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I.
Secondary Open-Angle Glaucoma
A. Pseudoexfoliation Syndrome and Pseudoexfoliative Glaucoma
1. Epidemiology
a.
At-risk populations
b.
Equal prevalence of the glaucoma males vs. females
c.
Increased prevalence with age
2. Pathogenesis
a.
Basement membrane disease
b.
Mechanism for IOP rise is not well understood
c.
Association with systemic vascular disease
3. Ocular Findings
a.
Gray-white material on the anterior lens capsule is diagnostic
b.
Material found on anterior segment structures
c.
Iris transillumination defects distinct from pigment dispersion
syndrome
d.
Pigment deposition distinct from pigment dispersion syndrome
i)
Patchy pigment deposition in the TM
ii)
Sampolesi line
e.
Poor pupillary dilation and weak zonular attachments affect cataract
surgery
i)
Increase risk of capsular rupture
ii)
Increase risk of lens or IOL dislocation
f.
Association with narrow angles
4. Treatment and Management
a.
Medical-similar to POAG
b.
ALT very effective
c.
Watch carefully-glaucoma can be very aggressive
B. Pigment Dispersion Syndrome and Pigmentary Glaucoma
1. Epidemiology
a.
Young, myopic males typically
b.
Caucasians
c.
AD
d.
Decrease incidence with age as decrease in pigment liberation
2. Pathogenesis
a.
Liberation of pigment from posterior iris pigment epithelium because of
rubbing of zonules on posterior iris surface
b.
IOP elevation probably due to TM dysfunction associated with pigment
accumulation-decrease outflow
3. Ocular Findings
a.
Pigment deposition on anterior segment structures
i)
Krukenberg’s spindle
ii)
Angle
iii)
Iris surface
b.
Gonioscopic findings
i)
Dense, regular deposition of pigment in angle
ii)
Concave iris
iii)
“Reverse papillary block”
c.
Pigment on the surface of the lens-Zentmayer’s ring or Scheie’s line
d.
IOP can be very elevated and some patients get significant IOP spikes
associated with pigment liberation
i)
Exercise
ii)
Pupil dilation
4. Treatment and Management
a.
Medical-similar to POAG
b.
ALT very effective
c.
Laser peripheral iridotomy (LPI)
i)
Relieve “reverse pupillary block”
ii)
Which patients should this be used for?
C. Uveitic Glaucoma
1. Epidemiology
a.
Can be associated with any uveitic condition
b.
The relationship of IOP and inflammation
2. Pathogenesis
a.
Acute IOP elevation
i)
TM outflow obstruction by uveitic debris
ii)
TM inflammation-trabeculitis
b.
Chronic IOP elevation
i)
Scarring
ii)
PAS
3. Ocular Findings
a.
Symptoms and signs consistent with acute and chronic uveitis
b.
Elevated IOP
4. Treatment and Management
a. Treat the uveitis-sometimes the only treatment necessary
b. Search for the underlying cause of the uveitis
c. Need for IOP control dependent on the level of IOP and the risk of
optic nerve damage in that patient
i)
Aqueous suppressants
ii)
Prostaglandins and miotics contraindicated
D. Uveitic Syndromes
1. Glaucomatocyclitic Crisis (Posner-Schlossman Syndrome)
a.
Marked elevation of IOP associated with mild anterior uveitis
b.
Recurrent
c.
High IOP, mild uveitis, fine KP, no PAS
d.
Treatment is with steroid drops and aqueous suppressants
2. Fuch’s Heterochromic Iridocyclitis
a.
Chronic, unilateral inflammation associated with elevated IOP
b.
Mild anterior uveitis
c.
Round KP
d.
Hypochromia (therefore, heterochromia)
e.
Iris nodules
f.
Vitreous opacities
g.
May not respond well to treatment
h.
Treatment is steroid drops and aqueous suppressants
E.
Steroid-Induced Glaucoma
1. “Is the IOP elevated because of the steroid or because of the uveitis?”
a.
If the inflammation gets better but the IOP goes up, probably steroidinduced
b.
Not always easy to tell
2. IOP elevation usually not seen until 1-2 weeks of topical treatment but may be
seen months later
3. IOP elevation more likely with certain steroids i.e. dexamethasone,
prednisolone than others e.g. loteprednol, rimexolone
4. Correlation of IOP rise with potency of drug and frequency of dosing
5. Some patients more susceptible-“steroid responders”
6. Correlation with POAG
F.
Glaucoma Associated with Trauma
1. Associated with uveitis and hyphema
2. Hyphema and Glaucoma
a.
IOP elevation due to blood and blood products obstructing TM
b.
Usually associated with re-bleed
c.
Aqueous suppressants, cycloplegics, anti-inflammatories
d.
Surgical evacuation may be necessary in cases of very high IOP, blood
staining of the cornea, non-clearing hyphema
3. Angle-Recession Glaucoma
a.
Epidemiology-Follows blunt trauma to the eye
b.
Pathogenesis-Trauma leads to tearing of the ciliary muscles and
damage to the TM
c.
Ocular Findings
i) Widening of ciliary body band in the involved eye
ii) Must compare to the opposite eye
iii) Greater amount of recession, greater risk for elevated IOP
iv) Usually associated with other signs of trauma
4. Treatment and Management
a.
Similar to treatment of POAG but ALT may be of less value
b.
Watch for the development of POAG in the opposite eye
G. Glaucoma Associated with the Lens
1. Phacolytic Glaucoma
a.
Protein leakage from a hypermature cataract
b.
IOP rise secondary to inflammation
2. Lens Particle Glaucoma
a.
Lens particles obstruct TM
b.
Following YAG or from lens
c.
IOP rise secondary to inflammation
II. SECONDARY ANGLE-CLOSURE GLAUCOMA
A. Phacomorphic Glaucoma
1. Pathogenesis
a.
Large, cataractous lens causes shallowing of chamber angle
b.
Acute angle closure or chronic angle closure
c.
Pupillary block mechanism
2. Treatment and Management
a.
Acute-as PACG
i) Medical treatment to quickly lower IOP
ii) LPI to reverse pupillary block
iii) Cataract surgery is ultimate treatment
b.
Chronic
i) Medical treatment as in OAG
ii) LPI to prevent or reverse pupillary block
iii) Cataract surgery is the ultimate treatment
c.
Should cataract surgery be done in lieu of LPI?
B. Aphakic and Pseudophakic Pupillary Block
1. Pathogenesis
a.
Usually associated with AC IOL and blocked iridectomy site
b.
Can also occur if pupil blocked by vitreous, posterior structures moving
forward, etc.
c.
Can be acute with very high IOP or chronic
2. Treatment and Management
a.
Medically lower IOP if high
b.
Laser PI
C. Neovascular Glaucoma
1. Pathogenesis
a.
Anterior segment neovascularization occurs secondary to posterior
segment hypoxia
i) Diabetic retinopathy
ii) Central retinal vein occlusion
iii) Central retinal artery occlusion
iv) Ocular ischemic syndrome
New vessel growth at pupillary margin, across iris, and in angle
Eventual development of fibrovascular membrane across TM reducing
outflow
2. Ocular Findings
a.
Often present with relatively acute onset of painful, red eye
b.
Iris and angle neovascularization
c.
Ectropion uveae
d.
High IOP
e.
Retinal ischemia
3. Treatment and Management
a.
Treat before PAS formation if possible
b.
PRP to reduce the stimulus for new blood vessel growth
c.
Medical treatment-no miotics or prostaglandins
d.
Surgical treatment-filtration surgery
e.
If vision lost, prevent pain
v)
Atropine
vi)
Topical steroid
vii)
Respond to bullous keratopathy
b.
c.
D. Other Secondary Angle-Closure Glaucomas
1. ICE syndrome
2. Ciliary block (aqueous misdirection)
3. Cysts and tumors
4. Ciliochoroidal effusion