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Glaucoma

Aqueous Humor

 Composition of Aqueous

The aqueous is a clear liquid that fills the anterior and posterior chambers of the
eye. The composition of aqueous is similar to that of plasma except for much
higher concentrations of ascorbate (Vit C), pyruvate, and lactate and lower
concentrations of protein (if protein increase in aqueous called plasmoid
aqueous ), urea, and glucose.

Aqueous humour secretion Decreased in


1- Hypoxia
2- Hypothermia
3- Drugs (beta-blokers,sympathomimetics and CAI)
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4- Cyclodestructive (cyclotherapy and laser ablation) 0912117973
5- Ciliary body shutdown ( Iridocyclitis and retinal detachment)

 Aqueous humor formed by

Ciliary body processes through


1-Active process (80%)
By Carbonic anhydrase enzyme ((IN non-pigmented ciliary epithelium))
2-Passive process (20%)
By Ultra-filtration, Diffusion

 Flow of Aqueous (Circulation)

Aqueous is produced by the ciliary body. Entering the posterior chamber, the
aqueous passes through the pupil into the anterior chamber and then to the
trabecular meshwork in the anterior chamber angle then to episcleral veins

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 Aqueous drainage

1-Major part (85%) (Trabecular outflow)


2-Minor part (15%) (Uveo-scleral outflow)

 Function of aqueous humour

1-Transport nutrients to avascular structure (e.g. Lens)


2-Maintenance of normal intraocular structure

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The angle of anterior chamber
It's the recess that lies between the periphery of the cornea & iris root.

The angle of anterior chamber examined by Goniolens (Gonioscopy)

Structures seen through Goniolens

1- Schwalbe's line (End of descement membrane)

2- Trabecular meshwork :- in cross section it's appear triangular with it's

Apex :- Attached to the Schwalbe's line

Base :- Attached to the sclera spur


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3- Sclera spure :- give origin to the longitudinal ciliary muscle
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4- Base of ciliary body

5- Root of the iris

The following structure are NOT seen by Gonioscopy ((Canal of schlemm))

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 Grading of angle width

Grade 0 Iridocorneal contact (NO angle structures can be identified)


Grade 1 Only Schwalbe's line
Grade 2 Grade 1 + trabecular meshwork
Grade 3 Grade 2 +sclera spure
Grade 4 Grade 3 + ciliary body

**N.B
Myopic eyes have wide angles, and Hypermetropic eyes have narrow angles.

Intraocular pressure (IOP)


-Normal range (11-21mmHg)
-Diurnal variation <4 mmHg (higher in the morning and lower in the
afternoon)
-Difference between two eyes is usually < 4mmhg
-Drinking 2 liters of water elevate the IOP within 30 minute (NOT exceeding
4mmhg)
-Factor affecting IOP:- Heart rate, Blood pressure, Body tempreture

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 Measurement of intraocular pressure

1- Digital palpation ((Rough test))

Value :- to test tension of sclera (rigidity)digitally


The patient is asked to look down, without closing his eyes; The eye is fluctuated
between both index finger of examiner.

2- Tonometry

Tonometry is measurement of intraocular pressure.

A- Applanation Tonometry (Goldmann tonometer)

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This is attached to the slit lamp and measures the force required to flatten a fixed
area of the cornea. (while patient is sitting )
Disadvantage: -need local anesthesia ,fluorescin stain ,cross infection, expensive
Advantage: - more accurate

B- Indentation Tonometry (Schiotz Tonometry)

Is portable and measures the corneal indentation produced by a known weight.


(while patient is supine )
Disadvantage: - Schiotz is less accurate, Cross infection. Need local anesthesia
Advantage: - Cheap, easy to use, does not require slit lamp, Used when it is not
possible to use the Applanation.

C- Tono-Pen Tonometry :- portable with contact

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D-Air-puff Tonometry :- portable without contact (low risk of infection)

Glaucoma
Triad

1- Pathological IOP 2- Visual field defect

3- Glaucomatous cupping of the optic disk (Optic nerve damage)

IOP Visual field Optic nerve damage

Glaucoma Increase Abnormal Present


Ocular Hypertension Increase Normal NO
Normal tension glaucoma NTG Normal or Abnormal Present
((low tension glaucoma)) Low

 Classification of Glaucoma

1- Congenital ‫ﻣدرﺳﺔ اﻟﻔراﺷﺔ‬


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2- Acquired
A- Primary (open) & (close)
B- secondary (open) & (close)
***N.B
In general, primary open-angle glaucoma is most common and accounts for about 55%
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of cases; secondary glaucoma are next (30%), followed by primary angle-closure
7
(12%) and congenital (3%).
Congenital Glaucoma
It can be subdivided into

(1) Primary congenital glaucoma

In which the developmental abnormalities are restricted to the anterior chamber


angle e.g.
1- Abnormal mesodermal membrane in the angle.
2- Failure of complete separation of iris from the cornea.
3-Absence of canal of schlemm's.

(2) Secondary congenital glaucoma


Including Aniridia, Sturge-Weber syndrome, Neurofibromatosis-1, Marfan's
syndrome, congenital rubella, Retinoblastoma, Uveitis, Trauma, Retinopathy of
prematurity

Primary Congenital Glaucoma (Buphthalmos)


 Epidemiology

Primary congenital glaucoma is an inherited Autosomal recessive (AR)


disorder. It is Bilateral in approximately 70% of all cases; boys are affected in
approximately 70% of all cases, congenital glaucoma is rare, congenital
glaucoma is manifest at birth in 50%, and diagnosed by the end of the first year
in 80%. Positive family history.

 Symptoms
The earliest and most common symptom is lacrimation. Photophobia may be
present (due to irritation of nerve ending)

 Signs

Eyeball Chronically elevated intraocular pressure in children under the age of three will lead
to enlargement of globe.
Cornea 1- Corneal edema (due to endothelium damage by increase IOP)

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2- Macrocornea (above 11.5 mm is considered signi icant)

3- Haab's striae (horizontal tears of Descemet's membrane)

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4- Curvature of cornea decreased (flat cornea)
Sclera Blue sclera

A/C Deep
Pupil Large
Iris Iridodenesis (iris tremulous)
Lens Flattened & displaced backward & displacement
Tension but less than expected (distended due to high sclera elasticity)
High
Fundus Glaucomatous cupping of the optic disk
Refraction Axial myopia (less than expected due to flat cornea, flat lens)

 Complication

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A- Decrease of vision
1- Subluxation 2- complicated cataract 3-myopia
4-optic nerve atrophy 5- corneal opacity

B- Unilateral: - Amblyopia

C-Bilateral: - Nystagmus

 Differential Diagnosis

1- Corneal enlargement: - Megalocornea, high myopia


2- Blue sclera
3- Watery eye: - Nasolacrimal duct obstruction.
4- Cloudy cornea: - Trauma at birth or keratitis (intra-uterine infection)

 Diagnosis

1- History
Positive family history
2- Examination
The enlarged corneal diameter is a characteristic finding. The cornea normally
Measures 9.5mm on average in normal newborn infants. Enlargement
to more than 10.5mm suggests childhood glaucoma
3- Measurement of intraocular pressure.
Measurement is facilitated by giving the hungry infant a bottle during the
examination. Feeding distracts the baby, and a measurement usually can be
obtained easily. Such a measurement is usually far more accurate than one
obtained under general anesthesia as narcotics, especially barbiturates and
halothane, reduce intraocular pressure.
4- Gonioscopy of the angle of the anterior chamber.
Examination of the angle of the anterior chamber provide etiologic information.
5- Optic disk ophthalmoscopy.
Glaucomatous cupping of the optic disk

 Prognosis

In untreated cases blindness occurs early. The eye undergoes marked stretching
and may even rupture with minor trauma.

 Treatment
Childhood glaucoma is treated surgically only.
Medical treatment only used before surgery to control IOP

If corneal diameter LESS than 13 mm do (goniotomy or trabeculotomy)

1- Principle of goniotomy
(Establish communication between A/C & canal of schlemm)

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With a gonioscope in place on the eye, the goniotomy scalpel is advanced
through the anterior chamber to the trabecular meshwork. The trabecular
meshwork can now be incised as far the canal of Schlemm over an arc of about
120 degrees to permit drainage of the aqueous humor
These operations can only be performed when the cornea is clear enough to
allow visualization of the structures of the anterior chamber.

2- Principle trabeculotomy
(Establish communication between A/C & canal of schlemm)
After split-thickness scleral flap have been raised, access to the canal of Schlemm
and the canal is probed with a trabeculotome. Then the trabeculotome is rotated
into the anterior chamber
This operation can also be performed when the cornea is opacified.

If corneal diameter MORE than 13 mm or (goniotomy & trabeculotomy


failed) then do Trabeculectomy

Goniotomy & trabeculotomy are useless if corneal diameter is more than


13 mm as the canal of schlemm's is usually absent

Primary Open-Angle Glaucoma ((POAG))


((Chronic simple glaucoma))
Primary open angle glaucoma is the most common form of glaucoma and
accounts for over 55% of adult glaucoma
The disease is four times more common and more likely to cause blindness in
blacks.
Bilateral but ((asymmetrical))
equal in both sex (slightly more common in male)

 Etiology
The cause of primary open angle glaucoma is not known
But maybe caused by sclerosis by trabecular meshwork lead to narrowing of
spaces of Fontana

 Risk Factors
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1-Age above 45
2- Race - more common, earlier onset and more severe in blacks
3-Inheritance (AD)
4- Positive family history
5-High Myopia , Ocular hypertension , DM ,HTN , Migraine
6-Retinal disease (CRVO, 5% of patient with rhegmatogenous RD , 3% RP )
7-Steroid (Topical > Systemic)

 Symptoms
((Asymptomatic)) The majority of patients with primary open angle glaucoma
do not experience any subjective symptoms for years. However, a small number
of patients experience occasional unspecific symptoms such as headache,
blurred or decreased vision that the patient may attribute to lack of eyeglasses
or insufficient correction. night blindness due to peripheral field defect

 Signs
1- High IOP
2- Glaucomatous cupping
3- Field defect.

 Diagnostic considerations

1- Measurement of intraocular pressure.


Elevated intraocular pressure in a routine ophthalmic examination is alarming
sign.
(A) Tension in both eyes: - normally the difference less than 4mmhg, bigger
difference more than (8mmhg) suggestive
(B) Diurnal variation: - normally less than 4mmhg if increased more than
(8mmhg) suggestive

2- Gonioscopy.
The angle of the anterior chamber is open and appears as normal as the angle in
patients without glaucoma.

3- Ophthalmoscopy.
Examination of the optic nerve for glaucomatous cupping

Glaucomatous cupping
Early changes Late changes
1- large C/D ratio (0.4) 1-large C/D ratio more than 0.7
2-Asymmetrical of C/D between 2 eyes 2-has over-hanging (undermined) edge
3- Vertical elongation of optic cup 3- the vessels appear as interrupted
4-splinter hemorrhage on disc 4-Nasal shift of the vessels

4- Visual field defect


Due to optic nerve damage
(Due to increase of IOP lead to mechanical pressure with ischemia on optic.N)
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Visual field measured by Perimetry

Changes in central field


1- Paracentral scotoma: - isolated, if connected with blind spot called arcuata
scotoma
2- Seidel scotoma: - it's elongation of blind spot above or below
3-Arcuata (bjerrum) scotoma
4-Ring (annular) scotoma: - due to fusion of 2 arcuata scotoma

Changes in peripheral field


1- Nasal field contraction
2-Roenne's nasal step
3- Marked contraction (more nasally) = Tubular field
4- At end macula involved lead to loss of vision

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 Treatment

1- Medical therapy
Medical therapy is the treatment of choice for primary open angle glaucoma with
regular follow up.

Drug Action Side effects


A- Adrenergic antagonist Decrease Production of Local:- superficial punctuate keratitis
beta blockers aqueous humor. & decrease of tear production
(FIRST line of treatment) Systemic:-bradycardia & hypotension
a-Timolol: 0.25 -0.5% and increase bronchospasms,
twice daily insomnia, depression, decrease libido
b-Betaxolol: 0.5% Contraindications:
Asthma , DM, Heart failure

B- Prostaglandin Increase uveo-scleral Local:- changes in the color of the iris


analogues: aqueous humor in 16% of all patients.(specially with

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Latanoprost (Xalatan) drainage latanoprost), eyelash hypertrichosis &
(FIRST line of treatment) hyperpigmentation of lashes and
0.0005 %drops periorbital skin
once daily systemic :- headache , nausea

C-Direct
Sympathomimetic agents
(adrenergic agonist)

Epinephrine (alpha –beta Improve drainage of Local:- (allergy) ,Macular &corneal


agonist) aqueous humor edema ,conjunctival pigmentation
1-2% twice daily Systemic:- 10–15% of patients
develop allergy. Hypertension,
headache

Brimonidine: 1-Improves drainage of Local:-allergy conjunctivitis


(alpha2 agonist) aqueous humor by Systemic: -hypotension & dry mouth.
0.5% twice daily reducing episcleral
venous pressure
2-Reducing aqueous
humor production by
decreasing ciliary body
perfusion
D-Parasympathomimetic Improve drainage of Local:- temporary myopia due to
Agents– aqueous humor contraction of the ciliary muscle &
Pilocarpine 1-4% The effect is probably headache. Miosis with worsening of
(3-4 drop daily) purely mechanical via the night vision and narrowing of
contraction of the the peripheral field of vision,
ciliary muscle lead to follicular conjunctivitis, Retinal
pulling on the Detachment (Very rare)
trabecular meshwork
and sclera spur lead to Systemic :- diarrhea , increase
increase aqueous sweating
outflow Contra-indication:- Pupillary block
glaucoma
E-Carbonic anhydrase Reduces aqueous
inhibitors: humor production.
–Topical Dorzolamide: ((By inhibition of Systemic :-Prolonged therapy causes
2% drop carbonic anhydrase malaise, nausea ,depression ,anorexia
2-3 times daily enzyme)) ,weight loss ,and decrease libido in of
chemically derived from Glaucoma patients
sulphonamides

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Systemic
–Systemic Acetazolamide paraesthesiae (hypokalemia),
(Dimox) renal stone , bone marrow
250mg with potassium depression(Aplastic anemia) , Steven
johansen syndrome(skin rash),
nausea, vomiting, diarrhea ,weight
loss, malaise, fatigue, depression, and
decreased libido
Contraindication
They have sickle cell anemia
They are allergic to sulfa medications
((which are chemically derived
from sulphonamides))

2- Laser Trabeculoplasty

Application of laser (usually argon) burns via a Goniolens to the trabecular


meshwork facilitates aqueous outflow by induced minimal scars at trabecular
meshwork lead to it's contraction so lead to widening of spaces of Fontana. Laser
Trabeculoplasty may be used in the initial treatment of primary open-angle
glaucoma. Treatments can be repeated

3- Surgical treatment of primary open angle glaucoma.

Indications

1- Medical therapy is insufficient.


2- The patient does not tolerate medical therapy.
3- The patient is not a suitable candidate for medical therapy due to lack of
Compliance

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A- Trabeculectomy is the procedure most commonly used to bypass the normal
drainage channels, allowing direct access from the anterior chamber to the
subconjunctival. (Bleb)

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The major complication is fibrosis in the episcleral tissues, leading to closure of
the new drainage pathway. Perioperative or postoperative adjunctive treatment
with antimetabolites such as 5-fluorouracil and Mitomycin C reduces the risk of
bleb failure.
***N.B
1-Implantation of a silicone tube (Ahmed Valve) to form a permanent channel for
aqueous flow out of the eye is an alternative procedure for eyes that are unlikely to
respond to trabeculectomy.

Normal tension glaucoma((NTG)) ((NTG = low tension glaucoma))


*Is a variant of POAG
*Predominantly a disease of the elderly and more common in females
*A mean IOP equal or less than 21mmHg
*Glaucomatous OD damage and visual field loss
*Open angle on Gonioscopy
*Absence of secondary causes for glaucomatous optic disc damage
*Above age of 40 years 0.2%
*Accounts for 16% of all cases of POAG

 Complications of Trabeculectomy
1- (((Intraoperative)))
A- Suprachoroidal hemorrhage B-Subconjunctival hemorrhage C-Hyphema
2- (((Early postoperative)))
A-Flat AC B-Endophthalmitis C-Suprachoroidal hemorrhage
D-Hyphema E-Cystoid macular edema
3- (((Late postoperative)))
A-Filtration failure B-Endophthalmitis C-Cataract progression
D-Refractive error E-visual field error

Primary closed angle glaucoma ((PCAG))


Definition: - is a condition in which elevation of IOP occurs as a result of
obstruction of aqueous outflow by partial or complete closure of the angle by
peripheral iris.

Bilateral but asymmetrical, more common in Elderly Nervous Female ,

 Etiology

(A) - Predisposing factor

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Narrow angle (shallow anterior chamber)

(1)- Hypermetropia

(2)- Old age (due to continuous increase of lens thickness)

(B) - Precipitating factors

Pupillary dilatation

Due to Mydriatic, Excitement, prolonged stay in dark lead to angle closure

Through TWO mechanism

1. Iris bombe (More important)

The pupillary border of the iris is close to anterior surface of the lens increase
of pressure in posterior chamber iris bomb contact between the root of the
iris & the cornea peripheral anterior synechiae closure of the angle

2. Iris crowding (Less important)

Root of dilated iris is crowded in angle, lead to obstruction of angle

 Clinical picture

***(1)- Prodromal stage ((Intermittent))

Transient mild attack of Headache, blurred vision & colored haloes around light
(due to corneal edema) due to increased IOP on top of precipitating factor. The
attack is relived by sleep & exposure to light (due to miosis, lead to open angle)

Diagnosis by

1- History

2- Tonometry Normal IOP between attacks elevated IOP during attack

3- Gonioscopy Narrow angle

4- Provocation tests

A- Mydriatic test

Intraocular pressure measured before & after mydriatic

If difference between two reading 8mmhg or more Diagnostic

B-Dark room test

Intraocular pressure measured before & after 1 hour in dark room

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If difference between two reading 8mmhg or more Diagnostic

***(2)- Acute stage (acute congestive glaucoma)

Symptoms Signs
* Rapidly progressive unilateral of Lid edema
headache & ocular pain Conjunctiva ciliary congestion
Cornea cloudy
*Decrease of vision ((due to corneal edema A/C shallow
,optic nerve ischemia)) Iris Iris bombe
Pupil semi-dilated non reactive oval vertical
*Nausea & Vomiting with abdominal pain IOP High
due to stimulation of vagus

 Fate

With TTT resolution

With delay TTT chronic glaucoma

With no TTT absolute glaucoma

***(3)-Chronic glaucoma

Due to peripheral anterior synechiae

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IOP decrease but not to normal due to anterior synechiae

Optic nerve glaucomatous cupping

Visual field visual defect

***(4)-Absolute glaucoma

Blind painfull eye, it’s the end stage of uncontrolled glaucoma

 Treatment

Stage Treatment
Prodromal stage 1- Peripheral iridoectomy or iridotomy for affected eye
2-Prophylactic iridoectomy or iridotomy to other eye

Acute stage Hospitalization


(Emergency) Treatment mainly surgery
preceded by medical treatment to decrease IOP within 24Hr
to avoid operative complication (expulsive hemorrhage, lens displacement)
If IOP decrease after 24Hr Gonioscopy is done
If no peripheral anterior synechiae or less than 180 degree peripheral
iridoectomy or iridotomy
If there is peripheral anterior synechiae or more than 180 degree
Trabeculectomy
If IOP not decrease after 24Hr
Surgical decrease of IOP (Vitreous Tap) then done trabeculectomy
*Prophylactic iridoectomy or iridotomy to other eye
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Chronic stage Trabeculectomy

Absolute  If painfull
glaucoma (1)- Retro-bulbar alcohol
Lead to destruction of myelinated sheath of nerves ,so loss of sensation
 Disadvantage :-
a- Recurrent of sensation due to re-mylination of nerve (after 6 months )
b- Proptosis due to retro bulbar hemorrhage
c-Paralytic squint due to damage of cranial nerve (3,4,6)
(2)- cyclo-destruction (induce by partial damage to ciliary body)
Cyclodiathermy (Heat),cyclocryotherapy(freeze)
,cyclophotocoagulation(Laser)
(3)- Enucleation
 If not painfull no treatment

 Medical Treatment of acute stage

Treatment is initially directed at reducing the intraocular pressure.

Topical drug
Pilocarpine (parasympathomimetic) Action
2-4% every 5min until miosis occur then every
3hrs 1-Lead to contraction of sphincter muscle
so lead to miosis ,open angle
2-Improve drainage of aqueous humor
The effect is probably purely mechanical via
contraction of the ciliary muscle and tension
on the trabecular meshwork and scleral spur.
Side effect :- AS previous
Timolol (Beta blocker) 0.5% twice daily Decrease production of aqueous humor

Side effect :- AS previous

Systemic drug
1- Dehydrating agent (Hyperosmotic Action :- Increase blood osmolarity
agent) (1) draw water out of eye >>> decrease IOP
- Mannitol (20-25%) IV ((Most widely used))
-Glycerin (50%) orally has a sweet and Administration :- once for fear of
sickening taste. Pure lemon (not orange) juice -Brain cell dehydration
has to be added to avoid nausea -Urinary retention
(it should be used with care in diabetics because -Circulatory overload (C/I in heart failure)
change to glucose inside body )
-Isosorbide orally

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2- Systemic carbonic anhydrase inhibitor Action
(CAI) prevent formation of aqueous humor by
e.g. Acetazolamide (Dimox) with potassium inhibition to carbonic anhydrase enzyme
dose 250mg tablet or IV(if there is vomiting) S/E :- AS previous
every 6 hour Contraindication:- AS previous
3- Analgesia For pain relive
4- Anti-emetic For vomiting relive

Secondary glaucoma
Secondary open angle glaucoma Secondary closed angle glaucoma
1-Pseudoexfoliative glaucoma. 1-Rubeosis iridis.

2-Pigmentary glaucoma. 2-Trauma.


A- Anterior lens dislocation
3-Cortisone glaucoma(Drug induced B- Traumatic iridocyclitis:- cause ring synechiae
glaucoma) & occlusion-pupillae
Increased deposits of mucopolysaccharides in
the trabecular meshwork. 3-lens –induce Glaucoma
A- Intumescent cataract (Phacomrphic
4-Inflammatory glaucoma. glaucoma)
1. The viscosity of the aqueous humor increases B- Lens displacement (Anterior lens
as a result of the influx of protein (Plasmoid dislocation)
aqueous)
2. The trabecular meshwork becomes congested 4-Mydriatic drug (drug induced glaucoma)
with inflammatory cells (Hypopyon)
5-Intra-ocular tumor induce glaucoma
5-lens –induce Glaucoma by forward displacement of lens lead to
1- Phacolytic glaucoma pupillary block
2- Phacotoxic uveitis
3- Lens displacement 6-Causes in iris
A-Chronic iridocyclitis:- cause ring synechiae &
6-Traumatic Glaucoma total posterior synechiae
1- Hyphema B-Iris tumor or cyst. May produce pupillary
2- Vitreous hemorrhage (Ghost cell glaucoma) block.
3- Angle recession glaucoma
4- Traumatic iridocyclitis

7-Intra-ocular tumor can induce glaucoma


by many ways
1- Rupture of blood vessels lead to hyphema
2-Uveitis lead to hypopyon
3-Obstruction of trabecular meshwork by
malignant cells
4-Obstruction of episcleral vein by malignant
cells

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 Pigmentary glaucoma

Pigment dispersion syndrome uncommon bilateral condition characterized by


the deposition of pigment granules throughout the anterior segments. Affected
individuals are typically myopic men in the third to fifth decades of life. The
male: female ratio is 5:1
The pigment granules are released into the aqueous humor and deposited on all
anterior chamber structures, including the trabecular meshwork. Elevation of
IOP appears to be caused by pigmentary obstruction.
Treatment is as for primary open-angle glaucoma.

 Pseudoexfoliation glaucoma

In pseudoexfoliation syndrome, fine white deposits of a amorphous acellular


material are seen on the anterior lens surface (in contrast to the true exfoliation
of the lens capsule caused by exposure to infrared radiation, ie, "glassblower's
cataract"), ciliary processes, zonule, posterior iris surface, loose in the anterior
chamber, and in the trabecular meshwork. The disease usually occurs in patients
over age 65 and is reported to be particularly common in Scandinavia. Treatment
is as for primary open-angle glaucoma.

 Neovascular glaucoma ((100day glaucoma))

Neovascularization of the iris (rubeosis iridis) and anterior chamber angle is


most often secondary to retinal ischemia
Causes
1- Advanced diabetic retinopathy
2- Central retinal vein occlusion ((Ischemic type))
3-long standing RD, intraocular tumors

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Glaucoma results initially from obstruction of the angle by the fibrovascular
membrane, but subsequent contraction of the membrane leads to angle closure.
Neovascularization draws the angle of the anterior chamber
The prognosis for eyes with neovascular glaucoma is poor.

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