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.
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
- Pathogenesis of Primary Open Angle Glaucoma
- Aetiology of Primary Open Angle Glaucoma
- Clinical features of Primary Open Angle Glaucoma
- Investigations of Primary Open Angle Glaucoma
- Management of Primary Open Angle Glaucoma
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
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.
Signs of Primary Open Angle Glaucoma
1. Anterior segment changes
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
NORMAL OPTIC DISC:-
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)
-hemorrhagic which appear broken like pieces
II. Advanced changes- Advanced changes in primary open angle glaucoma include:-
-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.
c. Small wing-shaped paracentral scotoma- it is earliest clinically significant field defect.
d. Seidel scotoma- paracentral scotoma + blind spot = sickle shaped scotoma
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
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
Management of Primary Open Angle Glaucoma
A. Medical treatment
(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.
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.
B. Laser trabeculoplasty
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.