids have the potential to affect IOP in the long term (systemic steroids are generally less likely to do so). Broadly speaking, the population can be divided into three groups according to their IOP response to a six-week course of steroids:[22] 
    • High responders - they show a marked elevation (>30 mm Hg). This occurs in 5% of the general population but in 90% of the POAG population (and in 30% of their siblings and 25% of their offspring).
    • Moderate responders - 35% of the general population will show a modest elevation in IOP (22 mm Hg-30 mm Hg), the figure dropping to 10% in POAG patients (and in 50% of their siblings and 70% of their offspring).
    • Non-responders - 60% of the population fall into this group. There are no POAG patients in this group (but 20% of their siblings and 5% of their offspring).

Unless treated, COAG is progressive. Treatment aims to stall this progression but cannot reverse it. However, if treatment is timely, appropriate and maintained, useful vision can be expected to be maintained throughout the patient's lifetime.

Factors involved in more rapid progression include myopia, the presence of optic disc haemorrhages, vascular factors and genetic factors. Although there is not an associated mortality per se, studies have shown cardiovascular mortality tending to increase in people of African ethnicity with previously diagnosed/treated POAG and ocular hypertension.[23]

POAG cannot be prevented but its progression can be slowed if it is detected and treated. By and large, the patient will not notice symptoms relating to POAG until the visual field changes are very advanced, at which point very little can be done. For this reason, screening remains the only tool for detection, with shared care between optometrists and ophthalmologists underpinning the detection and management. It should involve tonometry (measuring the IOP), visual fields and an examination of the optic disc.

Where there is no family history, opportunistic screening can be performed (ideally every two years) when the patient goes for a routine visit to their optician. From the age of 65 this should be carried out yearly.

In patients with a first-degree relative with POAG, a full specialist optician or ophthalmologist review should be carried out at the age of 40, with further screening every two years until the age of 50, and yearly thereafter. Shorter inter-screening intervals are recommended for patients with raised IOPs and patients considered otherwise at risk of POAG.

Further reading & references

  1. Kwon YH, Fingert JH, Kuehn MH, et al; Primary open-angle glaucoma. N Engl J Med. 2009 Mar 12;360(11):1113-24. doi: 10.1056/NEJMra0804630.
  2. Anderson DR; Normal-tension glaucoma (Low-tension glaucoma). Indian J Ophthalmol. 2011 Jan;59 Suppl:S97-101. doi: 10.4103/0301-4738.73695.
  3. Glaucoma; NICE Clinical Guideline (April 2009)
  4. Glaucoma referral and safe discharge - A national clinical guideline; Scottish Intercollegiate Guidelines Network - SIGN (March 2015)
  5. Glaucoma Staging System 2 (Brusini); OphthaClass
  6. Glaucoma Grading Scale (Hodapp-Parrish-Anderson); OphthaClass
  7. The Disc Damage Likelihood Scale (DDLS); OphthaClass
  8. The Glaucomatous Optic Nerve Head Classification; OphthaClass
  9. Ting NS, Li Yim JF, Ng JY; Different strategies and cost-effectiveness in the treatment of primary open angle glaucoma. Clinicoecon Outcomes Res. 2014 Dec 4;6:523-30. doi: 10.2147/CEOR.S30697. eCollection 2014.
  10. Burr J, Azuara-Blanco A, Avenell A, et al; Medical versus surgical interventions for open angle glaucoma. Cochrane Database Syst Rev. 2012 Sep 12;9:CD004399. doi: 10.1002/14651858.CD004399.pub3.
  11. Vass C, Hirn C, Sycha T, et al; Medical interventions for primary open angle glaucoma and ocular hypertension. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003167.
  12. McCarty CA, Mukesh BN, Kitchner TE, et al; Intraocular pressure response to medication in a clinical setting: the Marshfield Clinic Personalized Medicine Research Project. J Glaucoma. 2008 Aug;17(5):372-7.
  13. British National Formulary; NICE Evidence Services (UK access only)
  14. Rolim de Moura C, Paranhos A Jr, Wormald R; Laser trabeculoplasty for open angle glaucoma. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003919.
  15. Wang H, Cheng JW, Wei RL, et al; Meta-analysis of selective laser trabeculoplasty with argon laser trabeculoplasty in the treatment of open-angle glaucoma. Can J Ophthalmol. 2013 Jun;48(3):186-92. doi: 10.1016/j.jcjo.2013.01.001.
  16. Latina MA, Tumbocon JA; Selective laser trabeculoplasty: a new treatment option for open angle glaucoma. Curr Opin Ophthalmol. 2002 Apr;13(2):94-6.
  17. Martin KR, Broadway DC; Cyclodiode laser therapy for painful, blind glaucomatous eyes. Br J Ophthalmol. 2001 Apr;85(4):474-6.
  18. Canaloplasty for primary open-angle glaucoma; NICE Interventional Procedure Guidance, May 2008
  19. Trabecular stent bypass micro-surgery for open angle glaucoma; NICE Interventional Procedure Guidance, May 2011
  20. Trabeculotomy ab interno for open angle glaucoma; NICE Interventional Procedure Guidance, May 2011
  21. Assessing fitness to drive: guide for medical professionals; Driver and Vehicle Licensing Agency
  22. Tripathi RC, Parapuram SK, Tripathi BJ, et al; Corticosteroids and glaucoma risk. Drugs Aging. 1999 Dec;15(6):439-50.
  23. Wu SY, Nemesure B, Hennis A, et al; Open-angle glaucoma and mortality: The Barbados Eye Studies. Arch Ophthalmol. 2008 Mar;126(3):365-70.
  24. Higginbotham EJ, Gordon MO, Beiser JA, et al; The Ocular Hypertension Treatment Study: topical medication delays or prevents primary open-angle glaucoma in African American individuals. Arch Ophthalmol. 2004 Jun;122(6):813-20.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Olivia Scott
Current Version:
Peer Reviewer:
Dr Colin Tidy
Document ID:
670 (v29)
Last Checked:
25/06/2015
Next Review:
23/06/2020

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