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] ‫تحضير للعملية‬
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 ˂ ½ angle PAS  upper peripheral laser iridotomy
 If ˃ ½ 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)  ‫مهم جدا‬
  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 ‫مهم‬
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 glaucoma‫مهم جدا‬
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 α2 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