glaucoma & target iop

GlaucomaGlaucomaTarget IOPTarget IOP

Do Seiha, MDDo Seiha, MDPreah Ang Duong HospitalPreah Ang Duong Hospital

Department of Department of OphthalmologyOphthalmology

Mekong Sante 25 Jan, 2011Mekong Sante 25 Jan, 2011

Glaucoma Objectives:

1. Introduction to Glaucoma: Terminology, Epidemiology

2. Intraocular pressure and Aqueous humor dynamics

3. Clinical evaluation

4. Open-angle glaucoma

5. Angle-closure glaucoma

6. Childhood glaucoma

7. Medical management of glaucoma

8. Surgical theraphy for glaucoma


Definitions:

Glaucoma: A group of disease that have in common a

characteristic optic neuropathy with associated visual field loss for

which elevated IOP is one of primary risk factors.

Normal IOP: 10-22 mmHg.

Three risk factor determine the IOP:

- rate of aqueous humor production by ciliary body

- resistance to aqueous outflow across the

Trabecular meshwork-Schlemm’s canal system

- the level of epischeral venous pressure


Classification:

Open-angle glaucoma

- Primary open-angle glaucoma

- Normal-tension glaucoma

- Juvenile open-angle glaucoma

- Glaucoma suspects

- Secondary open-angle glaucoma

Angle-closure glaucoma

- Primary angle- closure glaucoma with relative pupillary block

- Acute angle closure

- Subacute angle closure

- Chronic angle closure

- Secondary angle- closure glaucoma with pupillary block

- Secondary angle- closure glaucoma without pupillary block

- Plateau iris syndrome


Classification:

Childhood glaucoma

- Primary congenital glaucoma

- Glaucoma associated with congenital anomalies

- Secondary glaucoma in infants and children


Epidemiology:

Primary open angle glaucoma:

WHO:- blindness prevelence of all type of glaucoma > 8 million

people with 4 millon cases caused by POAG.

- The third leading cause of blindness worldwide

Prevelence:- 1.1-2.1%

- blacks: 3-4 times highers

- age > 70 years: 3-8 times highers

Risk factor:- Advanced age

- decrease central corneal thickness

- race

- positive family history

- diurnal variation IOP

- DM and myopia ( controversy )


Epidemiology:

Primary angle closure glaucoma:

Prevelence: white 0.1%

arctic region 20-40 times higher than whites

Inuits > Asians > Whites

uncommon among blacks

Gender: women develop AACG 3-4 times more than men

Age: most common between 55-65 years

Refraction: hyperopia


Aqueous humor formation:

- Ciliary process (supply by major arterial circle of the iris)

- Aqueous humor is produced by 3 process

- active secretion

- ultrafiltration

- simple diffusion

- Aqueous humor:

- high H, Cl , ascorbate

- protein free

- Produced 2.0 microL/min (1% turnover/min)


Supression of Aqueous humor formation:

- Carbonic anhydrase inhibitors

- Beta-adrenergic antagonists

- Alpha2 agonists

Rate of Aqueous humor formation:

- affect by – integrity of blood-aqueous barrier

- blood flow to the ciliary body

- neurohumoral regulation of vascular tissue and the ciliary

epithelium

- decrease: - age

- sleep


Aqueous humor outflow:

0.22-0.28 microL/min/mmHg

decrease with age

affected by – surgery

- trauma

- medication

- endocrine factors


Aqueous humor outflow:

Trabecular outflow ( pressure-dependent outflow )

Trabecular meshwork: 3 parts

1. Uveal part

2. Corneoscleral meshwork

3. Juxtacanalicular meshwork (major site or outflow resistance)

Uveoscleral outflow ( pressure-independent outflow )

anterior chamber=> ciliary muscle=> supraciliary and

suprachoroidal spaces

5-15% of total aqueous outflow

increase outflow by cycloplegic, adrenergic agents,PGs analogs

cyclodialysis

decrease outflow by miotic


Episcleral venous pressure: (EVP)

- relatively stable except:

- body position

- orbit,head and neck obstruction venous return

- A-V shunt

- 8-10 mmHg.

- IOP rises 1 mmHg. for every 1 mmHg. increase in EVP

Intraocular pressure: normal 16+/- 6 mmHg.

- factor influencing IOP: - time of day

- heartbeat

- respiration

- excercise

- fluid intake

- systemic and topical medication


Diurnal variation: normal IOP varies 2-6 mmHg.

suggestive glaucoma: varies > 10 mmHg.

Clinical measurement of IOP:

Imbert-Fick principle:

pressure = force/area

Instrument:

1. Goldmann applanation tonometer

- flatten an area of cornea of 3.06 mm of diameter

- safe,easy and accuracy

2. Noncontact tonometer

3. Tonopen: very small area, useful in corneal scar or edema

4. Schiotz tonometry: indentation, known weight

5. Digital pressure


Clinical measurement of IOP:

Possible source of error in Tonometry

- sgueezing of the eyelids

- breath holding or Valsava maneuver

- pressure on the globe

- extraocular muscle force applied to a restricted globe

- tight collar or necktie

- obesity or straining to reach slit lamp

- an inaccuracy calibrated tonometer

- high corneal astigmatism

- corneal thickness greater or less than normal

- corneal scarring and irregularity

- technician error


1. History and general examination

2. Gonioscopy:

2.1 Direct gonioscopy:

- direct visualization of the chamber angle

- Koeppe, Barkan, Swan-Jacob,Richardson

- supine position ( OR room )

2.2 Indirect gonioscopy:

- inverted image

- upright position ( slit lamp )

- indentation gonioscopy : Zeiss-type

nonindentation gonioscopy: Goldmann-type


2. Gonioscopy:

Gonioscopic assessment

Grade 4: The angle between the iris and the surface of

the trabecular meshwork is 45*


the trabecular meshwork is greater than 20* but less than 45*


the trabecular meshwork is 20*. angle closure is possible


the trabecular meshwork is 10*. angle closure is probable in time

Slit : The angle between the iris and the surface of

the trabecular meshwork is less than 10*.

angle closure is very likely

Grade 0: The iris is against the trabecular meshwork. angle closure is present

Gonioscopic assessment


3. The optic nerve:

Anatomy and pathology:

compose: neural tissue

glial tissue

extracellular matrix

blood vessel

1.2-1.5 million axon of retinal ganglion cell

1.5 mm diameter

blood supply:

superficial nerve fiber layer: central retinal artery

prelaminar region: short posterior ciliary artery

laminar region: short posterior ciliary artery

retrolaminar region: short posterior ciliary artery

pial artery

Optic nerve pathway

Distribution of nerve fiber


3. The optic nerve:

Glaucomateous optic neuropathy:

Theory: Mechanical theory:

- direct compression of axonal fibers with distribution of

lamina cribosa plates

- interuption of axoplasmic flow => death of RGCs.

Ischemic theory:

- decrease optic nerve perfusion=> intraneural ischemia

Examination:

- slit lamp combined with 60,78 or 90 D lens


3. The optic nerve:

Glaucomateous optic neuropathy:

Clinical evaluation

normal disc: neural rim : ISN’T rule

color : orange to pink

vertical C:D : 0.1-0.4

black larger disc area and larger C:D than white

myopia larger disc area and larger C:D than normal and hyperopia

Sign of glaucoma

Generalized Focal

- large optic cup - notching of the rim

- Asymetrical of the cup - vertical elongation of the cup

- Progressive enlargement of cup - region pallor

- splinter hemorrhage

- nerve fiber layer loss

Glaucomateous optic neuropathy


4. The visual field :

An island hill of vision in a sea of darkness


4. The visual field :

Glaucomatous visual field defects:

- generalized depression

- paracentral scotoma

- arcuate scotoma

- nasal step

- altitudinal defect

- temporal wedge

Paracentral scotoma

Arcuate scotoma

Nasal step

Tubular field

Progression of glaucomatous damage


Primary open angle glaucoma(POAG):

Clinical feature:- insidous onset

- slow progression

- painless

- bilateral, can be asymmetrical

- IOP >22 mmHg.

- glaucomatous optic neuropathy

- visual field loss

- gonioscopy: opened angle

Risk factors: - age

- race : black > white

- family history

- controversy: myopia, DM, cardiovascular disease

CRVO


Normal- tension glaucoma:

Hypothesis: higher prevalence of vasospastic disorder such as migrain,

Raynaud phenomenon,ischemic vascular disease,

Autoimmune disease and coagculopathy

Diagnosis: - IOP < 21 mmHg.

- glaucomatous optic neuropathy

- visual field loss

- opened angle


Secondary open-angle glaucoma:

1.Pseudoexfoliation syndrome:

- deposition of a distinctive fibrillar material in anterior segment

- unilateral or bilateral

- common in Scandinavian

- age > 70 years

- target like pattern ( intermediate clear area)

- angle: - heavy pigment

- Sampaolesi’s line (anterior to Schwalbe’s line )

- often narrow ( anterior movement of lens-iris diaphragm)

- pupillary margin translumination

- poorly dilated pupils

- poor prognosis

- laser trabeculoplasty: very effective



2.Pigmentary glaucoma:

- pigment dispersion syndrome:

- Krukenberg spindle

- midperipheral iris transilumination

- reverse pupillary block

- Zentmayer’s line (pigment deposits near the equator of the lens)

- gonioscopy: homogeneous, densely pigmented TM.

- developing glaucoma 25-50% ( white, male,myopia)

- Management: - Medication

- laser peripheral iredectomy,laser trabeculoplasty

- surgery



3. Lens-induced glaucoma:

3.1 Phacolytic glaucona:

- leakage of lens protein through the capsule

- debris obstructs TM.

- mature or hypermature cataract

- elderly patients of history poor vision

- Management: cataract extraction

3.2 Lens particle glaucoma:

- lens cortex obstructs TM.

- occur within weeks of the initial surgery or trauma

- Management: - medication

- surgery if failed medication



3. Lens-induced glaucoma:

3.3 Phacoanaphylaxis:

- rare

- granulomatous inflammation

- sensitized to their own lens protein fellow surgery or trauma

- Management: - medication

- surgery if failed medication



4. Intraocular tumor :

- unilateral chronic glaucoma

- Mechanism: - direct tumor invasion

- neovascularization of angle

- deposit of tumor cell, inflammatory cell and debris

5. Ocular inflammation:

- Mechanism:- edema of the TM

- TM endothelial cell dysfunction

- blockage of the TM. by fibrin and inflammatory cells

- PGs-mediated breakdown of the blood-aqueous barrier

- steroid-induced reduction in aqueous outflow through

the TM.



6. Glaucomatocyclitic crisis :

- uncommon

- marked increase IOP

- low grade anterior chamber inflammation

- unilateral

- middle age

- trabeculitis

7. Elevated episcleral venous pressure:

- obstructs venous outflow

- chronic red eye

- gonioscopy: blood in Schlemm’s canal

- Management: reduce aqueous humor formation



8. Fuchs heterochromic iridocyclitis:

- chronic

- unilateral

- middle age

- iris heterochromia

- gonioscopy: multiple fine vessels that cross the TM

- open-angle glaucoma 15%

- Management:- steroid not effective

- aqueous supressant

9. Steroid induced glaucoma:

- prolonged used of topical,periocular,inhaled or systemic steroid

- increase resistance to aqueous outflow in the TM.



10.Accidental and surgical trauma:

10.1 Hyphema:

- more common following recurrent hemorrhage

- increase IOP: obstruction of TM. with RBC,inflammatory cell

direct injury of the TM.

- Sickle cell hemoglobinopathies: increase incidentof glaucoma

10.2 Angle recession:

- splits between the longitudinal and circular ciliary muscle fiber

- chronic unilateral

- greater extent of angle recession=>greater risk of glaucoma

10.3 Surgical trauma:

- usually transient

- retained viscoelastic substance


Pathogenesis and pathophysiology of angle closure:

angle closure: apposition of the peripheral iris to the TM. =>

reduced drianage of aqueous humor

Mechanism:

1. pupillary block: no movement of aqueous through the pupil as a

result of 360* posterior synechiae

2. without pupillary block: iridotrabecular apposition or synechiae from

iris +/- lens being pushed, rotated or pull forward

3. lens induced angle-closure glaucoma:

intrimescent or dislocated lens

4. Iris-induced angle closure:

- plateau iris syndrome

- peripheral iris configuration

- airidia

Acute angle closure glaucoma


Risk factor:

1. race : Inuits, East asians

2. ocular biometrics : shallow anterior chamber

thick lens

increase anterior curvature of the lens

short axial lenght

small corneal diameter and radius of curvature

3. age

4. gender: women 2-4 times common than men

5. family history

6. hyperopia


Acute primary angle closure:

- sign: - high IOP

- middilated,sluggish and often irregular pupil

- corneal epithelial edema

- congested episcleral and conjunctival blood vessels

- shallow anterior chamber

- a mild amount of aqueous flare and cell

- Diagnosis: gonioscopy

- Glaukomflecken: small anterior subcapsular lens opacities ( ischemia)

- Management: - iridectomy

- cholinergic agent

- high IOP (40-50mmHg) pupillary sphincter ischemia

and unresponsive to miotic agent

- fellow eye: prophylaxis PI


Subacute or intermittent angle closure:

Sign: - blurred vision

- halos

- mild pain

- resolve spontaneously ( during sleep-induced miosis )

- gonioscopy: narrow angle with/without peripheral anterior

synechiae

- can progress to chronic angle closure or acute attack

- Management: peripheral iridectomy


Chronic angle closure:

- major cause of blindness in Asia

- mechanism: creeping angle closure ( slow formation of PAS )

- sign: - permanent PAS

- rise IOP

- progressive cupping

- loss of visual field

- Management: peripheral iridectomy

antiglaucoma drug


The occludable or narrow angle :

- only small percentage develope angle-closure glaucoma

- iridectomy is not necessary in all patients

- indication for PI:- apposional angle

- PAS

- increase segmental TM.pigmentation

- history previous angle closure

- positive provocative test

- anterior chamber depth less than 2.0 mm

- strong family history

Plateau iris:

- anteriorly positioned ciliary process => pushing the peripheral iris

forward

- Management: laser iridectomy and iridoplasty

Plateau iris syndrome


Secondary angle closure with pupillary block:

Lens induced angle closure:

1. Phacomorphic glaucoma:

- rapid onset

- intrumescent lens

- different of anterior chamber depth between 2 eyes

2. Ectopia lentis:

- displacement of lens

- Management: iridectomy, lens extraction

3. Aphakia or pseudophakic angle-closure glaucoma

- pupillary block by intact viterous face

Phacomorphic glaucoma


Secondary angle closure without pupillary block:

1.Neovascular glaucoma:

- most common causes: DM,CRVO,ocular ischemic syndrome

- neovascularization of iris and TM. => PAS

- poor prognosis

- Management: - retinal ablation

- treat underlying disease

2. ICE syndrome:

- abnormal corneal endothelium

- 3 clinical variants: Chandler syndrome

Essential iris atrophy

Cogan-Reese syndrome

- unilateral

- women 20- 50 years

- glaucoma 50%

ICE syndrome



3. Tumor:

most common: - primary choroidal melanomas

- ocular metastasis

- retinoblastoma

4. Aqueous misdirection:

- rare

- present following ocular surgery with angle closure

- flat of both central and peripheral anterior chamber

- anterior rotated of ciliary process

- Management:- cycloplegic

- antiglaucoma drugs

- Yag anterior hyaloidectomy

- 50 % controlled by medication



5. Inflammation:

- formation of posterior synechiae, peripheral anterior synechiae

- Management: aqueous suppressant, corticosteriod

6. Trauma:

- peripheral anterior synechiae

7. Drug induced secondary angle closure glaucoma:

- antiepileptic, antidepressant


Classification:

1. Primary congenital glaucoma

2. Secondary infantile glaucoma: inflammation, neoplasm,metabolic

3. Juvenile glaucoma: onset after 3 years of age

4. Developmental glaucoma: other developmental anomalies

Primary congenital glaucoma:

- 50-70 % of congenital glaucoma

- 65 % male

- 70 % bilateral

- most case : sporadic

- genetic: GLC3A , chromosome 2 (2p21)

GLC3B , chromosome 1 (1p36 )


Primary congenital glaucoma:

Pathopysiology:

1. Cellular or membranous abnormality in the trabeccular meshwork

2. Widespread anterior segment anomaly, including abnormal insertion

of the ciliary muscle

Clinical features:

- Clinical triad: epiphora, photophobia, blepharospasm

- Buphthalmos : corneal diameter > 12 mm. during the first year of life

- corneal edema

- Haab’s striae: tear in Descemet’s membrane

- gonioscopy: open with high insertion of iris root

- cupping may be reversible if IOP is lower

- Management: goniotomy or trabeculotomy

medication ( B- blocker, carbonic anhydrase inhibitor )

Childhood glaucoma


Developmental glaucoma:

1. Axenfeld-Reiger syndrome:

- bilateral congenital anomalies ( angle, iris, TM )

- AD

- glaucoma 50 %

2. Peters anomaly:

- bilateral

- defect corneal endothelium and Descemet,s membrane

- central corneal defect with adhesion between central iris and

posterior cornea

- sporadic

- glaucoma 50 %


Developmental glaucoma:

3. Aniridia :

- bilateral

- iris hypoplasia

- AD

- 1/3 sporadic => 20 % Wilm’s tumor

- PAX 6 gene on 11p13 chromosome

- glaucoma 50 – 75 %

( rudimentary iris stump rotates anteriorly )

- WAGR syndrome :

Wilm’s tumor, aniridia, genitourinary anomalies, mental retardation

AD

13 % of aniridia

Aniridia


Goal of treatment: - lowest risk

- fewest side effect

- least disruption of patient’s life

Target IOP: - severity of the damage

- life expectancy

- associated risk factor

Medical agents: 1. Beta-adrenergic antagonists

2. Parasympathomimetic ( miotic ) agent

3. Carbonic anhydrase inhibitors

4. Adrenergic agonist

5. Hypotensive lipids

6. Combination medications

7. Hyperosmotic agents

“The facts are that people loss vision with glaucoma because of problems

with optic neuropathy, but they develop the optic neuropathy

because of the elevated IOP. For clinicians, the most important fact is that by controlling the pressure, we

currently have the best way of preventing the blindness.”

Ref: http://www.ophthalmologytimes.comRef: http://www.ophthalmologytimes.com

RELATIONSHIP BETWEEN INTRAOCULAR PRESSURE AND VISUAL FIELD LOSS

The Australian Blue Mountain study found the

odds ratio of developing glaucoma was 4.7

times higher in patients with a screening IOP of

greater than 21 mmHg than in patients with

lower IOP.

Ref: Surveys of Ophthalmology 2003; 48 (Suppl 1): 53-57Ref: Surveys of Ophthalmology 2003; 48 (Suppl 1): 53-57

RELATIONSHIP BETWEEN INTRAOCULAR PRESSURE

AND VISUAL FIELD LOSS

According to the AGIS study, reducing IOP in

glaucoma patients limits disease progression

and slows visual field loss.

Ref: Surveys of Ophthalmology 2003; 48 (suppl 1): 53-57Ref: Surveys of Ophthalmology 2003; 48 (suppl 1): 53-57

RELATIONSHIP BETWEEN INTRAOCULAR RELATIONSHIP BETWEEN INTRAOCULAR PRESSUREPRESSURE

AND VISUAL FIELD LOSS AND VISUAL FIELD LOSS

According to the EMGT study, for every 1 According to the EMGT study, for every 1

mm drop in IOP, a 10% reduction in risk of mm drop in IOP, a 10% reduction in risk of

glaucomatous progression was observed.glaucomatous progression was observed.

Ref: Surveys of ophthalmology 2003; 48 (suppl 1): 53-Ref: Surveys of ophthalmology 2003; 48 (suppl 1): 53-5757

Thus lowering IOP to an appropriate Thus lowering IOP to an appropriate level reduces the risk of further visual level reduces the risk of further visual

lossloss It is now agreed that using a number It is now agreed that using a number (e.g. < 21 mmHg) is obsolete, because (e.g. < 21 mmHg) is obsolete, because

it does not take into account the it does not take into account the individual variability for each patientindividual variability for each patient

Ref:1. Surveys of Ophthalmology 2003; 48 (suppl Ref:1. Surveys of Ophthalmology 2003; 48 (suppl 1): 53-571): 53-57

2. Bull. Soc. Belge Ophthalmol 1999; 274: 61-652. Bull. Soc. Belge Ophthalmol 1999; 274: 61-65

THE TARGET PRESSURE CONCEPT

A “target” pressure should be set as a goal of long term therapy: it should be chosen on an individual basis, weighing potential benefits and risks of treatment for each

patient.


TARGET IOP

The goal of the clinician while treating patients with glaucoma should be to lower the intraocular pressure to a level that is “safe” for that particular eye.


TARGET IOP: DEFINITION

Target IOP may be defined as a pressure, rather a range of intraocular

pressure levels within which the progression of glaucoma and visual field loss will be delayed or halted


SETTING TARGET IOP: FACTORS TO BE CONSIDERED

IOP level at which optic nerve damage occurred

Extent and rate of progression of glaucomatous damage, if known

Presence of other risk factors Patient’s age Expected life span Medical history

Ref: Surveys of Ophthalmology 2003; 48 (suppl 1); 53-57Ref: Surveys of Ophthalmology 2003; 48 (suppl 1); 53-57

HOW TO CALCULATE TARGET IOP

Target IOP = “Maximum IOP – Maximum IOP % - Z”Target IOP = “Maximum IOP – Maximum IOP % - Z”Z is an optic nerve damage severity factor.Z is an optic nerve damage severity factor.ZZ Optic Nerve damageOptic Nerve damage00 Normal disc and Normal Normal disc and Normal

visual fieldvisual field11 Abnormal Disc and Normal Abnormal Disc and Normal

visual fieldvisual field22 Visual field loss not threatening Visual field loss not threatening fixationfixation33 Visual field loss threatening or Visual field loss threatening or

involving fixation involving fixationRef: Bull Soc. Belge Ophthalmol 274, 61-65, 1999Ref: Bull Soc. Belge Ophthalmol 274, 61-65, 1999

HOW TO CALCULATE TARGET IOP

For e.g.: An eye with a maximum IOP of 30 mmHg, optic nerve damage and

visual field loss not threatening fixation would have a target set at 19 mmHg

(30-30%-2)

Ref: Bull. Soc. Belge Ophthalmol 274, 61-65, 1999Ref: Bull. Soc. Belge Ophthalmol 274, 61-65, 1999

AAO GUIDELINES: TARGET IOP

Glaucoma patients with mild damage (optic disc cupping but no visual field loss) Reduction of 20-30% from baseline

Glaucoma patients with advance damage Reduction of 40% or more from baseline

Normal pressure glaucoma Reduction of 30% from baseline

Ocular hypertension Reduction of 20% from baseline

Surveys of Ophthalmology 2003; 48 (suppl 1): 53-57Surveys of Ophthalmology 2003; 48 (suppl 1): 53-57

AAO GUIDELINES: TARGET IOP

Open angle glaucoma with IOP in the mid to high 20s Target IOP range 14-18 mmHg

Advanced Glaucoma Target IOP < 15 mmHg OHT whose IOP > 30 mmHg with no sign of optic

nerve damage Target IOP < 20 mmHg

Ref: Surveys of Ophthalmology 2003; 48 (suppl 1); 53-57Ref: Surveys of Ophthalmology 2003; 48 (suppl 1); 53-57

HOW TO USE A TARGET IOP

Recommended to record and highlight the target pressure in the chart of a patient

Draw an IOP curve for each glaucomatous patient and to highlight the target pressure on the curve

Ref: Bull. Soc. Belge Ophthalmol 274; 61-65, 1999Ref: Bull. Soc. Belge Ophthalmol 274; 61-65, 1999

HOW TO USE A TARGET IOP

Target pressures should be reevaluated periodically. This is because a target IOP that is appropriate when you first see a patient may not be safe pressure 10 years later when he or she may have developed systemic hypertension, diabetes, or some other condition that may affect the patient’s susceptibility to glaucomatous progression

Ref: Surv. Of Ophthalmology 2003; 48 (suppl 1): 53-57Ref: Surv. Of Ophthalmology 2003; 48 (suppl 1): 53-57

“ “ You’re not going to have one target pressure that’s appropriate for every patient. It is a dynamic process and you always have to be alert and open to modification.”

L. Jay Katz,

Professor of Ophthalmology

Jefferson Medical College

“Patients should be followed closely over time and their target pressures should be adjusted, depending upon how the patient is doing. If the patient progresses, the target pressure should be lowered. If the patient does very well, the target pressure should be lowered. If the patient does very well, the target might be raised.”

Stevens Simmons, Associate Clinical Professor,

Albany Medical College

TARGET IOP: SUMMARY AND RECOMMENDATIONS

Target IOP should be individualized as per patient and should be a flexible ever changing variable varying with the progression of the disease

The concept of a target IOP should be a part of the standard of care for physicians who treat glaucoma patients

The methods used to maintain the target pressure should be sustainable over the long term with minimal adverse effects


1. Beta-adrenergic antagonists:

- inhibiting cAMP production in ciliary epithelium

=> decrease aqueous humor secretion 20-50 %

=> decrease IOP 20-30 %

- peak 2-3 hours

- non selective beta-antigonist: carteolol, levobunolol, timolol maleate

selective beta1 antigonist: betaxolol

- side effect: bronchospasm, bradycardia, heart block, lower BP

CNS depression, punctate keratitis, impotence, allergy


2. Parasympathomimetic agents:

- Direct-acting cholinergic agents: affect the motor endplates

pilocarpine

Indirect-acting cholinergic agents:inhibit enzyme acethylcholinesterase

echothiophate iodide

- Contraction of the longitudinal ciliary muscle

=> increase outflow => decrease IOP 15-25 %

- Reduced uveoscleral outflow

- Disrupt the blood-aqueous barrier

- associated retinal detachment

- induced myopia


3. Carbonic anhydrase inhibitors:

- Direct antagonist activity on ciliary epithelial carbonic anhydrase

=> decrease aqueous humor

- Systemic CAI:

Acetazolamide ( 62.5 mg gid ) decrease IOP 15-20 %

Methazolamide ( 25-30 mg bid,tid )

side effect: ( dose relate )

acidosis, depression, numbness, renal stone, hypokalemia

bone marrow depression

- Topical CAI:

Dorzolamide, Brinzolamide, Sulfonamide

decrease IOP 14-17 %

side effect: bitter taste, punctate keratopathy


4. Adrenergic agonist:

- Nonselective Alpha agonist : epinephrine

Dipivefrin

increase conventional and uveoscleral outflow


side effect: headache, increase BP, tachycardia, arrhythmia

adrenocchrome depositsat the conjunctival and cornea

pupillary dilation, allergic blepharoconjunctivitis

cystoid macular edema

- Relative selective Alpha agonist : Alpraclonidine

Brimonidine

decrease aqueous production

increase uveoscleral outflow



5. Hypotensive lipids:

- increase uveoscleral outflow 50 %

Latanoprost, Travoprost, Bimatoprost decrease IOP 25-32 %

Unoprostone decrease IOP 13-18 %

- side effect: darkening of the iris and periocular skin

conjunctival hyperemia, hypertrichosis

Herpes keratitis, cystoid macular edema

uveitis

6. Combined medication:

- Cosopt: timolol maleate 0.5% + dorzolamide 2%

- Advantage: less confusion

increase compliance


7. Hyperosmotic agents:

- Osmotic gradient => drawing water from the vitreous cavity

- effect are transient => rebound elevation IOP

- oral glycerine, intravenous manitol

- side effect: headache

mental confusion

acute congestion heart failure

myocardial infarction

8. Surgical therapy for glaucoma

Open angle glaucoma:

Trabeculectomy:

- Indication: - Failed maximum medication

- progressive glaucomatous optic neuropathy

- Relative contraindication: - blind eye

- rubeosis iridis

- active iritis

- Less successful in younger, aphakia, pseudophakia

uveitis glaucoma, black, previously failed filtering

Trabeculectomy


Open angle glaucoma:

Trabeculectomy

Complication

Early Late

infection leakage

hypotony failure

flat anterior chamber cataract

aqueous misdirection blebitis

hyphema endophthalmitis

cataract dysesthetic bleb

cystoid macular edema bleb migration

hypotony maculopathy hypotony

choroidal effusion

suprachoroidal hemorrhage

loss of vision


Angle closure glaucoma:

1. Laser iridectomy:

indication: pupillary block

contraindication: active rubeosis iridis

systemic anticoagulants

complication: focal lens or corneal damage

retinal detachment

bleeding

IOP spike

2. Peripheral iridoplasty

3. Cataract extraction


Congenital glaucoma:

Goniotomy: clear cornea

Trabeculotomy: cloudy cornea

indication: childhood glaucoma

contraindication: - unstable health

- multiple anomalies with poor prognosis

complication: - hyphema

- infection

- lens damage

- uveitis

Thank you

glaucoma & target iop

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