Transcript Chapter 11 Glaucoma Primary Open Angle Glaucoma

Chapter 11. Glaucoma
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Concept:
Those suffer from pathologic high IOP
which is sufficient to cause excavation of
optic disc, optic atropy and characteristic
loss of visual field are called glaucoma.
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IOP is a major risk factor, but not always,
especially for open angle glaucoma,
normal tension glaucoma.
Vascular or ischemic factors
Neuroprotection
Primary angle closure glaucoma
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Etiology:
blockage or permennant synechia of
trabecular meshwork by peripheral iris.
narrow angle,
small eye,
shallow anterior chamber
Acute angle-closure glaucoma
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Etiology: still unknown
often induced by fatigue, anxiety, anger
small or crowded eye:
short axis of the globe
small cornea
shallow anterior chamber
narrow angle, thick lens
Clinical manifestation
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Staging:
1. Preclinical stage
2. Premonitory stage
3. Acute attack
4. Remission stage
5. Chronic stage
6. Absolute stage
Diagnosis and differential diagnosis
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Acute attack :nausea, vomitting,headache;
Congestion
Edematous cornea
Reduced vision
High IOP
Shallow chamber
Pupil dilated
feckle
1. Acute conjunctivitis
2. Acute iridocyclitis
Treatment
1. IOP controled with
20% mannitol, 1% pilocarpine
0.25% timolo, diamox, etc
2. Peripheral iridectomy
laser iridotomy
3. Trabeculectomy
Chronic angle-closure glaucoma
Etiology: still unknown
shallow chamber
narrowed angle
goniochia
Clinical manifestation
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IOP increase progressively
Excavtion of optic cup
Visual field loss
seidal scotoma
nasal step
arcute scotoma
circuit scotoma
tubular vision
Treatment
1. Medical treatment
0.25% pilocarpine
0.5% timolo
diamox
mannitol if necessary
2. Peripheral iridectomy or trabeculectomy
according to gonioscopy
Primary Open Angle Glaucoma
Etiology: still unknown
Characteristics:
high IOP
angle open
pathologic findings on trabecular
meshwork and Schlemm’s cannal
Clinical findings
Symptoms:
usually no symptoms
usually found at late stage
few blurred vision, pain of the eye
IOP:
fluctuated at early stage
high at late stage
24-hour IOP curve is important for
abnormal findings
Clinical findings
Anterior Segment of Eye:
usually no abnormal findings
Fundus Examination: key tips
1. optic cup enlarged and deepened
2. narrowing of neuroretinal rim
3. larger C/D ratio
4. unsymmetric C/D ratio
5. hemorrhage on or near optic disc
6. loss of optic nerve fiber
Clinical findings
visual function: loss of visual field
1. paracentral scotoma
2. arcuate scotoma
3. quadrant field loss
4. tubular visual field
Diagnosis
IOP: 24-hour IOP curve important
Optic cup changes:
Visual field loss:
any patient with either 2 of the 3 signs
mentioned above plus an open angle,
diagnosis can be made.
Treatment
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Medical:
target IOP: various,
individual
beta-blockers or alpha-excitors
diamox( carbonic anhydrase inhibitor)
latanoprost
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Laser : trabeculoplasty
Filtering surgery
trabeculectomy
nonpenetrating trabecular surgery
reversed trabeculectomy
Congenical glaucoma
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Infantile glaucoma
Juvenile glaucoma
abnormalities of angle
Surgery
trabeculotomy
goniotomy
Chapter 12. Uveal Diseases
Anatomy:
1. iris
2. ciliary body
3. choroid
Characteristics:
abundant in blood vessels
abundant in pigment
Uveitis
Etiology & Mechanism
1. Infection: bacteria, virus, fungus etc
2. Auto-immune factors: antigens
3. Oxidation damage
4. Arachidonic acid
5. Immuno-inheritance: HLA antigen
Anterior Uveitis
Including:
1.iritis: iris only
2. Iridocyclitis: iris + ciliary body
3. Cyclitis: ciliary body only
Classification:
1. Acute: HLA-B27 (+)
2. Chronic: Fuchs
3. Both acute and chronic
Clinical Manifestation
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Symptoms:
pain
photophobia
tearing
blurred vision
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Signs:
1. ciliary or mixed congestion
congestion near limbus
due to dilation of episcleral vessels
notice: keratitis and PACG
2. KP( keratic precipitate)
indicating endothelial damage and
inflammatory cell or pigment existing
dust KP: non-sarcoid uveitis
neutrocyte, lymphocyte, plasma
middle sized KP: Fuchs syndrome, HSK
mutton KP: sarcoid uveitis
mono-nuclear macrophage
3. Aqueous flare:
damage of blood-aqueous barrier,
protein entering into
anterior chamber;
no meaning of active inflammation
4. Aqueous cells:
indicating the severity of inflammation
inflammatory cells like white-greyish
dust going up near iris,
coming down near cornea
causing KP formation and hypopyon
5. Iris changes:
posterior synechia: iris to lens
anterior synechia: iris to cornea
iris nodules: Koeppe
Bussaca
irido-sarcoma
6. Pupil changes:
small pupil
irregular pupil
seclusion of pupil
occlusion of pupil
7. Lens changes:
pigment on lens
cataract
8. Vitreous changes:
inflammatory cell
Complications
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1. Cataract: aqueous changing leading to
abnormal metabolism of lens and longterm use of steroids
2. Glaucoma: obstruction of trabecular
meshwork, anterior iris synechia,
occusion or seclusion of pupil
3. Low IOP & atrophy: atrophy of ciliary
body leading to less secretion of aqueous
Differential Diagnosis
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1. Acute conjunctivitis
2. Acute angle closure glaucoma
3. Ocular tumour
4. Panuveitis
Treatment
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1. Cycloplegia: pain of the eye
homatropine is ideal, better, lasting
18~36 hours
atropine lasting longer,no recommendaed
1). prevent and treat posterior synechia
2). relieve ciliary and sphincter spasm
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2. Steroid eye drops:
predineson is the best owing to good
penetration into anterior chamber
sub-conjunctival injection should not be
used in anterior uveitis
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3. Nsaid eye drops: prostaglandin,etc.
4. Systemic use of steroids:
5. Etiologic treatment:
6. Treatment for complications
Sympathetic Ophthalmia
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Etiology: auto-antigen exposure after
penetrating wound or operation, resulting in
auto-immune response.
Clinical manifestation: severe uveitis
Treatment: large dose of steroids
other anti-immunologic drugs
Prognosis: used to be very poor
much better right now