NewGradOptometry the basics of glaucoma pdf

NEWGRADoptometry

The Basics of
Glaucoma for the
General Practitioner
Kevin Cornwell, OD


The Basics of Glaucoma for the General Practitioner

A Basic Introduction to Glaucoma Management
The glaucomas are a class of ocular disease characterized by progressive optic
nerve degeneration with subsequent loss in retinal nerve fiber layer (RNFL) and
retinal ganglion cells (RGCs). It is the leading cause of irreversible blindness
worldwide, affecting over 60 million people. As primary eye care providers on the
front lines of ocular disease management, it is important for us to have an arsenal
of management strategies at our disposal. By having a thorough understanding of
glaucoma’s pathophysiology and various treatment options, we are able to provide
better education and treatment options for our patients. In this article we will dive
a bit deeper into addressing a patient’s risk factors and specifically tailoring their
treatment plan.
At this time, there is no definitive cure for glaucoma; however, when caught early
in the disease process, most practitioners are able to preserve their patients’ vision
and quality of life. Currently, the reduction of intraocular pressure (IOP) is the only
evidence-based treatment for glaucoma.
The primary care optometrist will likely encounter two common types of glaucoma,
either primary open angle glaucoma (POAG), or normal tension glaucoma (NTG).
More rare are cases of acute angle closure glaucoma (AACG) and neovascular
glaucoma (NVG).

Pathophysiology

POAG pathogenesis is primarily thought to be caused from elevated eye pressure
or ocular ischemia, while NTG pathogenesis is more likely attributed to ocular
ischemia. Several causes of ocular ischemia are nocturnal hypotension, metabolic/
cardiovascular disease, and sleep apnea. For these reasons it is important to assess
a patient’s vasculopathic risk factors and treat/educate accordingly. While some
practitioners continue to refute the link between diabetes and glaucoma,2-14 the
American Academy of Ophthalmology agrees that type 2 diabetes is a risk factor
for POAG.1 Some commonly used POAG risk calculators are now even including
diabetes into their calculations for risk of developing glaucoma.28
AACG occurs when patients with narrow anterior chamber angles (eg. hyperopes or
advanced cataracts) have transient or permanent occlusion of the angle causing a
rapid spike in IOP and subsequent irreversible optic nerve damage (over hours to
days). It is best to refer patients with narrow angles for laser peripheral iridotomy
and/or cataract surgery if you feel they are at risk for angle closure (to prevent an
acute episode and permanent vision loss). Patients with untreated or recurring
uveitis/iritis are also at risk for AACG due to the formation of anterior or posterior
synechiae.
NVG occurs when the anterior chamber angle is partially or completely occluded
from the abnormal formation of blood vessels within the angle (eg. vein occlusions
or uncontrolled metabolic disease).

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Glaucoma (POAG/NTG) is often a slow, painless, progressive disease that takes
place over years to decades. However, some patients who experience acute angle

closure or NVG (of any etiology) will often complain of severe ocular pain, increased
pressure, photophobia, and hazy/cloudy vision.
Table 1. Evidence-based risk factors for the development of open angle glaucoma1
Myopia/peripapillary atrophy20

Age

Elevated IOP

Thinner central
corneal thickness (CCT)24

Metabolic syndrome/Diabetes2-14

Cup-to-disc asymmetry

Positive family history

Pseudoexfoliation29

Pigment dispersion syndrome

Reduced corneal hysteresis

Cardiovascular disease15

Smoking16-19

Latino/Hispanic or
African Ancestry22,23

Disc Hemorrhage21

Lower Systolic/Diastolic
Blood Pressure

Fig 1. Peripapillary atrophy and high myopia are considered risk factors for developing glaucoma20

Fig 2. Nerve fiber hemorrhages at the optic disc, aka “drance hemes” are also pathognomonic for glaucoma.
These can predict areas of impending nerve fiber damage, subsequent erosion of the neuroretinal rim, and
are also considered a strong risk factor for POAG progression.21

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TIP: Take advantage each time you have your patient
in your office to examine the disc for drance hemorrhages.
If found, this will be a red flag of an area to watch more
closely in the future for rim erosion, whether
through thinning of the rim on clinical exam, wedge
defects seen on fundus photography, RNFL thinning on
OCT or eventually visual field loss.

Another emerging field in the research of glaucoma pathophysiology is
investigating the relationship between intraocular pressure (IOP) and intracranial
pressure (ICP). While first described in the early 1970s, this theory suggests that
changes in ICP, relative to IOP, creates a difference in trans-lamina cribrosa
pressure (leading to optic nerve cupping). In other words, if IOP is greater than the
retrolaminar pressure (ICP), this pressure difference could result in glaucomatous
optic neuropathy.25, 26 There is also an age related decline in ICP which may partially
explain glaucoma being more prevalent in older populations.27
The relationship between IOP and ICP has also been of great interest as a means of
explaining the phenomenon of optic disc swelling and elevated ICP in astronauts.
This is referred to as spaceflight-associated neuro-ocular syndrome (SANS).
Another example of optic nerve pathology related to intracranial pressure is that
seen with cases of idiopathic intracranial hypertension (IIH).

Making a Diagnosis
When deciding when to make a diagnosis of glaucoma or initiate treatment based
on high risk, there are a number of factors to be accounted for.
1. Nerve appearance, specifically vertically elongated cup-to-disc ratios are
more suspicious of glaucoma. Now, a nerve can be vertically elongated
(especially if the disc is also vertically oval in shape) without being
glaucomatous. Examine for notches, early signs of thinning, bared vessels or
drance hemorrhages for additional signs of glaucoma.
2.A difference in vertical c/d of greater than 0.2 between right and left eye.
3.Intraocular pressure.

4.Central corneal thickness.
5.Visual field results.
6.RNFL OCT findings. If documented progression on repeated testing can be
proven, your case is much stronger for the patient having glaucoma.
According to the Ocular Hypertension Treatment Study (OHTS), central corneal
thickness (CCT) plays a significant role in determining a patient’s true IOP.
According to OHTS, physiologically thinner corneas, typically those less than 545550 micrometers, are an independent risk factor for developing glaucoma.24

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Fig. 3 Most OCT machines today have an anterior segment feature, which allows the
practitioner (or ophthalmic technician) to acquire non-invasive pachymetry readings
via the drawing tool (billable procedure).

It is also important to remember that POAG/NTG should never be diagnosed based
on only one visual field test, one IOP measurement, or one OCT scan. Results
from OHTS suggests performing 3 consecutive, reliable visual field tests prior to
definitively saying a patient has glaucomatous field loss.
Careful assessment for pigment dispersion syndrome is also important when
determining a patient’s overall risk for developing POAG. The presence
of krukenberg spindles – excessive pigment on corneal endothelium,
iris transillumination defects (best appreciated viewing undilated iris on
retroillumination), and excessive pigment within the angle, noted on gonioscopy,
all point to pigment dispersion syndrome and increased risk for elevated IOP.
The presence of pseudoexfoliation is another risk factor for elevated IOP and

POAG development and is best assessed with a dilated pupil. Patients with
pseudoexfoliation tend to have greater diurnal fluctuations in IOP.29
Patient ethnicity is another factor to consider when deciding to treat. Since the
African American population tend to have larger vertical cup-to-disc ratios and
thinner CCTs, they may benefit from earlier treatment of ocular HTN vs. patients of
other ethnicities.24



Stereoscopic evaluation of the optic nerve head should
be the foundation of the glaucoma work-up, since up to
40% of patients with “normal” IOP can have
glaucomatous optic neuropathy. This can be VERY difficult
to do with monocular, undilated views.






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Fig 4. Sometimes shallow cupping can make the neuroretinal rim appear deceptively normal. Utilizing the
slit lamp’s red-free filter during biomicroscopy can help practitioners better assess the patient’s rim tissue.
Obtaining photos of the fundus/optic nerves can also be a useful tool, providing an alternate perspective.

Remember that glaucoma produces the classic erosion/cupping of the rim tissue, while other etiology is
usually responsible for pallor/atrophy of the optic disc. Only in advanced stages of POAG will practitioners
appreciate a trace pallor of the neuroretinal rim. If disc pallor is present disproportionately to the amount of
cupping, it is prudent to shift your work up for non-glaucomatous optic neuropathy, instead of POAG.

Treatment Goals: What is “Target IOP”?
While every practitioner may have a slightly different approach for glaucoma
management, it is important to have one that is evidence-based while also realistic
for your individual patient’s lifestyle. Since the reduction of IOP is the only proven
treatment for glaucoma, it is important to have some type of criteria to use in
determining your goal IOP for that particular patient.
Some practitioners (including glaucoma specialists) will simply say, “I want to
achieve an eye pressure that stops the progression of glaucoma.” Others will have
a predefined formula, such as “30% reduction from the maximum IOP reading or
average of multiple readings.” The name of the game in treating glaucoma is to
prevent visual field degradation while also preserving quality of life. Having a goal
for the patient’s treated IOP is important and helps the practitioner assess whether
or not the current treatment strategy is effective or if it needs to be altered.

Fig. 5 In order to establish a target IOP for the patient, its best to obtain at least 3 or 4 untreated IOP
readings, preferably with Goldmann tonometry. For patients who strain to comfortably position themselves
in our slit lamp, practitioners may obtain more accurate IOP readings from handheld tonometers such as the
Perkins model.

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While “normal” IOP can range from 10mmHg to 21mmHg,30,31 the higher a
patient’s baseline IOP usually equates to a greater risk of glaucoma development.
Practitioners must also take into consideration a patient’s CCT in order to truly
assess IOP.30,31





There is no definitive study that says reducing a patient’s
IOP by X% is guaranteed to eliminate all risk of progression.
There is, however, a multitude of clinical pearls we can take
away from the major glaucoma treatment trials.

Table 2. Summary of major glaucoma treatment trials

Ocular hypertension
treatment study (OHTS)

Only ~10% of patients with ocular hypertension will develop glaucoma
over 5 years
20% IOP reduction results in half the risk of converting from ocular
hypertension to POAG over 5 years (from 9.5% risk vs. 4.4%)

Early manifest
glaucoma trial (EMGT)

Progression occurred in 45% of tx group vs. 62% w/o tx over 5 years
Tx group = IOP reduction of ~25% (5.2mmHg)

Pseudoexfoliation doubles the risk of converting from ocular hypertension to glaucoma (57.1% vs. 27.6%) – regardless of baseline IOP
>10% risk reduction per each 1mmHg reduction in IOP

Collaborative initial glaucoma
treatement study (CIGTS)

2 tx groups: Medical (>35% IOP reduction) vs.Surgical
(>40% IOP reduction)
10% of medical tx showed increased cupping vs. 1% of surgical tx, over 5
years
Overall visual field progression same in both groups
Optimal IOP reduction ~35% (diminished returns thereafter)
IOP deviations >8.5 mmHg had double the risk of progression

Advanced Glaucoma
Intervention Study (AGIS)

IOP < 18 mm Hg maintained over 8 years showed no VF progression
Mean IOP was 12.3 mmHg for group that did not progress
IOP deviations <3 mmHg progressed less vs. > 3 mmHg

Preferred practice guidelines from the American Academy of Ophthalmology
state that a target IOP reduction of 20% from baseline is recommended for
glaucoma suspects.1 The American Optometric Association recommends a 30% to
50% reduction of pre-treatment IOP for managing glaucoma, depending on the
patient’s stage/severity and rate of progression.32
Prostaglandin analogues have been shown to reduce IOP by 28-33%, while beta
blockers and carbonic anhydrase inhibitors have a slightly smaller IOP lowering
effect of just 15-20%.31
Unfortunately, despite significant IOP reduction, some glaucoma patients will

progress while other untreated patients will not.31

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Assessing our patient’s other comorbidities and systemic diseases is also important
with our glaucoma management plan. Addressing metabolic dysfunction,
cardiovascular disease, and smoking cessation can all help restore ocular perfusion
and potentially improve treatment outcomes. Referring patients to primary care,
behavioral health, and/or nutritionists can also help foster a multidisciplinary
approach in the management of glaucoma.
Table 3. Commonly prescribed eye drops in medical glaucoma treatment and management
Drug Class

Prostaglandin analogues

Carbonic anhydrase
inhibitors

Mechanism of action

Typical Dose

Contraindication

Increased uveoscleral

outflow

QHS

Uveitis/iritis/herpes simplex keratitis

Increased uveoscleral
outflow

BID

Periopertively (eg. before/after cataract
surgery) - increased CME risk
Sulfa allergy
Kidney stones
Aplastic Anemia, thrombocytopenia,
sickle cell disease

Beta Blockers

Increased uveoscleral
outflow

QD vs BID

Any breathing problems (eg. asthma
or COPD)
Bradycardia, hypotension, congestive
heart failure

Alpha-2 agonists

Increased uveoscleral
outflow

BID vs TID

Ocular hypersensitivity reaction from
A2 agonists
Monoamine oxidase inhibitor tx

Patients who you suspect may have NTG should have their blood pressure checked
in-office. Practitioners working in multidisciplinary settings can also review the EHR
for vital signs/BP taken at other encounters. It is important to assess a patient’s
risk for nocturnal hypotension. To your surprise, your NTG patient may be on 3 or
4 blood pressure medications, some of which are taken in the evening. Some of
these patients may achieve adequate blood pressure with less medication or an
alternative dosing schedule. It is important to communicate with the patient’s PCP
and explain your concern for mitigating risk of pathological nocturnal hypotension,
and subsequent glaucoma progression.

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Visual Field (VF) Testing & Optical
Coherence Tomography (OCT)

In the initial stages of monitoring patients who you suspect may have glaucoma,
obtaining a 24-2 Humphrey VF and OCT scan of the optic nerve/RNFL is a great
place to start. If the practitioner is concerned for any paracentral defects involving
fixation (eg. compromised ganglion cell count on macular OCT), it is prudent to
also perform a 10-2 VF. While most glaucoma patients will initially lose peripheral
vision (eg. nasal steps, arcuate scotomas) some patients may actually lose central
vision first (eg. paracentral, centrocecal scotoma) due to RNFL loss in the macular
vulnerability zone.33 Since 50% of all retinal ganglion cells are within the central 8
degrees of fixation, the 10-2 VF is more sensitive at detecting glaucomatous defects
involving fixation. The 24-2 VF spaces test points 6 degrees apart, while 10-2 VF
testing spaces points only 2 degrees apart.

Fig 6. With frank notching or erosion of the neuroretinal rim, patients will present with corresponding
visual field defects that mirror the glaucomatous optic neuropathy. Assessing the ganglion cell count
on macular OCT scan can also be a useful tool when assessing a glaucoma risk, or determining the
presence or progression of central visual field defects. The inferotemporal portion of the ganglion cell
layer within the macula is referred to as the macular vulnerability zone33 - correlating with superior
centrocecal defects as shown above.

During the initial glaucoma workup, it is not uncommon to conduct 3 or more 24-2
VF tests over the course of 12 months.
Patients who struggle with formal VF testing may benefit from repeated
explanations of the test, hearing a repeated dialogue during the test — “you’re
doing great, don’t move your eyes or head,” or even alternating testing spot size,
such as increasing to size 5 vs. size 3 default. Increasing spot size can also be
beneficial in monitoring patients with more advanced glaucoma. To avoid fatigue
and improve testing reliability, practitioners can also alternate which eye is tested
first, especially if you’re initially only concerned about one eye. Due to spectacle
mag and distortion of the visual field, patients with high refractive error (+/- 7.00
diopters) maybe perform better with a contact lens during the test.

When you’ve repeated numerous VF’s and continue obtain unreliable results, it may
be time to switch to relying on objective testing in your glaucoma management
plan. This primarily includes serial IOP readings and OCT scans, as well as
pachymetry and gonioscopy.

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Fig 7. Inferior notching with corresponding classic superior arcuate defect shown on 24-2 visual field
testing. Given this visual field defect involves fixation, periodic 10-2 visual fields will also be obtained
to better assess progression. Remember that glaucomatous VF defects will always respect the
horizontal meridian, while non-glaucomatous optic neuropathy typically respects the vertical meridian.

Fig. 8 Performing gonioscopy is also important as part of the diagnosis of primary open angle
glaucoma. Sure, the angle may look wide open on a Van Herick assessment, but performing
gonioscopy allows the practitioner to detect an angle abnormalities such as angle recession
or neovascularization, as well as determine level of pigmentation. More pigment present in the
angle can improve outcomes of SLT laser treatment.

Tips to Improve Compliance
Sometimes holding patients accountable for taking their glaucoma drops can
improve compliance. This can be done simply by making a spreadsheet/grid with
your office’s header at the top, and includes the names, dates, and times of all
drops prescribed (similar to a journal).
Collaborating with spouses, caretakers, or other family members can also be a
useful way to maintain compliance with topical glaucoma treatment.

Right off the bat, if patients flat out tell you they’re not interested in committing to
using eye drops on a routine basis, or you suspect there will be poor compliance,
a referral to ophthalmology is your best bet. Optometrists can explain other
treatment options to the patient and opt for referral to have the patient undergo
selective laser trabeculoplasty (SLT) or even MIGS if the patient will be undergoing
cataract surgery. Cataract surgery alone can also drop intraocular pressure by
several points, even putting the patient within your target IOP range.

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Minimizing the treatment burden for the patient is key to successful outcomes.
Unfortunately, most patients will not be compliant with taking three or more eye
drops on a daily basis. For this reason, most practitioners will always start with
a prostaglandin analogue (generic version ok) dosed just once in the evening.
Sometimes patients will ask if a specific time is really important, and most ODs will
agree simply 1 drop in each eye “in the evening” will suffice. Whether it’s before
or after dinner, walking the dog, or their favorite television show, is really up to
the patient. Also, the difference in therapeutic IOP reduction with prostaglandins
is somewhere around 1mm Hg when taken in the AM vs. PM, therefore taking
them ANY TIME of day is more efficacious than poor compliance in the evening as
typically directed.

Fig 9. Primary open angle glaucoma of the right eye, with superotemp RNFL wedge defect and
correlating RNFL thinning on OCT. Interpret OCT test results in context with the visual field and
your stereoscopic assessment of the patient’s optic nerve. Never diagnose glaucoma solely on the

OCT scan alone (eg. “red disease”). The reference ranges of the OCT do not scale across all patient
races/demographics, and therefore must be factored into the larger clinical picture.

Overall, treating glaucoma can be a challenging but rewarding experience for both
the practitioner and patient. Offering to manage and treat glaucoma can also be
an excellent practice builder. It is important to have the full clinical picture before
making a definitive diagnosis. While IOP reduction is currently the only evidencebased treatment for glaucoma, it is important to assess your patient’s other
systemic risk factors and comorbidities. With a thorough work up and systematic
approach, your patients with POAG or at risk for developing glaucoma will greatly
benefit from your expertise as their primary eye care provider.

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