Glaucoma, Open-Angle
than whites). There is a genetic tendency to
BASIC INFORMATION
DEFINITION
Glaucoma is a chronic degenerative optic neu-
ropathy (or the high potential for such degenera-
tion due to risk factors) in which the neuro-retinal
rim of the optic nerve becomes progressively
thinner, thereby enlarging the optic-nerve cup.
The classification of glaucoma is based on
the appearance of the iridocorneal angle (open
angle vs. closed angle) and is further subdi-
vided into primary and secondary types. Primary
open-angle glaucoma can occur with or without
elevated intraocular pressure (IOP). Normal ten-
sion glaucoma refers to primary open-angle
glaucoma without elevated intraocular pressure.
SYNONYMS
Primary open-angle glaucoma (POAG)
Open-angle glaucoma (OAG)
Secondary open-angle glaucoma (e.g., pseu-
doexfoliation, pigment dispersion, trauma,
inflammatory)
Chronic open-angle glaucoma
ICD-10CM CODES
H40.10X0 Unspecified open-angle glaucoma,
stage unspecified
H40.10X1 Unspecified open-angle glaucoma,
mild stage
H40.10X2 Unspecified open-angle glaucoma,
moderate stage
H40.10X3 Unspecified open-angle glaucoma,
severe stage
H40.10X4 Unspecified open-angle glaucoma,
indeterminate stage
H40.11X0 Primary open-angle glaucoma,
stage unspecified
H40.11X1 Primary open-angle glaucoma,
mild stage
H40.11X2 Primary open-angle glaucoma,
moderate stage
H40.11X3 Primary open-angle glaucoma,
severe stage
H40.11X4 Primary open-angle glaucoma,
indeterminate stage
EPIDEMIOLOGY &
DEMOGRAPHICS
INCIDENCE (IN U.S.): Third most common
cause of vision loss (75% to 95% of all forms of
glaucoma are open angle)
PEAK INCIDENCE:
• Increases after age 40 yr
• Three million cases expected by 2020 because
of the rapid increase in aging population
PREVALENCE (IN U.S.):
• Overall prevalence in U.S. population aged
>40 yr is estimated to be 1.86%, with 1.57
million white and 398,000 black patients
affected. By 2020, we may expect more than
3 million cases in the U.S.
• 150,000 patients have bilateral blindness.
• Prevalence is higher in diabetics, those with
high myopia, and older persons.
• More common in African-American popula-
tion (three times the age-adjusted prevalence
Descargado para Felipe Calderón Avendaño (felipe.calderon.a@usach.cl) en Universidad de Santiago de Chile de ClinicalKey.es por Elsevier en junio 21, 2017.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2017. Elsevier Inc. Todos los derechos reservados.
519
IMAGING STUDIES
OAG; multiple genes have been isolated that
are associated with development of high IOP
and optic nerve damage.
PREDOMINANT AGE:
• Persons >50 yr
• Can occur in 30s and 40s, and juvenile forms
are rare
PHYSICAL FINDINGS & CLINICAL
PRESENTATION
• High intraocular pressures and/or large optic
nerve cup (Ocular Hypertension Treatment Study
results help to delineate important risk factors).
• Abnormal visual fields (with advanced glau-
coma damage to the optic nerve).
• Open anterior chamber angle—evaluated
with gonioscopy.
• Since early treatable stages of OAG normally
have no symptoms, it’s important to have
routine eye exams, especially patients with
family history and patients over 60 yr.
• Secondary forms of OAG may exhibit ocular
findings such as pseudo-exfoliation, pig-
ment dispersion, blood in anterior chamber,
inflammation.
ETIOLOGY
• Uncertain hereditary tendency (multifactorial
genetics).
• Topical steroids can induce high IOP and
cause glaucoma.
• Trauma.
• Inflammatory (e.g., history of uveitis).
• High-dose oral corticosteroids taken for pro-
longed periods.
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
• Other optic neuropathies (previous retinal vas-
cular disorders, optic nerve pits, or coloboma).
• Physiologic cupping of the optic nerve: The
optic nerve may appear similar to glaucoma
damage but does not progress. This is fol-
lowed for any signs of progression.
• Ocular hypertension: IOP is chronically ele-
vated, but not causing optic nerve damage,
must monitor closely.
• Secondary glaucoma from inflammation and
steroid therapy.
• Trauma.
WORKUP
• Comprehensive eye examination
• Intraocular pressure
• Slit lamp examination
• Visual fields
• Gonioscopy: to determine the type of glaucoma
• Nerve fiber analysis (e.g., GDx, OCT, and HRT)
• Corneal thickness (thick central cornea will
result in possible overestimation of the true
physiologic IOP, and vice versa, so this is
important information in diagnosis and treat-
ment of OAG)
LABORATORY TESTS
Blood sugar
• Optic nerve photography—stereo photo-
graphs (Fig. E1).
G
• Visual field testing.
• Laser scan of nerve fiber layer, OCT, HRT.
Rarely, MRI of orbits if the glaucoma findings
are atypical or suspicious of other causes of
optic nerve atrophy (Fig. E1).
TREATMENT
ACUTE GENERAL Rx
and Disorders
Diseases
• β-blockers (e.g., timolol) qd to bid depending
on individual response to drug.
• Carbonic anhydrase inhibitors (e.g., Diamox
250 mg qid or 500 mg bid).
• Prostaglandin analogues (latanoprost, bima-
toprost, travoprost, tafluprost) are commonly
used as first-line treatment. They lower intra- I
ocular pressure by 25% to 30% by increasing
uveoscleral outflow and reducing aqueous
production.
• Alpha-2 agonists and cholinergic agonists.
• Hyperosmotic agents (mannitol) in acute
treatment (IV).
• Selective laser trabeculoplasty (SLT) may
delay or forestall need for second eyedrop.
The effect may be temporary but the laser
can be repeated.
CHRONIC Rx
• At least biannual checks of intraocular pres-
sure and adjustment of medication.
• Surgical trabeculectomy and filter valve sur-
geries can be considered for glaucoma that
progresses (optic nerve changes or visual
field progression) despite maximal toler-
ated medical therapies. Recently, minimally
invasive glaucoma surgeries (MIGS) have
been advocated for IOP control. Some are
performed at the time of cataract procedures
and some are independent procedures. The
effort is to reduce the risks associated with
traditional trabeculectomy.
DISPOSITION
Must be followed by ophthalmologist.
REFERRAL
Immediately to ophthalmologist.
PEARLS &
CONSIDERATIONS
COMMENTS
• Glaucoma is a serious blinding disease that
must be monitored professionally by an
ophthalmologist. It is mostly asymptomatic
until late in the disease when visual problems
arise. Even in developed countries half of
glaucoma cases are undiagnosed.
• Risk factors that should prompt referral to an
ophthalmologist for evaluation of glaucoma
are high intraocular pressure, family history
of glaucoma, use of systemic or topical corti-
costeroids, older age, and black race.
520 Glaucoma, Open-Angle
• Vision loss from glaucoma cannot be recov- Potential sites of increased resistance to SUGGESTED READINGS
ered. Early diagnosis and treatment may aqueous flow are described in Fig. 2. Available at www.expertconsult.com
minimize visual loss.
• Glaucoma is not solely caused by increased RELATED CONTENT
intraocular pressure because approximately EVIDENCE Glaucoma (Patient Information)
20% of patients with glaucoma have normal
Available at www.expertconsult.com
intraocular pressure. However, high pressure AUTHOR: R. SCOTT HOFFMAN, M.D.
is definitely a risk factor to be considered.

2 3 4 5

1 Ciliary body processes (when ciliary body swollen by congestion), fibrin

debris, vitreous face against the lens equator
2 Pupillary block by anterior position of lens or swollen lens
3 Pretrabecular by neovascular or cellular membranes
4 Trabecular by abnormal accumulation of extracellular matrix
5 Post-trabecular by increased episcleral venous pressure

FIG. 2  Potential sites of increased resistance to aqueous flow. (From Yanoff M, Duker JS: Ophthalmology, ed 2,
St Louis, 2004, Mosby.)

Descargado para Felipe Calderón Avendaño (felipe.calderon.a@usach.cl) en Universidad de Santiago de Chile de ClinicalKey.es por Elsevier en junio 21, 2017.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2017. Elsevier Inc. Todos los derechos reservados.
Glaucoma, Open-Angle
EVIDENCE
Abstract[1]
Ocular hypertension is a common and important problem seen by eye
care providers. This review presents a practical approach to individuals
with ocular hypertension. It describes the common functional and struc-
tural investigations used in evaluation, as well as the advantages and
disadvantages of each test. This review also discusses several landmark
studies on ocular hypertension and provides a practical guide to the
management of this problem.
This article is an excellent review of the pertinent information we use
to guide management of glaucoma suspects. Although the factors
weighed to determine treatment decisions for these patients are familiar,
it is helpful to flesh out the details. As an example, central corneal thick-
ness (CCT) is well known to influence the risk of glaucoma. However, its
application may be variable in clinical practice. The clinical definition of
thin vs thick CCT is not standardized, and different practitioners may use
different thresholds. Although no algorithm has been proven useful for
adjusting intraocular pressure measurement for CCT, some doctors still
use them. Controversy may be found in the fine points of even broadly
accepted tenets of glaucoma care, and looking at a review of the evi-
dence is enlightening. The authors take on risk calculators, disc photog-
raphy, Heidelberg retinal tomography, optical coherence tomography
(including recent and important work regarding new ways to define the
optic disc margin using Bruch membrane opening), and perimetry. In a
perfect world, specific evidence-based guidelines would make it simple
to analyze the risk to an individual patient and the most cost-effective
way, on a societal basis, to determine when and whom to treat. We are
not there yet.
S. Fudemberg, MD
Abstract[2]
Purpose:
To investigate clinical characteristics and progression rates of the initial
central scotomas (ICS) compared with the initial peripheral scotomas
(IPS) in normal-tension glaucoma (NTG) patients.
Methods:
Among NTG patients showing a single hemifield defect and who per-
formed more than five reliable standard visual field (VF) tests, medical
records of ICS (involvement of ≥3 adjacent points with P<5% within the
central 12°of fixation and one point with a P < 0.01 within the central 6°
of fixation) (n=32) or IPS (no VF abnormality within the central 6° of
fixation) (n=34) were retrospectively analyzed. The changes of mean
Descargado para Felipe Calderón Avendaño (felipe.calderon.a@usach.cl) en Universidad de Santiago de Chile de ClinicalKey.es por Elsevier en junio 21, 2017.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2017. Elsevier Inc. Todos los derechos reservados.
520.e1
thresholds from 10 zones of the glaucoma hemifield test, central 6° and
12° zones, peripheral zones other than central 6° and 12°, and the entire
hemifield were inspected. To calculate the progression rates, linear
mixed-effect model was employed.
Results:
There were no significant differences between the two groups in age,
gender, ocular factors including baseline/mean treated intraocular pres-
sure, and systemic factors including systolic or diastolic blood pressure/
perfusion pressure, mean ocular perfusion pressure (all P > 0.05). There
were no significant differences in baseline mean deviation and pattern
standard deviation (P>0.05) between the two groups, but VF index was
significantly lower in ICS group than in IPS group (P=0.001). The pro-
gression rates between the two groups were not significantly different in
all zones we investigated (all P>0.05).
Conclusions:
Newly diagnosed cases of NTG with ICS may not differ from those with
IPS in clinical characteristics and progression rates under treatment. B
Evidence-Based References
1. Boey PY, Mansberger SL: Ocular hypertension: an approach to assessment and
management, Can J Ophthalmol 49:489–496, 2014.
2. Cho H-K, Lee J, Lee M, et al.: Initial central scotomas vs peripheral scotomas
in normal-tension glaucoma: clinical characteristics and progression rates, Eye
28:303–311, 2014. B
SUGGESTED READINGS
Gupta D, Chen PP: Glaucoma, Am Fam Physician 93(8):668–674, 2016.
Quigley HA: Glaucoma, Lancet 377:1367–1377, 2011.
Weinreb RN, et al.: The pathophysiology and treatment of Glaucoma, JAMA
311(18):1901–1911, 2014.
 A B
Single Field Analysis Eye: Left
Name:
ID:
Central 24-2 Threshold Test

Fixation Monitor: Gaze/Blind Spot Stimulus: III, White Pupil Diameter: 4.8 mm Date: 02-09-2013
Fixation Target: Central Background: 31.5 ASB Visual Acuity: Time: 9:04 AM
Fixation Losses: 9/14 xx Strategy: SITA-Fast RX: +2.75 DS +1.50 DC X 158 Age: 79
False POS Errors: 0%
False NEG Errors: 15%
Test Duration: 05:51

Fovea: OFF
8 <0 5 7

20 24 11 13 <0 7

23 25 23 25 21 16 <0 <0

23 20 20 28 27 12 14 11 2
30
∇
30
<0 0 27 30 29 26 25 24 22

<0 28 27 28 28 26 23 18

21 25 23 26 27 23

<0 3 7 <0

-17 -28 -21 -19 -13 -24 -17 -15

-6 -4 -17 -15 -30 -21 -3 0 -14 -11 -27 -17 *** Low Test Reliability ***
-5 -4 -7 -5 -9 -14 -31 -30 -1 0 -3 -1 -6 -10 -28 -26
GHT
-6 -11 -3 -5 -19 -16 -18 -24 -3 -7 0 -1 -15 -13 -14 -20
Outside Normal Limits
-31 -4 -2 -3 -5 -6 -5 -4 -28 -1 2 0 -2 -2 -1 0

-31 -2 -4 -3 -3 -5 -7 -10 -28 1 0 0 0 -1 -4 -7

VFI 75%
-8 -5 -7 -4 -3 -6 -5 -1 -4 0 1 -3

-31 -26 -22 -30 -27 -22 -19 -27 MD -11.85 dB P < 0.5%
PSD 10.02 dB P < 0.5%

Total Deviation Pattern Deviation

< 5%
< 2%
< 1%
< 0.5%

 2010 Carl Zeiss Meditec

C HFA II 750-41202-5.1.2/5.1.2

FIG. E1  Moderate to marked glaucoma. A and B, Stereo disc photographs showing inferior neuroretinal rim
shelving; C, visual field from the same eye showing superior arcuate scotoma and nasal step (but note sub-
optimal reliability);
Descargado para Felipe Calderón Avendaño (felipe.calderon.a@usach.cl) en Universidad de Santiago de Chile de ClinicalKey.es por Elsevier en junio 21, 2017.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2017. Elsevier Inc. Todos los derechos reservados.
Glaucoma, Open-Angle 520.e3

Patient: Disease: Operator:

DOB(age): Ethnicity: Caucasian Algorithm Ver: A6, 11, 0, 12
ID: Gender: F Physician:

OD GCC Significance Optic Nerve Head Map

ST SN RNFL Parameters OD OS
140 113 Avg. RNFL 96.92 84.80
Sub. Avg 104.50 104.97
Inf. Avg 89.33 64.62
NU
TU
93 71
Nerve Head Parameters OD OS

Rim Volume (mm ) 0.135 0.066

Nerve Head Vlm (mm ) 0.308 0.157

T N
Fovea Cup Volume (mm ) 0.031 0.052
71 55
TL NL
Nerve Head Parameters OD OS
Optic Disk Area (mm ) 1.87 1.56
127 104 Cup/Disc Area Ratio 0.31 0.32

IT IN Horizontal C/D Ratio 0.61 0.97

Vertical C/D Ratio 0.56 0.74

TU ST SN NU NL IN IT TL Rim Area (mm ) 1.29 1.07

200
Cup Area (mm ) 0.58 0.49
100
p >5% within Normal
0
T S N I T p <5% Borderline
p <1% Outside Normal
Exam Date: 01/10/2013, SSI= 44.7 Exam Date: 01/10/2013, SSI= 40.7
OS GCC Parameters OD OS
Optic Nerve Head Map GCC Significance Avg. GCC(µm) 83.24 73.76
Sup. GCC(µm) 81.59 83.95
SN ST Inf. GCC(µm) 84.88 63.58
150 123 FLV (%) 2.165 10.912
GLV (%) 13.274 23.241

TU
NU 72 75

N T
Solid line-OD
81 60 TL Fovea
Dash line-OS
NL
TU ST SN NU NL IN IT TL

86 81 200
IN IT

TU ST SN NU NL IN IT TL
100
200
100

0 0
T S N I T T S N I T
D Exam Date: 01/10/2013, SSI= 41.8 Exam Date: 01/10/2013, SSI= 64.7
FIG. E1  cont’d  D, OCT from the same patient—note inferior abnormality on ganglion cell complex analysis
of the left eye corresponding to the superior nasal step. (From Bowling B: Kanski’s clinical ophthalmology: a
systemic approach, ed 8, 2016, Elsevier.)

Descargado para Felipe Calderón Avendaño (felipe.calderon.a@usach.cl) en Universidad de Santiago de Chile de ClinicalKey.es por Elsevier en junio 21, 2017.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2017. Elsevier Inc. Todos los derechos reservados.