Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

‫د دمحم قاسم النويني‬

Glaucoma /2

Primary Angle Closure Glaucoma (PACG)

Definition: is a condition in which there is obstruction to aqueous outflow due
to partial or complete closure of the angle by peripheral iris.
Unlike POAG, the diagnosis is by examination of anterior segment and
gonioscopy. Presence of a normal optic disc and absence of visual field loss
does not preclude (exclude) diagnosis of PACG (as it is acute so the damage
doesn’t occur unless the condition left without treatment and blindness happen
within few days or even hours). In addition, there are shallow AC and convex
iris-lens diaphragm.
Risk factors:
1- Age: average age 60 years, usually it rarely occur before this age, as the
AC is still deep.
2- Gender: ♀/♂ = 4/1.
3- Race: whites 6% of glaucomas, more common in South East Asians,
Chinese and Eskimos, uncommon in Blacks.
4- Family history: ocular anatomical features are inherited, 1st degree relatives
are at increased risk.
Anatomical predisposing factors:
1- Relative anterior location of iris-lens diaphragm.
2- Shallow anterior chamber (AC).
3- Narrow entrance to anterior chamber angle.

Classification of PACG:
1- Latent PACG: the asymptomatic phase of PACG.
Signs: slit-lamp examination:
a- Shallow AC. b- Convex-shaped iris-lens diaphragm.
c- Close proximity of iris to cornea. d- Normal IOP.
Gonioscopy: shows an occludable angle (grades 2,1 & 0).
Management:
An eye that has latent PACG (which is detected by routine examination ±
family history) needs bilateral YAG laser PI (peripheral iridotomy) as
prophylactic treatment.
If no treatment done the following may happen:

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

a- Remain normal for long life.

b- Acute or intermittent PACG.
c- Develop chronic PACG without passing through acute or sub-acute phase.
2- Intermittent (sub-acute) PACG:
In patient with anatomical predisposing factors of PACG and an occludable
angle, the mid-dilated position of the pupil is critical position as pupillary block
can happen due to direct contact between the iris and lens at the pupillary
margin. Pupillary block leads to increase IOP in the PC more than AC and
anterior bowing of iris periphery (iris bombe) toward corneal periphery till it
occlude the angle of the AC which causing sudden rising of IOP. Then the
pupillary block is spontaneously broken duo to exposure to bright light, the
pupil is miosed, angle opens and IOP drops.

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

Attack could be precipitated by:

a- Physiological mydriasis (e.g. watching TV in dark room, emotional stress).
b- Physiological shallowing of AC (prone or semi-prone position; as reading
or sewing), as the lens moves forwards.

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

c- Iatrogenic; by using mydriatic drugs. These drugs should be avoided in

patients with shallow AC and Narrow angles.
Clinical features:
- Transient obscuration of vision.
- Halos around light due to corneal edema.
- Eye ache (due to rapid elevation of IOP).
- Frontal headache.
- Recurrent attacks, broken after 1-2 hours by physiological miosis (exposure
to bright sunlight or sleep).
Treatment:
YAG laser PI to the affected eye and prophylactic PI to the fellow eye.
Without treatment, acute or chronic PACG will develop.
3- Acute congestive angle-closure glaucoma:
This condition is caused by a sudden total closure of the angle.
Clinical features:
Symptoms: a- Rapidly progressive impairment of visual acuity, due to corneal
oedema.
b- Periocular pain + congestion.
c- Nausea and vomiting in severe cases.
Signs seen with slit-lamp:
a- Ciliary flush due to injection of limbal and conjunctival blood vessels.
b- IOP severely elevated (>50mmHg).
c- Corneal oedema with epithelial vesicles.
d- Shallow AC + peripheral iridocorneal touch.
e- Aqueous humour flare (protein) + cells.
f- Pupil vertically oval + fixed in mid-dilated position, not reactive to light
and accommodation.
Treatment is surgical….
,but initially we start medical treatment to control elevated IOP which is by:
a- IV acetazolamide: 500mg followed by 250mg q.i.d orally.
b- Hyperosmotic agents: - IV Mannitol 1g/kg(5cc/kg) of 20%.
- Oral glycerol 1g/kg of 50% with orange juice.
c- Topical therapy:
i- Pilocarpine 2% x4 to affected eye, it causes miosis and pulls iris periphery
away from cornea.
ii- Pilocarpine 1% x4 to unaffected eye (as prophylaxis).
iii- Beta-blocker x2, only for the affected eye.
iv- Topical steroid: to avoid permanent adhesion between the periphery of
iris and the cornea (peripheral anterior synechia)( PAS).

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

Surgical treatment:
a- We do bilateral YAG PI, then we stop Pilocarpine to fellow eye
(unaffected) and we decrease medication of affected eye, 1 st we stop IV
Mannitol, then oral acetazolamide, if IOP is elevated again (due to peripheral
anterior synechiae (PAS) formation) go to:
b- Trabeculectomy is indicated, which means that 50% of the angle is already
closed by permanent anterior synechiae and YAG laser PI with topical
medications alone cannot control IOP.

4- Chronic angle closure glaucoma:

Types:
a- Creeping synechial obstruction of the angle, gradual and progressive
(narrow angle is closed by gradual formation of synechiae).
b- Synechial obstruction of the angle as a result of intermittent (sub-acute)
attacks.
c- Mixed combination of POAG + narrow angles usually associated with long
use of miotics (pilocarpine).
Treatment:
a- PI (YAG laser) for both eyes.
b- If IOP is not controlled with PI alone, the trabeculectomy is indicated to
one or both eyes.
NOTE
In general, the most common type of glaucoma is POAG 65%, followed by
secondary glaucomas 20%, then comes PACG 12% (especially the acute
one) then and the least common ones are the congenital glaucomas 3%.

Congenital glaucomas
They are uncommon (not rare), sever and potentially blinding disease.
Types:
1- True congenital glaucoma: represents (40%) of all congenital glaucoma,
the IOP is elevated during intra-uterine life.
2- Infantile glaucoma: represents (55%) of congenital glaucomas, the disease
is manifested before 3 years age, but the patient was born with normal IOP.
3- Juvenile glaucoma: represents (5%) of congenital glaucomas, least
common, present after 3 years but before reaching 16 years (>16 → adult
glaucoma).
In general, congenital glaucoma:
- It occurs 1 in 10,000 births.

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

- Most cases are sporadic, some are inherited as autosomal recessive trait.
- 65% in boys and 35% in girls.
- Bilateral in 75% and 25% unilateral.

Aetiology:
Anterior segment dysgenesis, defect in cleavage during fetal development,
so we have abnormal angle and abnormal development of anterior chamber, so
there will be no trabecular meshwork and the angle is completely obstructed.

Clinical Features:
The first sign noticed by parents is the corneal haze:
1- Corneal haze (or opacity): caused by epithelial oedema and corneal
clouding secondary to elevated IOP.
2- Photophobia, lacrimation and blepharospasm: due to damage of corneal
endothelium producing corneal oedema.
3- Buphthalmus: a large eye due to elevated IOP prior to the age of 3 years,
so we should expect elevated IOP in every child with large eye below age of 3
years.
- Sclera also enlarges becoming stretched and takes blue appearance due to
the enhanced visualization of underlying uvea.
- Corneal enlargement leading to deep AC (Anterior chamber), zonule
becomes stretched, rarely lens becomes subluxated .
- Ocular enlargement leads to axial myopia.
4- Breaks in descemet's membrane (Haab striae). (due to stretching).
5- Optic disc cupping, C/D >0.3, it is not a reliable sign, as stretching of
sclera will cause enlargement of scleral canal and cupping due to separation of
nerve fibers, and as soon as we control IOP, C/D will return to normal.
Reversible cupping
6- Visual field: cannot be done as majority of cases are under 3 years and the
diagnosis is straight forward by clinical signs.
* The intraocular pressure should be check under general anesthesia by using
Perkins hand-held applanation tonometer or Schiøtz tonometer.
Management: is always surgical, and no role for medical treatment, and
surgery should be done as early as possible. (On day of delivery)
Diagnosis:
1- Signs.
2- Checking IOP.
3- Corneal diameter: normally, corneal diameter at delivery is ≤ 10 mm, if
corneal diameter was > 12mm at age of 1 year, or 13mm at any age, then it is

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

viewed with suspicion. In children, corneal diameter is regarded as visual

field assessment in adults to follow patients with glaucoma.
Surgery:
1- Goniotomy. We incised the trabecular meshwork to create a direct
communication between the anterior chamber and schlemm's canal bypassing
the trabecular meshwork, this operation needs clean cornea to use the
instruments and visualized the structures of the angle of the AC. successful
rate is 80%.
2- Trabeculotomy. From the limbus, we introduce a probe inside the
schlemm's canal and then we open the inner wall of it toward the AC. Also
here there is a direct communication between the anterior chamber and
schlemm's canal bypassing the trabecular meshwork
3- Trabeculectomy: same operation discussed in previous lecture, but there is
high failure rate due to very high activity of fibroblast cells.

The motto is: "Operate as soon as possible even a one day old baby" .

Secondary glaucomas

1- Lens-related glaucoma:
a- Phacolytic glaucoma (lens protein glaucoma):
It occurs in association with hypermature cataract (leakage of lens materials
and shrinkage of lens). Leaked lens material is engulfed by microphages. The
trabecular obstruction is caused by high molecular weight lens proteins which
have leaked through the intact capsule into the aqueous humour or by
microphages laden with these proteins.
Treatment: control IOP medically, then surgery (cataract extraction).

b- Phacomorphic (Intumescent) glaucoma:

Is acute secondary angle-closure glaucoma precipitated by an intumescent
cataractous lens. Swelling of lens pushes the lens-iris diaphragm forward to
occlude the angle of the anterior chamber. Presentation is the same like that of
PACG but with significant cataract.
Treatment: surgery (cataract extraction).

c- Phacoanaphylactic (phacoantigenic) glaucoma:

Is an autoimmune reaction to lens proteins occurring in an eye with a
traumatic ruptured anterior capsule (large lens matter passing through a
rupture in capsule, this matter is regarded as foreign body and antibodies

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

against it is produced). Therefore, there will be occlusion of the pores of

trabecular meshwork by immune complexes and cells.
Treatment: cataract extraction.

2- Neovascular glaucoma (NVG):

Is a relatively common and serious condition, which occurs as a result of iris
neovascularization (Rubeosis iridis).
The common aetiopathogenic factor is severe, diffuse and chronic retinal
ischaemia.
Retinal ischaemia leads to hypoxic retina which tend to produces
vasoproliferative growth factors in an attempt to revascularize hypoxic areas
(form new blood vessels to compensate for hypoxia), but unfortunately these
blood vessels are very fragile, so they may rupture suddenly and patient get
sudden blindness due to retinal or vitreous hemorrhage. These vessels may
rupture spontaneously or during valsalva manoeuvre. However, these factors
also diffuse in to the anterior segment and initiate Rubeosis iridis
(neovascularization of iris) and neovascularization in the angle of the anterior
chamber (leading to occlusion of trabecular meshwork).
* If you see rubeosis iridis in any person, you can say without any doubt that
there is retinal ischaemia.

Causes of retinal ischaemia (causes of NVG):

a- Central retinal vein occlusion(CRVO). (commonest cause)
b- Diabetes mellitus (proliferative diabetic retinopathy).
c- miscellaneous, e.g.: - Carotid obstructive disease.
- Central retinal artery occlusion.
- Intraocular tumours.
- Long standing retinal detachment.
- Chronic intraocular inflammation.
Treatment:
1- Medical treatment is initially with topical beta-blockers and
acetazolamide. Topical atropine and steroids may decrease inflammation
and make the eye more comfortable and less congested, even if IOP
remains high.
2- Panretinal photocoagulation(PRP) by laser: We destruct retinal tissue
in order to decrease O2 consumption and control hypoxia. We
photcoagulate the mid periphery and the periphery of retina and we
preserve the macula only.
3- Filteration surgery may be consider if still there is useful vision either by
trabeculectomy with anti- metabolite or by use artificial filtering shunts.

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

4- Cyclodestruction by trans-scleral diode laser or trans-scleral

cyclocryotherapy which lead to destructs part of Ciliary body and
decrease aqueous production.
5- Retrobulbar alcohol injection is useful in relieving pain by destruction
of sensory enervation.
6- Enucleation (evacuation of all intraocular contents and we leave just the
sclera) may be considered if all else fails.

3- Inflammatory glaucomas
Glaucomas secondary to intraocular inflammation frequently present a
considerable diagnostic and therapeutic challenge. Although in some cases
the elevation of IOP is transient and innocuous, often it is persistent and
severely damaging.

A/In acute anterior uveitis, the IOP is usually normal or subnormal as a result
of concomitant ciliary shutdown. Occasionally, however, a trabecular-block
open angle glaucoma develops secondary to obstruction of aqueous outflow,
most commonly just as the acute inflammation is and ciliary body function
returning to normal. The block may be caused by either inflammatory cells
and debris or acute trabeculitis. The IOP usually returns to normal once the
inflammation has subsided.

B/ Secondary angle closure is caused by 360° iridolenticular adhesions

(seclusio pupillae), The pupil block obstructs the passage of aqueous humour
from the posterior to the anterior chamber, and the increased pressure in the
posterior chamber causes an anterior bowing of the peripheral iris (iris
bombé), If severe, iris bombé is associated with a shallowing of the anterior
chamber, and apposition of the peripheral iris to the trabeculum and
peripheral cornea. If this occurs in an eye with active inflammation, the iris
sticks to the trabeculum and the iridocorneal contact becomes permanent
with the development of peripheral anterior synechiae (PAS).

Slit lamp examination shows seclusio pupillae, iris bombé and a shallow
anterior chamber.

Gonioscopy shows angle closure from irido-trabecular contact.

Treatment involves the following measures:

1. Prevention of synechial angle closure can be effective by a reduction in

the 'stickiness' of the peripheral iris using a combination of intensive
topical steroids and anterior sub-Tenon's injection of a long-acting
depot steroid preparation.

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Glaucoma/5th year/2021-2022 Dr Mohammed Qasim AL NUWIANI

2. Lowering of IOP with topical ß-blockers and/or sympathomimetics or .

Carbonic anhydrase inhibitors. never by prostaglandin analogue

3. Nd-YAG laser iridotomy may be required if medical therapy fails.

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