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Tiêu đề Glaucoma
Tác giả Harold E. Cross M.D., P. Tsai, MD, T. Altenbernd, MD
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GLAUCOMA GLAUCOMA Harold E Cross M D , Ph D (With contributions by T Altenbernd, MD, and P Tsai, MD) Brought to you by GLAUCOMA What is it? A disease of progressive optic neuropathy with loss of ret.

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GLAUCOMA GLAUCOMA

Harold E Cross M.D., Ph.D.

(With contributions by T Altenbernd, MD, and P Tsai, MD)

Brought to you by

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GLAUCOMA GLAUCOMA

What is it?

A disease of progressive optic

neuropathy with loss of retinal

neurons and their axons (nerve

fiber layer) resulting in blindness if

left untreated.

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“Glaucoma describes a group of diseases that kill retinal

ganglion cells.”

“High IOP is the strongest known risk factor for glaucoma

but it is neither necessary nor sufficient to induce the

neuropathy.”

Libby, RT, et al: Annu Rev Genomics Hum Genet 6: 15, 2005 Brought to you by

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GLAUCOMA GLAUCOMA

There is a dose-response

relationship between intraocular

pressure and the risk of damage to

the visual field.

What causes it?

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GLAUCOMA

How do we diagnose it?

IOP is not helpful diagnostically until it reaches

approximately 40 mm Hg at which level the

likelihood of damage is significant.

Visual fields are also not helpful in the early stages

of diagnosis because a considerable number of neurons

must be lost before VF changes can be

detected.

Optic nerve damage in the early stages is difficult

or impossible to recognize.

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GLAUCOMA

Intraocular pressure is not the only factor

responsible for glaucoma!

95% of people with elevated IOP will never have

the damage associated with glaucoma.

One-third of patients with glaucoma do not have

elevated IOP.

Most of the ocular findings that occur in people

with glaucoma also occur in people without

glaucoma.

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• Diurnal flucuation normally < 6 mmHg

• Women have slightly higher pressures

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Iris bombé

GLAUCOMA

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Population distribution of IOP

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IOP Variables

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Angle Anatomy

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Schiotz Air

Non-contact

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Goldmann applanation

tonometer

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Tonopen

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GLAUCOMA GLAUCOMA

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The normal visual field: an island of

vision in a sea of darkness:

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THE VISUAL FIELD

Humphrey automated perimetry

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Cup-to-disk ratio

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Normal

DISK CUPPING

Glaucoma

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Glaucomatous cupping

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GLAUCOMA GLAUCOMA

Optic nerve signs of glaucoma progression

Increasing C:D ratio

Development of disk pallor

Disc hemorrhage (60% will show progression of

visual field damage)

Vessel displacement

Increased visibility of lamina cribosa

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GLAUCOMA

Ocular hypertension treatment study

(OHTS study)

GOALS: To evaluate the effectiveness of topical ocular hypotensive

medications in preventing or delaying visual field loss

and/or optic nerve damage in subjects with ocular

tension at moderate risk for developing open-angle

glaucoma (POAG).

POPULATION: 1636 participants aged 40-80 years with IOP 24-32

mm HG in one eye, and 21-32 in the other, randomly

assigned to observation and treatment groups.

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GLAUCOMA GLAUCOMA

TREATMENT GOALS: Reduce pressure to less than or

equal to 24 mm Hg with a minimum pressure reduction of

20% from the baseline.

OUTCOME MEASURES: Development of reproducible

visual field abnormality or development of optic disc

deterioration.

MEDICATIONS USED: beta-adrenergic antagonists,

prostaglandin analogues, topical carbonic anhydrase

inhibitors, alpha-2 agonists, parasympathomimetic agents, and epinephrine.

OHTS parameters

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OHTS parameters that

influence the risk of

developing POAG

IOP Age Cup-disk ratio

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Percentage of OHTS participants in

observation group who developed POAG

(mean follow-up = 72 mo)

IOP vs central

corneal thickness

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Normal central corneal thickness: 545 – 550 u

Add or subtract 2.5 mmHg for each 50 u

change in central corneal thickness

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Congenital Glaucoma

Congenital Glaucoma

Buphthalmos and cloudy corneas

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Narrow Angle Glaucoma

Onset: 50+ years of age

Nausea and vomiting

Halos around lights

Intermittent eye ache

at night

Signs Red, teary eye Corneal edema Closed angle Shallow AC Mid-dilated, fixed pupil

“Glaucomflecken”

Iris atrophy

AC inflammation Brought to you by

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GLAUCOMA

Angle anatomyGrade I Grade 0 Grade III Grade II

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Anatomy of Angle Closure Glaucoma

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Narrow Angle Glaucoma

Mid-dilated, fixed pupil

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Narrow Angle Glaucoma

Narrow Angle Glaucoma

Treatment: Peripheral

Iridotomy

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Open Angle Glaucoma

Aka: chronic simple glaucoma (CSG)

IOP Diabetes

Age Myopia

Race Gender

Family history Cardiovascular

Central corneal disease

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Open Angle Glaucoma

Onset: 50+ years of age

Symptoms

Usually none

May have loss of central

and peripheral vision

late

Signs Elevated IOP Visual field loss Glaucomatous disk changes

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Normal Tension Glaucoma

(NPG, LTG, LPB, NTG)

Similar to OAG but IOP always < 21 mmHg

Higher prevalence of vasospastic disorders,

blood dyscrasias, autoimmune diseases

May be related to episodic hypotension,

hyopthyroidism

A diagnosis of exclusion!!!

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Open Angle Glaucoma

Risk factors

EXAMINATION:

C/D 0.6 or greater

Vertical elongation of disc

Inf rim thinner than sup.

C/D asymmetry >

0.2 Brought to you by

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Treatment

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GLAUCOMA

Filtration blebs

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This platform has been started by

Parveen Kumar Chadha with the

vision that nobody should suffer the

way he has suffered because of lack

and improper healthcare facilities in

India We need lots of funds

manpower etc to make this vision a

reality please contact us Join us as

a member for a noble cause.

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Our views have increased the

mark of the 25,000

collaboration, partners.

Brought to you by

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011-25464531 ,

011-41425180

,

91-9818308353 +,

Saxbee Consultants Details :-www.parveenchadha.com

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THANK YOU ALL FOR LISTENING!

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