Glaucoma

Aqueous formation by ciliary process

A. TM outflow B. uveoscleral outflow C. iris crypts

 Introduction
Aqueous humor
Definition It is a transparent fluid that fills the anterior & posterior chambers.
Formation by the non-pigmented epithelium in ciliary processes through:
Active secretion: needs ATP & carbonic anhydrase enzyme [60%]
Ultra-filtration by difference in hydrostatic pressure (Passive process)
Diffusion by difference in osmotic pressure 40%

Ciliary processes
75 plications project into posterior chamber
Each major process consists of:
Inner capillary core & stroma
2 layers of epithelium
Outer pigmented
Inner non-pigmented
Blood aqueous barrier
Formed of tight junctions in the apical region of the non-pigmented epithelial cells

Circulation
Aqueous is secreted into the posterior chamber pass through pupil anterior chamber

Drainage
Direct outflow pathway (trabecular meshwork outflow) 80% of drainage
Indirect outflow pathway: 20% of drainage
Uveo-scleral outflow: through interstitial spaces of the C.B. & choroid
supra-ciliary & supra-choroidal spaces choroidal circulation
Through iris crypts via iris stroma.

Function
Maintenance of I.O.P important for structure integrity of globe
Nutrition for avascular structures (cornea & lens)
Optical function
 Angle

Angle by goniolens
Notice that angle is 360o
 Anatomy of the angle
Definition Recess between the root of iris & cornea.

Angle structures Scheme

I Can See Till
1- Schwalbe's line Thickened termination of Descemet's membrane
Schwalbe's line
2- Trabecular meshwork
- Sponge-like with holes (spaces of Fontana) [Holes in size towards Schlemm's canal]
- In cross section, it appears triangular:
o Apex: attached to the Schwalbe's line
o Base: attached to the scleral spur
- It is connected to Schlemm's canal collector canals aqueous veins episcleral
veins

3- Scleral spur small ridge of sclera projecting into A.C.

It is attached to the longitudinal ciliary muscle
(contraction of longitudinal muscle opening spaces of Fontana)
4- Ciliary body band small part of the ciliary base.
5- Root of iris

How to evaluate AC angle = Gonioscopy

By goniolens

The angle can NOT be seen

Principle of gonioscopy
directly using torch or slit lamp
Elimination of this refractive interface
because light emanating from
by a contact lens (goniolens)
angle undergoes total internal
permits visualization of the angle
reflection at the corneal-air
interface.
 Intraocular pressure (IOP)
Normal IOP it is the pressure under which the eye functions normally
(Average I.O.P is 10-21 mmHg)
Eye to eye variation > 4 mmHg
Diurnal variation = fluctuation > 4 mmHg
Highest in the morning & lowest in the evening; d.t. :
Venous stagnation during sleeping aqueous outflow
Extra-ocular muscle massage aqueous outflow
Circadian rhythm of steroid
Measurement of IOP see page 247

Glaucoma
Definition progressive optic neuropathy (leads to field defect), in which IOP is a major
risk factor
In glaucoma, IOP is higher than what nerve fibers can tolerate

I.O.P Optic neuropathy Filed defect

Normal N. NO NO
Glaucoma
Normotensive glaucoma N.
Ocular hypertension NO NO

Theories of optic nerve fibers damage in glaucoma

1. Mechanical theory
I.O.P posterior bowing of lamina cribrosa damage of nerve fiber layer
2. Ischemic theory
I.O.P pressure on blood vessels supplying optic nerve fibers ischemia
3. Neurotoxic theory ganglion cells apoptosis release cytokines that kill healthy cells
 Classifications of glaucoma
According to age
o Congenital
o Acquired

According to etiology
o 1ry
o 2ry

According to angle
o Open
o Closed (by iris)

Absolute glaucoma
The end stage of any glaucoma (glaucomatous optic atrophy + no PL)
 1ry angle-closure glaucoma (PACG)
Definition of I.O.P d.t. closure of angle by iris periphery, in absence of other causes of
angle closure.
Incidence
Age: Old age
Sex: : = 4:1
Laterality: Bilateral (one eye precedes other)
Etiology
(A) Predisposing factors shallow A.C narrow angle
Hypermetropia (small eyes) shallow A.C
Old age: progressive in lens thickness pushing iris forward shallow A.C
Nervous individuals: imbalance between sympathetic & parasympathetic tone
unstable vasomotor reaction C.B. congestion pushing iris forward shallow A.C
(B) Precipitating factors mid-pupillary dilatation by:
Mydriatic drugs e.g. atropine, adrenaline, phenyl ephrine .
Prolonged stay in dim illumination [most attacks occur at evening]
Excitement (sympathetic)
(C) Mechanism of IOP
Iris bombe (The most common mechanism)
Tight apposition of iris to the lens (in eyes with narrow angle) relative pupillary block
collection of aqueous in posterior chamber pushing of iris forward iris bombe
Why this occur in mid-pupillary dilatation?
As iris is relaxed in this position, so can be easily pushed forward.
If the attack does NOT relieved P.A.S. formation permanent closure of angle
Iris crowding (plateau iris): (less common mechanism)
In which the root of dilated iris is crowded at the angle occluding it.

Iris bombe
 Clinical picture (stages) of 1ry angle-closure glaucoma
Prodromal stage = Intermittent = Sub-acute P.A.C.G
Acute (congestive) stage of P.A.C.G
Chronic stage = Chronic angle-closure glaucoma
Absolute glaucoma
Atrophic stage

Prodromal stage = Intermittent = Sub-acute P.A.C.G

Definition Mild transient attack of I.O.P,
Which stopped spontaneously by miosis (on exposure to light or sleep)
Triggered by: dim light
Relieved by: exposure to bright light
Symptoms
- Pain (dull aching)
- Headache
- Vision: mild blurring of vision d.t. corneal odema
- Colored haloes around light d.t. diffraction of light by corneal odema
Signs
IOP: normal! (in between attacks)
Gonioscopy: narrow angle.
Fate either,
Attack of acute congestive glaucoma.
Chronic angle closure glaucoma (d.t. PAS) after repeated sub-acute attacks
(Without passing through an acute stage)
Treatment Bilateral upper peripheral laser iridotomy

Upper peripheral laser iridotomy

Aim: allowing a way for aqueous from posterior chamber to AC
Why upper? to be covered by lid; cosmetically & to avoid diplopia
Why peripheral? to avoid lens injury
 Acute (congestive) stage of P.A.C.G
Definition Acute of I.O.P d.t. sudden total closure of the angle.
Symptoms
Severe bursting pain referred to temple
Headache
Reflex lacrimation Reflex blepharospasm Reflex photophobia
Rapid painful of vision d.t. corneal edema optic nerve ischemia
Colored haloes around light d.t. diffraction of light by corneal odema
Nausea, vomiting & abdominal colic:
d.t. irritation of 5th nerve vagal stimulation (at brain stem)
Redness
Signs
Visual acuity: Rapid of vision (down to H.M.)
Lid: oedema
Conjunctiva: ciliary congestion + conjunctival congestion
Cornea: odema
A.C: shallow
Angle: closed
IOP: (stony hard)
Iris: iris bombe
Pupil: semi-dilated, vertically oval (d.t. iris sphincter ischemia) & irreactive (fixed)

At the attack, angle & fundus can NOT be examined d.t. corneal odema,
if we put glycerin drops odema
Fundus: congestion
Angle: closed

D.D.
Causes of red eye page 237
2ry glaucomas: e.g.
Phacomorphic glaucoma (intumescent cataract)
Glaucomato-cyclitic crisis = Posner-Schlossman syndrome:
Angle is open during attack deep A.C. Kps
2ry inflammatory glaucoma (uveitis): Kps miosis aqueous cells, flare - hypopyon

Neo-vascular glaucoma: rubeosis irides

 Treatment
It is an ocular emergency; if untreated optic nerve ischemia & CRAO
Essentially surgical

Hospitalization
Medical treatment pre-operative [given for 24 hours]
1. IOP to avoid expulsive hemorrhage
Hyper-osmotic agents e.g. mannitol 20%
Action: draw water from vitreous
Carbonic anhydrase inhibitor
Action: aqueous formation
Beta blockers
Action: aqueous formation
Miotics as pilocarpine
Action: T.M outflow + misosis (draws iris away from angle)
Pilocarpine should be started after the I.O.P. is bit lowered
At higher IOP, constrictor pupillae muscle is ischemic & unresponsive to pilocarpine

2. Inflammation steroid: inflammation & synechia formation

3. Pain systemic analgesics
Evaluate
- IF IOP vision improves, pupil constricts & congestion do gonioscopy
If angle PAS upper peripheral laser iridotomy
If angle PAS trabeculectomy
- IF failed to IOP
Trabeculectomy proceeded by posterior sclerotomy to IOP during operation
Other eye prophylactic upper peripheral laser iridotomy because it has an occludable angle

Upper peripheral laser iridotomy

Aim: allowing a way for aqueous from posterior chamber to AC
Why upper? to be covered by lid; cosmetically & to avoid diplopia
Why peripheral? to avoid lens injury

Lens extraction is an option of treatment!

Fate either,
- Resolution: if the patient gets the proper treatment
- Post-congestive stage "Posner's triad"
Glaucoma-flecken of Vogt: anterior sub-capsular lens opacity
(d.t. necrosis of sub-capsular epithelium)
Patches of iris atrophy
Presence of PAS
- Chronic angle closure glaucoma
- Absolute glaucoma

Chronic stage = Chronic angle-closure glaucoma

Definition Slowly progressive closure of the angle sustained IOP
Symptoms
Asymptomatic
Symptomatic:
- Headache
- Gradual of vision & field defect
Signs
- IOP:
- Optic nerve: glaucomatous cupping (as in POAG)
- Field: field defects (as in POAG)
- Gonioscopy:
Early cases: appositional angle-closure (NO PAS)
Late cases: PAS
Apposition can be differentiated from PAS by indentation gonioscopy
Treatment
Laser iridotomy if IOP is still elevated give anti-glaucomatous medication
if IOP is still elevated trabeculectomy
Other eye prophylactic upper peripheral laser iridotomy because it has an occludable angle
 Primary open angle glaucoma = Chronic simple glaucoma
Definition bilateral disease of adult onset characterized by:
- Open AC angle
- IOP > 21 mmHg
- Glaucomatous optic nerve damage
- Characteristic visual field defects
- NO 2ry cause for glaucoma

Incidence the most common 1ry glaucoma

Etiology Genetically-determined,
Age-related thickening and sclerosis of the TM aqueous outflow

Pathogenesis see page 6

Risk factors
1. IOP: the higher the IOP, the greater the risk (the most important risk factor)
2. Age: risk with age
3. Race: more common & more severe in black races
4. +ve family history of glaucoma
5. Myopia
6. D.M.
Clinical picture
Symptoms
Asymptomatic as the disease is:
- Gradual
- NOT painful
- Late affection of macula (=late affection of vision)
Symptomatic:
- Headache
- Dark adaptation d.t. peripheral retinal ischemia
- Early presbyopia d.t. ischemia of ciliary muscle
- Late: field defect & loss of vision
 Progressive optic nerve cupping

Undermining of disc edge angulation of blood vessels = bayoneting sign

 Signs
Gonioscopy open angle
IOP > 21 mmHg (Best measured by Goldmann applanation tonometry)
Glaucomatous optic neuropathy
Cup
C/D ratio > 0.5
Asymmetry of C/D between the 2 eyes > 0.2
Vertical elongation of optic cup
d.t. selective loss of neural rim tissue in the inferior and superior poles.
[Do NOT obey I.S.N.T rule]
Rim
Thinning of neuro-retinal rim
Notching of the rim
Lamina cribrosa
Visibility & posterior bowing
Blood vessels
Nasal shift of the vessels d.t. loss of nasal neuroretinal rim
Angulation of blood vessels: blood vessels appear as if interrupted d.t. undermining
of disc edge
Background
Peri-papillary chorio-retinal atrophy
Splinter hemorrhage
Nerve fiber layer (NFL) defect detected by red free filter

Detection of early loss of the NFL (nerve fiber layer)

By quantitative assessment of NFL thickness using:
- OCT (optical coherence tomography)
- HRT (Heidelberg retinal tomography)
Arrangement of retinal fibers

Normal field

Field defect
 Field changes
(done by automated perimetry)

The most crowded fibers are affected first

Arcuate fibers (nasal field) nasal fibers (temporal field) papillo-macular fibers

1. Generalized of sensitivity

2. Early changes in the central field (30 o)

Para-central scotoma: a small isolated scotoma (above or below the fixation point)
Seidel scotoma: elongation of the para-central scotoma (along the distribution of the
arcuate fibers) to join the blind spot.
Arcuate (Bjerrum) scotoma: arcuate defect arches (above or below the fixation point)
reaching (but NOT exceeding) the horizontal raphe
Ring (Double arcuate) scotoma: when the lower & upper arcuate scotomas fuse.
Ronne's nasal step: d.t asymmetry between upper & lower field defects as they meet
each other along the horizontal meridian (NOT exceeding the horizontal raphe)

3. Late changes (in advanced cases) concentric contraction of the peripheral field that fuse
with the central field defect with preserved small island of central vision (tubular field) +
temporal island.

4. End stage (absolute glaucoma) total loss of vision (NO PL)

 Diagnosis of a patient with POAG
1. History family history ocular or systemic diseases drugs ..
2. Examination
Visual acuity: normal except in advanced glaucoma
Pupil reflex: normal except in advanced glaucoma
Slit lamp: to exclude causes of 2ry glaucoma.
Fundus examination: examine optic disc & retinal nerve fiber layer..
IOP: preferable measured by Goldman tonometer
Gonioscopy
3. Investigation
Visual field
Pachymetry: for central corneal thickness
OCT: evaluation of NFL thickness

Argon laser trabeculoplasty (ALT)

Trabeculectomy Aqueous shunt

 Treatment
Essentially medical
IOP is lowered to the required level (target pressure)

Target pressure: IOP that can prevent further optic nerve damage

Medical treatment 1st option used for life

- Beta blockers (1st choice) .
- Prostaglandins (1st choice) .
- Carbonic anhydrase inhibitors
- Alpha agonist.
- Miotics
Write details from page 30
Laser trabeculoplasty
Mechanism of action: aqueous outflow by the following mechanisms:
Mechanical tightening of the T.M opening of the adjacent untreated trabecular spaces
Inducing cell division & migration of macrophages to clear T.M. debris.
ALT (Argon laser trabeculoplasty)
Use thermal energy (by argon laser) to cause coagulative damage to T.M.
SLT (Selective laser trabeculopalsty)
Non-thermal treatment
Double frequency YAG laser affects only the melanin-rich cells in the T.M.

Surgical treatment
Indications:
1. Failure of medical treatment to control I.O.P.
2. Significant side effects.
3. The patient is poor, negligent or can NOT be followed up.
Options:
A. Trabeculectomy with or without anti-metabolites e.g. mitomycin C
I.O.P. by creating a fistula which allows aqueous outflow from the A.C. to sub-
conjunctival space
B. Aqueous shunting procedure
 Buphthalmos

Horizontal corneal diameter

Haab's striae
 1ry congenital glaucoma = 1ry buphthalmos
Definition I.O.P in infancy or early childhood d.t. anomalies at angle.
Etiology Trabecular dysgenesis
- Barkan's membrane covering the TM.
- Anterior insertion of C.B.
- Absent Schlemm's canal
Incidence rare
o Age: 65% of cases presents in the 1st year of life
o Sex: : = 2:1
o Laterality: Bilateral (75% of cases)
o +ve family history: (autosomal recessive)
Clinical picture
Symptoms Given by the mother
o Early: irritation of cornea (by corneal odema)
Pain (irritability) + reflex (lacrimation photophobia blepharospasm)
o Late: large eye (buphthalmos = ox eye), hazy cornea & poor vision
Signs
Eye will distend with I.O.P as the outer coat is still elastic

Cornea
Horizontal corneal diameter:
If > 12 mm suspect buphthalmos in 1st year Normal horizontal corneal
If > 13 mm suspect buphthalmos at any age diameter at birth = 10 mm

Curvature:
Transparency:
Corneal oedema (earliest sign) d.t. fine breaks in Descemet's membrane aqueous
influx into cornea
Haab's striae: Horizontal striae d.t. stretch & breaks in Descemet's membrane

Corneal opacity (at advanced stage)

Sclera bluish (stretch of sclera thin showing the underlying choroid)
Limbus stretched
A.C. deep
Gonioscopy anomalies at angle (trabecular dysgenesis)
IOP
 Iris tremulous iris + iris atrophy
Lens flattened & displaced backward + subluxated or dislocated d.t. stretching of zonule.
Fundus Optic nerve: cupping d.t. either: C/D > 0.3 is
- Loss of nerve fibers (irreversible) suspicious in infants
- Widening of scleral canal (reversible)

Cupping may reversible if I.O.P is lowered before atrophy of nerve fibers

Refraction myopia (but NOT proportionate to axial length) as:

o Corneal curvature:
o Lens: flattened & displaced backward

Causes of poor vision in buphthalmos

1. Optic nerve damage
2. Corneal cloudiness
3. Irregular astigmatism
4. Progressive myopia
5. Amblyopia

D.D.
(A) A child with lacrimation (watery discharge)
Secretion of tears:
- Corneal ulcer/ abrasion/ foreign body
- Iridocyclitis
- Congenital glaucoma
- Viral conjunctivitis
Drainage of tears most commonly NLD obstruction (+ve regurge test)
(B) Corneal oedema or opacification
1- Storage diseases (e.g. mucopolysaccharidosis)
2- Corneal dystrophies (e.g. congenital hereditary endothelial dystrophy)
3- Birth trauma
(C) Isolated corneal enlargement
1- Megalocornea
2- Congenital high myopia
(D) Other causes of optic nerve abnormalities
Congenital pits Coloboma Tilted disc syndrome Large physiological cup
(E) Blue sclera d.t. thin sclera showing the underlying uvea
o Physiological: in children
o Pathological:
High myopia
Buphthalmos
Over a staphyloma
Ehler Danlos syndrome
Osteogenesis imperfect
(F) Other causes of IOP in infancy = 2ry buphthalmos
Tumors: retinoblastoma
Inflammation: uveitis
Traumas: hyphema, angle recession glaucoma
Surgery: After congenital cataract surgery
Glaucomas associated with congenital ocular disorders: e.g. Peters' anomaly, aniridia
Glaucomas in the phakomatoses: Sturge-Weber syndrome, neurofibromatosis

Fundus examination should be done in any case of

buphthalmos to exclude retinoblastoma
 Goniotomy

Trabeculotomy

Trabeculectomy Aqueous shunt

 Treatment of 1ry congenital glaucoma
Treatment is essentially surgical
Medical treatment carbonic anhydrase inhibitor (drug of choice)
Indications: 1- Preparation for surgery
2- Adjuvant after surgery
Surgical treatment
Early cases: corneal diameter is < 13 mm
- If the cornea is clear, do Goniotomy
Incision is done through the internal layer of TM

- If the cornea is hazy, do Trabeculotomy

1. Partial thickness scleral flap is done to reach Schlemm's canal
2. Introduce the trabeculotome to cannulate Schlemm's canal, to be swept towards the AC

Late cases: corneal diameter is > 13 mm

(Schlemm's canal is absent or fibrosed)
1. Trabeculectomy: creating a fistula which allows aqueous outflow from the A.C. to sub-
conjunctival space
o Trabeculectomy alone: high failure rate is due to scar formation
o Trabeculectomy with adjuvant use of antimetabolites e.g. mitomycin C.
Indication: if goniotomy & trabeculotomy failed

2. Aqueous shunting procedures e.g. Ahmed valve

Absolute stage
Cyclo-destruction: cyclo-cryopexy or cyclo-photocoagulation (by diode laser)
 2ry glaucoma
Definition I.O.P 2ry to ocular or non-ocular causes.
Causes
1. Corneal causes
Open angle glaucoma
Corneal ulcer toxic iridocyclitis plasmoid aqueous & hypopyon
Closed angle glaucoma
Corneal perforation P.A.S, leucoma adherent or anterior staphyloma
Corneal fistula (after its closure) P.A.S
2. Iris causes
Open angle glaucoma
Iridocyclitis
Acute uveitis: d.t.
- Trabecular obstruction by inflammatory cells & plasmoid aqueous.
- Acute trabeculitis inter-trabecular pores aqueous drainage
Chronic uveitis d.t. scarring aqueous drainage
Prolonged use of steroid
Specific hypertensive uveitis syndromes as Posner-Schlossman syndrome & Fuchs
heterochromic uveitis
Rubeosis iridis hyphema
Pigmentary dispersion syndrome: dispersion of pigments (from back surface of iris) into:
o T.M. glaucoma
o Cornea Krukenberg spindle
o Lens pigments on lens
+ Iris shows: Trans-illumination defects (T.I.D)
Closed angle glaucoma
Iridocyclitis
Angle closure with pupillary block d.t. seclusio pupillae & occlusio pupillae
iris bombe progressive shallowing of the AC
Angle closure without pupillary block: d.t. contraction of inflammatory debris
P.A.S (PAS is more common in shallow AC & granulomatous uveitis)
Iris tumor or cysts
Irido-corneal endothelial (ICE) syndrome: progressive iris atrophy
+ corneal endothelial abnormalities + glaucoma (severe PAS)
 3. Lens causes = Lens-induced glaucoma
Open angle glaucoma
Phacolytic glaucoma (in hypermature cataract): lens proteins leave intact capsule &
engulfed by macrophage obstruction of T.M.
Phacotoxic = Phaco-anaphylactic glaucoma: lens proteins leave ruptured capsule
(after trauma or surgery) hypersensitivity to patient's own lens proteins
pahcoanphylactic uveitis 2ry glaucoma
Lens particle glaucoma: lens proteins (after trauma or surgery) obstruct TM
Subluxated or dislocated lens iridocyclitis 2ry glaucoma
Pseudo-exfoliative glaucoma (glaucoma capsulare)
Pseudo-exfoliative glaucoma
Formation & deposition of fibrillo-granular materials in the AC
+ Dispersion of pigment
Clinical picture
Lens:
- White material on anterior lens capsule (gives 3 distinct zones)
- Subluxated lens d.t. degenerating, weakened zonule
T.M. obstruction (by material) I.O.P (as POAG)
Iris: Trans-illumination defects (T.I.D)
Pupil: Poor pupil dilatation

Closed angle glaucoma

Phaco-morphic glaucoma (in intumescent cataract or micro-spherophakia)
pupillary block I.O.P
Anterior dislocation pupillary block I.O.P
Posterior dislocation: vitreous herniation pupillary block I.O.P
Pupillary block glaucoma = Glaucoma inversus
Closed angle glaucoma worsens by miotics & improves with mydriatics !

Aphakic glaucoma
I.O.P in aphakia, may be d.t. either:
Post-operative iridocyclitis
Post-operative hyphema
Pupillary block by vitreous, air or I.O.L
Steroid-induced
 4. Retinal causes
Proliferative diabetic retinopathy & ischemic CRVO neovascular glaucoma
Retinal detachment treatment: d.t.
tight scleral buckle silicon oil pneumatic retinopexy
5. Intra-ocular tumor
Space occupying lesion
Tumor may push iris forward closure of the angle
Seedling of malignant cells
Direct invasion of angle
Vitreous hemorrhage ghost cell glaucoma
Neovascular glaucoma
2ry uveitis
6. Elevated episcleral venous pressure
e.g. carotid cavernous fistula, cavernous sinus thrombosis & Sturge Weber syndrome
Episcleral venous drainage back pressure I.O.P.
7. Drugs
Mydriatics: may precipitate angle-closure glaucoma
Steroid-induced glaucoma: open angle glaucoma associated with topical use of steroid

How steroid I.O.P ?

Glycosaminoglycans (GAG) theory
Corticosteroids stabilize lysosomal membrane inhibit the release of hydrolases.
So, GAGs (present in the T.M.) can be NOT depolymerized retention of water
in the extracellular space narrowing of trabecular spaces aqueous outflow.
Treatment
1. Prevention (the most effective) by:
Judicious use of steroid
Frequent monitoring of IOP
in patients who require prolonged steroid therapy.
2. Curative:
Stop steroid
If IOP remains elevated treat as 1ry open-angle glaucoma
 8. Trauma
- Hyphema
- Angle recession glaucoma (see page 177)
- Iridocyclitis
- Lens dislocation
- Ghost cell glaucoma
- Siderosis bulbi
9. Malignant glaucoma = Aqueous misdirection syndrome
Definition Post-operative condition characterized by: central & peripheral shallow or flat A.C
with I.O.P in presence of a patent iridectomy & no response or even aggravation by miotics.
Incidence rare
It may occur in patient undergoing trabeculectomy operation, cataract surgery, surgical
iridectomy!
Pathogenesis unknown!
Anterior rotation of the ciliary processes and iris root aqueous circulates into the posterior
segment pushing vitreous-lens-C.B.-iris diaphragm shallow A.C. (peripheral & central)
Treatment
Medical: (usually fails)
Mydriatic-cycloplegic (Atropine + phenyl epherine): move C.B. outward away from
vitreous allowing passage of aqueous from the dilated pupil.
Drug I.O.P: Beta blockers + C.A.I
YAG laser: disruption of anterior vitreous face (allow aqueous to leave the posterior
segment & enter anterior segment break the attack)
Pars plana vitrectomy (if previous measures fail)
 Medical treatment of glaucoma
Formation
1. Alpha agonist
2. Beta blockers (BB)
3. Carbonic anhydrase inhibitor (CAI)
4. Osmotic agents
Drainage
5. Pilocarpine (Miotics)
6. Prostaglandin

Alpha agonist
Action
Formation: stimulation 2 receptors cAMP.
Uveo-scleral outflow
Side effects
- Allergy
- Mydriasis
- Dry mouth & nose
Beta blockers
Action: formation
Side effects
- Bradycardia
- Hypotension
- Heart block
- Bronchial asthma

Carbonic anhydrase inhibitors

Action: formation
Side effects
Parasthesia
Acidosis
Malaise complex
 Osmotic agents e.g. mannitol 20 %
Action: Draw water from vitreous
Side effects
Circulatory overload:
- Congestive heart failure
- Pulmonary odema
Urine retention
Miotic e.g. Pilocarpine
Action: T.M outflow
Side effects
Miotic life!
Retinal detachment (in predisposed patients)
Prostaglandins
Action: Uveo-scleral outflow
Side effects
Hyperemic conjunctiva
Iris pigmentation d.t. melanin production
 Surgical treatment of glaucoma

External fistulizing operation = Trabeculectomy = Filtration operation

With or without anti-metabolites e.g. Mitomycin C & 5-Fluorouracil

Definition I.O.P. by creating a fistula which allows aqueous outflow from the A.C. to sub-
conjunctival space (where it is absorbed by conjunctival blood vessels)
Technique
1. Open conjunctiva
2. A partial thickness scleral flap is done
3. Excision of T.M.
4. Peripheral iridectomy
5. Closure of scleral & conjunctival flap.

Aqueous shunting procedures

e.g. Ahmed, Molteno implants