Open Angle Glaucoma: POAG

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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 are 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.

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

Primary Open Angle Glaucoma

Primary open angle glaucoma or POAG is a type of primary glaucoma (and not as complication of other 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 onset occurs in 5th-7th decade (50-70 years) of life. The aqueous humor slowly gets accumulated in posterior chamber, followed by anterior chamber filling. This filling compresses the lens which in turn compresses backwards, affecting optic disc and thus causing visual field defects.

Pathogenesis of Primary Open Angle Glaucoma

open angle glaucoma largo images
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There is indeed rise in intraocular pressure, but exact cause is not known. The decreased outflow facility of intraocular pressure is attributed to increased resistance due to age related thickening, sclerosis of trabecula and absence of giant cell in schlemn canal.

Aetiology of Primary Open Angle Glaucoma

Etiology of POAG includes risk factors 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 of having POAG.
  • Other risk factors- include patient with myopia, diabetics, high b.p, cigarette smoking and thyrotoxicosis (grave ophthalmopathy)

Clinical features of Primary Open Angle Glaucoma

Clinical feature are individual symptoms and signs which appear on clinical investigations.

Symptoms of Primary Open Angle Glaucoma

  • Asymptomatic- in the earlier stages, it is asymptomatic. This is because the chamber (anterior and posterior) fill slowly. Hence, the patient remains asymptomatic while the disease grows insidious. The sudden visual defects appear when POAG reaches near end stage and are critically severe, often Blindness.
  • Visual field defects- Scotoma (visual field defects) are ignored, usually noticed on observant patient only.
  • Headache and pain in 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 close objects, hence he often has to change his presbyopic glasses.
  • Dark adaptation- Patient faces difficulty in adapting quickly to dark surrounding.
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Signs of Primary Open Angle Glaucoma

1. Anterior segment changes

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

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

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

C. Pupil reflexes- sluggish

2. Intraocular pressure changes

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


For this test, repeated observations of IOP of patient are done at frequent intervals, usually every 3 hours for 24hrs. The IOP falls mostly at night time.
The IOP is measured by tonometry, applanation tonometer is preferred. Following are 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 as early changes, advanced changes and Late changes (glaucomatous optic atrophy).

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

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

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

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


Diagram depiction
Fundus examination

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


-slightly oval cups
-difference in symmetry of cups
-increase in 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:-


-marked cupping
-shifting of retinal vessels towards nasal side
-crescent shadow due to thinning of neuroretinal rim
-pulsation of retinal arterioles
-laminar dot sign- from lamina cribrosa.

III. Glaucomatous optic atrophy- Late changes in primary open angle glaucoma include:-


-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


-These appear only when 40% of axons of 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 degree from fixation) and relate with optic disc changes.

The sequence of visual field loss due to glaucoma are:-

a. Isopter contraction- earliest field defect occurring in glaucoma. There is mild and not diagnostic constriction of central and peripheral field.

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

baring of the blind spot in glaucoma

c. Small wing-shaped paracentral scotoma- it is earliest clinically significant field defect.


d. Seidel scotoma- paracentral scotoma + blind spot = sickle shaped scotoma

Seidel scotoma in glaucoma poag

e. Arcuate or Bjerrum’s scotoma- extension of seidel scotoma


f. Double arcuate scotoma or Ring scotoma- joining of two arcuate scotoma


g. Roenne’s central nasal step. It is created when the two arcuate scotomas run in different arcs and join.


h. Peripheral field defects

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i. Advanced glaucomatous field defects- visual field defects continue to progress until a small part of central vision (tubular vision) is left.

Investigations of Primary Open Angle Glaucoma

1. Gonioscopy- Clearly reveals Open Angle Glaucoma.
2. IOP investigations:- These include Tonometry, Diurnal variation and Water drinking test:-
a. Tonometry- Applnation 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:-
a. Slit lamp biomicroscopy- show normal anterior segment.
b. 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:-
a. Perimetry- to detect visual field defects
b. 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 Water drinking test, other provocative tests include combined water drinking and tonography, bulbar pressure test, prescoline testand caffeine test.

Management of Primary Open Angle Glaucoma

These include Medical treatment, Laser trabeculoplasty and Surgery:-

A. Medical treatment

Drugs which Increase flow of aqueous humour- LAP

(i) Latanoprost(0.005%: once daily)- drug of first choice for the treatment of POAG (provided patient can afford to buy it). It increase the uveo-scleral outflow of aqueous humor.

(ii) 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).
(iii) 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 spasm of accommodation and miosis. Pilocarpine acts by contracting longitudinal muscle of ciliary body and opening spaces in trabecular meshwork, thereby mechanically increasing aqueous outflow.
Drugs which Decrease production of aqueous humour- BD
(i) Topical Beta blocker- these are drugs of choice and are affordable by everyone. Reduce IOP due to their 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)
-Cartelol- patient with hyperlipidemias or atherosclerotic cardiovascular disease-(1%: 1-2 times/day)
(ii) 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, also called Filtration surgeries. These include most popular- Trabeculectomy and others like Viscocanalostomy and Deep sclerectomy.

A very wonderful video of Trabeculectomy is shown here:-

So, this was all about Primary Open Angle Glaucoma. To check out basics again, click Basics of Glaucoma.

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