This document discusses various types of glaucoma including primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and ocular hypertension. It defines these conditions and describes their signs, risk factors, treatments, and etiologies. POAG is the most common type and usually presents with asymptomatic, progressively worsening vision loss and characteristic optic nerve cupping. Risk factors include older age, family history, and elevated intraocular pressure (IOP). NTG is similar to POAG but occurs in patients with normal IOP. The cause is believed to involve vascular dysregulation but lowering IOP remains important for treatment and prevention of progression. Ocular hypertension refers to elevated IOP without optic nerve

1. By
Mutahir Shah
M Phil Vision Sciences
Pakistan Institute of Community
Ophthalmalogy
Introduction to Glaucoma
POAG, NTG and Ocular
Hypertension

2. Normal disc that obeys the ‘ISNT’ rule

3. Intra Ocular Pressure
 Intraocular pressure (IOP) is determined by the
balance between the rate of aqueous production and
its outflow
 The average IOP in the general population is around
16 mmHg on applanation tonometry, and a range of
about 11–21 mmHg
 Some patients develop glaucomatous damage with
IOP less than 21 mm Hg whilst others remain
unscathed with IOP well above this level.
 These include features influencing the IOP reading,
such as corneal rigidity, and probably factors affecting
the susceptibility of the optic nerve to damage,
 Such as the integrity of its blood supply and structural
vulnerability to mechanical stress at the optic nerve

4. Fluctuation
 Normal IOP varies with time of day (diurnal
variation), heartbeat, blood pressure and
respiration.
 The diurnal pattern varies, with a tendency
to be higher in the morning and lower in the
afternoon and evening.
 Glaucomatous eyes exhibit greater than
normal fluctuation,
 The extent of which is directly proportional
to the likelihood of progressive visual field
damage,

5. Definition of Glaucoma
 A characteristic potentially progressive optic
neuropathy that is associated with visual field loss as
damage progresses, and in which IOP is a key
modifiable factor.
 Classification of Glaucoma:
 Glaucoma may be congenital (developmental) or
acquired.
 Open-angle and angle-closure types are distinguished
based on the mechanism by which aqueous outflow is
impaired with respect to the AC angle configuration.

6. Epidemiology
 Glaucoma affects 2–3% of people over the age of 40
years; 50% may be undiagnosed.
 Primary open-angle glaucoma (POAG) is the most
common form in white, Hispanic/Latino and black
individuals;
 The prevalence is especially high in the latter.
 Primary angle closure (PAC) constitutes up to half of
cases, and has a particularly high prevalence in
individuals of Asian descent,

7. Risk factors of POAG
• IOP. The higher the IOP, the greater the likelihood of
glaucoma. Asymmetry of IOP of 4 mmHg or
more is also significant.
• Age. POAG is more common in older individuals.
• Race. It is significantly (perhaps four times) more
common, more difficult to control in black
individuals than in whites.
• Family history of POAG. First-degree relatives of
patients with POAG are at increased risk. An
approximate risk to siblings is four times and to
offspring twice the normal population risk, though
surveyed figures vary.
• Diabetes mellitus. Many studies suggest a correlation
between diabetes and POAG.
• Myopia is associated with an increased incidence of

8.  Contraceptive pill. Long term use of OC use may
substantially increase the risk of glaucoma.
 Optic disc area. Large discs may be more vulnerable
to damage,
 Ocular perfusion pressure is the difference between
the arterial BP and the intraocular pressure (IOP), and
has been shown in population studies to be linked to
increased risk for the development and progression of
glaucoma.

9. Primary Open Angle Glaucoma
 Primary open-angle glaucoma (POAG) is a commonly
bilateral disease of adult onset.
 Symptoms:
 Usually Asymptomatic until the later stage.
 Early Symptoms may include parts of a page missing.
 Tunnel vision and loss of central fixation typically do not
occur until late.
 Signs:
 Raised IOP (Half the patient have an IOP of higher than
21mmHg.
 But still half of the patient have and IOP of 21 or lower at
any one screening.
 Normal Angle Appearance

10.  Disc Cupping & Notching usually follow ISNT rule.
concentrically enlargingFocal ischaemic – inferior notch and disc
haemorrhage;

11.  Characteristic visual field loss as damage progresses.
 CDR asymetry >0.2 in the absence of a cause(e.g.
anisometropia, Different nerve sizes.
 Bayoneting ( Sharp angulations(deviation from a straight
line) of blood vessels as they exit the nerve)
Others include Large fluctuation in IOP
bayoneting of blood vessels;

12. DD of POAG
 Ocular Hypertension : Normal VF and Optic Nerve
 Physiological Cupping: static Enlarged CDR without
rim notching and VF defects.
 Low Pressure Glaucoma: Same as POAG except
normal IOP
 Secondary Open Angle Glaucoma: Have an
identifiable cause may be lens induced , Inflammatory
Exfoliative, Pigmentary or steroid induced.
 Optic Atrophy : Characterized by disproportionally
more optic nerve pallor than cupping IOP normal color
vision and central vision are usually affected
 Congenital optic nerve defect(tilted disc, colobomas
Optic nerve pit

13. Ocular Hypertension
In the general population the mean IOP is 16 mmHg; two
standard deviations either side of this gives a ‘normal’ IOP
range of 11–21 mmHg
It is estimated that 4–10% of the population over the age of
40 years have IOP >21 mmHg without detectable
glaucomatous damage: ‘ocular hypertension’ (OHT).
 Intraocular pressure. The risk of developing glaucoma
increases with increasing IOP.
 Age. Older age is associated with greater risk.
 Central corneal thickness (CCT). The risk is greater in
eyes with low CCT and lower in eyes with higher CCT.
 This is probably due to resultant under- and over-
estimation of IOP
 Cup/disc (C/D) ratio. The greater the C/D ratio the higher
the risk. This may be because an optic nerve head with a
large cup is structurally more vulnerable, or it may be that

14. Treatment
 No treatment in the absence of Optic nerve
damage and VF loss if IOP is less than 24mmHg.
Close observation is necessary.
 Patient having an IOP of greater than 24 to
30mmHg but otherwise normal examinations are
candidates for pressure lowering therapy.

15. Normal Tension Glaucoma
 PAOG occurring in patients without IOP elevation
usually regarded as a variant of POAG.
 It is characterized by:
• IOP consistently equal to or less than 21 mmHg.
• Signs of optic nerve damage in a characteristic
glaucomatous pattern.
• An open anterior chamber angle.
• Visual field loss as damage progresses, consistent in
pattern with the nerve appearance.
• No features of secondary glaucoma or a non-
glaucomatous cause for the neuropathy.

16.  The distinction between NTG and POAG is based on
an epidemiologically derived range of normal IOP
 Clinical features
 History and examination are essentially the same as for
POAG but specific points warrant attention.
 • History
 ○ Migraine and Raynaud phenomenon.
 ○ Episodes of shock.
 ○ Head or eye injury.
 ○ Headache and other neurological symptoms
(intracranial lesion).
 ○ Medication, e.g. systemic steroids, beta-blockers.

17.  • IOP is usually in the high teens, but may rarely be in the
low teens.
 In asymmetrical disease the more damaged disc typically
corresponds to the eye with the higher IOP.
 • Optic nerve head
○ The optic nerve head may be larger on average in NTG
than in POAG.
○ The pattern of cupping is similar, but acquired optic disc
pits and focal nerve fibre layer defects may be more
common.
○ Peripapillary atrophic changes may be more prevalent.
○ Pallor disproportionate to cupping should prompt a
suspicion of an alternative diagnosis.
 • Visual field defects are essentially the same as in POAG
although there is some evidence that they tend to be
closer to fixation, deeper, steeper and more localized.

18. ○ Disc (splinter, Drance – see Figs A B and C) haemorrhages may be
more frequent than in POAG, and are associated with a greater likelihood
of progression.

19. Etiology
 Controversial: Most investigators believe that IOP play
an important role in LTG.
 Other proposed that include vascular dysregulation(e.g.
systemic or nocturnal hypotension, vasospasm or loss
of autoregulation) microischemic disease and
autoimmune disease.
 Treatment:
 Research suggests that further lowering of IOP plays
an important role in preventing progression of low
pressure POAG.
 Target IOPs are at least 30% lower than the level at
which progressive damage was occurring.
 Avoid use of Antihypertensive drugs at bedtime and

20. Refrences J Kanski 8th Edition and Wills Eye Manual