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GLAUCOMA Aqueous Outflow Pathway:

Maribel Castro – Enano, M.D. 1. Conventional (trabecular) route


<Team Rochas> • 90% of aqueous flow
• aqueous produced by the ciliary
Glaucoma epithelium is secreted into the
- Includes a complex of eye diseases which posterior chamber→ anterior
have in common an abnormal intraocular chamber passing through the
pressure that causes organic changes in the pupil→anterior chamber angle→
optic nerve and produces irreversible fenestrated layers of the trabecular
blindness through progressive loss of the
meshwork→ Schlemm’s canal→
field of vision
- many forms are asymptomatic as they venous tributaries →venous
destroy the optic nerve circulation of the eye
- if detected and IOP is reduced to normal 2. Unconventional (uveoscleral) route
by medication or surgery, the progression of • remaining 10%
blindness can be stopped • aqueous passes caross the ciliary body
- Pathophysiology, clinical presentation and into the suprachoroidal space and is
treatment of the different types of drained by the venous circulation in
glaucoma are so varied, there is no single the ciliary body, choroid and sclera
definition that adequately encompasses all *some aqueous drains via the iris
forms
- In the broadest terms, glaucoma involves a
study of the following: Pathogenesis of glaucomatous damage
1. IOP
2. optic nerve head damage 1. The Ischemic Theory – compromise of the
3. visual field loss microvasculature of the axons in the optic
4. drainage angle nerve head plays a role in the pathogenesis
of glaucomatous damage
Aqueous Secretion
1. Active Secretion – 80% of aqueous Possible Mechanisms:
production, aqueous secreted by the non- a. loss of capillaries
pigmented ciliary epithelium via an active b. alteration of capillary blood flow
metabolic process that is dependent on a c. changes that interfere with the
number of enzymatic systems delivery of nutrients or removal of
2. Passive secretion – 20% of aqueous metabolic products from the axons
production, aqueous produced by passive d. failure of regulation of blood flow
process such s ultrafiltration and diffusion e. delivery of injurious vasoactive
which are dependen, the on the level of substances to blood vessels of the
blood pressure in the ciliary capillaries, the optic nerve head
plasma oncotic pressure and the level of IOP
2. The Direct Mechanical Theory
Aqueous secretion is diminished by: - elevated IOP directly damages the retinal
1. Drugs – B- blockers, sympathomimetics, nerve fibers as they pass through the lamina
carbonic anhydrase inhibitors cribrosa
2. Cyclodestructive procedures
3. Ciliary body shutdown – detachment of Determinatuion of normal IOP is by the
ciliary body, inflammation of secretory following factors:
ciliary epithelium in iridocyclitis and retinal 1. Rate of aqueous secretion
detachment 2. Resistance encountered in outflow
channels
3. Level of episcleral venous pressure
• The rate of aqueous outflow is as well as though a bandage
proportional to the IOP minus the contact lens
episcleral venous pressure
• The distribution of IOP within the
general population has a range of
10 – 12mmHg 2. Gonioscopy
• Normal IOP varies with the time of Purposes:
the day, heart beat, blood a. Diagnostic – to identify abnormal angle
pressure level, and respiration structures and to estimate the width of the
• IOP has a tendency to be higher in chamber angle
the morning and lower in the b. Surgical- to visualize the angle during
afternoon and evening procedures such as laser trabeculoplasty and
• Mean range of diurnal IOP goniotomy
fluctuations in normal eyes is 5
mmHg Type of Goniolenses:
1. Indirect – provides a mirror image of the
Diagnostics: opposite angle and can be used only in
1. Tonometry conjunction with a slitlamp for diagnostic
a. Goldmann applanation tonometry purposes
gold standard a. Goldmann 3 – mirror goniolens
measures the force applied per unit b. Zeiss 4 – mirror goniolens
area c. Posner 4 – mirror goniolens
IOP is proportional to the pressure 2. Direct – provides a diect view of the angle
applied to the radius of curvature of and can be used for both diagnostic and
the globe (cornea) and thickness of surgical purposes
the globe does not require a slitlamp and used
b. Schiotz tonometry with patient in supine position
indentation tonometry, a plunger with a. Koeppe – dome-shaped goniolens
a preset weight indents the cornea which comes in several sizes
handy and cheap b. Swan- Jacob – surgical poniolens
c. Perkins tonometry which is held on the cornea by a
hand- held applanation tonometer handle
which uses a Goldmann prism adapted 3. Perimetry – a method of evaluating the
to a small light source visual field
d. Air – puff tonometry e.g. Humphrey perimeter, Octopus
noncontact tonometer which uses the 4. Other imaging procedures
Goldmann applanation principle but, Optical Coherence Tomography (OCT)
instead of using a prism the cntral Heidelberg Retinal Tomography (HRT)
part of the cornea is flattened by a GDx Nerve Fiber Analyzer
jet of air
does not require use of anesthetic Grading of Angle Width
e. Tono – Pen Grade 4 – (35- 45°), widest angle, ciliary
hand- held, self-contained battery body can be visualized with ease
powered, miniaturized portable Grade 3 – (25- 35°), open angle in which
tonometer the scleral spur can be identified
correlate with the Goldmann although Grade 2 – (20°), moderately narrow angle in
it slightly overestimates a low which only the trabeculum can be identified
IOP and underestimates a high Grade 1 – (10°), very narrow angle in which
IOP only the Schwalbe line can be identified
can take measurements in an eye with Slit angle – no obvious iridocorneal contact
distorted or edematous cornea, but no angle structures can be identified
Grade 0- (0°), closed angle due to 3) hemolyzed red cells (e.g. ghost cell
iridocorneal contact glaucoma)
4) macrophages (e.g. phacolytic
Classification: glaucoma)
- According to manner by which aqueous 5) proteins (e.g. acute anterior uveitis)
outflow is impaired 6) pseudoexfoliative material (e.g.
1. Open – angle pseudoexfoliation glaucoma)
2. Angle – closure c. Post – trabecular glaucoma- trabeculum
is normal but aqueous outflow is impaired
- (+)/ (-) of associated factors contributing due to elevated episcleral venous pressure
to the rise in IOP 1) Carotid – cavernous fistula and dural
1. Primary shunts
2. Secondary 2) Sturge – Weber Syndrome
3) Obstruction of the superior vena cava
- According to onset
1. Congenital Glaucoma Symptoms:
2. Infantile • asymptomatic until a significant visual
3. Juvenile field loss has occurred
4. Adult • initial VF loss – nasal field
• rare: eye pain, headache, halos due
A. Open – angle Glaucoma to transient corneal epithelial edema
1. Primary Open- angle Glaucoma
- generally bilateral, although not generally Signs:
symmetrical characterized in at least one • raised IOP, fluctuations IOP, optic disc
eye by the following: changes, glaucomatous field changes,
a. adult onset open angle on gonioscopy
b. an IOP > 21mmHg at some point
in the course of the disease Evaluation:
c. an open angle of normal ▪ Hx, PE
appearance ▪ visual acuity
d. glaucomatous optic nerve head ▪ slit lamp biomicroscopy
damage ▪ tonometry – note time of day
e. visual field loss ▪ gonioscopy
▪ ophthalmoscopy – note appearance of
2. Secondary Open- angle Glaucoma the disc
a. Pre- trabecular glaucoma – aqueous ▪ check visual fields perimetry
outflow is obstructed by a membrane
covering the trabeculum Management:
1) fibrovascular tissue (e.g. neovascular 1. Medical Therapy – topical B blocker,
glaucoma) prostaglandin analogue, carbonic anhydrase
2) endothelial cells (e.g. iridocorneal inhibitor, alpha- agonist, miotics
endothelial syndrome) 2. Laser trabeculoplasty – application of
3) epithelial cells (e.g. epithelial discrete burns to the trabeculum enhances
ingrowth) aqueous outflow and lowers IOP
b. Trabecular glaucoma – obstruction occurs a. uncontrolled glaucoma
as a result of clogging up of the meshwork b. primary therapy for pxs with poor
1) pigment particles (e.g. pigmentary compliance to medical therapy
glaucoma)
2) red blood cells (e.g. red cell
glaucoma)
c. nocturnal systemic hypotension
3. Trabeculectomy – conventional filtering as well as overtreated systemic
(drainage) procedure by creating a new hypertension
channel ( fistula) for aqueous outflow d. reduced blood flow velocity in
between the anterior chamber and sub- the ophthalmic artery when
Tenon space without the use of an artificial measured with transcranial
device Doppler ultrasonography
e. paraproteinemia and the
Indications: presence of serum
a. failed medical therapy and laser autoantibodies
trabeculoplasty
b. lack of stability for laser therapy due Management of NTG:
to 1. History
• poor patient cooperation 2. Reduction of IOP – indicated only in
• inability to adequately patients with documented progressive field
visulaize the trabeculum due to loss
narrow angle or corneal aim is to reduce IOP by atleast
opicification 30 %
c. eyes with advanced disease – very low 3. Systemic calcium – channel blockers
IOP is required considered in younger patients
and in those with early disease
NORMAL TENSION GLAUCOMA (NTG) 4. Monitoring of systemic BP (24 hrs)
• low- tension glaucoma if a significant nocturnal drop
• used to describe a type of POAG is detected, medication for
hypertension should be avoided
Characteristics:
1. a mean IOP =/< 21mmHg on diurnal B. Angle – Closure Glaucoma
testing • glaucoma due to obstruction of
2. glaucomatous optic disc damage and trabecular meshwork by peripheral
visual field loss Iris
3. open angle on gonioscopy • may be primary or secondary, with or
4. absence of secondary causes for without papillary block
glaucomatous optic disc damage • may be acute, subacute,
intermittent, or chronic
NTG Risk Factors:
1. Age – elderly 1. Primary Angle- Closure Glaucoma with
2. Gender – females greater risk at 2:1 Pupillary Block
ratyion - lens- iris apposition, which interferes
3. Race – more common in Japan than in with aqueous flow and causes the iris
either Europe or North America to bow forward and occlude the
trabecular meshwork
Clinical Features: 2. Primary Angle – Closure Without Pupillary
1. IOP in high teens Block
2. optic nerve head is larger in NTG than in - Plateau iris syndrome
POAG and incidence of splinter hges at the 3. Secondary Angle- Closure with Pupillary
disc margins is higher in NTG Block
3. visual fields defcts are essentially the - -lens-induced (e.g., phacomorphic,
same as in POAG dislocated lens), secclusio pupillae,
4. others aphakic/pseudophakic papillary block,
a. peripheral vascular spasm nanopthalmos, ciliary block/
b. migraine headaches
malignant glaucoma due to ROP, • IV hyperosmotic agent (Mannitol)
trauma, miotic therapy • argon laser trabeculectomy, Nd: YAG
4. Secondary Angle- Closure Without laser iridectomy, laser pupilloplasty,
Pupillary Block laser gonioplasty
- -due to posterior pushing mechanisms • trabeculectomy with or without use of
from tumors, choroidal hemorrhage or antimetabolites
effusion, scleral buckle, swelling after • artificial filtering shunts
PRP, post-inflammatory with posterior • cyclodestructive procedures,
synechiae and iris bombe; or anterior cyclocryotherapy, Nd:YAG
pulling mechanism in neovascular cycloablation
glaucoma, post- inflammatory
peripheral anterior synechiae GLAUCOMA DRUGS
1. Beta-blockers – decrease aqueous
Symptoms: secretion with little effect on episcleral
AACG- pain, red eye, photophobia, venous pressure
decreased/blurred vision, halos around
lights, headache, nausea, vomiting 2. Sympathomimetics – alpha and beta
*CACG- asymptomatic, may have decreased adrenergics agonists – increase aqueous
vision, constricted visual fields outflow

Signs: 3. Miotics – in PAOG, increase aqueous


Decreased VA, increased IOP, ciliary outflow
injection, corneal edema, AC cell/flare, - in ACG, opens the angle which results from
shallow AC, narrow angles on gonioscopy, the mechanical contraction of the pupil
mid-dilated nonreactive pupil, iris bombe; pulling the peripheral iris away from the
signs of previous attacks including sector iris trabeculum
atrophy, anterior subscapular lens opacities
glaucoma/flecken), dilated irregular pupil, 4. Prostaglandins derivatives – enhances
and PAS uveoscleral outflow without altering aqueous
outflow through the TM
Evaluation:
• Hx, PE 5. Carbonic anhydrase inhibitor
• visual acuity - reduce aqueous secretion through direct
• slit lamp biomicroscopy inhibition of carbonic anhydrase
• tonometry- note time of day *production of aqueous humor in the ciliary
• gonioscopy epithelium is a function of the production of
• ophthalmoscopy – note appearance of bicarbonate
the disc 6. Hyperosmotic agents
• check visual fields/perimetry - increase blood osmolality thereby creating
• consider provocative testing (prone an osmotic gradient between the blood and
test, prone dark-room test, and vitreous so that water is drawn from the
pharmacologic dilation; IOP increase vitreous
of > 8mmHg is considered positive

Management:
• topical B-blocker, topical
sympathomimetics (a- and B-
adrenergic agonists, topical miotics,
topical carbonic anhydrase inhibitor.
Topical prostaglandin analogue
• oral CAI, oral hyperosmotic agents

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