1. Glaucoma Suspect - Shields Textbook of Glaucoma, 6th edition - 녹내장 개정5판, 한국녹내장학회
부천성모병원 안과 Ap.홍승우/R3 이국

2. 고안압증(녹내장 의증)
녹내장 의증 정의 녹내장 의증 유병율 녹내장 의증 위험인자 녹내장 의증 치료 OHTS, BISED, VIP, RES, EGPS 등 각종 study 결과 인용

3. Introduction Ocular hypertension Glaucoma suspect
1970s : IOP greater than 21 mmHg, increased risk for COAG
Chandler and Grant : early open-angle glaucoma without damage
Glaucoma suspect
Advocated by Shaffer
Consistently elevated IOP
Optic nerve features suggestive of early glaucoma or suspicious visual field defects

4. Definition of Glaucoma Suspect
Open angle by gonioscopy
One of the following in at least one eye
IOP consistently >21 mm Hg by applanation tonometry
Appearance of the optic disc or retinal nerve fiber layer suggestive of glaucomatous damage
Diffuse or focal narrowing or sloping of the disc rim
Diffuse or localized abnormalities of the nerve fiber layer, especially at superior and inferior poles
Disc hemorrhage
Asymmetric appearance of the disc or rim between fellow eyes (e.g., cup-to-disc ratio difference > 0.2), suggesting loss of neural tissue
Visual fields suspicious for early glaucomatous damage
Adapted from AAO, 2005

5. Prevalence & Development of COAG
Prevalence rate
Wales, England, Sweden : 4-10% (IOP greater than or equal to 21 mmg, with normal visual fields and optic nerves)
Tajimi study : OHT 0.8%, glaucoma suspect 2.9%
Namil study : OHT 0.6%, glaucoma suspect 2.7%
Progression to COAG
1% per year over 5 to 15 years : glaucoma suspect on the basis of elevated IOP

6. Incidence of COAG among Persons with OHT
Study
Patients with Ocular Hypertension, n
Observation Period, y
Patients Developing COAG, n (%)
Perkins, 1973
124
5-7
4 (3.2)
Walker, 1974
109 11
11 (10.1)
Wilensky et al., 1974 50 6
3 (6.0)
Norskov, 1970 68 5
Linner, 1976 92 10
Kitazawa et al., 1977 75
9.5
7 (9.3)
David et al., 1977 61
3.3 (1-11)
10 (16.4)
Hart et al., 1979
33 (35.9)
Armaly et al., 1980
5886 13
98 (1.7)
Lundberg et al., 1987 41 20
14 (34.1)
Kass et al., 2002
819
89 (10.9)

7. Prevalence & Development of COAG
OHTS (ocular hypertension treatment study)
Randomized trial of topical ocular hypotensive treatment versus close observation in ocular hypertension
Cumulative probability of developing COAG over 5 years
1% per year in the medication group
About 2% per year in the observation group
3-5% per year in patients at higher risk for developing glaucomatous optic nerve damage

8. Screening & Early detection
Best method to detect early glaucoma (AAO)
Assessment of IOP, optic nerve, visual field
Screening
IOP value of more than 21 mmHg
Skilled optic nerve examination
Standard automated perimetry (SAP)
Short-wavelength automated perimetry (SWAP)
Frequency doubling technology (FDT)
Defects on SWAP & FDT can precede develoment of SAP-detected defects

9. IOP & Pachymetry Worthwhile to measure CCT with pachymeter
Glaucoma suspects : higher CCT than COAG or healthy
42% of glaucoma suspects : CCT greater than 585 μm
GAT was calibrated for CCT of 530 μm
Corrected IOP
mmHg per 50 μm of difference from 550 μm

10. Slitlamp Biomicroscopy & Gonioscopy
To exclude secondary causes of glaucoma
Angle closure
Angle recession
Pigment dispersion
Inflammatory forms of glaucoma

11. Fundus Examination Appearance of optic nerve head
Small hemorrhage (precede VF loss, future optic nerve damage)
Nerve fiber layer (NFL) defect
Red-free(green) light
Laser polarimetry with nerve fiber analyzer (GDx)
Scanning laser ophthalmoscopy (HRT)
Optical coherence tomography (OCT)

12. Visual Fields To obtain two or three baseline visual fields
24-2 SITA standard
24-2 full threshold or equivalent on different automated perimeter
FDT or SWAP
If abnormality, need to be confirmed on repeated test
In OHTS, 748 abnormal visual fields
On retesting, 604 (85.9%) were not confirmed abnormalities
Due to learning curve or long-term variability

13. Imaging of the Optic Nerve & NFL
Topographic features of optic nerve head and thickness of retinal NFL
Confocal scanning laser ophthalmoscope (HRT)
Optical coherence tomography (OCT)
Scanning laser polarimetry (GDx)
Evidence-based review of AAO
There is no single imaging device that outperforms the others in distinguishing glaucoma from controls
In conjunction with other parameters to define glaucoma diagnosis and progression

14. Ocular Blood Flow
Whether reduction in blood flow to optic nerve damage to optic nerve early : need to be proven
Laser Doppler flowmetry
Optic nerve head blood velocity, volume, flow in 4 quadrants of nerve
Glaucoma suspects vs controls
Significantly lower in superotemporal rim(16%), cup(35%), inferotemporal neuroretinal rim(22%)
Glaucoma suspects vs COAG : no significant difference

15. Risk Factors
Risk for glaucoma increases with number & strength of risk factors
Longitudinal population studies to evaluate risk factors
Barbados Incidence Study of Eye Diseases (BISED1), Melbourne Visual Impairment Project (Melbourne VIP2), Rotterdam Eye Study (RES3)
Older age, increase in IOP (1,2,3)
Family history of COAG, thinner CCT, lower ocular hypertension pressure (1)
Exfoliation, large cut-to-disc ratio, use of systemic α-agonist blocker (2)
Use of systemic CCB (3)

16. High-Risk Glaucoma Suspects
Include patients who have one or more of the following:
IOP consistently >30 mm Hg
Thin central corneal thickness (dependent on ethnicity)
Vertical cup-to-disc ratio >0.7
Older age
Abnormal visual field, e.g., increased pattern standard deviation on Humphrey Visual Field testa
Presence of exfoliation or pigment dispersion syndrome
Disc hemorrhagea
Family history of glaucoma or known genetic predisposition
Fellow eye of patient with severe unilateral glaucoma (excluding secondary unilateral glaucoma)
Additional ocular (e.g., suspicious disc appearance, myopia, low optic nerve perfusion pressure, steroid responder) or systemic risk factors that might increase the likelihood of developing glaucomatous nerve damage (e.g., African ancestry, sleep apnea, diabetes mellitus, hypertension, cardiovascular disease, hypothyroidism, myopia, migraine headache, vasospasm)

17. When To Treat
Consider visual, physical, medical, psychological, social circumstances
Stratify patients into low, moderate, high risk for progression
High risk : suggest treatment be initiated
Moderate risk : can initiate treatment if appropriate, or monitor closely
Low risk : monitor IOP as well as optic nerve structure and function, and treat if evidence of progression
Chandler & Grant
If IOP ≥ 30 mmHg (prevalence of glaucoma 11-29%)
If IOP mmHg with one or more risk factors

18. When To Treat
OHTS : reducing IOP by at least 20% in OHT can reduce the COAG over 5 year period (9.5%  4.4%)
In fact, most elevated IOP did not progress to glaucoma over 5 year follow up  not all patients should receive medication
Kass : lower threshold for treatment
Only one functional eye
Not possible to obtain reliable visual fields
Optic disc cannot be visualized
AAO : risk-benefit analysis
Likelihood of development of glaucomatous optic nerve damage should be carefully weighed against the risks of treatment

19. Approach To Treatment
Choice of treatment : selecting a topical medication
To achieve target IOP range
Least risk to ocular or systemic health and quality of life of patient
Laser trabeculoplasty
If target IOP range cannot be achieved with medication
Surgery
Rarely indicated as first-line therapy in glaucoma suspect
If extremely high, uncontrolled IOP to cause glaucomatous damage
Poor adherence to medical therapy
Inability to tolerate medical therapy

20. Guidelines For Follow-up
To determine whether change in IOP, optic nerve head, visual field status
Frequency of follow-up depend on…
Whether receiving medical therapy
Whether target IOP range be achieved
Number of risk factors for COAG

21. Recommended Guidelines for Follow-up of a Glaucoma Suspect (AAO)
Treatment
Target IOP Achieved
High Risk
Follow-up Interval, mo
Examination
ONH/VF Evaluation No
N/A
6-24
Yes
3-21
6-18
3-12 ≤4
Modified from American Academy of Ophthalmology. Primary Open-Angle Glaucoma Suspect,
Preferred Practice Pattern