Primary Open-Angle Glaucoma

Original article
Anthony Khawaja MA(Cantab), MB BS, MRCOphth
contributed by:
Alex Kozak, Anjana P. Jindal, Anthony Khawaja MA(Cantab), MB BS,
All contributors: MRCOphth, Dale Fajardo, Ed.D., M.B.A., Dylan Griffiths,
Ryan.C.Plumb.AAO, Sarwat Salim MD, FACS and WikiWorks Team
Assigned editor:
Review: Not reviewed

Contents

Summary
Glaucoma continues to be a major public health problem. It is the second leading cause of
blindness worldwide after cataracts. In the United States, primary open-angle glaucoma is the
most common form of glaucoma and is the leading cause of irreversible blindness in African
Americans. This disease is typically asymptomatic until advanced visual field loss occurs. Some
of the risk factors for primary open-angle glaucoma have been extensively described and studied,
including elevated intraocular pressure, advancing age, family history, African ancestry, myopia,
and perhaps presence of certain systemic diseases, such as diabetes and hypertension. The
precise mechanism of increased resistance to aqueous outflow remains unclear and is currently
an active focus of research. At present, all our treatment strategies are directed at lowering
intraocular pressure. Initial treatment is usually started with topical or oral medications.
However, with progressive damage, laser trabeculoplasty may be considered as an adjunctive
therapy, followed by incisional glaucoma surgery, either with trabeculectomy or glaucoma
drainage implant.

Disease Entity
Primary open angle glaucoma

Disease
Glaucoma describes a group of conditions in which there is characteristic cupping of the optic
disc with corresponding visual field defects, due to retinal ganglion cell loss. It is a progressive
condition and is the most common cause of irreversible blindness worldwide. Primary open
angle glaucoma (POAG) is a subset of the glaucomas defined by an open, normal
appearing anterior chamber angle and raised intraocular pressure (IOP), with no other underlying
disease. If there is an identifiable underlying cause for raised IOP, this is termed secondary

glaucoma. If the IOP is within normal limits, this is termed normal tension glaucoma (NTG).
Secondary glaucoma and NTG are not discussed in this section.

Etiology
The final common pathway for all potential etiologies of POAG is optic nerve head damage.
This is thought to be secondary to primarily ganglion cell axon loss, although loss of blood
vessels and glial cells has also been observed. There are many postulated mechanisms of
ganglion cell damage.
IOP related etiology
There is good evidence that IOP related mechanisms of optic nerve damage are very important in
the pathogenesis of POAG. By definition, patients with POAG have raised IOP. Raised IOP is an
important risk factor for the progression to POAG from ocular hypertension (OHT), and is the
only common clinical finding in a wide variety of secondary glaucomas. IOP seems to be
important even in NTG, as reduction of IOP was shown to reduce the risk of progression in these
patients in the Collaborative Normal Tension Glaucoma Study. In animal models, raised IOP
always precedes glaucomatous nerve damage. It is thought that raised IOP primarily affects the
optic nerve via the mechanical changes at the lamina cribrosa. There is consensus that the
etiology of raised IOP is due to reduced aqueous outflow, rather than over-production of
aqueous. Several theories exist as to the cause of reduced aqueous outflow (see below).
Non-IOP related etiology
A proportion of patients develop glaucoma and continue to progress despite low IOP. Equally, a
proportion of patients with elevated IOP never develop POAG. This supports the theories of IOP
independent mechanisms of glaucomatous nerve damage. These include ischemia, loss of
neurotrophic factors, neurotoxicity, and failure of cellular repair mechanisms.

Risk Factors
IOP
IOP is considered the most important risk factor for the development of POAG, and remains the
only known modifiable risk factor. Raised IOP in animal models results in glaucomatous optic
neuropathy. Population studies have shown increased prevalence of glaucoma with increasing
IOP. In patients with OHT (raised IOP but no signs of glaucomatous optic disc or visual field
changes), higher IOP is associated with a higher risk of developing POAG. This has been shown

in the OHTS (Ocular Hypertension Treatment Study) and the EGPS (European Glaucoma
Prevention Study). IOP is also thought to be a risk factor for NTG, despite IOP never being
higher than the normal range.
Age
The prevalence of POAG increases with age, even after compensating for the association
between age and IOP. Age was also found to be an important risk factor for the conversion of
OHT to POAG in both OHTS and EGPS.
Race
Several studies have shown POAG to be more prevalent in people of African-Caribbean descent
compared with Caucasians. Not only is POAG more prevalent in black race, its onset is earlier,
and disease progression has been shown to be faster and more refractory to treatment. Black
patients with OHT have been found to be more likely to progress to POAG. The prevalence of
POAG in Hispanics is thought to be between that of African-Caribbean and Caucasian
populations.
Refractive error
Myopia has been shown to be a risk factor for POAG in several studies. However, it can be
difficult to diagnose true POAG in myopic patients and controversy exists over whether it is real
risk factor. Myopic optic discs are notoriously difficult to assess, and myopic patients may have
visual field defects unrelated to any glaucomatous process.
Central corneal thickness
A thinner cornea has been shown to be a risk factor for OHT patients developing POAG. This
may be in part due to IOP measurement error (IOP tends to be read lower in patients with thinner
corneas), but there are also theories that a thinner cornea may indicate less rigid support
structures around the optic nerve head, and a resultant increased propensity to damage.
Family history
A first-degree relative with POAG is a risk factor for the development of POAG. This has been
reported in several studies with the odds ratio varying from 3 to 13. The risk is thought to be
higher still if the affected relative is a sibling. Several genes associated with POAG have been
identified, though these account for less than 5% of all POAG in the general population. It is
therefore thought that the hereditary aspect of POAG is likely to be polygenic and that geneenvironment interactions are important.

Other risk factors

A high prevalence of POAG has been found in diabetic patients, and a high prevalence of
diabetes has been found in POAG patients. However, controversy exists as to whether diabetes
truly is a risk factor for POAG, as several large population studies have found no association.
The role of blood pressure in the development of POAG is complicated and there is no
consensus. Hypertension may predispose to glaucomatous damage via increased peripheral
vascular resistance in small vessels, while a low blood pressure may reduce the perfusion
pressure of the optic disc. There is a relative paucity of data regarding the lifestyle and nutritional
epidemiology of POAG. There is a suggestion that exercise and a diet high in green collards and
with a high omega 6 to omega 3 fatty acid ratio are protective against POAG.

General Pathology
Many different abnormalities have been noted on histopathological examination of the drainage
angle in patients with POAG. These include narrowed intertrabecular spaces, thickened basement
membranes, fused trabecular beams, reduction in trabecular endothelial cells, reduction in actin
filaments, narrowing of collector channels, foreign material accumulation, scleral spur
thickening, and closure of Schlemms canal.

Pathophysiology
A commonly held view is that glaucoma is a group of conditions with varying
pathophysiological processes that share a common end-point of optic nerve head damage. There
are multiple proposed mechanisms of damage, some of which are IOP- dependent, and others are
IOP- independent.
IOP related mechanisms of damage
As discussed above, raised IOP is thought to damage the optic nerve head via induced
mechanical changes at the lamina cribrosa, or via vascular dysfunction and resultant ischemia.
There are several postulated mechanisms as to the cause of elevated IOP, the majority of which
are related to reduced aqueous outflow. Structural changes include:
Trabecular meshwork obstruction by foreign material (e.g. glycosaminoglycans, pigment, red
blood cells)
Trabecular endothelial cell loss (resulting in trabecular beams fusing)

 Loss of trabecular endothelial cell phagocytic activity

Loss of giant vacuoles from Schlemms canal endothelium
Reduced pore size and density in the wall of Schlemms canal
It has been suggested that these changes may be brought on by altered endogenous corticosteroid
metabolism (with secondary trabecular meshwork changes) or oxidative damage.
IOP independent mechanisms of damage
These include:
Reduced ocular perfusion pressure (and hence the association with vascular diseases such as
diabetes, hypertension and migraine)
Excitotoxic damage from excessive glutamate
Autoimmune-mediated nerve damage
Loss of neurotrophic factors
Failure of cellular repair mechanisms
Abnormal autoregulation of retinal and choroidal vasculature

Primary prevention
Visual loss from glaucoma is irreversible, and therefore prevention is a key strategy to
preventing morbidity from this condition.
It is recommended that people over 40 years of age should receive a baseline examination. The
patient's underlying characteristics and risk factors determine the frequency of follow-up visits.
Primary prevention of POAG has been shown to occur in the setting of OHT patients. These
patients have elevated IOP but no structural or functional evidence of optic nerve damage. Data
from OHTS and EGPS have shown that the risk of developing POAG in OHT patients can be
reduced by using topical therapy to lower IOP. Please see the table below on evidence-based
guidelines in terms of risk factors.

Not enough is currently known about the lifestyle or nutritional epidemiology of glaucoma to
inform the public of any health strategies for the prevention of glaucoma. Additional research is
required in this area.

Diagnosis
Diagnosis of POAG requires assessment of :
1. Intraocular pressure
2. Open- normal appearing anterior chamber angle
3. Characteristics signs of optic disc damage
4. visual function loss on perimetry
Frequently, the diagnosis is not clear-cut and the patient may present with some risk factors and
signs, but not others. In such cases, the patient may be labeled as a glaucoma suspect. These
patients require repeat assessments at regular intervals with the frequency of visits dependent
upon index of suspicion.

History
The majority of patients with POAG are asymptomatic. Typically, patients are only symptomatic
in late disease, when they may become aware of constricted visual field or blurred vision.
Occasionally, patients become aware of earlier visual field defects when performing monocular
tasks (such as using the viewfinder of a camera). More frequently, patients are usually diagnosed
as part of a routine eye test or as an incidental finding when presenting with another ophthalmic
condition (e.g. diabetic retinopathy). A detailed general history would reveal any causes of
secondary glaucomas (and therefore refuting POAG), such as steroid usage.

Physical examination
Physical examination consists of assessment of IOP, anterior chamber angle, optic disc and
visual field.
IOP

The gold standard for IOP measurement is Goldmann Applanation Tonometry (GAT). This is not
available in all instances, and non-contact tonometry is also frequently used. In the UK, this is
certainly true in the community where optometrists preferred method of IOP measurement is
non-contact.
Almost standard now, in conjunction with tonometry, is the measurement of central corneal
thickness (CCT). Theoretically, a thinner cornea may lead to measurements that under-estimate
true IOP and vice versa. However, the effect of CCT on IOP measurement is not predictable, and
there is no consensus as to the degree of under- or over-estimation of IOP that occurs with
thinner or thicker corneas. Moreover, CCT is only one biomechanical attribute of a cornea. For
example, a thin cornea that is very stiff may still result in over-estimation of IOP.
Newer methods of IOP measurement aim to overcome variations in corneal biomechanics and
give a more accurate estimate of true IOP. These include the Reichert Ocular Response Analyzer
(ORA) and the Pascal Dynamic Contour Tonometer (DCT). The ORA is a non-contact tonometer
that measures a biomechanical attribute of the cornea termed hysteresis. The DCT uses uses
principle of contour matching instead of applanation to reduce the effect of corneal
biomechanics.
For more information on tonometry, please see the section Intraocular Pressure and Tonometry.
Anterior chamber angle
The anterior chamber angle is assessed clinically using the slit lamp (Van Herick technique) and
with gonioscopy. Newer techniques for angle assessment include UBM (Ultrasound
Biomicroscopy) and AS-OCT (Anterior Segment Optical Coherence Tomogaphy).
Optic disc
Clinical examination of the optic disc is a very important part of the assessment of patients with
POAG. Direct ophthalmoscopy offers the most magnified view of the optic disc, but the view is
not stereoscopic. Slit lamp biomicroscopy with a lens that offers large magnification (e.g. 60
dioptre or super 66) has the advantage of giving a stereoscopic view. Stereoscopic disc
photographs offer a useful documentation of optic disc status, and also allow masked assessment
in trials. Clinical assessment of an optic disc is still considered the gold standard in the diagnosis
of POAG, though the inter-observer agreement is notoriously variable. Therefore, there is a drive
for more objective optic disc assessment such as Heidelberg Retinal Tomography (HRT) and
Ocular Coherence Tomography (OCT). Assessment of the nerve fiber layer surrounding the disc
by the GDx is also useful.
Visual field

Automated static threshold perimetry (e.g. Humphrey field analysis) is the gold standard for
diagnosis and monitoring of POAG. Various testing algorithms have been validated for POAG
and allow reduced testing time for patients (e.g. Swedish Interactive Threshold Algorithm,
SITA). Patients with early POAG may have normal visual fields on testing, and it has been
estimated that 50% of ganglion cells need to be lost before a field defect becomes apparent. This
rationale has led to development of new perimetric tests such as short-wavelength automated
perimetry (SWAP) and frequency doubling technology (FDT), which may be able to enhance
earlier detection of functional loss by targeting a specific subset of ganglion cells that have
sparse distribution.

Signs
IOP
The International Society for Geographical and Epidemiological Ophthalmology has published a
consensus definition for POAG. This definition does not include IOP - i.e. POAG is diagnosed
based on signs of glaucomatous optic neuropathy regardless of the level of IOP. Patients can be
classified as normal tension glaucoma (NTG) or high tension glaucoma (HTG) based on the
IOP. Sometimes an IOP spike may be missed in a clinical setting. In these cases, if HTG is
suspected, measurement of IOP at hourly intervals throughout the day, beginning in the early
morning, may be indicated. This is termed phasing. If a patient has all the features of POAG but
consistently normal IOPs (less than or equal to 21 mmHg), this is considered NTG (discussed
further in another section).
Anterior chamber angle
By definition, the anterior chamber angle of POAG patients is open. The Van Herick
test provides an estimate of anterior chamber depth peripherally and reveals an irido-corneal
distance of greater than 25% of corneal thickness. Gonioscopy is essential to make the diagnosis
of POAG and should be performed on the initial visit. Various classifications systems have been
described to assess the extent of an open angle. Gonioscopy helps to differentiate
POAG from secondary open angle glaucomas (such as pigment dispersion in pigmentary
glaucoma or neovascularization of the angle in neovascular glaucoma).
Optic disc
Optic disc changes seen on clinical examination of patients with POAG include:
High cup:disc ratio (Figures 1 and 2)
Cup:disc ratio asymmetry between eyes (usually considered significant if greater than 0.2)
Vertical elongation of cup

 Focal neuro-retinal rim thinning or notching (Figure 1)

Vessel bayoneting (Figure 2)
Beta-zone peripapillary atrophy
Disc hemorrhage
Photos Courtesy of Anthony Khawaja, MD, Royal Free Hospital, London, UK and Sarwat
Salim, MD, University of Tennessee, Memphis, TN, USA

Symptoms

See the section History above.

Clinical diagnosis
Advanced POAG is a relatively clinical diagnosis. Patients will have undisputable characteristic
optic nerve damage and restricted visual fields. However, visual function loss from POAG is
irreversible; therefore, it is critical to diagnose this disease as early as possible and prevent
further loss of vision. Diagnosis of early POAG is more difficult. Optic disc changes or visual
field abnormalities may be more equivocal. When the evidence for POAG is not compelling
enough to commence therapy, the patient is referred to as a glaucoma suspect and reviewed
regularly to watch for any signs of progression. An experienced clinician is able to assess clinical
examination findings in conjunction with investigation results and make a decision as to the
diagnosis. Clinical findings corresponding with investigative findings add weight to the
diagnosis of POAG. For example, Figure 1 shows the left optic disc of a patient, and Figure 3
shows the left visual field of the same patient. The thinning of the superior neuro-retinal rim of
the optic disc corresponds well with the dense inferior arcuate scotoma in the visual field. This
provides strong evidence for glaucoma.
Another important characteristic of POAG is that it is a progressive disease. If optic disc
appearances and visual field changes are static on no therapy, this would count against a
diagnosis of glaucoma.

Diagnostic procedures
Optic disc
Diagnostic procedures such as HRT, OCT and GDx are useful objective adjuncts to clinical optic
disc assessment. Quantitative measures such as neuro-retinal rim area or volume and retinal
nerve fiber layer thickness are useful for monitoring and assessing progression. Also, when
compared with normal population values, they may give some indication of diagnosis (e.g.
Moorfields Regression Analysis for HRT). This is discussed in more detail in the section Optic
Nerve and Retinal Nerve Fiber Imaging.
Visual Field
Features of visual field defects, detected on automated threshold perimetry, that are characteristic
of POAG include:
Localized defects respecting the horizontal meridian

 Nasal step
Arcuate scotoma (Figure 4)
Generalized depression
Abnormal Glaucoma Hemifield Test

Visual field testing is also useful for assessing progression. The video below shows progression
of an inferior arcuate scotoma in a patient with glaucoma over a 4 year period.

For more information, please see section Standard Automated Perimetry.

Laboratory test
At present, no laboratory tests are routinely used in the diagnosis or management of POAG.

Differential diagnosis
Differential diagnoses to consider include:
Ocular hypertension (elevated IOP but no definite signs of glaucomatous optic neuropathy)

 Normal tension glaucoma (all the features of POAG but IOP always measured within normal
limits)
Primary angle closure glaucoma (narrow drainage angle on gonioscopy)
Pigment dispersion glaucoma (Krukenberg spindle, iris transillumination, heavily pigmented
angle in all 360 degrees)
Pseudoexfoliation glaucoma (pseudoexfoliative material seen on pupil margin and lens)
Steroid-induced glaucoma (history of topical or systemic steroid usage)
Posner-Schlossman Syndrome (mild inflammation, unilateral)
Physiological cupping (normal large optic disc with large cup:disc ratio; should be symmetric)
Myopia (optic discs can be very difficult to assess, and may be associated visual field
defects which are not generally progressive)

Management
Vision loss from POAG is irreversible. Management is, therefore, aimed at slowing the
progression of the disease, thereby maintaining optimum visual function.

General treatment
The only proven treatment for POAG is lowering IOP. There is now substantial evidence from
randomized trials that lowering IOP reduces the risk of progression of POAG (Advanced
Glaucoma Intervention Study AGIS, Early Manifest Glaucoma Trial EMGT) and reduces the
risk of conversion from OHT to POAG (OHTS, EGPS). However, to date, there is no controlled
trials for POAG, with randomization to treatment or observation. A multicenter clinical trial
based in the UK is under-way which will hopefully address this. The study is comparing the rate
of progression in early POAG between patients receiving latanoprost or placebo.
IOP may be lowered by medical therapy (topical and systemic), laser therapy and surgical
procedures. There is no strong evidence supporting which of medical, laser or surgical therapy
should be given initially. For example, the CIGTS (Collaborative Initial Glaucoma Treatment
Study) showed no significant difference in outcome between patients randomized to either
medical therapy or trabeculectomy. Commonly, patients are started on medical therapy with
possible adjunctive laser therapy, and only if these measures fail is surgery considered.

Unfortunately, some POAG patients continue to progress despite lowering of IOP. This provides
some evidence that there are IOP-independent mechanisms at play. Therefore, searching for
other reversible risk factors for POAG is essential. For example, this may come from
epidemiological study of POAG and identifying lifestyle or nutritional risk factors associated
with POAG.

Brief Overview of Guidelines from Glaucoma Clinical Trials

Ocular Hypertension Study: Risk factors for development of POAG
1. Older age
2. Higher IOP
3. Greater pattern standard deviation
4. Thinner central corneal thickness
5. Larger vertical cup-disc ratio
Collaborative Normal Tension Glaucoma Study: Risk factors for progression
1. Female gender
2. Recurrent disc hemorrhages
3. History of migraines
Early Manifest Glaucoma Treatment Trial: Risk factors for progression
1. Higher IOP
2. Exfoliation
3. Older age
4. Bilateral disease
5. Worse mean deviation on VF
6. Recurrent disc hemorrhages

The Collaborative Initial Glaucoma Treatment Study (CIGTS)

1. Medical therapy was as effective as trabeculectomy
2. Quality of life surveys were similar with the two groups, with the exception of more local symptoms with trab
Glaucoma Laser Treatment Trial (GLT)
Initial laser trabeculoplasty was as effective as medical therapy
Flourouracil Filtering Surgery Study
The success of trabeculectomy was improved with postoperative use of 5FU

The Advanced Glaucoma Intervention Study (AGIS)

1. African Americans had less progression with initial laser treatment while Caucasians had better outcomes with
2. Higher IOP fluctuation was associated with VF progression
3. Reduced risk of progression was noted with IOP consistently below 18
mm Hg or largely below 14 mm Hg.

Medical therapy
Medical therapy may be topical or systemic. However, it is important to appreciate that topical
medication may cause significant systemic side effects, especially beta-blockers.
Topical therapy includes:
Alpha-agonists (apraclonidine, brimonidine)
Beta-blockers (timolol, betaxolol, carteolol, levobunolol,etc.)
Carbonic anhydrase inhibitors (brinzolamide, dorzolamide)
Miotics (pilocarpine,etc.)
Prostaglandins (latanoprost, bimatoprost, travoprost, etc.)
The most efficacious class of drops is the prostaglandin analogues. They are also the most
convenient drops with once nightly dosage. Side effects are mainly local and include hyperemia,
lengthening of lashes, darkening of iris color and peri-ocular skin pigmentation. These are
reversible on stopping the medication. The second most efficacious class of drops is the betablockers. Topical alpha-agonists, carbonic anhydrase inhibitors and miotics are much less
efficacious, rarely achieving a drop in IOP of greater than 3 mmHg.
The best locally tolerated drops are the beta-blockers, with very few patients experiencing ocular
discomfort or redness. However, beta-blockers also cause the most systemic side-effects. There is
a significant amount of systemic absorption following passage through the nasolacrimal duct.
Side effects include breathlessness, reduced exercise tolerance and falls. This is especially true
for elderly patients, which is a significant proportion of the POAG population. Therefore, nonselective beta blockers are contraindicated in patients with respiratory diseases and some cardiac
conditions.

Typical first line therapies are prostaglandin analogues and beta-blockers. Prostaglandin
analogues are more efficacious and have less systemic side effects. Beta-blockers may be
preferred in younger patients due to less local side effects, or in unilateral glaucoma to avoid
cosmetically undesirable asymmetrical side-effects (such as lash growth).
Systemic therapy includes acetazolamide (carbonic anhydrase inhibitor given orally or
intravenously) and the hyperosmotic agents (glycerin, mannitol). Oral beta-blockers lower IOP,
though are not used for this indication. However, it is important to appreciate that a patient
taking an oral beta-blocker, for hypertension for example, may have masked ocular hypertension.
Furthermore, there may be little additional benefit in prescribing a topical beta-blocker for
someone already taking an oral beta-blocker, though this may cause significantly worse sideeffects.
Please see section Medical Management for Primary Open Angle Glaucoma for more detailed
information.

Medical follow up
Once the diagnosis of POAG has been established, it is important to carefully counsel the
patient. They need to be informed of the natural history of the condition, initial asymptomatic
presentation of the disease with irreversible visual loss in cases which are not treated or under
treated. When starting a topical medication, the patient needs to understand the probability of
life-long therapy, potential side-effects, the need to use the drops every day, and the fact that they
will not notice any benefit the treatment is preventative. It is important to teach patients how to
administer drops effectively.
It is popular practice to define a target IOP for IOP lowering. This would be based on current
evidence, the stage of the patients POAG and other risk factors for progression. A reasonable
initial target is for at least 20%-30% reduction in IOP. A larger reduction may well be needed for
patients presenting with advanced disease. AGIS showed reduced risk of progression for patients
whos IOPs were consistently below 18 or largely below 15.
First review after commencing a new therapy should occur within 6-8 weeks, though the patient
should understand to present sooner if they develop any side-effects. Thereafter, 3-4 monthly
review is sufficient if the patient remains stable. At each review, the patient needs the following
assessed:
Any subjective change in vision or any side-effects
IOP is it within target?

 Signs of progression standard automated perimetry, optic disc assessment (clinical +/- HRT,
OCT)
If the patient has no side effects, the IOP is within target level and there are no signs of
progression, then a routine 3-4 month review can be arranged. If the initial therapy was not at all
effective, it should be swapped for an alternative class of drop. If the initial therapy significantly
reduced IOP, but not to target level, then an additional drop should be prescribed (or a
combination drop used). If there are signs of progression despite target IOP, the target should be
lowered further, and the patient more closely followed. If target IOP is not reached despite fully
tolerated topical medications, laser or surgical therapy should be considered.

Surgery
Non-medical interventions for POAG include:
Laser trabeculoplasty (see Laser Trabeculoplasty: ALT vs SLT)
Trabeculectomy +/- augmentation (see Trabeculectomy)
Non-penetrating drainage surgery
Shunt procedures (see section Glaucoma Drainage Implant Surgery)
Cyclodestructive procedures (cyclodiode, cyclocryotherapy)
All these therapies aim to lower IOP. Laser trabeculoplasty is a reasonable initial therapy,
especially for patients in whom compliance may be an issue. It is particular effective in patients
with pigmented drainage angles, though its long term success rate is limited. With the advent of
anti-scarring agents (5-fluorouracil, mitomycin C) for augmentation, trabeculectomy remains a
successful surgical treatment for POAG. Some studies comparing trabeculectomy to drainage
device implantation suggest improved outcomes for drainage devices, though the evidence is still
somewhat equivocal and shunt surgery is generally reserved for patients with high risk of failure
from trabeculectomy (e.g. previous trabeculectomy, uveitis, aphakia). Non-penetrating drainage
surgery is thought to be safer that standard trabeculectomy, but less efficacious in IOP lowering.
Cyclodestructive procedures are generally reserved for eyes in which all other measures have
failed, or in eyes with poor visual potential. This is due to the risk of long-term hypotony.

Surgical follow up

Early surgical follow up is discussed in the individual sections on the surgical procedures.
Longer term surgical follow up is similar to the assessment described above under Medical
follow up. Essentially, 3-4 month review is sufficient for patients with target IOP and no signs of
progression. If target IOP is not reached, or there are signs of progression, further therapy is
required.

Prognosis
Untreated POAG can lead to irreversible blindness. There is not much data on the natural history
of POAG, as it is considered unethical to not treat patients with advanced disease. One study in
St Lucia found that 35% of untreated eyes progressed to end-stage disease over 10 years. There
is strong evidence that lowering IOP can reduce the rate of progression significantly. During 6
years of the EMGT, 53% progressed, though treatment reduced the rate of progression by half,
and for each mmHg of IOP lowering achieved, the rate was reduced by 10%. Progression is
noted to be worse in patients with more advanced disease at baseline. This may be because an
already damaged disc is more susceptible to further damage, or simply that as there are fewer
ganglion cell axons, each further one lost has a greater impact on function.
The rate of progression and risk of blindness may be hard to predict in individual patients. Some
patients progress despite strict target IOPs, whereas others may remain static despite higher IOP.
Observing a patients rate of progression and tailoring therapy according to this is a pragmatic
approach to POAG. Risk factors for progression include:
Higher degree of optic nerve damage
Higher IOP
Positive family history of visual loss from POAG
Presence of a recognized gene for POAG
Poor compliance and access to good health care
Longer life expectancy
Presence of systemic cardiovascular disease

Additional Resources
International Glaucoma Association
NICE (National Institute for Health and Clinical Excellence) guidelines

European Glaucoma Society

References
Denniston A, Murray P. Oxford Handbook of Ophthalmology. Oxford, United Kingdom: Oxford
University Press; 2006:276-277.
Rhee D. Glaucoma: Color Atlas and Synopsis of Clinical Ophthalmology. New York, NY:
McGraw-Hill; 2002:204-229.
Schacknow P, Samples J. The Glaucoma Book: A Practical, Evidence-Based Approach to
Patient Care. New York, NY: Springer; 2010:399-420.
Stamper R, Lieberman M, Drake M. Becker-Shaffers Diagnosis and Therapy of the Glaucomas.
8th Edition. New York, NY: Mosby; 2009:239-265.
Categories:

Articles

Glaucoma

What links here

Related changes

Special pages

Printable version

Permanent link

Page information

This page was last modified on September 30, 2014, at 10:33.

This page has been accessed 49,965 times.

Privacy policy

About EyeWiki

Disclaimers