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Glaucoma, Open-Angle 519

than whites). There is a genetic tendency to IMAGING STUDIES


BASIC INFORMATION OAG; multiple genes have been isolated that
are associated with development of high IOP
• Optic nerve photography—stereo photo-
graphs (Fig. E1).
G
DEFINITION and optic nerve damage. • Visual field testing.
Glaucoma is a chronic degenerative optic neu- PREDOMINANT AGE: • Laser scan of nerve fiber layer, OCT, HRT.
ropathy (or the high potential for such degenera- • Persons >50 yr Rarely, MRI of orbits if the glaucoma findings
tion due to risk factors) in which the neuro-retinal • Can occur in 30s and 40s, and juvenile forms are atypical or suspicious of other causes of
rim of the optic nerve becomes progressively are rare optic nerve atrophy (Fig. E1).
thinner, thereby enlarging the optic-nerve cup.
PHYSICAL FINDINGS & CLINICAL
The classification of glaucoma is based on
the appearance of the iridocorneal angle (open
PRESENTATION TREATMENT
angle vs. closed angle) and is further subdi- • High intraocular pressures and/or large optic
nerve cup (Ocular Hypertension Treatment Study ACUTE GENERAL Rx

and Disorders
Diseases
vided into primary and secondary types. Primary
open-angle glaucoma can occur with or without results help to delineate important risk factors). • β-blockers (e.g., timolol) qd to bid depending
elevated intraocular pressure (IOP). Normal ten- • Abnormal visual fields (with advanced glau- on individual response to drug.
sion glaucoma refers to primary open-angle coma damage to the optic nerve). • Carbonic anhydrase inhibitors (e.g., Diamox
glaucoma without elevated intraocular pressure. • Open anterior chamber angle—evaluated 250 mg qid or 500 mg bid).
with gonioscopy. • Prostaglandin analogues (latanoprost, bima-
SYNONYMS
Primary open-angle glaucoma (POAG)
• Since early treatable stages of OAG normally
have no symptoms, it’s important to have
toprost, travoprost, tafluprost) are commonly
used as first-line treatment. They lower intra- I
Open-angle glaucoma (OAG) routine eye exams, especially patients with ocular pressure by 25% to 30% by increasing
Secondary open-angle glaucoma (e.g., pseu- family history and patients over 60 yr. uveoscleral outflow and reducing aqueous
doexfoliation, pigment dispersion, trauma, • Secondary forms of OAG may exhibit ocular production.
inflammatory) findings such as pseudo-exfoliation, pig- • Alpha-2 agonists and cholinergic agonists.
Chronic open-angle glaucoma ment dispersion, blood in anterior chamber, • Hyperosmotic agents (mannitol) in acute
inflammation. treatment (IV).
ICD-10CM CODES • Selective laser trabeculoplasty (SLT) may
H40.10X0 Unspecified open-angle glaucoma, ETIOLOGY delay or forestall need for second eyedrop.
stage unspecified • Uncertain hereditary tendency (multifactorial The effect may be temporary but the laser
H40.10X1 Unspecified open-angle glaucoma, genetics). can be repeated.
mild stage • Topical steroids can induce high IOP and
H40.10X2 Unspecified open-angle glaucoma, cause glaucoma. CHRONIC Rx
moderate stage • Trauma. • At least biannual checks of intraocular pres-
H40.10X3 Unspecified open-angle glaucoma, • Inflammatory (e.g., history of uveitis). sure and adjustment of medication.
severe stage • High-dose oral corticosteroids taken for pro- • Surgical trabeculectomy and filter valve sur-
H40.10X4 Unspecified open-angle glaucoma, longed periods. geries can be considered for glaucoma that
indeterminate stage progresses (optic nerve changes or visual
field progression) despite maximal toler-
H40.11X0 Primary open-angle glaucoma,
stage unspecified
DIAGNOSIS ated medical therapies. Recently, minimally
H40.11X1 Primary open-angle glaucoma, invasive glaucoma surgeries (MIGS) have
DIFFERENTIAL DIAGNOSIS been advocated for IOP control. Some are
mild stage
H40.11X2 Primary open-angle glaucoma, • Other optic neuropathies (previous retinal vas- performed at the time of cataract procedures
moderate stage cular disorders, optic nerve pits, or coloboma). and some are independent procedures. The
H40.11X3 Primary open-angle glaucoma, • Physiologic cupping of the optic nerve: The effort is to reduce the risks associated with
severe stage optic nerve may appear similar to glaucoma traditional trabeculectomy.
H40.11X4 Primary open-angle glaucoma, damage but does not progress. This is fol-
indeterminate stage lowed for any signs of progression. DISPOSITION
• Ocular hypertension: IOP is chronically ele- Must be followed by ophthalmologist.
vated, but not causing optic nerve damage,
EPIDEMIOLOGY &
must monitor closely. REFERRAL
DEMOGRAPHICS
• Secondary glaucoma from inflammation and Immediately to ophthalmologist.
INCIDENCE (IN U.S.): Third most common steroid therapy.
cause of vision loss (75% to 95% of all forms of • Trauma.
glaucoma are open angle) PEARLS &
PEAK INCIDENCE: WORKUP CONSIDERATIONS
• Increases after age 40 yr • Comprehensive eye examination
• Three million cases expected by 2020 because • Intraocular pressure COMMENTS
of the rapid increase in aging population • Slit lamp examination • Glaucoma is a serious blinding disease that
PREVALENCE (IN U.S.): • Visual fields must be monitored professionally by an
• Overall prevalence in U.S. population aged • Gonioscopy: to determine the type of glaucoma ophthalmologist. It is mostly asymptomatic
>40 yr is estimated to be 1.86%, with 1.57 • Nerve fiber analysis (e.g., GDx, OCT, and HRT) until late in the disease when visual problems
million white and 398,000 black patients • Corneal thickness (thick central cornea will arise. Even in developed countries half of
affected. By 2020, we may expect more than result in possible overestimation of the true glaucoma cases are undiagnosed.
3 million cases in the U.S. physiologic IOP, and vice versa, so this is • Risk factors that should prompt referral to an
• 150,000 patients have bilateral blindness. important information in diagnosis and treat- ophthalmologist for evaluation of glaucoma
• Prevalence is higher in diabetics, those with ment of OAG) are high intraocular pressure, family history
high myopia, and older persons. of glaucoma, use of systemic or topical corti-
• More common in African-American popula- LABORATORY TESTS costeroids, older age, and black race.
tion (three times the age-adjusted prevalence Blood sugar

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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.
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Glaucoma, Open-Angle 520.e1

EVIDENCE 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
Abstract[1] hemifield were inspected. To calculate the progression rates, linear
Ocular hypertension is a common and important problem seen by eye mixed-effect model was employed.
care providers. This review presents a practical approach to individuals Results:
with ocular hypertension. It describes the common functional and struc- There were no significant differences between the two groups in age,
tural investigations used in evaluation, as well as the advantages and gender, ocular factors including baseline/mean treated intraocular pres-
disadvantages of each test. This review also discusses several landmark sure, and systemic factors including systolic or diastolic blood pressure/
studies on ocular hypertension and provides a practical guide to the perfusion pressure, mean ocular perfusion pressure (all P > 0.05). There
management of this problem. were no significant differences in baseline mean deviation and pattern
This article is an excellent review of the pertinent information we use standard deviation (P>0.05) between the two groups, but VF index was
to guide management of glaucoma suspects. Although the factors significantly lower in ICS group than in IPS group (P=0.001). The pro-
weighed to determine treatment decisions for these patients are familiar, gression rates between the two groups were not significantly different in
it is helpful to flesh out the details. As an example, central corneal thick- all zones we investigated (all P>0.05).
ness (CCT) is well known to influence the risk of glaucoma. However, its Conclusions:
application may be variable in clinical practice. The clinical definition of Newly diagnosed cases of NTG with ICS may not differ from those with
thin vs thick CCT is not standardized, and different practitioners may use IPS in clinical characteristics and progression rates under treatment. B
different thresholds. Although no algorithm has been proven useful for
adjusting intraocular pressure measurement for CCT, some doctors still Evidence-Based References
use them. Controversy may be found in the fine points of even broadly 1. Boey PY, Mansberger SL: Ocular hypertension: an approach to assessment and
accepted tenets of glaucoma care, and looking at a review of the evi- management, Can J Ophthalmol 49:489–496, 2014.
dence is enlightening. The authors take on risk calculators, disc photog- 2. Cho H-K, Lee J, Lee M, et al.: Initial central scotomas vs peripheral scotomas
raphy, Heidelberg retinal tomography, optical coherence tomography in normal-tension glaucoma: clinical characteristics and progression rates, Eye
(including recent and important work regarding new ways to define the 28:303–311, 2014. B
optic disc margin using Bruch membrane opening), and perimetry. In a
perfect world, specific evidence-based guidelines would make it simple SUGGESTED READINGS
to analyze the risk to an individual patient and the most cost-effective Gupta D, Chen PP: Glaucoma, Am Fam Physician 93(8):668–674, 2016.
way, on a societal basis, to determine when and whom to treat. We are Quigley HA: Glaucoma, Lancet 377:1367–1377, 2011.
not there yet. Weinreb RN, et al.: The pathophysiology and treatment of Glaucoma, JAMA
S. Fudemberg, MD 311(18):1901–1911, 2014.
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

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Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2017. Elsevier Inc. Todos los derechos reservados.
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.