Chapter 11 Glaucoma Primary Open Angle Glaucoma
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Transcript Chapter 11 Glaucoma Primary Open Angle Glaucoma
Chapter 11. Glaucoma
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.
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
Etiology:
blockage or permennant synechia of
trabecular meshwork by peripheral iris.
narrow angle,
small eye,
shallow anterior chamber
Acute angle-closure glaucoma
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
Staging:
1. Preclinical stage
2. Premonitory stage
3. Acute attack
4. Remission stage
5. Chronic stage
6. Absolute stage
Diagnosis and differential diagnosis
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
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
Medical:
target IOP: various,
individual
beta-blockers or alpha-excitors
diamox( carbonic anhydrase inhibitor)
latanoprost
Laser : trabeculoplasty
Filtering surgery
trabeculectomy
nonpenetrating trabecular surgery
reversed trabeculectomy
Congenical glaucoma
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
Symptoms:
pain
photophobia
tearing
blurred vision
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
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
1. Acute conjunctivitis
2. Acute angle closure glaucoma
3. Ocular tumour
4. Panuveitis
Treatment
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
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
3. Nsaid eye drops: prostaglandin,etc.
4. Systemic use of steroids:
5. Etiologic treatment:
6. Treatment for complications
Sympathetic Ophthalmia
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