Open Angle Glaucoma: POAG

As discussed earlier, Glaucoma is a group of disorders characterized by optic neuropathy associated with visual field defects and elevated intraocular pressure. Glaucoma is divided into three types, namely, Primary Glaucoma and Secondary Glaucoma and Congenital Glaucoma.

Primary Adult Glaucoma has mainly two types, Primary Open Angle Glaucoma and Primary Angle Closure (or Closed Angle) glaucoma. The other one, Primary mixed mechanism glaucoma, we wouldn’t be discussing.

Previously, we discussed Understanding the basics before Glaucoma. In this blog, we will be focusing on Primary Open Angle Glaucoma or POAG. Later we will follow up on Congenital glaucoma, Closed angle glaucoma and secondary glaucoma with surgeries as a follow-up.

Primary Open Angle Glaucoma

Primary open-angle glaucoma or POAG is a type of primary glaucoma (and not as a complication of another disease) where intraocular pressure progressively and slowly increases without any obvious ocular or systemic causes.

The intraocular pressure rise is generally more than 21mm hg with characteristic optic cupping and specific visual field defects. It is also called chronic adult glaucoma since its onset occurs in the 5th-7th decade (50-70 years) of life. The aqueous humour slowly gets accumulated in the posterior chamber, followed by the anterior chamber filling. This filling compresses the lens which in turn compresses backwards, affecting the optic disc and thus causing visual field defects.


Open Angle Glaucoma Mechanism
Open Angle Glaucoma Mechanism

There is indeed a rise in intraocular pressure, but the exact cause is not known. The decreased outflow facility of intraocular pressure is attributed to increased resistance due to age-related thickening, sclerosis of the trabecula and absence of giant cells in schlemn canal.


The Aetiology of POAG includes risk factors such as:-

  • Hereditary- 10% chances in siblings and 4% in children from parents.
  • Age- most common in 50-70 years of age.
  • Race- black people are more prone to white people having POAG.
  • Other risk factors- include patients with myopia, diabetics, high b.p, cigarette smoking and thyrotoxicosis (grave ophthalmopathy)

Clinical features

Clinical features are individual symptoms and signs which appear in clinical investigations.


  • Asymptomatic- in the earlier stages, it is asymptomatic. This is because the chamber (anterior and posterior) fills slowly. Hence, the patient remains asymptomatic while the disease grows insidious. The sudden visual defects appear when POAG reaches the near-end stage and are critically severe, often Blindness.
  • Visual field defects- Scotoma (visual field defects) are ignored, usually noticed on the observant patient only.
  • Headache and pain in the eye- This occurs due to slow compression and mild compression of optic structures.
  • Frequent changes of glasses- The person is unable to adjust his eyes in reading and closing objects, hence he often has to change his presbyopic glasses.
  • Dark adaptation- The patient faces difficulty in adapting quickly to dark surroundings.


1. Anterior segment changes

These are changes in the anterior segment of the eye which involve the anterior chamber, cornea and pupil.

A. Slit lamp biomicroscopy- It reveals a normal anterior segment.

B. Central corneal thickness (CCT)- It becomes low, usually less than 555 micrometres.

C. Pupil reflexes- sluggish

2. Intraocular pressure changes

There is significant variation in the IOP of patients at different day times. This is referred to as the Diurnal variation of IOP.

Diurnal Variation Open Angle Glaucoma
Diurnal Variation in Open-Angle Glaucoma

For this test, repeated observations of the IOP of patients are done at frequent intervals, usually every 3 hours for 24hrs. The IOP falls mostly at night time.
The IOP is measured by tonometry, an applanation tonometer is preferred. The following are the changes observed:

  • Morning rise- 20%
  • Afternoon rise- 25%
  • Biphasic rise- 55%

A variation of 5mm Hg is a suspect case of POAG while a variation of more than 8mm Hg confirms the primary open-angle glaucoma.

In later stages, there is more than 2mm Hg rise permanently, rising the IOP to 30-45mm Hg.

3. Optic disc changes

The routine fundus examination reveals optic disc changes. These are further divided into early changes, advanced changes and Late changes (glaucomatous optic atrophy).

Various examination techniques used for demonstrating optic disc changes include direct/indirect ophthalmoscopy, and slit lamp biomicroscopy with +90D or Goldmann lens.

The recording and documentation include serial drawings, photography and photogrammetry.

The changes observed, as said, are as follows:-

I. Early stage
II. Advanced stage
III. Optic atrophy

Normal Optic Disc

This is what a normal optic disc in the eye looks like:

Normal Optic Disc- Diagram
Normal Optic Disc- Diagram
Normal Optic Disc Fundus Examination
Normal Optic Disc Fundus Examination

I. Early changes

Early changes of the optic disc in primary open-angle glaucoma include:

Early Glaucoma Changes in Optic Disc
Early Glaucoma Changes in Optic Disc
Early Glaucoma Changes in Optic Disc- Fundus Examination
Early Glaucoma Changes in Optic Disc- Fundus Examination
  • slightly oval cups
  • the difference in symmetry of cups
  • increase in the size of cups (0.6 when normal is 0.3-0.4)
  • pallor areas
  • hemorrhagic which appear broken like pieces

II. Advanced changes

Advanced changes in primary open-angle glaucoma include:

Advanced Glaucomatious Optic Disc Changes
Advanced Glaucomatous Optic Disc Changes
Advanced Optic Disc Changes in POAG- Fundus Examination
Advanced Optic Disc Changes in POAG- Fundus Examination
  • marked cupping
  • the shifting of retinal vessels towards the nasal side
  • crescent shadow due to thinning of the neuroretinal rim
  • pulsation of retinal arterioles
  • laminar dot sign- from lamina cribrosa

III. Glaucomatous optic atrophy

Late changes in primary open-angle glaucoma include:

Glaucomatous Optic Disc Atrophy
Glaucomatous Optic Disc Atrophy

As the damage, progresses, all the neural tissue of the disc is destroyed and the optic nerve head appears white and deeply excavated.

4. Visual field defects

Glaucoma Visual Field Defects
Glaucoma Visual Field Defects
  • These appear only when 40% of the axons of the optic nerve have been destroyed. These continue to progress with untreated IOP rise.
  • These visual field defects in glaucoma are observed in Bjerrum’s area (10-25 degrees from fixation) and relate to optic disc changes.

Sequence of Visual Field Loss

The sequence of visual field loss due to primary open glaucoma is:

a. Isopter contraction

Earliest field defect occurring in glaucoma. There is mild and no diagnostic constriction of the central and peripheral fields.

b. Baring of blind spot

Again non-specific and not diagnostic, it means the exclusion of blind spot from the central field due to the inward curve.

c. Small wing

Shaped paracentral scotoma- it is the earliest clinically significant field defect.

d. Seidel scotoma

Paracentral scotoma + blind spot = sickle-shaped scotoma

Seidel Scotoma
Seidel Scotoma

e. Arcuate or Bjerrum’s scotoma

Extension of seidel scotoma

Bjerru M Scotoma
Bjerru M Scotoma

f. Double arcuate scotoma or Ring scotoma

Joining of two arcuate scotoma

Double Arcuate Scotoma
Double Arcuate Scotoma

g. Roenne’s central nasal step

It is created when the two arcuate scotomas run in different arcs and join.

Double Arcuate Scotoma
Double Arcuate Scotoma

h. Peripheral field defects

i. Advanced glaucomatous field defects

The visual field defects continue to progress until a small part of central vision (tubular vision) is left.


1. Gonioscopy

It clearly reveals Open Angle Glaucoma.

2. IOP investigations

These include Tonometry, Diurnal variation and Water drinking test:

a. Tonometry

Applanation tonometry is preferred to measure IOP.

b. Diurnal variation

IOP variations are noted.

c. Water drinking test

8 hours fast, drink 1 Ltr water and then IOP measured every 15 mins for 1 hour. 8mm rise is diagnostic.

3. Anterior segment investigations

These include Slit lamp biomicroscopy and CCT:

  • Slit lamp biomicroscopy- show normal anterior segment.
  • Central corneal thickness- less than 545.

4. Optic disc investigations

These include Documentation of optic disc changes.

5. Visual field defects

These include Perimetry and NFLA:

  • Perimetry- to detect visual field defects
  • Nerve fibre layer analyzer (NFLA)- helps in detecting the glaucomatous damage to the retinal nerve fibres before the appearance of actual visual field changes and/or optic disc changes.

6. Provocative tests

  • In suspicious cases with borderline intraocular pressure, provocative tests are carried out to establish a degree of probability that a patient does or does not have glaucoma. Apart from the Water drinking test, other provocative tests include combined water drinking and tonography, bulbar pressure test, prescoline test and caffeine test.


The management of Primary Open Angle Glaucoma includes Medical treatment, Laser trabeculoplasty and Surgery:

A. Medical treatment

  1. Drugs which Increase the flow of aqueous humour- LAP
    • Latanoprost(0.005%: once daily)- drug of the first choice for the treatment of POAG (provided patient can afford to buy it). It increases the uveo-scleral outflow of aqueous humour.
    • Adrenergic drugs
      • Epinephrine hydrochloride (0.5, 1, 2%: 1-2 times/day) and dipivefrine hydrochloride (0.1%: 1-2 times/day)
      • Brimonidine (0.2%: 2 times/day).
    • Pilocarpine(1, 2, 4%: 3-4 times/day)- Second/Adjunctive drug of choice, it is avoided in young patients because it causes problems due to spasms of accommodation and miosis. Pilocarpine acts by contracting the longitudinal muscle of the ciliary body and opening spaces in the trabecular meshwork, thereby mechanically increasing aqueous outflow.
  2. Drugs which Decrease the production of aqueous humour- BD
    • Topical Beta-blockers- these are the drugs of choice and are affordable for everyone. Reduce IOP due to its effect on beta receptors in the ciliary processes.
      • Timolol- not used in bronchial asthma and/or heart blocks-(0.25, 0.5%: 1-2 times/day)
      • Betaxolol- preferred in cardiopulmonary problems-(0.25% : 2 times/day)
      • Levobunolol- long-lasting action-(0.25, 0.5% : 1-2 times/day)
      • Carteolol- patient with hyperlipidemias or atherosclerotic cardiovascular disease-(1%: 1-2 times/day)
    • Dorzolamide(2%: 2-3 times/day)- carbonic anhydrase inhibitor which lowers IOP by decreasing aqueous secretion.

B. Laser trabeculoplasty

  • Argon Laser Trabeculoplasty (ALT) or Diode Laser Trabeculoplasty (DLT).
  • It is done when medical treatment fails.
  • It reduces 8-10mm Hg IOP in patients with medical treatment.
  • It reduces 12-16mm Hg IOP in patients without medical treatment.

C. Surgery

  • Fistulising is also called Filtration surgery. These include the most popular- Trabeculectomy and others like Viscocanalostomy and Deep sclerectomy.
  • A very wonderful video of Trabeculectomy is shown here:
Credits: Alila Medical Media

So, this was all about Primary Open Angle Glaucoma. To check out basics again, click Basics of Glaucoma. Please leave any reviews in the comments section below.

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