Glaucoma
Definition
of Glaucoma
- Acquired optic
neuropathy characterized by optic cupping and loss of nerve tissue.
- IOP elevation is a risk factor
- Visual field loss is a late finding
- Leading cause of
irreversible blindness in the world (66.8 million cases; 6.7 mil bilateral)
- Second leading
cause of permanent blindness in US and leading cause among
African-Americans
- Prevalence in
American Adults: 1.7% whites, 5.6% blacks (2.3 million: 3-5% of these are
blind)
Glaucoma Basics
Optic Nerve Head Anatomy & Physiology
- Optic disc:
1.5-1.9 mm in diameter and wide range of disc areas
- Axons: 1.2
million. divided by septa into 1,000 fascicles,
cell bodies in ganglion layer, synapse in lateral geniculate body (LGB).
- Parvocellular cell axons (P cells): axons more numerous but smaller diameter,
sensitive to color and detail information, small receptive fields and
slow conduction velocities
- Magnocellular cell axons (M cells): fewer, larger diameter, sensitive to
changes in luminance in dim environments, larger receptive fields, faster
conduction velocities, may be more susceptible to glaucomatous damage
- Topographic organization: fibers that arc around the papillomacular bundle and
enter superotemporal and inferotemporal are most susceptible to damage, peripheral
axons travel deeper in the nerve fiber layer and exit eye in outer
portion of optic nerve.
Optic nerve- four regions
- surface nerve fiber
layer: visible, almost completely axons.
Covered by layer of astrocytes: inner limiting membrane of Elsching- this
layer thickens over cup: central meniscus of Kuhnt.
- prelaminar: between surface and lamina cribrosa. Axons in bundles,
separated by glial septa, border of astrocytes separate axons from retina
tissue
- laminar: visible in deep large cups as laminar dots. Axons
travel through pores in lamina cribrosa. Pores are larger superio- and
inferiotemporally- perhaps contributing to greater sensitivity to
glaucoma damage
- retrolaminar: behind lamina cribrosa. Axons
supported by fibrous tissue lined by astrocytes and axons myelinated by
ogliodendrocytes doubling the diameter.
- Blood supply of
optic nerve
- surface nerve fiber
layer: branches of central retinal
artery through recurrent branches in peripapillary retina
- prelaminar: peripapillary choroidal arteries and short posterior
ciliary arteries
- laminar: short posterior ciliary arteries; rich anastomoses
form "circle of Zinn-Haller"
- retrolaminar: centripetal
branches of pial vessels and anastomose with peripapillary choroid,
circle of Zinn-Haller, and central retinal artery branches.
- venous drainage:
central retinal vein
Theories of Glaucomatous Optic nerve damage
- Mechanical- compression of axons against lamina cribrosa
compromises axoplasmic flow and causes apoptosis
- Vascular- optic nerve ischemia possibly by an abnormality in
autoregulation, cannot accommodate for variations in perfusion pressure
Aqueous System
Anatomy & Physiology
Aqueous composition
- Derived from
plasma
- Almost devoid of
protein (<1% of plasma levels)
- Contains 10X -
50X more ascorbate
- Slightly more
acidic and hypertonic than plasma
- Less calcium,
glucose, bicarbonate and carbon dioxide than plasma
- More lactic acid
and chloride than plasma
Aqueous production
- Produced in the
non-pigmented epithelium of ciliary body processes
- The
non-pigmented epithelium have "leaky" tight junctions allowing
passage of ions and water
- Active transport: (secretion) energy expended to drive sodium into
posterior chamber. This sodium gradient causes water to follow. Large
highly charged molecules are also transported actively. Uses ATPase and
carbonic anhydrase
- Ultrafiltration:
driven by hydrostatic pressure and
osmotic gradient, small water soluble molecules pass through micropores in
cell membrane in this way
- Diffusion: concentration gradients drive flow, important for
lipid-soluble molecules
- Decreased by age
(2% per decade), sleep (45%), inflammation, general anesthetics, poor
blood supply, glaucoma medications
Aqueous Outflow
o
"conventional
outflow"
o
increases
as IOP increases
- Pressure-
independent: ciliary body face and iris root (10%)
o
"uveoscleral
outflow" into the suprachoroidal space
o
increased
by latanoprost, anticholinergics (atropine)
o
uveovortex
outflow- minor pathway through iris, ciliary body and choroidal blood vessels
into the vortex veins.
IOP Determinants
- Goldmann
equation: Po = (F/C) +Pv where Po = IOP, F = rate of aqueous formation, C
= facility of outflow, Pv = episcleral venous pressure.
- Normal values:
- IOP (Po); Mean
=16 mm Hg, Range = 10-21 mm Hg
- Rate of
production (F); Mean = 2 µl/min, Range 1.8-4.3 µl/min
- Facility of
outflow (C); 0.22-0.28 µl/min/mm Hg
- Episcleral
venous pressure (Pv); 8-12 mm Hg
Trabecular Meshwork
- Sits within the
scleral sulcus
- Anterior border
is Schwalbe's line: a 50 to 150 µ transition zone between TM and Decemet's
membrane
- Posterior border
is scleral spur attached to it is the longitudinal muscle of ciliary body
- Three layers; 1) uveal meshwork, 2) corneoscleral meshwork 3)
juxtacanalicular tissue- provides majority of outflow resistance
- Most flow is
through posterior portion of TM hence more pigmentation
Schlemm's Canal
- Vein-like tube
(190-350 µ) at base of scleral sulcus
- Occasionally
forms a plexus instead of one canal
- Perforated on
the scleral side intermittantly by 25 to 35 aqueous collector channels
leading to intrascleral and deep scleral plexi
- from scleral plexi
aqueous passes through the aqueous veins into the venous system
- glycosaminoglycans are found in TM
and increased in POAG
Perimetry
Gonioscopy
Glaucomas
of Infancy and Childhood
Aniridia
Anaridia- Genetics
- Autosomal
Dominant (Chromosome 11p, PAX6 gene) or Sporadic, rarely AR
- PAX6 is a homeobox gene regulating expression of structural
genes in time and space
- Sporatic cases
from deletion of portions of Chromosome 11p
- some of these
deletions can result in WAGR complex: Wilms tumor, Anaridia,
Genitourinary abnormalities and mental Retardation
Anaridia- Glaucoma pathogenesis
- Iris stub
attached to angle structures by fine strands that cause stub to cover
angle causing glaucoma
Anaridia- Signs
- Bilateral
involvement
- Glaucoma in
50-66%, most in late childhood or early adulthood with closure of angle
- Cornea:
epithelium develops abnormally with scarring and pannus: difficult to
treat, abnormal stem cells
- Iris: lack of
iris tissue, stub visible on gonioscopy, can have iris present with all
the other signs of aniridia
- Lens: cataract
common
- Retina: foveal
hypoplasia causing nystagmus with VA potetial of 20/200.
- Systemic: WAGR
complex: most important Wilms tumor in sporatic forms
- Four varieties
of aniridia:
- Mostly iris abnormalities and normal vision
- Associated with corneal pannus, glaucoma, foveal
hypoplasia and poor vision
- Wilms tumor and other kidney or GU abnormalities
- Mental retardation
Anaridia- Treatment
Axenfeld-Rieger
Syndrome
Also known as iridocorneal dysgenesis or anterior chamber cleavage syndrome.
Pathophysiology
- Arrest of
anterior segment development late in gestation
- Glaucoma from
compact, ineffective trabecular tissue
Genetics
- Autosomal
Dominant
- Chromosome 4q
(REIG1 or called PITX2 gene)
- PITX2 gene is a paired homeobox gene controlling
expression of other genes
- Chromosome 13q
- Chromosome 6p
(FKHL7) some cases of Axenfeld anomaly and Rieger anomaly without systemic
abnormalities
Signs
- Bilateral,
Glaucoma in 50%- related to level of iris insertion, higher = greater risk
- Cornea: Posterior
Embryotoxin: glassy, white line on corneal endothelium = prominent
anterior Schwalbe's line. (Seen in 15% of normals). By itself not
associated with glaucoma. Not necessary for diagnosis but seen in nearly
all.
- Iridocorneal
angle: prominent iris processes. Iris may insert high in the angle. Axenfeld
anomaly: posterior embryotoxin + iris processes
- Iris: thin and
hypoplastic. Sphincter stands out as a ring, corectopia, polycoria,
changes are usually static. Rieger anomaly: posterior embryotoxin +
iris processes + iris hypoplasia, corectopia, or polycoria
- Non-ocular
findings: mid-face flattening, maxillary hypoplasia, hypertelorism,
telecanthus, broad & flat nasal bridge, hypodontia (too few),
microdontia, redundant periumbilical skin, hypospadias, growth hormone
deficiency, empty sella
Treatment
- Glaucoma treated
like POAG except colinergics and ALT ineffective.
- Early cases
might respond to goniotomy or trabeculotomy, but less effective than for
primary congenital glaucoma
Differential Diagnosis
Inherited Disorders Assoicated
with Glaucoma- in most cases disease is rare or glaucoma is
uncommon
Inherited Ocular Disease associated
with Glaucoma
Inherited Chromosomal absence
or duplication with Glaucoma
- Turner syndrome
(XO)
- Patau syndrome
(Trisomy 13-15)
- Edward syndrome
(Trisomy 18)
- Down syndrome
(Trisomy 21)
Inherited/ Congenital
Systemic disease associated with Glaucoma
Iris Hypoplasia
- Autosomal
dominant, rare
- Iris stroma thin
allowing visualization of the sphincter muscle- similar to iris hypoplasia
in Axenfield-Rieger syndrome
- Distinct dark grey
or chocolate-brown irises
- Angles open and
eye otherwise normal
- RIEG1 (PITX-2)
gene mutation found in one family
Juvenile Primary Open-Angle
Glaucoma
Lowe Syndrome
- Oculocerebrorenal
Syndrome
- Cataracts almost
100%
- Glaucoma 66%
- Systemic
findings: mental retardation, aminoaciduria, renal rickets, hypotonia
- X-linked
recessive; Mutation on OCRL-1 gene.
- Poor TM
development
Peters
Anomaly- Rare disease with central corneal opacities
- Pathophysiology-
Corneal endothelium does not
develop. Absent Decemet's as well. If no other AC abnormalities called- Internal
ulcer of von Hippel. Cataracts from failure of separation of cornea
and lens during embryogenesis. Can rarely occur with Axenfield-Rieger's syndrome
- Genetics- Most cases sporadic, Autosomal recessive and dominant
pedigrees reported. One case of PAX-6 gene mutation found (same as aniridia)
- Signs-
o
80% bilateral.
o
Glaucoma 50% and can be present at
birth.
o
Central white corneal opacitiy.
Perepherial cornea clear. Adhesions of iris tissue to edges of central corneal
lesion
o
Cataract in some
o
Usually isolated finding
Phakomatoses-
Three are associated with glaucoma
Encephalotrigeminal
Angiomatosis- (see path notes: Sturge-Weber)
- Born with
visible port-wine lesion on one side of face in trigeminal distribution
- Pathophysiology-
increased IOP from resistance to
aqueous outflow from elevated
episcleral venous pressure OR congenital abnormality of angle
- Genetics- No
heriditary pattern
- Signs- Unilateral, Glaucoma in 50% especially in those with
upper lid angiomas
o
Conjunctiva- large tortuous episcleral
vessels
o
Retina- choroidal
hemangiomas
o
Associated findings- angiomas of CNS
leading to seizures or other neurologic signs or symptoms, some are
developmentally delayed
Oculodermal Melanocytosis
- Marked
pigmentation throughout involved eye, face and mucosa of mouth
- Without dermal
involvement: ocular melanocytosis
- Skin involvement
follows trigeminal distribution
- 10% have
elevated IOP in the involved eye
- Heavy TM
pigmentation from accumulation of melanocytes
Primary Congenital Glaucoma
Develops within first 3 years of life, not associated with any other
abnormality or cause
Pathophysiology
- Isolated
abnormality of angle development
- Posterior
migration of trabecular tissue continues through the first year of life
- Posterior
migration is arrested in congenital glaucoma
- Iris inserts
high in the angle, compressing trabecular beams
- Deep derangement
of TM and Schlemm's canal can occur
Epidemiology &
Genetics
- Approx 1 in
30,000 (general ophthalmolgist sees 1 case every 5 yrs)
- 1 in 10,000 have
a pediatric glaucoma
- 60% diagnosed by
age 6 months, 80% by age 1
- 65% male
- Genetics: most
cases sporatic
- Most common
inheritance pattern: autosomal recessive: Chromosome 2p (CYP1B1)
and 1p
Symptoms
- Triad : photophobia,
epiphoria, blepharospasm
- noticed in bright
environment
Signs
- 70% bilateral
- Buphthalmos
("ox eye"): large eye, excessive growth in response to elevated
intraocular pressure
- Axial eye length
charted along normal growth curves
- Cornea: Enlarged
corneal diameter >12. Normal is 10.0 to 10.5mm in newborn. Corneal edema.
Haab's striae = horizontal or circumferential cracks in Decemet's.
- Anterior
chamber: deep chamber (normal is shallow)
- Iridocorneal
Angle: iris inserts high (at level of scleral spur or TM), compacting TM
creating appearance of a membrane. Iris vessels prominent: "Loch Ness
Monster" vessel
- Optic nerve: Cup
>0.3 is suspicious (normal £ 0.1). Much more reversable
- Refractive
error: myopia can be high
Treatment
- IOP will be
lowered after a few minutes of general anesthesia (except with Ketamine
& trichloroethylene)
- Chloral Hydrate
doesn't lower IOP significantly
- Use Perkins
tonometer or pneumotonometry
- Normal IOP in
newborn = 11 mm Hg (11-17 with Chloral hydrate)
- EUA: IOP before intubation, horizontal corneal diameter,
anterior segment, gonioscopy, MRx, Axial eye length, optic nerve head
& fundus
- Koeppe or
Swan-Jacobs lens can be used with operating microscope
- 70% ethanol to
remove edematous epithelium
- Goniotomy
- Trabeculotomy
Prognosis / Sequelae
- the earlier the
onset = poorer prognosis
- later the delay in
diagnosis = poorer prognosis
- Diagnosis
between 8 months and 2 years- good prognosis
- Large thin
globes lead to: high myopia, easy globe rupture, retinal detachment, corneal
exposure, ectopia lentis
- Cataracts
common, corneal decompensation from endothelial loss
- Risk of
ambylopia and anisometropia
Primary Congenital Glaucoma-
Differential Diagnosis
- Tearing
- Bupthalmos
- High myopia
- Exophthalmos
- Shallow orbits
- Large Cornea
- Megalocornea- X linked, bilateral
- Corneal breaks
- Trauma (forceps)- usually unilateral and OS
Cloudy Cornea- DDX
Open-Angle Glaucomas
Primary Open-Angle Glaucoma (POAG)
Optic nerve head cupping and VF loss with IOP > 21 mm
Hg. Normal angle anatomy.
POAG Epidemiology
- Increased risk
with age >50, family history, increasing IOP, black race, steroid use
POAG Signs/Symptoms
- IOP >21mm Hg
with:
- Open anterior
chamber angle on gonioscopy
- Thinning of
optic nerve rim over time
- Acquired optic pit
- Notching
- More thinning in superior or inferior nerve rim
- Optic disc
hemorrhages (more common in Normal tension Glaucoma)
- Nerve fiber
layer thinning or defect
- Cup to disc
asymmetry between the two eyes
- Bayoneting of
the blood vessels entering the optic nerve (diving at acute angles into
the deep cup)
- Visual Field
loss
- Nasal step
- Paracentral scotoma
- Arcuate scotoma
- only temporal
island remains in late glaucoma
- Cornea usually
clear
- Largely
asymptomatic with insidious onset
POAG Treatment
- Rule out
atypical cases of glaucoma by working up other causes of optic neuropathies
- Pallor out of proportion to the degree of cupping
- Visual field defects respecting the vertial meridian,
hemaniopic loss or central loss
- Disproportionate vision loss
- Early color vision loss
- Consider diurnal
pressure readings if progression noted with normal IOP on clinic visits
- Treat in a
stepwise, logical fashion. One eyed trials give the most information
about drug effectiveness
- Punctal
occlusion allows better ocular penetration and less systemic side effects
- Regular Goldman
or Humphrey visual fields are obtained
- Nerve fiber
layer thickness analysis by optical coherence tomography or Heidleberg
scan can obtain sensitive measures of nerve fiber layer and perhaps help
detect changes earlier.
- Visual field
changes usually are a late sign of nerve fiber layer loss.
Normal Tension Glaucoma (NTG)
Optic nerve head cupping and VF loss without documented IOP > 21. Possibly vascular etiology more
likely.
NTG- Epidemiology
- Elderly
- IOP's in normal
range but usually slightly higher than average
- Associated vasospastic
diseases: Migraine HA and Raynaud's phenomenon
- Increased
incidence of autoimmune disease and hypercoagulopathy
- Possibly systemic
hypotension, often when sleeping.
- History of
severe systemic hypotension associated with blood loss and may be
non-progressive.
NTG- Symptoms / Signs
- Visual symptoms
occur earlier than with POAG but most asymptomatic
- Notching of cup
and disc hemorrhages more common than with POAG.
- VF loss deeper,
steeper and closer to fixation than POAG.
NTG- Treatment
- Rule out other etiologies
of glaucoma or evidence of previously high IOP- trauma, inflammation,
burned out pigmentary glaucoma
- Diurnal curve
testing
- Neurologic
evaluation in cases of unilateral cupping, atypical visual field loss,
pallor in excess of cupping
- Some patients
will not progress- serial evaluations are indicated before treatment begun
- Fixation
splitting VF loss requires prompt treatment
- Collaborative
NTG Treatment Trial: 30% reduction in IOP slowed progression vs.
non-treated. If there is damage at this target IOP adjust target lower.
- Usual medications are used, but theoretical risk of ß-blockers
reducing blood flow to optic nerve
- ALT
can be useful in IOP high normal
- Trabeculectomy
Ocular Hypertension
Exfoliation Syndrome and Glaucoma
Pigment Dispersion Syndrome/ Pigmentary Glaucoma
PDS- Pathophysiology
- Abnormal amounts
of pigment are liberated from posterior surface of iris and deposited
throughout eye.
- During blink
(while awake) or jarring exercise
PDS- Epidemiology
- Diagnosed second
and third decades of life, more common in whites, myopes, males
- 25%-50% of those
with PDS will progress to pigmentary glaucoma.
- Cases of
glaucoma can "burn out" with age and increased thickening of
lens reversing backbowing of iris
- 6%-8% develop
retinal detachment
Pigmentary Glaucoma- Symptoms
- Early: none or
blurred vision with jarring exercise (not: jogging, bicycling, swimming) .
- Later:
perepherial vision loss.
- Very late: loss
of central vision.
PDS- Signs
- Cornea:
Krukenberg spindle
- Gonioscopy:
backbowing of iris causing reverse pupillary block, dense trabecular
pigment, Sampaolesi's line
- Pupil: radial
transillumination defects & pupil irregularities, more affected eye
has darker iris and larger pupil,
- Scheie stripe or
Zentmeyer line: pigment at junction of posterior lens capsule and zonules
- Elevated IOP
- Cupped optic
nerve.
Pigmentary Glaucoma- Treatment
PDS- Prognosis
- 25-50% of PDS
develop glaucoma
- With age and
lens thickening, aqueous is trapped in posterior chamber to such a degree
to eliminate backbowing
- When pigment is
no longer liberated, disease "burns out"
- 6-8% develop
retinal detachment
Steroid Induced Glaucoma
- Topical,
subconjunctival, oral or inhaled steroids can be responsible
- After 6 weeks:
IOP rise of <5mm Hg in 60%, rise of 6-15mm Hg in 30% and >15mm Hg in
5%.
- Etiology of IOP
not known
- Possible
increase in glycosaminoglycans in TM or inhibition of phagocytosis of TM
endothelial cells
- IOP rise in POAG, relatives of those with POAG, diabetics and myopes
- IOP rise can
occur after many months
- Depot steroids
can cause IOP rise even if no rise with topical steroid
- medrysone and
fluorometholone cause less IOP elevation and less anti-inflammatory effect
Glaucoma from Elevated Episcleral
Venous Pressure
DDX
- IOP is at least
as high as episcleral venous pressure (see IOP
formula)
- Signs:
unilateral glaucoma, dilated episcleral veins, proptosis, chemosis, blood
in Schlemm's canal
- If AV fistula:
ocular pulsations (seen also on tonometry), audible pulse-synchronous
bruit, dilated superior ophthalmic vein on echo
- Treat underlying
cause
- Treatment of
glaucoma is very difficult: medications usually are not sufficent.
- ALT
is ineffective.
- Surgical
procedures have high risk of choroidal effusion and suprachoroidal
hemorrhage
- Angle
closure from choroidal effusion or hemorrhage or neovascular glaucoma
from ischemia also occur
Causes of Elevated
Episcleral Venous Pressure
- Carotid-Cavernous
sinus fistula
- Dural sinus
fistula
- AV malformation
in the orbit
- Venous
compression- mass or Thyroid ophthalmopathy
- Orbital varices
- Sturge-Weber
- Idiopathic and
familial
- Superior vena
cava syndrome
Angle-Closure Glaucomas-
Iris obstructs the trabecular meshwork in one of several ways.
Pupillary Block Glaucomas- forward
bowing of iris: iris bombé
Synechial Angle Closure: perepherial
anterior synechiae adherent to TM or scleral spur
Iridocorneal-endothelial
syndromes (ICE)
ICE- General facts
- Rare diseases of
the corneal endothelium
- Unilateral
- Usually in women
in 4th or 5th decade of life
- Sporadic (no
inheritance pattern)
- Possibly due to
Herpes simplex virus infection - Viral DNA found on PCR of corneas with
ICE
- No Systemic
associations
- Abnormal
cellular endothelial membrane coats trabecular meshwork and iris
- Three types of
presentations: Chandler syndrome, essential iris atrophy, Cogan-Reese are
not discrete or mutually exclusive
- Can have signs of any one or of a combination of the
three
- Treatment:
- Aqueous suppressants
- Surgical management difficult: abnormal endothelium
can close off sclerostomies, blebs and anterior chamber tubes
- Cholinergic agonists and laser trabeculoplasty have no
role in this condition
- Do not confuse
with Reiger anomaly and syndrome:
- Axenfield-Reiger: dominant, bilateral, early onset
with posterior embryotoxin
ICE- Chandler Syndrome
- Corneal changes
are most prominent
- Hammered silver
appearance and corneal edema
- Iris changes
less prominent: with mild iris atrophy and corectopia possible
- Angle synechaie
ICE- Cogan-Reese Syndrome
- Appearance of
multiple fine iris nevi
- This is in reality abnormal endothelium covering the
iris has fenestrations allowing normal iris to prolapse through
- Most consider
this synonymous with Iris nevus syndrome
- Hammered silver
appearance to corneal endothelium
- Angle synechaie
ICE- Essential Iris Atrophy
- Iris changes
predominate
- Extensive atrophy
- Corectopia
- Polycoria: Stretch Holes & Melt holes
- Hammered silver
appearance to the corneal endothelium
- Angle synechaie
Posterior Polymorphous
Corneal Dystrophy
see: PPMD in
cornea notes
Nanophthalmos
- Eye extremely
small but near normal lens size
- Crowding of
anterior chamber and risk of pupillary block and angle closure
- Thick sclera
prevents normal flow of aqueous form suprachoroidal space
- Intraocular
surgery can lead to unrelenting suprachoroidal effusions
- Prophylactic LPI if any risk of angle compromise
- Prophylactic
scleral windows for intraocular surgery
Ciliary Body Swelling
- Caused by
interruption of the vasculature or inflammation of ciliary body
- After Scleral
buckle, extensive PRP, or with inflammation
- Avoid
cholinergics- further rotates ciliary body forward
- LPI has no role
- Treat with
anticholinergics and corticosteroids
Neovascular Glaucoma
- Associated conditions
- Treatment
- Typically
develops in response to retinal ischemia
- Vasogenic
factors stimulate anterior segment vessel growth (theory): vascular
endothelial growth factor (VEGF) found in animals
- New vessels are
accompanied by a membrane that can obstruct aqueous outflow
- In diabetes with
AC neovascularization but no PDR, consider carotid disease
- gonioscopy: vessels cross
scleral spur and arborize over TM, membrane can pull iris over angle
- PAS develops
Neovascular Glaucoma- Treatment
- Treat underlying
retinal ischemia (PRP in Diabetes)
- Even with
synechial closure, PRP
allows for more successful filtering surgery
- Medical
treatment: aqueous suppressants
- Cholinergic agnoists are ineffective
- ALT
has no role
- Trabeculectomy with active neovascularizaton
poorly successful, use antimetabolite
- Seton
more successful
- Cyclodestructive procedure- often good option
given poor visual potential
Conditions associated with Neovascular
Glaucoma
Primary Pupillary Block Glaucomas-
hyperopic, crowded eyes
Acute
Angle-Closure Glaucoma (AACG)- iris suddenly driven over TM
with dramatic rise in IOP. Mid-dilated pupil.
AACG- Epidemiology
- Elderly with
small hyperopic eyes and shallow anterior chambers
- Thicker lens
with age predisposing narrow angles
- Women higher
risk
- More common in
Asians and Eskimos
- African-Americans
have more chronic angle closure than acute
AACG- Symptoms
- Sudden severe
pain, blurred vision, nausea, vomiting, diaphoresis
AACG- Signs
- Eye injected
- Corneal edema
- AC shallow with
mile reaction.
- Pupil mid-dilated,
fixed and may be irregular
- TM is covered by
the iris
- Glaucomfleckin-
necrosis of lens epithelium
- Van Herick Test
can be used to determine angle depth
- Indentation
gonioscopy to test for appositional or synechial closure
- High IOP (over
60 not uncommon)
- If attack breaks
spontaneously an AC cellular reaction and hypotony can result mimicking
uveitis
- Provocative
tests: (positive if greater than 8mm Hg of IOP rise): 1) pharmocologic
mydriasis. 2) sitting in a dark room for 1 hour
without sleeping. 3) lying prone for a period of
time without sleeping.
AACG- Treatment
- Laser
iridotomy or surgical iridectomy
- usually angles open to
grade 2 after LPI
- If corneal edema
precludes LPI: use osmotic agents (mannitol), carbonic anhydrase
inhibitors (acetazolaminde), ß- blockers and a 2- agonists.
Colinergic agonists only after IOP has decreased
to permit perfusion of the iris.
- Pressing on the
central cornea has broken attacks
- Consider
prophylactic treatment in the opposite eye
- Pilocarpine is
not effective in preventing an attack
- Laser iridoplasty can pull iris away from TM
temporarily
AACG- Sequelae
- Iris atrophy-
sectoral atrophy produces a swirl appearance
- Cataract and
glaukomflecken (necrosis of anterior lens capsule)
- Perepherial
anterior synechaie
- Optic nerve
cupping
- Risk of Angle
closure in fellow eye is 40-80% in 5-10 years
Intermittent Angle-Closure Glaucoma
Intermittent ACG: Epidemiology
Intermittent ACG: Symptoms
- Episodes of
blurred vision with headache
- Colored halos
- Can be confused
with migraine headache
Intermittent ACG: Signs
- Narrow angles
may be only sign
- Optic cupping
and VF loss later
Intermittent ACG: Treatment
Chronic ACG
Chronic ACG: Epidemiology
Chronic ACG: Symptoms
- Insidious and
asymptomatic
Chronic ACG: Signs
- Increased IOP
- Optic cupping
- Visual field
loss
- Closure of
angles by extensive perepherial anterior synechiae especially superiorly
Chronic ACG: Treatment
Aqueous Misdirection- (also
called ciliary block glaucoma or malignant glaucoma)
- Acqueous travels
into the posterior chamber rather than the anterior
- Vitreous moves
forward and collapses the iris and lens into the AC
- Ciliary body
forms seal around lens or vitreous trapping aqueous posteriorly
- Trapped aqueous
compacts the anterior hyaloid face making it impermeable to fluid
- Typically after
glaucoma surgery in those with angle-closure glaucoma
- Can occur after
other procedures
- Characteristics:
totally flat AC with lens touching
cornea, elevated IOP
- DDX: Pupillary block (bombé and some AC
under center of cornea), suprachoroidal hemorrhage (seen on fundus exam or
echo
- Medical
Treatment: atropine (for up to a year), corticosteroids,
CAI's, burst of an osmotic agent. Effective 50%.
- Surgical
Treatment: 1) Nd:YAG
laser to rupture anterior hyaloid face. 2) Argon to shrink ciliary
body processes if visible through an iridectomy. (same
settings as ALT) 3) Pars plana vitrectomy with
attention to removing anterior hyaloid from perepherial iridectomy.
Secondary Pupillary Block
Glaucomas
LPI indicated in these cases
Plateau Iris Syndrome
- Younger adults
- Prominent,
forward ciliary body, holding iris anterior
- Plateau Iris
configeration: iris on the same plane as Schwalbe's line but steep
drop-off right before TM.
- Part of this
configuration is due to pupillary block therefore LPI
is indicated
- Plateau Iris
syndrome: IOP remains high despite LPI
- Typically
asymptomatic unless attack of angle closure occurs
- AC appears deep by
slit lamp
- "Sine
wave" appearance on indentation gonioscopy
- Cholinergic
agonists (pilocarpine) or ALT to shrink peripheral iris
Glaucoma
with Open and Closed-Angle mechanisms
Inflammatory
Glaucoma
Inflammatory Glaucoma- Open Angle
Mechanisms
- Trabeculitis
decreases aqueous outflow
- Inflammatory
debris can clog TM
- Aqueous protein
and decrease aqueous outflow
- Theoretic
basement membrane substance covers TM in chronic uveitis
- Scleritis can
result in increased episcleral venous pressure
- Corticosteroids
Inflammatory Glaucoma- Angle-Closure
Mechanisms
- PAS can develop
with inflammation in the angle
- Neovascularization
of the angle
- Central
posterior synechiae can cause pupillary block
- Uveitis causes
swelling and anterior rotation of the ciliary body closing the angle
Inflammatory Glaucoma-
Treatment
- Decrease
inflammation: main goal
- Topical,
periocular, systemic steroid in light of inflammation and high IOP, treat
inflammation with more steroid
- Aqueous
suppressants to decrease IOP
- Avoid cholinergic agonists because they cause
breakdown of blood/aqueous barrier, they can induce miosis and anterior
movement of lens-iris diaphram causing adhesions between pupil and lens
- Hyperosmotic agents are likely to be
ineffective due to leaky blood-aqueous barrier
- Any iris bombe
should be treated with an LPI- larger than usual to
avoid closing
- Goniosynechialysis
can break synechaie that are less than 6 months old
- Trabeculectomy with antimetabolites have a high
failure rate
- Setons
or valves
Uveitis and
Keratouveitis associated with Glaucoma
- Uveitis
associated with Joint disease
- Uveitis
associated with Infectious disease
- Herpes Simplex keratouveitis
- Herpes Zoster keratouveitis
- Congenital rubella
- Leprosy
- Syphilis
- Cytomegalic inclusion retinits
- Toxocariasis
- Meningococcal endophthalmitis
- Mumps
- Nephropathia epidemica
- Onchocerciasis
- Toxoplasmosis
- Coccidioidomycosis
- Uveitis
associated with other disorders
Fuchs
Heterochomic Iridocyclitis
Fuchs Heterochromic Iridocyclitis-
Epidemiology
- Diagnosed
between age 30-60
- No gender
predilection
- Sporadic (rare
familial cases)
Fuchs Heterochromic
Iridocyclitis -Signs / Symptoms
- Symptoms: Insidious, many are asymptomatic, some have blurred
vision or floaters
- Signs:
- Unilateral (10% bilateral)
- Glaucoma 50%
- Cornea: stellate
keratic precipitates with fine filaments distributed over entire
epithelium
- Anterior chamber: chronic
low-grade uveitis
- Angle/ TM: fine
neovascularization, NO PAS
- Iris:
- Heterochromia 80%- usually light eyes affected
- Affected eye lighter: 67%
- Affected eye darker: 11%
- No difference: 22%
- Loss of normal iris architecure, neovascularization
(can bleed with minor insult like gonioscopy), occasionally inflammatory
nodules like Koeppe nodules
- Lens: posterior
subcapsular cataracts
- Vitreous: cells in
anterior vitreous
- Retina: some claim toxo
like lesions are present (one study)
Fuchs Heterochromic Iridocyclitis- Treatment
Glaucomatocyclitic Crisis
(Posner- Schlossman syndrome)
- Bouts of
increased IOP with mild AC reaction
- IOP can reach
levels of 40 to 60 mmHg
- Surprisingly few
symptoms: hazy vision or halos
- Almost always
unilateral
- Mild injection
of conjuctiva
- Corneal edema
- Hypochromia of
the iris in 40%
- Etiology
unknown: possible viral, vascular, allergic or developmental process
- Treatment: topical
corticosteroids and aqueous supressants during episodes. Usually between
episodes no treatment necessary. Chronically elevated IOP treated like
other chronic glaucoma
- Higher risk of POAG in fellow eye
Syndrome of Precipitates on the Trabecular
Meshwork
- Precipitates
develop on the face of the TM, solid to confluent, gray or yellowish in
color
- Bilateral in 86%
- Develops after
age 50
- Often otherwise
indistinguishable from POAG
- IOP does not correlate
with precipitate appearance
- PAS develop in
areas of precipitates
- Cholinergic agonists can raise IOP
- Cause unknown
- Treatment: intensive
topical steroids, aqueous suppressants, can recur so long term follow-up
is necessary
Lens-Induced Glaucoma
Phacolytic Glaucoma
- Develops when
long-standing cataract becomes hypermature
- Eye red,
painful, long history of decreasing vision
- Conjunctival
injection, corneal edema, high IOP
- Dense AC flare,
large cells, and debris or refractile bodies, keratic precipitates not
common
- Cataractous lens
often Morgagnian (liquified cortex allows nucleus to drop inferiorly)
- White deposits
on anterior lens capsule represents either calcium oxylate or cholesterol
crystals
- Soluable
proteins leak through microscopic defects in grossly intact lens
capsule
- Macrophages
accumulate in the TM
- High molecular
weight protein released from lens can cause elevation in IOP
- Treatment: decrease IOP and reduce inflammation medically, ECCE
or Phaco with indocyanin green, irrigation of AC.
Phacomorphic Glaucoma
- Large lens
causes angle-closure glaucoma by pupillary block or by collapsing
peripheral AC
- Patients usually
have thick, mature cataracts and shallow AC
- LPI
can deepen chamber and lower IOP
- Aqueous
suppressants and cataract removal
Lens Particle Glaucoma
- Ruptures lens
capsule releases lens material which obstructs TM
- Inflammation
invariably present
- AC tap may
demonstrate lens fiber fragments
- Aqueous
suppressants and corticosteroids
- Lens or lens
fragments may need to be surgically removed
Phacoanaphylactic (Phacoantigenic) Glaucoma
- Also called:
Phacoantigenic endophthalmitis
- Disruption of
the lens by trauma
- Sensitization
period of hours to years
- Eye develops
inflammatory reaction to the retained lens material
- Zonal
granulomatous inflammation forms around lens material containing PMN's,
macrophages, and multinucleated giant cells.
- Eye inflammed
often with hypopion
- Mutton-fat
keratic precipitates, congestion of iris vessels.
- Posterior
synechiae with dense flare and cells
- Most cases have
low IOP but in some glaucoma develops
- Treatment:
- Aqueous suppressants, corticosteroids
- Retained lens material should be removed when
necessary
- Some risk of
sympathetic ophthalmia in fellow eye
Ectopia Lentis
- DDX
- Crystalline lens
becomes partially (subluxed) or completely displaced (dislocated)
- Glaucoma caused
by pupillary block if lens pushes against iris, is trapped in pupil, or
dislocated entirely into AC allowing vitreous to become trapped in pupil.
- Iridotomy or LPI to relieve pupillary block
- If lens in AC:
use cholinergics to constrict the pupil
then remove lens or dilate the pupil, allowing it to fall into PC,
then add cholinergics
- Phacolytic glaucoma can develop prompting removal
of lens usually by pars plana lensectomy and vitrectomy
- Simple Ectopia
lentis- Autosomal dominant, dislocation
congenitally or later in life
- Ectopia lentis
et pupillae- Autosomal recessive, pupil and
lens grow in different directions, usually bilateral
- Buphthalmos- eyes become so large that zonules break
- Exfoliation syndrome- weak zonules
- Marfan syndrome-
Autosomal dominant, defect in fibrillin
gene, chromosome 15
- tall, thin, long
fingers and toes
- cardiovascular abnormalities
- some have eyes with
increased axial length
- lens subluxes
superiorly and rarely dislocated completely
- Weill-Marchesani
syndrome- small round lenses (spherophakia), short, stocky, short fingers
- Homocystinuria- Marfan-like features, at risk of thromboembolic
episodes, test homocystine in urine
- Hyperlysemia
- Sulfite oxidase
deficency
Spherophakia
- Lens has
abnormally large A-P dimension and small equatorial dimension
- Association with
Weill-Marchesani syndrome
- Pupillary block
can develop
- Pilocarpine
brings lens forward and make pupil constrict around lens causing pupillary
block
- LPI
should relieve the block
- Cycloplegic
agents pushes lens back and can help break pupillary block
Glaucoma From Tumors or Cysts
Tumors causing Glaucoma
Cysts causing Glaucoma
- Primary iris
cysts: Spontanous or Familial cysts of
the iris can cause angle-closure glaucoma
- Laser can be used to rupture these cysts
- Secondary iris
cysts: inplanted epithelial cells from
trauma or surgery
- lead to angle
closure, inflammation and glaucoma
- rupturing of these cysts
can can lead to epithelial downgrowth
- they should be
removed intact
Mechanisms of Tumors Causing Glaucoma
- Direct invasion into the TM
- Melanoma of iris or ciliary body
- Metastatic tumor
- Leukemia
- Juvenile xantogranuloma
- Posterior Pressure closing angle
- Melanoma of ciliary body or choroid
- Retinoblastoma-
large exudative retinal detachment can be present
- Pigment cells and necrotic debris clogging TM
- Melanoma of ciliary body (A.K.A. melanomalytic
glauoma)
- Retinoblastoma
- Neovascularization
- Hemorrhage
- Uveitis
Glaucoma after Trauma- trabecular contusion
= high IOP and no inflammation after trauma. AC cells common after trauma with
high or low IOP
Other processes that can arise from severe trauma: lens-particle glaucoma, phacoanaphylaxis, ectopia lentis
Angle Recession Glaucoma
- Blunt trauma
- Shearing injury
through the ciliary body face, splitting the longitudinal and circular
muscles
- Adjacent
trabecular meshwork is damaged causing elevated IOP
- Elevated IOP can
develop months or years after injury
- Signs: very deep
AC and wide ciliary body face that is lighter in color, ruptured iris
processes
- In Ddx of unilateral glaucoma
- 6% of eyes of
180 degrees or more of recession will develop glaucoma
- Treatment: usual
medications, ALT is usually not effective, Trabeculectomy has increased
risk of vitreous loss due to zonular loss
Hyphema (Blood induced
Glaucoma)
Hyphema- Risk of Glaucoma
- Related to size
of hyphema
- Less than 50% hyphema - 14% risk
- More than 50% hyphema - 27% risk
- 100% (not 8 ball) - 52% risk
- 100% (8-ball) - almost 100% risk
- Rebleeding confers even higher risk: 20% rebleed (3rd
to 5th day)
- 8-ball hyphema- no aqueous
circulation, blood becomes black
- Sickle-cell disease-
more difficulty clearing blood from AC, more likely to develop high
IOP, and optic nerves more sensitive to damage: see treatment
- Adhesion to iris
and angle can occur
Corneal Blood Staining
- large hyphema and
high IOP.
- sometimes difficult to
see due to AC blood.
- clears from periphery
first, and can take months or years
- in young children
can lead to ambylopia
- hemoglobin in corneal
stroma, iron in keratocytes
Hyphema- Treatment
- Controversial
and often debated
- Avoid aspirin
- Reliable patient/ parents: home bed rest may be adequate
- Otherwise: hospitalization
for bedrest, bilateral eye patching, and dilation.
- Aminocaprioic
acid (Amicar) or tranexamic acid- antifibrinolytic agents that inhibit
resorption of clot and prevent rebleeding. More useful in cases with large
risk of rebleeding
- Corticosteroids:
variable results
- Aqueous
suppressants to decrease IOP
- AVOID: carbonic
anhydrase inhibitors and adrenergic agonists in Sickle Cell: promote
sickling
- AC washout for severe IOP
elevation and large hyphema:. Optimal time is day
4. Removing all the blood is usually not possible,
removing the majority is usually all that is necessary.
- Trabeculectomy and AC
washout: eliminates risk of angle closure
and iridectomy will allow passage of large amount of acqueous.
- Other surgical procedures: urokinase or fibrinolysin injected in AC,
cryoextraction of clot, phacoemulsification of clot. However, surgical
instruments in the AC in this setting (no view) is dangerous
Ghost Cell Glaucoma
- Develops after
large vitreous
hemorrhage
- RBC become
round, rigid, empty except for marginated, denatured hemoglobin (Heintz
bodies)
- If there is
communication with the AC, these cells can obstruct the TM
- Most common in
setting of Trauma with zonule and anterior hyloid disruption
- Khaki-colored
pseudohypopyon can form which sometimes has a red stripe of fresh blood (candy
stripe sign)
- Elevated IOP
treated with usual medications
- If large
hemorrhage and no response, pars plana vitrectomy may be required
Chemical Burns
- Two phases of
IOP rise; 1) initially shrinkage of cornea and sclera cause decreased eye
volume and increased IOP. 2) Later, IOP rises due to inflammation and
prostaglandin release.
- In severe burns,
damage to aqueous outflow channels in the sclera, episclera and
conjunctiva. This can preclude filtering surgery and necessitate a cyclodestructive procedure
Epithelial Downgrowth
- Poorly closed
wounds from surgery or truama
- Epithelilal
cells proliferate through wound into the anterior chamber
- Growth over
endothelium- corneal edema
- Growth over TM-
intractable glaucoma
- Management is
difficult. Some advocate en block excision of involved anterior segment
structures
- Setons
can be used
- Fibrous Downgrowth- acts like and
is treated as epithelial downgrowth but is less severe. Still somewhat
poor prognosis
Flat anterior chamber
- If chamber
remains flat long enough (trauma, wound leak ect.), extensive peripheral anterior
synechiae can develop leading to chronic angle
closure glaucoma
- Synechiae
develop quickly if eye is inflammed
- Best prevented
by meticulous closure of traumatic and surgical wound openings
- Synechiae can be
broken by laser or surgical goniosynechialysis
- If chamber
reforms quickly PAS can be prevented
Siderosis
- Retention of
Iron foreign body or intraocular hemorrhage
- Damage to
photoreceptors, trabecular meshwork, cataract and iris hyperchromia
Glaucoma Following Surgery-
DDX
- Early IOP
elevation following surgery
- Late IOP
elevation following surgery
Iridoschisis
- Anterior iris
stroma splits from deeper iris
- Elderly, usually
> age 70
- Glaucoma 50%
- Mechanisms of
glaucoma
- angle closure with a
component of pupillary block
- open angle glaucoma
from debris and pigment in TM
- Iris touching
cornea may cause decompensation
Differential Diagnoses
Unilateral Glaucoma- DDX
Iris Heterochromia with Glaucoma- DDX
- Ligher eye with glaucoma
- Darker eyes with high IOP
Ectopia Lentis- DDX (see ectopia lentis information)
- Primary ocular
- Systemic
- Marfan syndrome
- Weill-Marchesani syndrome
- Homocystinuria
- Hyperlysemia
- Sulfite oxidase deficency
- Ehlers-Danlos syndrome type 1
- Syphilis
Drugs
Drugs- General Principles
- Average drop
contains 20-50 microliters
- Tear lake holds
7-10 microliters (20% of a drop)
- Tears turn over
16% per minute
- 42% of the
medication remains in tears for 5 minutes
- Drugs are highly
concentrated: e.g. one drop of 1% atropine = 0.5mg (preanesthesia dose is
0.4mg)
- Drugs must be
lipid soluable and water soluable to penetrate epithelium, stroma and
endothelium
- Preservatives increase penetration through
the epithelium
- Inflamed eyes
can also have increased penetration
Drug List
Generic Drug Names (A-Z)
Trade Drug Names (A-Z)
Cholinergic
Agonists
- Action
- Application
- Agents / Dose
- Adding other agents
- Side Effects
- Nicotinic
receptors- autonomic nerve synapses, striated
muscles
- Muscarinic
receptors cause contraction of pupillary
sphincter (miosis), circular fibers of ciliary body (accommodation), and
longitudinal fibers of ciliary body (increased outflow through ciliary
body) as well as other smooth muscle and secretory glands
- Direct acting
drugs e.g. pilocarpine stimulate muscarinic receptors
- Indirect acting
drugs e.g. echothiophate stimulate both muscarinic and nicotinic receptors
Cholinergics - Action
- Enhance or
stimulate action of acetylcholine at the neuromuscular junction
- Acetylcholine
stored in postganglionic neuron, once released it is rapidly hydrolyzed by
acetylcholineesterase
- Acetylcholine
itself cannot be used as a drop because of rapid deactivation
- Direct acting
agents: Miochol (acetylcholine) can be used in the eye for rapid
miosis, Pilocarpine mimics miochol effects, peak effect at 2 hours,
duration 8 hours
- Indirect acting
medications are more potent, longer lasting and block breakdown of
acetylcholine at the juntion
- Contraction of
longitudinal muscle of ciliary body opening TM, increasing conventional outflow.
- Increase
uveoscleral outflow
- Cause miosis and
accommodation by causing contraction of pupillary sphincter and circular
muscle of ciliary body
Cholinergics - Application
Cholinergics - Agents / Dose- using
direct and indirect agent together concurrently is not helpful because of
competition for receptor sites
Direct-Acting Agents
- Pilocarpine hydrochloride, QID, (generic
avail.), no added benefit above 4% unless dark iris, start on low dose,
start with solution and move to Ocuserts,
o
Adsorbocarpine (Alcon); Solution 1, 2,
4%
o
Akarpine (Akorn); Solution 1, 2, 4%
o
Isopto Carpine (Alcon); Solution 0.25,
0.5, 1, 2, 3, 4, 6, 8, 10%
o
Pilopto-Carpine (Lebeh); Solution 4%
o
Pilocar (Ciba); Solution 0.5,1, 2, 3,
4, 6%
o
Piloptic (Optopics); Solution 0.5, 1,
2, 3, 4, 6%
o
Pilostat (Bauch & Lomb); Solution
0.5, 1, 2, 3, 4, 6%
o
Pilagan (Allergan); Solution 1, 2, 4%
o
Pilopine HS Gel (Alcon); Gel 4%
o
Ocusert (Alza); Pilo-20: 20
micrograms/hr (equivalent to 1-2% gtts), Pilo-40: 40 micrograms/hr (equivalent
to 2-4% gtts)
Indirect Acting Agents-
aphakics or pseudophakics who need additional IOP effect than with
pilocarpine,
o Humorsol
(Merck); Solution 0.125, 0.25%;
- Echothiophate iodide, BID, no added benefit above 0.125%,
irreversible with atropine
o Phospholine
iodide (Wyeth-Ayerst); Solution 0.03, 0.06, 0.125, 0.25%
- Physostigmine, BID, (generic avail.), partially
reversible with atropine
o Eserine
sulfate (Ciba) Ointment 0.25%
Both Direct and Indirect
o
Carboptic (Optopics); Solution 3%
o
Isopto Carbachol (Alcon); Solution
0.75, 1.5, 2.25, 3%
Cholinergics - Adding other agents
- Add well to
aqueous suppressants e.g. Beta-blockers, CAI's and alpha-adronergic
agonists
- Interaction with
prostaglandin analogues is less understood, in animal studies pilocarpine
completely blocked effect of prostaglandin analogues, however in some
people an additive effect has been found
Cholinergics - Side Effects
Cholinergics- Systemic Side-Effects
- Uncommon with
direct agents
- pralidoxime chloride
(Protopam) taken within 4 hours can reverse oral ingestion of physostigmine
- General:
weakness, fatugue, diaphoresis, muscle tremor, salivation
- CNS:
deterioration of mental status in Alzheimer's patients
- Pulmonary:
bronchospasm, pulmonary edema, cough
- Cardiovascular:
hypotension, bradycardia, 1 case of 3rd degree heart block
- GI: diarrhea,
nausea, vomiting, cramping
- Other:
leukocytosis, prolonged respiratory paralysis with succinylcholine
(indirect agents inhibit pseudocholinesterase which metabolizes
succinylcholine), decreased ability to metabolize some local anesthetics
(indirect agonists)
Cholinergics- Ocular Side
Effects
- Ocular and brow
ache
- Miosis:
decreases visual field sensitivity & requires dilation
- Accommodative
spasm with induced myopia (up to 15 diopters)
- central posterior
synechiae, frequently after LPI
- Retinal
detachment
- Worsening of
inflammation (breakdown of blood-aqueous barrier), stop few weeks before
surgery
- Cataract
(particulary in indirect agents
in adults)
- Iris cysts in
iris pigment epithelium (indirect
agents in children)- preventable by using 10% phenylephrine
- Cicatricial
pemphigoid
- Conjunctival
hyperemia
- Punctal stenosis
- Increased tear
production
- Hypersensitivity
- Superficial
corneal haze (pilocarpine gel)
Adrenergic
Agonists
Adrenergic Agonists- Action
- Act on aqueous
inflow and outflow
- a - Adrenergic stimulation
decreases aqueous production- short lived
- Late increase in
aqueous outflow by altering metabolism of glycosaminoglycans in TM
Adrenergic Agonists- Application
- Good for most
forms of glaucoma
- Avoid in aphakic
patients- risk of reversable CME
- Acute
angle closure attack could be caused by pupillary dilation in
unrecognized narrow angles
Adrenergic Agonists- Agents / Dose
Nonselective Adrenergic Agonists
Nonselective Adrenergic Pro-drug
- Dipivefrin hydrochloride- BID (generic
avail.), penetrates lipid barrier 17 fold easier, less systemic side
effects
- Propine (Allergan) 0.1% solution
Selective alpha-2 Adrenergic Agonists
Adrenergic Agonists- Adding other agents
Adrenergic Agonists- Side Effects
Nonselective Adrenergic
agonists- Side effects
- Systemic
- Ocular
- Epinepherine
poorly tolerated because of both systemic and ocular side effects
- Dipivefrin has
few systemic effects
Nonselective Adrenergic
Agonists- Systemic Side effects
- Applicable to
Epinepherine not dipivefrin
- General: headaches, nervousness
- Cardiovascular: HTN, tachycardia, arrhythmia
- Systemic
toxicity a concern for those taking tricyclic antidepressants or drugs
that deplete catecholamines (reserpine and guanethidine)
Nonselective Adrenergic
Agonists- Ocular Side effects
- Burning
sensation and tearing
- Blurred vision
- Rebound
hyperemia
- Follicular
conjunctivitis
- Adrenochrome
deposits: palpebral conjunctiva, cornea, contact lens, nasolacramal ducts
- CME in aphakics and
pseudophakics (20%)
- Madarosis (loss
of eyelashes)
- Shedding of
latent herpes virus
- Corneal
endothelial toxicity or epithelial edema
- Mydriasis with angle closure
- Cicatricial
pemphigoid
- Suggestion of
reduced optic nerve perfusion (not proven)
Selective Adrenergic
Agonists- Side effects
- apraclonidine has few
systemic side effects
- briminodine has fewer
ocular side effects but cross the blood brain barrier
- Systemic:
- General: lethargy, fatigue and drowsiness with
brimonidine; dry mouth; dry nose
- Cardiovascular: decreased blood pressure with
brimonidine, vasovagal reaction, one case of chest tightness and near
syncope
- Infants: respiratory depression
- Ocular: irritation,
follicular conjunctivitis, blanching, lid retraction, mydriasis, hyperemia
ß-Adrenergic
Antagonists
Timolol is usually the gold standard against which other drugs are compared
ß-Blockers- Action
- Decrease aqueous
production by one third assuming presence of sympathetic tone
- Peak effect 2
hours lasts 24 hours
- Effect may
diminish over time
- Do not lower IOP
during sleep
ß-Blockers- Application
ß-Blockers- Agents / Dose
Nonselective ß-Blockers
- Carteolol hydrochloride BID, intrinsic
sympathomimetic activity so has short-lived beta blockade effect, less
effect on serum lipids than timolol
- Ocupress (Otsuka) 1% solution
- Levobunolol hydrochloride BID (generic
avail.)
- AKBeta (Akorn) 0.25, 0.5% solution
- Betagan (Allergan) 0.25, 0.5% solution
- Metipranolol hydrochloride BID, occasional granulomatous AC inflammation
- OptiPranolol (Bausch & Lomb) 0.3% solution
- Timolol hemihydrate BID
- Betimol (Ciba) 0.25, 0.5%
- Timolol maleate BID, QD for gel (generic avail.)
- Timoptic (Merck) 0.25, 0.5% solution
- Timoptic XE (Merck) 0.25, 0.5% gel, preservative:
benzododecinium bromide
- Ocudose (Merck) 0.25. 05%; single use packaging
without preservative
Selective ß-Blockers
- Betaxolol hydrochloride BID, less IOP
lowering effect that timolol
- Betoptic (Alcon) 0.5% solution
- Betoptic S (Alcon) 0.25% suspension
ß-Blockers- Adding other agents
ß-Blockers- Side Effects
- Systemic
- Ocular
- Can have severe
or fatal systemic side effects
- Avoid in
patients with asthma, CHF (relative), bradycardia and heart block
- Bradycardia more
likely in those taking quinidine and verapamil
- Carteolol has less effect on serum lipids
- Side effects can
develop insidiously
ß-Blockers- Systemic Side
Effects
- General: lethargy
- CNS: depression, confusion, impotence, decreased libido,
psychosis, anxiety, hallucinations, emotional liability
- Pulmonary: bronchospasm
- Cardiovascular: bradycardia, decreased target heart rate in exercise,
hypotension, decreased myocardial contractility, worsening CHF, decreased
HDL, increased triglicerides, worsening heart block, syncope
- GI: nausea, diarrhea, abdominal cramping
- Other: exacerbation of Myasthenia Gravis, masked
hypoglycemic symptoms in brittle diabetics, reduced glucose tolerance in
diabetics
ß-Blockers- Ocular Side
Effects
- Burning and
hyperemia
- Corneal
anesthesia, punctate keratopathy
- Visual
disturbance
- Intraocular
inflammation (metipranolol)
- Cictricial
pemphygoid
- Allergic
conjunctivitis
Carbonic Anhydrase
Inhibitors
CAI- Action
- Decrease aqueous
production by inhibiting ciliary body carbonic anhydrase
- Carbonic
anhydrase catalyzes the reversible conversion of CO2 and H2O to
bicarbonate (H2C03)
- Bicarbonate
formation is coupled to the secretion of sodium
- Results in
decrease of aqueous production by 25%
- Peak effect 2
hours
- Decrease aqueous
production during sleep as well as wake
CAI- Application
- Used in all
forms of glaucoma
CAI- Agents / Dose
Oral CAI's
o Dazamide
(Major) 125, 250 mg tabs
o Diamox
(Storz) 125, 250 mg tabs
o Diamox
SR (Storz) 500 mg sustained release capsules BID
o Diamox
Powder (Storz) 500 mg/vial to mix for injection IV or IM
o Diamox
Syrup 5-10 mg/kg Q 4-6 hours
o Daranide
(Merck) 50 mg tabs
- Methazolamide BID-TID (generic avail), fewer systemic side effects,
less IOP lowering effect, mostly metabolized in liver- less renal stones
o Glautabs
(Akorn) 25, 50 mg tabs
o MZM
(Ciba) 25, 50 mg tabs
o Neptazane
(Storz) 25, 50 mg tabs
Topical CAI's
o Azopt
(Alcon) 1% suspension
o Trusopt
(Merck) 2% solution
o Cosopt
(Merck) combination Timolol & dorzolamide
CAI- Adding other agents
- Adds well to
other glaucoma drops
CAI- Side effects
Oral CAI- Side effects
- Systemic
- General: parasthesias in
hands and feet, metallic taste in mouth, carbonated beverages taste flat,
malaise, weight loss, headache
- CNS: depression,
loss of libido
- Pulmonary: respiratory
decompensation in COPD
- Cardiovascular: mild decreased
blood pressure
- GI: nausea, cramps,
epigastric burning
- Renal/genitourinary: nephrolithiasis (calcium oxalate/phosphate stones),
frequency (early), renal failure
- Hematologic: aplastic
anemia, agranulocytosis, thrombocytopenia, neutropenia, pancytopenia,
hemolytic anemia, acute leukemia, (most do not do routine blood counts
for monitoring)
- Other: hypokalemia
(esp. in combination with thiazides), increased serum uric acid,
metabolic acidosis (esp in combination with salicylates, renal, pulomary
or hepatic disease
- Ocular- rare induced
myopia
Topical CAI- Side effects
- Any of oral CAI side effects possible but much
less likely
- 25% with dorzolamide have bitter taste in mouth
- Superficial
punctate keratitis
- Corneal
decompensation in Fuchs' endothelial dystrophy
- Local allergic
reaction
Prostaglandin
Analogues
Prostaglandins- Action
- Prostaglandins
are local hormones that act locally in tissues
- At high
concentrations cause conjunctival hyperemia, breakdown of blood-aqueous
barrier, miosis, and increase IOP
- At low
concentrations, prostaglandin F2a decreases IOP and not inflammatory
- Increases uveoscleral outflow through ciliary body and
iris root
- Relaxes ciliary
body musculature or causes loss of extracellular matrix
Prostaglandins- Application
Prostaglandins- Agents / Dose
- Latanoprost QD (Qhs may be more effective)
o
Xalatan (Pharmacea) 0.005% solution,
30% reduction in IOP
o
Rescula (Ciba) 0.15% solution, 13-15%
reduction in IOP
Prostaglandins- Adding other agents
- In animals,
cholinergic agonists completely blocked the pressure lowering effect
- In humans,
however, these drugs have been shown to be additive
Prostaglandins- Side Effects
- Very short half
life, very small concentration
- Systemic: case reports of migraine
- Ocular:
- increased iris
pigmentation with darkening of iris (10%), more frequent in iris of mixed
colors (blue-brown, green-brown, yellow-brown)
- conjunctival hyperemia
- punctate epithelial
erosions
- increased number of,
thickened and curled eyelashes
- reports of anterior
uveitis and CME
Hyperosmotic
Agents
Hyperosmotics- Action
- Systemically
induce rapid but transient reduction in IOP
- Create an
osmotic gradient between blood and intraocular contents
- High osmolarity
of blood draws water into into bloodstream
- Larger molecules
that cannot enter eye have longer effect (glycerol, isosorbide, mannitol)
- Smaller
molecules diffuse into eye and limit duration of action (ethanol or urea)
- Onset of action
10min to 1 hr (isosorbide and glycerine fastest), duration of effects 4-8
hours
Hyperosmotics- Appliction
- Used in
situations where IOP is very high
- No role in long
term management of glaucoma
- Acute
angle closure glaucoma
- Used in OR to
bring IOP down to a safe level to perform intraocular surgery (IV
mannitol)
- Less useful in
inflamed eyes where there is breakdown of blood-aqueous barrier
Hyperosmotics- Agents / Dose
o
Osmoglyn (Alcon) 50% solution
o
Ismotic (Alcon) 45% solution
o
Osmitrol (Baxter) 5-25% solution
- Urea, IV causes tissue necrosis if extravasation from IV
site
o
Ureaphil (Abbott) powder or 30%
solution
Hyperosmotics- Adding
other agents
- Effects are
additive to other agents
- Usually used in
situations where other meds are being employed
Hyperosmotics- Side Effects
- Bad taste: give
over ice with lemon juice.
- Can become
thirsty but avoid drinking and diluting osmotic effect.
- Increased vascular
volume and strain on renal system account for most side effects
- Glycerol is the
only agent metabolized, since it is broken down into sugar it can cause
trouble for diabetics
- Shrinking the
brain can stretch blood vessels causing hemorrhage
- Systemic
- General: headache, back
pain, chills, fever, dry mouth
- CNS: subarachnoid
and subdural hemorrhage, obtundation, seizure, disorientation, confusion
- Pulmonary: pulmonary edema
- Cardiovascular: vascular
overload, hypovolemia, CHF, hypertension
- GI: nausea,
vomiting, diarrhea
- Renal/ GU: diuresis, renal
insufficency, electrolyte imbalance, ketoacidosis in diabetics (glycerol), acidemia
- Other: tissue necrosis
if urea extravasation
- Ocular: blurred vision
Combination Drugs
o
E-Pilo-1, E-Pilo-2, E-Pilo-4, E-Pilo-6
Preservatives
- All drops
contain benzalkonium except:
o Phospholine iodide (chlorbutanol)
o Timoptic XE (benzododecinium)
o Timoptic Ocudose (preservative free)
o Pilocarpine Ocuserts (preservative free)
Glaucoma meds in
Pregnancy
Glaucoma meds in
Lactation
Glaucoma meds in
Children
Laser Treatments
Laser Trabeculoplasty
ALT- Mechanism
- Thinning and
scarring of the TM at sites of laser uptake cause adjacent areas to widen
and become clear of debris
- Increased cell
division and phagocytosis improving TM function
- Alteration of
extracellular matrix improving TM function
ALT- Indications
- Open
angle glaucoma with adequate TM pigment
- 80% have IOP
drop of 7 to 13 mm Hg. The higher the pre-treatment IOP the greater the
drop.
- Has be shown to be effective as an initial treatment
modality. Most use it after meds have failed to lower IOP.
- Can decrease IOP
in NTG if IOP is near the higher end of normal
- Exfoliative and
pigmentary glaucoma
- Less effect in
aphakic and pseudophakic eyes
- Not indicated in
angle recession, developmental glaucoma, juvenile glaucoma, inflammatory
glaucoma, or synechial angle closure
ALT- Technique
- Prophylactic
treatment with Alpha-2 Adrenergic agonist,
pre- and post laser
- 16x or 25x
magnification
- Lenses: Goldmann 3-mirror lens, Goldmann 1-mirror lens, Ritch
lens, Trokel lens, others
- Wavelength: Argon green or blue-green
- Spot size: 50 microns
- Duration: 0.1 second
- Power: 200-1200 mW (cause blanching or a small bubble in the
TM, 600-700 for lighter pigment, 200-300 for heavier pigment)
- Applications: 40-50 spots per 180 degrees or 80-100 spots per 360
degrees
- Diode laser red
settings are the same except use 75 micron spot size
- Aim at the
junction of the pigmented and non-pigmented TM
- Check IOP 1-2
hours after the procedure. If IOP elevated treat with aqueous
suppressants until controlled
- Topical
corticosteroids QID for 4 days in addition to preexisting glaucoma meds
- See patient in 6
weeks to measure pressure lowering effect
ALT- Complications
- Elevated IOP in
20%
- Transient
corneal opacities
- Mild iritis
- Peripheral
anterior synechiae
- Loss of pressure
lowering effect: gradual loss of control occurs in 7-10% of eyes over the
first 5 years
- Retreatment of
eyes with 360 treatment causes many to have higher IOP
Laser Perepherial Iridotomy (LPI)
LPI- Indications
LPI- Technique
- Argon Laser
- Nd:YAG laser
- Clear corneal
edema using topical or systemic drugs or topical
glycerin
- Pilocarpine 1% thins the iris and puts it on
stretch
- Prophylactic alpha 2-adrenergic agonist
- Topical
anesthesia
- Abraham (66
diopter) or Wise (103 diopter) lens
- Iridotomy in
mid-peripheral iris under upper eyelid
- Signs of
completion: flow of aqueous from posterior chamber is seen and deepening
of AC
LPI- Argon laser
- Requires pigment
in the iris for adequate uptake
- Color: Green
- Spot size 50
microns
- Duration:
0.02-0.2 seconds
- Power: 1 watt
- Lens: Abraham or
Wise
- Single round
area is treated until perforation is obtained
- Upon reaching
the pigment epithelium and difficulty arises in penetrating, transfer to
the YAG laser
LPI- Nd:YAG laser
- Can be used on
iris of any color
- Spot size: fixed
- Duration: fixed
- Energy: 1-12 mJ
- Lens: Abraham or
Wise
- Enlarge hole at
edges not in center
LPI- Post-op
- Add second drop
of Alpha-2 agonist
- Check IOP 1-2
hours
- Topical
Prednisolone QID for 4 days
- Continue pre-op
glaucoma meds except pilocarpine which can cause central posterior
synechiae
- Determine
patency by transillumination and documenting deeping of angle
LPI- Complications
- Iritis
- IOP elevation
- Corneal
epithelial opacities- no long-term sequelae
- Anterior Capsule
rupture with Nd:YAG laser
- Bleeding with Nd:YAG laser: stopped by applying pressure to eye with
the contact lens
- Retinal/ foveal
laser damage (Rare)
- Iridotomy
closure if small and inflammation present. Argon more likely to close
- Monocular
diplopia or see a line under their vision- often transient
Laser Iridoplasty
- Used in plateau
iris syndrome or before laser trabeculoplasty to
provide better view of angle
- Spot size:
200-500 microns
- Duration:
0.2-0.5 seconds
- Power: 150-300
mW
- Contact lens:
None or Goldmann 3-mirror
- Aim for far
peripherial iris and cause visible shrinking of iris tissue
- 4-6 applications
per quadrant
- Pred Forte QID
for 4 days
Laser Suture Lysis
- Hoskins, Ritch
or corner of Zeiss 4 mirror lens
- Argon or Krypton
(red wavelength-if blood present): 50-100 microns, 0.02 sec, 250-500 mW
- Compress
conjunctiva, blanching vessels
- Check IOP and
Seidel test afterwards
Surgical Treatments
Full Thickness Filtering Procedures
- Process:
- Limbus based conjuctival flap
- Direct opening is made through the sclera using: Elliot
trephination, posterior lip sclerectomy, anterior lip sclerectomy or
Scheie thermosclerostomy (cutting and cauterization)
- Iridectomy is made through the sclerostomy
- Conjuctiva is closed
- Post-op
complications are common from excessive aqueous outflow: hypotony, flat
anterior chamber, suprachoroidal effusion, suprachoroidal hemorrhage
- High rate of
cataract formation
- Tall filtering
blebs from flow perpendicular to the limbus that are prone to leaking and
infection
- Nd:YAG and holmium laser have been used to create a
sclerostomy without manipulating conjuctiva and no iridectomy. They have
same problems as other full thickness procedures plus risk of iris
incarcerated in the wound
Goniotomy
Trabeculotomy
Trabeculectomy
- Anesthesia: peri or
retrobulbar injection. Topical anesthesia in severely damaged optic
nerves.
- Exposure: lid speculum and 7-0 Vicryl corneal traction
suture pulled inferiorly.
- Conjunctival incison: limbus based flap. Incision 10mm from limbus following
curvature of the limbus with Wescott
scissors. Handle conjunctiva with serrated, non-toothed
forceps. Grasp Tenon's capsule wherever possible. Tenonectomy only if
there is a very thick capsule that could
interfere with suture lysis post-op. Use bipolar cautery for careful
hemostasis.
- Exposure of the Limbus: Conjunctiva and Tenon's capsule are dissected forward
with Wescott scissors or
a Gill knife.
Expose the gray zone where sclera and cornea meet.
- Scleral Flap: Trapezoidal
flap: 3 mm at the limbus and 2 mm in anterior-posterior dimension. 1/2 to
3/4 depth in the sclera. Make the initial incisions with a #75 blade. Raise the corner of
the flap with the blade and retract it back with Bonn forceps. Dissect the flap
anteriorly to the cornea with the blade.
- Antimetabolite:
optional. Mitomycin C (0.2
mg/ml to 0.5mg/ml) soaked in a cellulose sponge under the scleral flap and
Tenon's capsule. (Suggested doses: 0.2 mg/ml for 2 minutes
for low risk cases, 0.35 mg/ml for 3.5 minutes for repeat filters and high
risk cases) Rinse with balanced salt solution thoroughly.
- Paracentesis: :Using a small sharp
blade (#75 or others). Inject Miochol to pull iris taut if patient not
taking pilocarpine. Some inject viscoelastic into the anterior chamber at
this time.
- Sclerostomy: Make an
incision as far forward under the scleral flap with a #75 blade. Remove
the posterior tissue with a Kelly
Decemet's punch.
- Peripherial iridectomy: grasp the iris with fine forceps. Cut across the iris
with Vannas scissors
ideally so no iris is visible through the sclerostomy. Place Atropine 1%
on the cornea helping to move the lens-iris diaphragm posteriorly and to
prevent aqueous misdiretion
- Scleral flap closure: 10-0 nylon suture through the
corners of the trapezoid. After two sutures are placed, inflate the
anterior chamber to a normal depth and IOP. Check the flap
for flow- without Mitomycin C maintain a small amount of flow; with
Mitomycin very little flow should be present. Add more sutures if flow is
excessive. A safety suture can be passed parallel to the tightest suture
preventing the flap from lifting in the event of laser suture lysis. Try
to make the more superior suture the tighter on and therefore the one that
would be cut first. Remember to draw the location of the sutures in the
medical record and the order in which they should be cut.
- Conjunctival closure: 8-0 vicryl suture (BV 130-4
needle) in a running horizontal mattress style, intermittantly incorporating a small amount of Tenon's capsule.
Some close Tenon's and conjunctiva in two layers.
- Test the bleb: Fill the
anterior chambe with BSS to raise the bleb. If it does not raise spontaneously, push posterior to the lip of the
scleral flap to raise it. Inspect the bleb for leaks with fluorescein and
cobalt blue light.
- Medications:
Subconjunctival injection of corticosteroids and tobradex ointment. When
the patch is removed used Prednisolone acetate 1% Q 2 hours (taper
depeding on the bleb appearance), Atropine
1% BID (stop at 1 week check if AC deep), Tobradex ointment at bedtime.
- Post-op visits: Routine: Day
#1, Day #5 then weekly or biweekly for 6-8 weeks. Lengthen follow-up after
that time.
Setons
Indications for Seton implantation
Setons with Valves
- Ahmed
- Model S-3, pediatric, (96 square mm)
- Model S-2 (184 square mm)
- Krupin (180 square mm)
Setons without Valves- need to
be disabled until eye has encapsulated the plate (absorbable suture ligation,
suture cut with laser in AC, or large prolene suture coursing
subconjunctivally)
- Baerveldt
- Molteno
- Single plate (135 square mm)
- Double plate (270 square mm)
- Schocket to an
encircling band (300 square mm)
Seton implantation
- Limbus or fornix
based incisions
- Inserted below
Tenon's capsule and behind the rectus muscle insertions
, anterior margin is about 10 mm from limbus
- Sutured to
sclera with non-absorbable suture.
- Ligate tube if a
non-valve system
- Irrigate through
tube if valved system to prime
- Tube trimmed to
length
- 22-gauge needle
inserted posterior to the limbus parallel to the iris and tube inserted
through tract
- Scleral (or dura
or pericardium) patch graft to cover the tube at the limbus
- Reposition and
suture conjuctiva with 9-0 polyglactin (Vicryl) sutures
Seton- Post-op complications
- Similar to trabeculectomy
- Tube obstruction
- Echography can
help determine whether fluid is flowing to the plate: fluid pockets and
flattened sclera
- Tenon's cysts:
either transient (high bleb phase) or permanent
- Tube can erode
through patch or conjunctiva: risk of endophthalmitis and epithelial
downgrowth
- Large blebs can
cause strabismus
Cataract surgery in glaucoma
patients
- Combined small
incision phacoemulsification and trabeculectomy with Mitomycin C is a
reasonable option in most cases except those with the most severe optic
nerve damage
- Two approaches:
- Trabeculectomy preformed and phacoemulsification done
beneath the scleral flap
- Tempoal scleral tunnel or clear corneal incision and
superior trabeculectomy at a second site (allows for a smaller scleral flap)
- In those who
have had previous trabs: clear cornea or scleral tunnel
phacoemulsification preformed later is usually safe for the bleb.
- Exfoliative
glaucoma patients have lax zonules and increased risk of zonule dehiscence
- Miotic pupils
from cholinergic therapy requires surgical pupillary enlargement with
sphincterotomies, iris retractor hooks, or streached with Kuglen hooks and
supported with viscoelastic
- Cataract surgery
combined with seton implantation can also be
done.
Other Surgical Procedures for Glaucoma
Surgical peripherial iridectomy
- Creates a hole
in the iris with Vannas scissors through a small limbal wound
- Almost
completely replaced by laser iridotomies
- Indications:
- In cases of severe inflammation with pupillary block
from central posterior synechiae, LPI's can repeatedly close from
inflammation
- Patients that cannot cooperate with laser iridotomy
because of age or mental disablility
- Laser is not available
Iridencleisis
- No longer
performed
- Filtering
procedure is performed and iris tissue is pulled up into the sclerostomy
to act as a wick an keep sclerostomy open
- Theoretic risk
of sympathetic ophthalmia
- Superior sector
iridectomy, updrawn pupil and pigment in bleb are all signs that a
iridencleisis has been done
Goniosynechialysis
- Irrigating
spatula is used to strip recently formed peripheral anterior synechiae
from the TM
- Can effectively
open an angle that has been closed for less than one year
Cyclodialysis
- Ciliary body is
surgically detached from the scleral spur
- Allows flow of
aqueous directly into suprachoroidal space
- Process:
- An incision is created over the ciliary body
- A spatula is inserted into the suprachoroidal space
- The spatula is used to strip the ciliary body form the
scleral spur
- Complications:
bleeding and hypotony
- The cleft can
close spontaneously causing a sudden increase in IOP
- Rarely used
because of it's unpredictable nature
Complications of Filtering Procedures
- Hypotony
- Blebitis- may be
treated with topical fortified antibiotics
- Bleb associated
Endophthalmitis
- Often caused by: Strep
pneumoniae or Haemophilus
influenzae
- Often poor outcome
Cyclodestructive
Procedures
Cyclocryotherapy
- Probe placed
over the ciliary body, 1-1.5 mm from limbus
- Transillumiation
can be used to mark out the position of the ciliary body
- 5-7 spots over
180 degrees
- Temperature: -60
C to -80 C
- Duration 1
minute
- Firm pressure
decreases blood flow to ciliary body and makes treatment more effective
- Record clock
hours treated
- Some avoid 3 and
9 o'clock because of the long ciliary nerves
Laser Cyclophotocoagulation
Transscleral Laser
Cyclophotocoagulation
Nd:YAG laser
Cyclophotocoagulation
- Destroys ciliary
body epithelium and vasculature
- Minimal damage
to overlying stroma
- Pulsed mode or
continuous mode not Q-switched
- Non-Contact
system:
o
Spot size: fixed 70 microns
o
Energy 4-8 joules
o
Duration: 10-20 msec
o
Applications: 32
o
Treat 360 degrees, look for blanching
of conjunctiva
o
Fixed quartz fiberoptic probe
o
Power: 4-9 watts
o
Duration: 0.5-0.7 msec
o
Applications: 32
o
Treat 360 degrees,
o
Uses less energy than the non-contact
system
o
Causes coagulation necrosis and has
less pain, inflammation and vision loss
Diode laser
Cyclophotocoagulation
- Energy
penetrates less efficiently than the YAG laser
- Fixed quartz
probe
- Power: 1750-2000
mW
- Duration: 2
seconds
- Application:
17-24
- Treat 270-360
degrees
- Popping sound
means power should be decreased by 200-250 mW
- Non-contact
diode lasers are available
Endoscopic Argon Laser
Cyclophotocoagulation
- Laser delivered
through a 20-gauge fiberoptic probe through the pars plana
- Scleral
indentation brings the ciliary processes into view through a dilated pupil
- Endoscopic
viewing systems are available
- The end of the
probe is placed about 3mm from the ciliary body
- Done at time of
vitrectomy
- Spot size: 20
gauge probe
- Power: 500-1000
mW
- Duration:
0.1-0.2 sec
- Applications:
3-5 per ciliary body process
- Treat 180-360
degrees
Transpupillary
Cyclophotocoagulation
- In traumatic
anaridia or large sector iridectomies, ciliary body may be seen and
treated
- Congenital
anaridia often have too much corneal pannus by the time they develop
glauomca
- Short lived
effect
- Slit lamp
delivery system with Goldmann 3-mirror lens
- Spot size:
50-200 microns
- Power: 500-1000
mW
- Duration:
0.1-0.2 sec
- Applications:
3-5 per ciliary body process
- Treat up to 180
degrees, limited by view
Theraputic Ultrasound
- Not widely used
because of complications
- Thins sclera
- Post-op IOP
spikes
- Occasional
severe uveitis
Cyclodestructive Procedures- Post-op
management
- Retrobulbar
anesthesia
- Subconjunctival
steroids
- Topical
anticholinergics and corticosteroids
- Glaucoma
medications are continued except cholinergics until effect can be
determined
- Narcotic
analgesics
- Laser procedures
usually cause less pain
Cyclodestruction- Complications
- Decreased visual
acuity from hypotony, macular edema, and cataracts
- Hypotony higher
in cyclocryotherapy than laser CPC
- Risk of phthisis
increased with each procedure preformed
- Inflammation,
esp. from cyclocryo and ultrasound
- Chronic aqueous
flare (breakdown of blood aqueous barrier)
- Pain, greater
with cryo
- Hyphema in neovascular glaucoma
- IOP spikes, peak
at 6 hours, less common in laser procedures
- Surface burns
- Scleral thinning
esp. with ultrasound
- Sympathetic
ophthalmia very rare (perhaps related to incision surgery), more common in
laser procedures
Hypotony
Hypotony- Definition
- IOP below the
level at which the eye functions normally
Hypotony- Causes
- Ocular causes
- Systemic Causes- bilateral
- Myotonic dystrophy- rarely symptomatic
- High serum osmolality: dehydration, uremia,
hyperglycemia
- Systemic acidosis
Hypotony- Evaluation
- If AC is flat,
falsely high IOP because of corneal-lens touch
- Seidel testing
of conjunctival or bare scleral wound
- AC examination
for inflammation
- Gonioscopy to
rule out cyclodialysis cleft- can inflate AC with viscoelastic
- Flourescein can
be instilled in AC and scleral cutdown 4-5 mm posterior to limbus. Dye in
suprachoroidal fluid is evidence of a cyclodialysis cleft
Hypotony- Sequelae
- Cornea: Decemet's folds,
edema, astigmatism from eyelid pressure
- Anterior chamber: cellular reaction
(photophobia), shallowing (lens-cornea touch harmful, lens-iris is better
tolerated)
- Iris: perepherial
anterior synechiae
- Lens: cataract
- Fundus: ciliochoroidal
effusions, maculopathy (including choroidal folding), suprachoroidal
hemorrhage, disc edema (pseudoreverasal of cupping), CME
- General: discomfort,
phthisis bulbi
Hypotony- Treatment
- Directed at
underlying cause
- Early
overfiltering bleb: reduce steroid, pressure
patching, Simmons shell under patch (uncomfortable)
- Late
overfiltering bleb:
- tichloracetic acid or laser
to shrink bleb.
- Autologous blood patch- simulates scarring and
decreases outflow, can lead to elevated IOP and bleb failure.
- Revise bleb by resuturing flap or scleral
(pericardial) patch grafting
- Leaking bleb: pressure patching, bandage contact lens, aqueous
suppressants, Simmons shell, tissue glue (less effective on conjunctiva
than cornea), suture leak (9-0 vicryl or 10-0 nylon on BV needle),
compression suture, bleb revision, observation
- Cyclodialysis
cleft: laser treatment (Argon laser,
100µ, 0.1-0.2 sec, 500-1000 mW), in and around cleft, penetrating
diathermy, cryotherapy, surgical closure, buckling element at limbus
- IOP can go very high after closure but drops in a few
days when TM function returns
- cholinergics
can reopen clefts
- Rhegmatogenous retinal
detachment
- Uveitis- vigerous steroid
- Ciliochoroidal
effusions- corticosteroids (topical or
oral) and anticholinergics, if persistant surgical drainage
Preoperative Drop orders
- Cataract
Extraction
- Flurbiprofen 0.03% (Ocufen) 1 gtt q5 min x 3, 1 hour preop
- Cyclopentolate 1% 1gtt q 5 min x 3, 1 hour preop
- Phenylephrine 2.5% 1 gtt q 5 min x 3, 1 hour preop
- Trabeculectomy
with Mitomycin C
- 0.2 mg/cc (or other dose) send 1/2 cc sterile in TB
syringe to OR