Diagnosis and Management of Primary Open Angle Glaucoma

 A Photo-Essay for Health Professionals

John G. O'Shea MD,  Robert B. Harvey FRCSEd, David A. Infeld FRCSEd


It is estimated that approximately 50% of patients with primary open angle glaucoma( POAG ) remain undiagnosed in most Western communities. This review encompasses recent scientific advances in the diagnosis and treatment of POAG these include elucidation of the genetic mechanism behind the disease and the study of haemodynamic co-factors in the development of glaucomatous optic neuropathy.  New types of topical medication have recently developed for therapy of glaucoma. The impact of these therapies and their cost effectiveness remains yet to be fully evaluated. There are widely differing regimes which effectively treat glaucoma, some ophthalmologists prefer early surgical intervention whilst others reserve surgery for relatively advanced disease.  All methods of current treatment rely on the reduction of intraocular pressure- as yet there is no medication which has been consistently proven as neuro-protective or will favourably influence optic nerve perfusion.

Glaucoma can be considered a generic name for a group of diseases causing optic neuropathy ( disc cupping ) and visual field loss usually , but not always,  in the presence of raised IOP, it is increasingly being realised that other factors- such as optic nerve head perfusion, are concomitantly responsible for optic neuropathy in adult glaucoma. (1) The most common type of glaucoma in Western societies is Primary open angle glaucoma (POAG). (2)  This review will emphasise the diagnosis, morbidity and treatment of POAG and normal tension glaucoma ( NTG).

New strategies in glaucoma management

Glaucoma is a major cause of blindness and also lesser degrees of visual  impairment. Glaucoma and its management has an enormous impact in our society in terms of the number of loss of productivity, number of ophthalmic consultations and health costs. (2,3,4)  World-wide, glaucoma is the third leading cause of blindness with 22.5 million affected and  an estimated more than five million blind from glaucoma. (2)

 Shared care of glaucoma by ophthalmologists and optometrists,  has been internationally postulated by many learned bodies as a mechanism of reducing the high cost of glaucoma management and increasing the quality of patient care. (2,3,4)

Prevalence of glaucoma

The prevalence of primary open angle glaucoma (POAG) is estimated as being from 1.1-3 % of Western populations, over the age of 40 years, in both  past and more recent population surveys.

These surveys all use differing diagnostic criteria (1) - however, the inescapable conclusion is that POAG is an increasingly common disease in our ageing population.  (1,4,5,6,7,8,9 )  The prevalence of POAG is commonly thought of higher in men than in women (although some studies do not support this). (8)

A recent study from the Netherlands found overall prevalence of POAG was 1.10% (95% confidence interval [CI]: 1.09, 1.11). Age-specific prevalence figures increased from 0.2%in the age group of 55 to 59 years to 3.3% in the age group of 85 to 89 years. Men had a more than three times higher risk of having POAG than women (odds ratio, 3.6). In 8.8% of the eyes (2.9% of patients), visual acuity was 6/ 60 or less due to POAG.  (7 )

The Blue Mountains Eye Study provided detailed age and sex-specific prevalence rates for open-angle glaucoma and ocular hypertension in an older Australian population found  a prevalence of 3.0% for POAG. Ocular hypertension, defined as an intraocular pressure in either eye greater than  21 mmHg, without matching disc and field changes, was present in 3.7% of this population (95% CI, 3.1-4.3), but there was no significant age-related increase in prevalence. ( 8 ) This correlates with the original Framingham Eye Study (1977) which found a prevalence of POAG in an aged population of 3.3%. (5)



Table- Estimates of the Prevalence of Glaucoma


Baltimore (1990 ) 1.3% ; 50% undiagnosed

Ireland  (1992) 1.9% ; 49% undiagnosed

Beaver Dam (1992) 2.1%

Rotterdam (1996) 1.1% ; 53% undiagnosed

Blue Mountains (1996 ) 2.4% ; 51% undiagnosed

Melbourne VIP (1997) 1.7% ; 50% undiagnosed


( Source 1,2 )




Ethnicity affects both the chance of an individual developing glaucoma and the prognosis of his or her disease. The Barbados Eye Study highlighted the public health importance of POAG in the Afro-Caribbean region and has implications for other populations. The prevalence of POAG by self-reported race was 7.0% in black, 3.3% in mixed-race, and 0.8% (1/133) in white or other participants. In black and mixed-race participants, the prevalence reached 12% at age 60 years and older and was higher in men (8.3%) than in women (5.7%), with an age-adjusted male-female ratio of 1.4. Among participants 50 years old or older, one in 11 had POAG, and prevalence increased to one in six at age 70 years or older.  (10 )

Glaucoma is still considered to be under- diagnosed. In the United Kingdom it was recently concluded that glaucoma screening of people over age 40 years is economically justifiable, and should now form part of the standard optometric examination. (1,4)  Estimates infer that approximately 50% of patients who suffer from glaucoma still remain undiagnosed. (1,2)


Optometrists and the diagnosis of Glaucoma

Hitchings noted that in the United Kingdom optometric screening is the principal

modality of glaucoma diagnosis and the trend in Europe and the United States is that

optometrists are becoming far more directly involved in the care of their patients. (1)


The model proposed in the United Kingdom by the Royal College of

Ophthalmologists for the interaction between ophthalmologists and optometrists in

glaucoma management is that of ‘shared care’, namely the optometrist refers the

patient to an ophthalmologist for confirmation of the diagnosis and initiation of



The optometrist then takes over the subsequent care of  the patent serially evaluating

intraocular pressures and visual fields and monitoring the progression of the disease.

If he is unhappy with any aspect of the patient’s care he refers back to the

ophthalmologist for another opinion. (3)  Studies undertaken in Bristol showed this to

be an effective regime.


Diagnosis of Glaucoma


The diagnosis of glaucoma is based upon;

1. Intraocular pressure ( IOP ) and its measurement. (tonometry)

2. Optic disc examination.

3 Visual Field examination ( perimetry ) (4)


Factors which determine intraocular pressure ( IOP )

The aqueous humour is produced by non- pigmented epithelium of the ciliary processes of the ciliary body. The aqueous flows through the pupil from the posterior chamber to the anterior chamber and leaves the eye via the trabecular meshwork, Schlemm’s canal and episcleral veins. (12,13) IOP is determined by the rate of aqueous production, the rate of aqueous outflow and the episcleral venous pressure. Many factors affect the IOP, these include age, systemic blood pressure, genetic factors and topical or systemic medications.(13,12)

Factors that affect the level of recorded IOP include the time of day, season, respiration and method of measurement.  Recent studies have indicated that IOP can be lowered by regular aerobic exercise. (12)

The measurement of IOP and its significance

The measurement of IOP ( tonometry ) can be performed using one of several instruments. Commonly used devices are the Goldmann applanation tonometer (used in conjunction with a slit lamp biomicroscope), the Perkins tonometer (a hand-held applanation tonometer) and the non-contact air-puff.  There are inaccuracies inherent with all methods of  tonometry that may contribute to the varying IOP measurements seen in individual patients. Most optometrists will already be familiar with the advantages and disadvantages of these methods so that it is not felt necessary to present a detailed overview of  the various techniques currently employed. (13)

 The mean IOP is 16mm Hg; the arbitrary “normal” range is 10-21 mm Hg. IOP must be evaluated in a clinical context. (1,13) Approximately  6.6% % of the population have an IOP above 21mmHg.

 There is no clearly defined level of safe IOP; some individuals may develop optic nerve damage with an IOP of 12mm Hg whilst others may not  develop damage with an IOP of 30mm Hg. (13)

Elevation of IOP is regarded as a very important risk factor for the development of glaucoma. However, it is only a risk factor and is present in about 80% of patients with POAG (so-called “high tension” glaucoma in contrast to “normal tension” glaucoma ).(14)

Ocular Hypertension

Ocular hypertension can be defined as IOP greater than 21mmHg where the optic disc and visual field are normal. (8) ( The Baltimore Eye Survey, found 6.6% of people had an intraocular pressure greater than 22mmHg in one or both eyes.[15] )

  'Target Pressure ’.

A useful clinical concept is that each eye treated for glaucoma has a target pressure, this is based upon a general assessment of each individual patient’s disease burden. (13,14)


2. Optic disc examination

The optic disc and nerve fibre layer are examined for signs of glaucoma damage. The slit lamp biomicroscope offers a far superior view compared with the direct ophthalmoscope because of stereo-visualisation, favourable illumination and high magnification. (13)

The normal optic disc is round or slightly oval.  It contains a central physiological cup which is devoid of optic nerve fibres and of a different colour. The ratio of optic cup diameter to optic disc diameter (cup to disc ratio, CDR) is usually 0.3A CDR of greater than 0.5 is seen in 6% of the normal population. (13)


Progressive enlargement of the optic cups documented with periodic follow-up is a most important sign of uncontrolled glaucoma ( table ).


TABLE-  Optic disc changes in Glaucoma


Notching of neuroretinal rim, Pallor, Splinter haemorrhage, Progressive enlargement , vertical elongation,  Asymmetry (between the left & right eyes), Nasal displacement of central retinal vessels, baring of lamina cribrosa. (21)


Atrophy of the Retinal Nerve Fibre Layer may be detectable using the green ( red-free) light of the slit lamp biomicroscope. (13)



Notching of the neuro-retinal tissue of the optic disc is characteristic. 

A so-called splinter haemorrhage located at the optic disc margin is characteristic of glaucoma. It is more commonly seen in normal tension glaucoma. (21)

Other conditions that may mimic glaucomatous optic neuropathy include a large physiological cup and congenital optic disc abnormalities such as coloboma. (13)

Recent scientific work has been devoted to determining the role of optic disc perfusion in glaucoma. Most authorities now agree that there are abnormalities of the ocular circulation which contribute to the pathogenesis of the disease although the precise significance of these abnormalities is not understood and there are some inconsistencies of results between major research centres. There are as yet no drugs available which have been consistently shown to aid optic nerve perfusion. (16-20)


3. Visual field examination  ( Perimetry )


Visual field examination is important in glaucoma management in order to detect and quantify any deficits of the patient’s peripheral vision and to quantify any progressive changes seen with repeated follow-up. (1,21)  Several perimeter machines are available, the Humphrey 24-2  Fastpac  being currently the most popular method of field analysis. (22,23) Others include the Octopus, the Henson and the Dicon. The machines basically test the patient’s ability to detect a target stimulus against a darker background. Testing conditions that can be varied include the number, duration and light intensity of the target stimulus. (21-23)


Factors that can affect the result include patient fatigue or lack of concentration, the spectacle frame, miosis ( from pilocarpine drops) and opacities of the ocular media (such as cataract). (21-23)


The two basic types of perimetry used are static and kinetic perimetry. (21-23)

Static perimetry is  the basis of computerised supra-threshold perimetry, a stationary target is presented and its intensity varied to determine retinal sensitivity. (21-23)


Table- Field Analysis

Tangent  screen, 

Manual kinetic perimetry,

Fields:- baring of blind spot, generalised constriction earliest findings

Bjerrum scotoma (10-20 degrees), arcuate scotoma, temporal wedge, nasal step

Static automated perimetry, (Humphrey, Octopus, Henson etc.)

Blue target against a yellow background help to identify damage to the larger ganglion cells (magnocellular loss).


Other Tests

Confocal laser scanning ophthalmoscopy

Pulsatile ocular blood flow

Ultrasound Doppler velocimetry  

In kinetic ( isopter ) perimetry a moving target of differing sizes is presented. (21-23) This article discuss the many techniques and types of perimetery and their relative advantages and disadvantages but rather presents a photographic atlas of common glaucoma defects.


Hitchings notes that motion detection perimetry, performed on a laptop computer may be of help to optometrists undertaking glaucoma screening. (1) Blue on yellow perimetry has recently been shown to detect nerve fibre defect s significantly earlier then conventional suprathreshold perimetry.


Table- Some Associations of POAG with systemic or ocular pathology


High myopia, diabetes mellitus, retinal vein occlusion,

Peripapillary atrophy

Fuchs endothelial dystrophy, retinitis pigmentosa


4. Gonioscopy

Examination of the anterior chamber angle with a gonioscopic contact lens (gonioscopy) is also very important in determining the aetiology of glaucoma, for example- chronic angle closure glaucoma versus POAG. (13)


Table- Gonioscopy



Gonioscopy to visualise the iridocorneal angle utilises a contact lens

 to avoid the problem of total internal reflection which normally makes all angle

structures invisible. ( The large difference in refractive index between the cornea and air has to be minimised. ) 


The Goldmann gonioscope has a highly curved anterior surface which needs

to be filled with about 3 drops of normal saline or hypromellose before application

to the anaesthetised cornea.


It is best to ask the patient to look down whilst the lens is applied to prevent spillage.


Each quadrant of angle can be examined by rotating the lens. Typically the upper quadrant is narrowest.


Under the Shaffer angle grading system each quadrant is given a grade from:-

0 is closed (either contact or adhesion)

I 10-15 degrees

II 15 to 25 degrees

III 25 to 35 degrees

IV 40 or more degrees

Evaluation includes the assessment of peripheral anterior synechiae (adhesions)

or any neovascular membranes which can also obstruct aqueous drainage.


Illustration courtesy of  Dr. Robert Harvey FRCSE, from Practical Ophthalmology CD ROM, 2002  Palmtrees Publishing. (13)

Primary open angle glaucoma (POAG)


The most common type of glaucoma in Western societies is primary open angle glaucoma. The resistance of the trabecular meshwork increases, typically as an ageing or involutional change leading to increased IOP. It is now recognised that intrinsic factors within the optic nerve are also important in the development of POAG as are genetic factors. Older definitions of the disease have often put undue stress in the role of raised intraocular pressure ( IOP ) in the pathogenesis of open angle glaucoma. Recent scientific studies have revealed the situation to be more complex and that other factors, both vascular and biochemical, are likely involved in the pathogenesis of glaucomatous optic neuropathy.


In glaucomatous optic neuropathy there is optic disc cupping and atrophy and apoptosis of retinal ganglion cells and their axons,  and possibly other retinal elements, leading to irreversible visual field loss. The intraocular pressure (IOP) is usually elevated. Glaucoma can thus be considered a generic name for a group of diseases causing optic neuropathy ( disc cupping ) and visual field loss usually, but not always,  in the presence of raised IOP, other factors- such as optic nerve head perfusion, are concomitantly responsible for optic neuropathy in adult glaucoma. Some authors postulate a disturbance of the mechanism of autoregulation of blood flow to the optic nerve whilst head other authors describe glaucomatous optic neuropathy as an intrinsic optic neuropathy due to localised vascular disease and to other biochemical mechanisms which have yet to be fully elucidated.(1,16-20)


Increased IOP may cause glaucomatous damage by a mechanical and/or ischaemic effect upon the optic nerve. There may be direct mechanical compression of optic nerve fibres from the increased IOP. Increased IOP may also interrupt the blood supply of the optic nerve fibres. (16-20)


Glaucomatous optic neuropathy usually has an insidious onset. It is often bilateral; it may be highly asymmetrical. It is more prevalent and more severe in black individuals. It is about 5 times more prevalent in individuals whose close relatives have POAG. Corticosteroid eye drops may cause glaucomatous damage by producing an elevation of IOP as a side effect. This side effect of IOP elevation, known as steroid response, is more common in patients with POAG. (13)


Normal tension glaucoma ( NTG)


Elevated IOP is a major risk factor for the development of glaucoma. However, 20% of patients do not have an elevated IOP. This is referred to as normal tension glaucoma. It is commoner in females. In normal tension glaucoma optic nerve damage and visual field loss occur despite a “normal” IOP. (24)  A CT scan should performed before a diagnosis of  NTG is made to exclude possible optic nerve compression by a tumour. (13)





Glaucomatous disc and field changes with IOP consistently < 22

20% of newly diagnosed glaucoma patients have IOPs less than 21 mm Hg at presentation.



? Decreased perfusion of disc (arteriosclerosis, low BP)



NON PROGRESSIVE-Due to transient vascular shock (single event of systemic hypotension)


PROGRESSIVE- Chronic vascular insufficiency



POAG with wide diurnal fluctuation

Resolved secondary glaucoma (non-progressive)  steroid related, pigmentary, intermittent ACG

Compressive optic neuropathy

Prior vascular insult- AION- non-progressive



History of CVS disease, diabetes, hypertension / hypotension, steroid use, vasospastic disease (Raynaud’s, migraine)

IOP < 22

Large cup relative to field loss

Disc haemorrhage is common.

Field loss closer to fixation and steeper.



Phasing- excludes POAG, shows diurnal range to decide on target IOP

CVS- BP, carotids, ECG, FBC (anaemia), ESR (GCA), cholesterol and triglyceride, BSL

Neuro-exam:  CT scan for compressive lesion.



1.  Correct any underlying abnormality such as anaemia

2.  Assess for progression and treat only if progression

3.  Reduce IOP maximally, aim for 10 mmHg (medical and laser treatment have only a limited role)Often come to surgery:-  trabeculectomy + 5FU,  Or  Scheie thermosclerostomy, rarely a seton.Treat one eye as a therapeutic trial as there is no definite evidence that reducing IOP prevents progression.

4.  Consider aspirin and calcium channel blockers for vasospastic disease.



 Other risk factors

Other factors which may contribute to the development of glaucoma include diabetes,

cardiovascular disease, myopia and a positive family history of glaucoma. There may be at least two primary open-angle glaucoma genes, the GLC1A gene on chromosome 1q and other genes located elsewhere in the genome. The TIGR gene is responsible for the phenomenon of steroid response.  ( 6, 25-28 ) In all, about seventeen candidate genes have been identified as possible associates in POAG. The ongoing elucidation of the genetic mechanism responsible for POAG and the possibilities of detecting glaucoma early in phenotypes  predisposed to POAG and tailoring therapy based upon genetic information is one of the most exciting areas of ongoing research.


Summary- Classic Risk factors for Glaucoma ( POAG)

Strong Association

Intraocular pressure



Family History


Moderate association




Weak Association

Systemic Hypertension





Less Common types of chronic glaucoma


Secondary open angle glaucoma

In secondary open angle glaucoma decreased outflow of aqueous results

from other conditions such as corticosteroid administration, pigmentary glaucoma or phacolytic glaucoma, or neovascularication of the iris ( rubeotic glaucoma ) (13).


TABLE  Causes of Secondary Open Angle Glaucoma include:

Psedoexfoliative glaucoma

Pigmentary glaucoma

Topical Corticosteroids

Phacolytic glaucoma                                                                   (13)



TABLE- Paediatric  glaucoma  

Paediatric  glaucoma can be congenital or develop during infancy or later childhood.

It is most commonly primary (i.e. isolated).  Secondary glaucoma can be associated with ocular conditions (such as aniridia, trauma or ocular tumour) or with systemic conditions (such as rubella).  A neonate or young child with glaucoma may present with epiphora, photophobia, blepharospasm, enlargement of the cornea or of the globe. Bupthalmos, enlargement of the globe, is not uncommon.

  IOP can be measured in infants and young children using a Perkins tonometer or Tono-Pen. In older children a Goldmann applanation tonometer can be used.  Many types of paediatric glaucoma are genetically determined. (25,26,27,28 )



Differential diagnosis of Glaucoma

  Conditions that can mimic glaucoma include carotid artery stenosis and optic nerve compressive lesions. The need for ophthalmic evaluation should be considered particularly for patients with atypical features (such as unilateral optic

neuropathy). (13,21)


Management of glaucoma- therapeutic paradigms


It can be difficult to distinguish clinically between the patient with early glaucoma and the patient with no glaucoma, experience is clearly needed in deciding when to treat. Issues in the management of glaucoma include both the indications for treatment and the type of treatment. (13)


This difficulty leads to the dilemma of determining which patients should be treated . Patients that do not have glaucoma may be subjected to the inconvenience, expense and possible toxicity of treatment. The unfortunate corollary is that treatment may be withheld from patients who have early glaucoma or who may develop glaucoma. (13)


The ultimate goal in glaucoma management is the preservation of vision. Factors to be considered include the initial IOP, the patient’s life expectancy and the degree of optic nerve damage. (13)


TABLE - Factors to consider in glaucoma  management include;


Initial IOP

Life expectancy


Extent  of optic nerve damage



A target IOP should be determined. This represents the IOP aimed for following therapy. For example, a patient with advanced glaucomatous optic neuropathy may require a target IOP of 12 mmHg. A patient with an initial IOP of 45 mmHg may possibly preserve vision with a target IOP of 25 mmHg.




A patient with a long life expectancy may require more frequent follow-up and more aggressive therapy. More aggressive therapy may be similarly required for patients with extensive optic nerve damage.



Table- Compliance is a very important issue in glaucoma management. Patients may be have no symptoms from glaucoma. Medication may cause various side effects. It may be difficult to comply with treatment regimes, for example, forgetting to administer midday doses of eye drops or falling asleep before taking the evening dose.   (3)


The options for treatment of glaucoma include one or more of the following:

1. medication

2. laser trabeculoplasty

3. filtration and other surgery.

Topical Anti-glaucoma Medication


Eye drops (and gel preparations) are the most common form of therapy to treat glaucoma. They are often prescribed to prevent glaucoma in patients who are regarded as being glaucoma suspects.

The choice of medication depends on how well the eye drop reduces the IOP and how well the medication is tolerated. Many possible ocular and systemic side effects can occur. Compliance is a very common and often overlooked source of failure of medical therapy. (1,13)


TABLE   Commonly  prescribed Anti-glaucoma Eye Drops


Timoptol (Timolol maleate),

Levobunolol (Betagan)

Betaxalol ( Betoptic )

Carteolol ( Teoptic)

 Other Common Medications

Brimonidine (Alphagan)

Dorzolamide (Trusopt)

Latanaprost (Xalatan)


Dipivefrin  (Propine)                              (13)



Beta Adrenergic Antagonists (Beta Blockers)

Side effects include asthma, bradycardia, reduction in  exercise tolerance, altered mentation, impotence, drowsiness and fatigue.  A topical beta blocker is usually the first line therapy in patients over the age of 40 years unless there are systemic contraindications such as asthma or bradycardia. (13,13 29-31)

Levobunolol (Betagan)

Once-daily administration may be effective in about 70% of patients,

thereby improving compliance and safety. In view of the diurnal variation in IOP with the peak occurring in the morning, instillation of the eye drop after awakening is advisable. . (13 29-31)

Timolol LA

This was designed for once-daily administration. It appears to be very similar in efficacy to twice-daily administration of Timoptol 0.5% drops. (13 29-31)

Carteolol ( Teoptic)

Carteolol 1%- A non-selective beta blocker with intrinsic sympathetomimetic activity.


Betaxolol (Betoptic)

This is a selective beta blocker. It can cause side effects seen with other beta blockers although less frequently and less severely.

Betaxalol is a popular cost effective choice as a first line drug in POAG. (13 29-31)

 Brimonidine (Alphagan)

This agent is an alpha 2-agonist. It appears to be as effective as timolol in controlling glaucoma but does not cause a significant reduction in heart rate.

Side effects include dry mouth ( 10% of patients ), allergy (seen in 10% of patients in 1 year trial), drowsiness, depression and fatigue. (32)


  TABLE-  Administering eyedrops

f more than one type of eye drop is being prescribed the patient should be instructed to wait  5 minutes between the instillation of eye drops in order to maximise ocular absorption. The eyelids should be gently closed after instillation. Patients may also find administration easier in front of a mirror.    (3)


  Dorzolamide, Brinzolamide

Dorzolamide and Brinzolamide are topical carbonic anhydrase inhibitors.

They have additive effects in IOP reduction when combined with beta blockers.

They lack the side effects of systemic carbonic anhydrase inhibitors. (29)

Dorzolamide requires three times a day instillation whether prescribed alone or twice daily in combination. (29)

Latanaprost (Xalatan)

Latanaprost is a prostaglandin analogue. Its action is  increases aqueous drainage vie the uveoscleral route. It is effective with once daily instillation; it is about as effective as Timolol. (24)


Muscarinic agonists derived from the pilocarpus plant have been in use in ophthalmology for over a century and are still efficacious in the treatment of acute and chronic glaucoma. (11,13, 31)

Side effects are common and include brow ache, blurred vision (from spasm of accommodation) and decreased night vision (from miosis).

Dipivefrin (Propine)

This is a pro-drug, converted to adrenaline inside the eye. Ocular side effects are common, including redness and stinging. If a patient is already using a topical beta blocker then adding propine usually does not significantly lower the IOP further. (13)

 Long term therapy with topical medication can cause histological damage to the conjunctiva. This secondary change may be responsible for failure of trabeculectomy surgery performed at a future stage. (33,34)



  TABLE  Practice point- Pupil mydriasis.


It is well justified that medical practitioners and optometrists routinely perform pupil dilation (mydriasis) provided patients are instructed on the risks and benefits of the procedure.


Encourage patients to seek urgent ophthalmic care if they develop a red painful eye. It may be worthwhile medico-legally giving written advice detailing symptoms of angle closure and giving a contact number or alternately, detailing the address of the nearest ophthalmic casualty.


The risks of provoking angle closure glaucoma  are, in fact, very small (15)  Of  4,870 subjects whose eyes were dilated on screening examination ( many of whom had previously diagnosed open angle glaucoma) none developed acute angle-closure glaucoma.(15) It has been recommended that the depth of the anterior chamber depth be estimated on the slit lamp prior to mydriasis. ( 15 )


Guttae tropicamide 0.5 %, which lasts 4-6 hours, is the preferred mydriatic for routine examinations.


Be careful in elderly patients, especially with cataracts.(15) Females are more prone to PACG. Patients should be instructed not to drive home. (15)



Argon laser trabeculoplasty


This treatment involves the application of laser energy (usually argon green) to the trabecular meshwork, thereby improving the rate of outflow of aqueous humour. Laser therapy and surgical therapy for glaucoma have an advantage over

medical therapy by sometimes obviating the problem of compliance. Several weeks may be required before the effects of argon laser trabeculoplasty (ALT) become evident. Complications include transient IOP elevation in the first few hours  postoperatively and also permanent IOP elevation. The IOP is usually reduced by 25%. 80% of patients show an initial beneficial effect. In at least 50% of these patients the effect is lost in the first 5 years. (13,35)

In black patients the benefit is lost earlier (35) another study yielded a success rate for ALT of 46% for 3-year follow-up.. ALT is less successful following cataract surgery.  Re-treatment in general is associated with a low success rate.(35) ALT is not useful in certain types of glaucoma, for example paediatric glaucoma.


Glaucoma surgery

Topical medication is the conventionally  initial type of therapy for POAG. There is increasing evidence, particularly from studies undertaken at Moorfields Eye Hospital (Moorfields Primary Treatment Trial )  that initial or early  therapy in the form of surgery may have significant advantages over initial medical therapy even when the patient presents with early glaucoma. (1,33,34)



The most common surgical procedure for glaucoma is trabeculectomy. In trabeculectomy an ostium is made in the inner sclera, a fistula covered by a flap fashioned in the outer sclera, thereby providing an alternative drainage site for aqueous humour.  (13,33,34,36,37)


Trabeculectomy lowers the intraocular pressure more consistently than anti-glaucoma eye drops or laser trabeculoplasty.  Some authorities consider performing trabeculectomy as primary therapy . (13,33,34,36, 37)

However, glaucoma surgery may also be associated with complications. The trabeculectomy fails usually because of scarring around the scleral flap or due to closure of the internal ostium. (33 )



TABLE  Surgical Procedures for Glaucoma

Trabeculectomy ( with or without antimetabolites )

     Filtration devices

     Combined procedure (glaucoma/cataract surgery)

     Goniotomy/Trabeculotomy (paediatric glaucoma)

     Peripheral Iridectomy (surgical)

     YAG laser Cyclodestruction

    Cyclodestruction (cyclocryotherapy)


Cataracts may progress rapidly after trabeculectomy. Age 61 years or older, exfoliative glaucoma, postoperative hypotony, and IOP peaks were identified as risk factors for accelerated cataract progression after trabeculectomy. (36)


Topical antimetabolites, such as 5-fluorouracil and mitomycin, can be used intraoperatively or immediately postoperatively in order to increase the success rate of the trabeculectomy procedure. Antimetabolite use, however, may increase the risk of complications such as ocular hypotony, wound leakage and infection. (37,38)


Microtrabeculectomy, usually  performed under local anaesthesia, is a less invasive variant of the trabeculectomy procedure which is gaining popularity. Reverse trabeculectomy, deep sclerectomy and viscocanalostomy are also other novel procedures which are currently being evaluated in the treatment of POAG. (38,39,40,41)



 Increased community awareness of glaucoma, and earlier detection of the condition, will doubtless result in decreased morbidity due to glaucoma. (1,4,8)   Shared care has been postulated as a model for interaction between optometrists and ophthalmologists by the Royal College of Ophthalmologists and will result in a more comprehensive, efficient and cost effective service for patients. (3,13)


Recent scientific advances include elucidation of the genetic mechanism behind the disease (6,27-29) and the study of haemodynamic and biochemical co-factors in the development of glaucomatous optic neuropathy,  particularly in relation to the pathogenesis of normal tension glaucoma. (16-20,42) Several new types of topical medication have recently developed for therapy of glaucoma (24,29-32) and both the impact of these therapies and their cost effectiveness remains to be evaluated. (41)

All methods of current glaucoma treatment rely on the reduction of intraocular pressure- as yet there is no medication which has been proven as neuro-protective or will favourably influence optic nerve perfusion. 

World-wide, glaucoma is reckoned the third leading cause of blindness with an estimated five million blind from the disease.  (2,43) Glaucoma and its management therefore has  an enormous impact in our society. (1,2,3,4). Topical medication is conventionally the initial type of therapy for POAG. There is evidence, particularly from studies undertaken at Moorfields Eye Hospital (Moorfields Primary Treatment Trial ) that early therapy in the form of surgery may have advantages over initial medical therapy.(1,33,34)-this, however, is still regarded as controversial by other authors. (40,42)


International Glaucoma Association
King's College Hospital
Denmark Hill
London, SE5 9RS,  UK




1. Hitchings, RA The Duke Elder Lecture, Flying  Blind 1997 Eye ; 11: 773-8


2. Wensor MD et al.  The Prevalence of Glaucoma in the Melbourne Visual Impairment Project Ophthalmology 1998 ; 5 : 733-9


3.  Hume J, Setting up a shared care glaucoma clinic.  Nursing Standard 1995 ; 10 : 34-36


4. Tuck MW, Crick RP, The cost-effectiveness of various modes of screening for primary open angle glaucoma. Ophthalmic Epidemiology. 1997 ; 4 :3-17.


5. Kahn HA, The Framingham Eye Study- Outline of Major Prevalence Findings  American Journal of  Epidemiology 1977 106 17-32


6. Sack J,  Healey DL,  de Graaf AP,  Wilkinson RM,  Wilkinson CH, Barbour

 JM,  Coote MA,  McCartney PJ,  Rait JL,  Cooper RL,  Ring MA,  Mackey DA,

The problem of overlapping glaucoma families in the Glaucoma Inheritance

 Study in Tasmania (GIST). Ophthalmic Genetics. 1996 ; 17 :209-14.


7. Dielemans I,  Vingerling JR,   Wolfs RC,   Hofman A,   Grobbee DE,  de Jong

 PT,  The prevalence of primary open-angle glaucoma in a population-based study

 in The Netherlands. The Rotterdam Study. Ophthalmology. 1994; 101:1851-5.


8. Mitchell P,   Smith W,  Attebo K, Healey PR, Prevalence of open-angle glaucoma in Australia. The Blue Mountains Eye Study. Ophthalmology. 1996;  103:1661-9.


9. Coffey M,  Reidy A,  Wormald R,  Xian WX,   Wright L.   Courtney P, Prevalence of glaucoma in the west of Ireland. British Journal of Ophthalmology 1993 ; 77:17-21.


10. Leske MC,  Connell AM,  Schachat AP,  Hyman L, The Barbados Eye Study. Prevalence of open angle glaucoma. Archives of Ophthalmology. 1994 112: 821-9.


11. Baume P, A Cutting Edge- Australia’s Surgical Workforce. 1994, Canberra, Australian Government Publishing Service ; 68-69, 117-120,


12. Larsson LI,  Rettig ES,  Brubaker RF, Aqueous flow in open-angle glaucoma. Archives of Ophthalmology. 1995 113(3): 283-6.


13. Harvey RB, Practical Ophthalmology- CD ROM 1998 Birmingham;  Palmtrees Publishing.


14. Odberg T, Visual field prognosis in early glaucoma. A long-term clinical follow-up.Acta Ophthalmologica 1993;  71:721-6.

15. Patel KH, Javitt JC,  Tielsch JM,  Street DA,  Katz J,  Quigley HA, Sommer A Incidence of acute angle-closure glaucoma after pharmacologic mydriasis

American Journal of Ophthalmology. 1995;  120: 709-17.


16. Hitchings RA.Intraocular pressure and circulation at the disc in glaucoma. Acta Ophthalmologica Scandinavica Supplement. 1997 ; 220: 15-20; 20-2


17. Hollo G,  van den Berg TJ,  Greve EL, Scanning laser Doppler flowmetry in glaucoma. International Ophthalmology. 1997 ; 20 : 63-70


18. Butt Z,  O'Brien C,  McKillop G,  Aspinall P,  Allan  Color Doppler imaging in untreated high- and normal-pressure open-angle glaucoma Investigative Ophthalmology & Visual Science. 1997 ; 38 : 690-6.


19. Kaiser HJ,  Schoetzau A,  Stumpfig D,  Flammer J, Blood-flow velocities of the extraocular vessels in patients with high-tension and normal-tension primary open-angle glaucoma. American Journal of Ophthalmology. 1997; 123(3): 320-7.


20. Ulrich A,  Ulrich C,  Barth T,  Ulrich WD, Detection of disturbed autoregulation of the peripapillary choroid in primary open angle glaucoma. Ophthalmic Surgery and Lasers. 1996; 27 :746-57


21. Bajandas FJ, Kline LB Neuro-ophthalmology review manual  1988 Thorofare N.J.,  Slack Incorporated ; 1-42


22. Stewart WC, Chauhan BC, Newer visual function tests in the evaluation of glaucoma. Survey of Ophthalmology 1995. 40: 119-35.


23. Chen YF,  Wang TH,  Hung PT, Automated perimetry in primary open-angle glaucoma.  Journal of the Formosan Medical Association. 1997 ; 96 :441-5


24. Greve EL,  Rulo AH,  Drance SM,  Crichton AC,  Mills RP,  Hoyng  Reduced intraocular pressure and increased ocular perfusion pressure in normal tension glaucoma: a review of short-term studies with three dose regimens of latanoprost treatment. Survey of Ophthalmology. 1997 ; 41 Suppl 2: S89-92.


25. Richards JE,  Lichter PR,  Herman S,  Hauser ER,  Hou YC,  Johnson AT,

Boehnke M, Probable exclusion of GLC1A as a candidate glaucoma gene in a family with middle-age-onset primary open-angle glaucoma.Ophthalmology. 1996 ; 103 :1035-40.


26. Lichter PR,  Richards JE,  Boehnke M,  Othman M,  Cameron BD,  Stringham

 HM,  Downs CA,  Lewis SB,   Boyd BF,  Juvenile glaucoma linked to the GLC1A gene on chromosome 1q in a Panamanian family. American Journal of Ophthalmology. 1997 ; 123(3):413-6.

27. Johnson AT,  Drack AV,  Kwitek AE,  Cannon RL,  Stone EM, Alward WL Clinical features and linkage analysis of a family with autosomal dominant

 juvenile glaucoma. Ophthalmology. 1993 ; 100 : 524-9


28 . Abecia E,  Martinez-Jarreta B,  Casalod Y,  Bell B,  Pinilla I,  Honrubia Genetic markers in primary open-angle glaucoma. International Ophthalmology. 1997;  20 :79-82


29. Strahlman E,  Tipping R, Vogel R, A double-masked, randomized 1-year study comparing dorzolamide (Trusopt),timolol, and betaxolol. International Dorzolamide Study Group Archives of Ophthalmology. 1995; 113 :1009-16.


30. Diggory P,  Cassels-Brown A,  Fernandez C, Topical beta-blockade with intrinsic sympathomimetic activity offers no advantage for the respiratory and cardiovascular function of elderly people. Age & Ageing. 1996 ; 25(6): 424-8.


31. Robin AL, Ocular hypotensive efficacy and safety of a combined formulation of

betaxolol and pilocarpine. Transactions of the American Ophthalmological Society. 1996 ; 94 : 89-101; discussion 101-3,.


32. Schuman JS,  Horwitz B,  Choplin NT,  David R,  Albracht D, Chen K,  A 1-year study of brimonidine twice daily in glaucoma and ocular hypertension. A controlled, randomized, multicenter clinical trial. Chronic Brimonidine Study Group. Archives of Ophthalmology. 1997 ; 115 :847-52


33. Broadway DC,  Grierson I,  O'Brien C,  Hitchings RA,  Adverse effects of topical antiglaucoma medication.  The conjunctival cell profile.  Archives of Ophthalmology. 1994 112 :1437-45


34. Migdal C, Gregory W, Hitchings R, Long-term functional outcome after early surgery compared with laser and medicine in open-angle glaucoma. Ophthalmology. 1994 ; 101 :1651-6; discussion 1657


35. Ustundag C,  Diestelhorst M,  Efficacy of argon laser trabeculoplasty: 3-year preliminary results of a prospective placebo-controlled study. Graefes Archive for Clinical & Experimental Ophthalmology. 1997 ; 235 :354-8,


36. Vesti E,  Raitta C, A review of the outcome of trabeculectomy in open-angle glaucoma. Ophthalmic Surgery and Lasers. 1997 ; 28(2):128-32


37. Vernon SA,  Spencer AF, Intraocular pressure control following microtrabeculectomy. Eye. 1995; 9 :299-303


37. Andreanos D,  Georgopoulos GT,  Vergados J,  Papaconstantinou D,  Liokis

  N,  Theodossiadis P, Clinical evaluation of the effect of mitomycin-C in re-operation for primary open angle glaucoma. European Journal of Ophthalmology. 1997 ;7 : 49-54

38. Robin AL,  Ramakrishnan R,  Krishnadas R,  Smith SD,  Katz JD,  Selvaraj

 S,  Skuta GL,  Bhatnagar R,  A long-term dose-response study of mitomycin in glaucoma filtration Archives of Ophthalmology. 1997 ; 115(8):969-74


39. Kosoko O. Gaasterland DE.  Pollack IP.  Enger CL. Long-term outcome of initial

ciliary ablation with contact diode laser transscleral cyclophotocoagulation for severe glaucoma. Ophthalmology. 1996 ; 103 :1294-302


40. Stewart WC,  Sine CS,  LoPresto C, Surgical vs medical management of chronic open-angle glaucoma. American Journal of Ophthalmology. 1996 ; 122(6):767-74.


41. Wishart P, Therapeutic options in primary open-angle glaucoma. ActaOphthalmologica Scandinavica Supplement. 1997 ; 220:23-8; 28-9


42 Kaiser HJ,  Schoetzau A,  Stumpfig D,  Flammer J, Blood-flow velocities of the extraocular vessels in patients with high-tension and normal-tension primary open-angle glaucoma. American Journal of Ophthalmology. 1997 ;  123 : 320-7


43. Foster A,  World distribution of blindness. Journal of Community Eye Health 1988 ; 1 : 2

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