Professional Documents
Culture Documents
Anterior Segment Examination &
Gonioscopy
Dr Simon Barnard
Lecture objectives
• To
To describe a best‐practice clinical anterior
describe a best practice clinical anterior
segment examination relevant to the
identification of features associated with
glaucoma, using a slitlamp biomicroscope
• To explain gonioscopic principles and anterior
chamber angle grading
chamber angle grading
• To enable readers to differentiate between
physiological and pathological anterior segment
and gonioscopic features
1
4/2/2008
Introduction
• Although glaucoma is an optic neuropathy,
examination of the anterior segment is
i ti f th t i ti
essential in the work‐up of these patients, and
those suspected of having a glaucoma
• Assessment of anterior segment is required to
differentiate between open‐angle and closed‐
p g
angle glaucoma, and can reveal secondary
causes of intraocular pressure (IOP) elevation
Gross external examination
• Before looking in detail with a slit lamp, a general
non magnified examination is necessary
non‐magnified examination is necessary
• Make mental note of age, race, and gender
• This is because the following are influenced by
these variables
– the risk of developing glaucoma
– likelihood of a particular disease subtype
– prognosis
– response to treatment
2
4/2/2008
Example
40 year old African with mild glaucoma has a
greater risk of developing significant visual
t i k fd l i i ifi t i l
loss in their lifetime than an elderly Caucasian
with a similar degree of glaucomatous
damage, and consequently requires more
aggressive therapy.
Non‐ocular signs ‐ general
• Casual inspection of the patient’s physique, limbs,
hands, and skin may detect relevant systemic
hands, and skin may detect relevant systemic
disease
• In younger individuals with glaucoma,
developmental anomalies may be seen, for
example,
– hypoplasia of the maxilla (flattening of the mid‐face)
and dental abnormalities in Rieger
g syndrome
y
• Signs of arthritis in the hands → difficulty
instilling eye‐drops
– undesirable to use medications that require frequent
dosing or multiple treatments.
3
4/2/2008
Non‐ocular signs ‐ Skin
• Phakomatoses
– facial haemangiomas (port‐wine stains) suggest
encephalotrigeminal angiomatosis (Sturge‐Weber
syndrome)
4
4/2/2008
– Neurofibromas suggest neurofibromatosis type‐1
(von Recklinghausen disease)
• A red, scaly, itchy rash is suggestive of atopic
d
dermatitis. Affected individuals may have a
titi Aff t d i di id l h
greater risk of developing an allergy to topical
medications
5
4/2/2008
Ocular Signs – Infantile glaucoma
• <Below the ages of 3‐4 years, immature elasticity
of connective tissue causes elevated IOP to
of connective tissue causes elevated IOP to
produce global enlargement (buphthalmos)
• Ocular stretch is most pronounced at the corneo‐
scleral junction, manifesting as corneal
enlargement.
• Corneal diameters exceeding 12 mm, particularly
when asymmetrical, are suspicious of glaucoma
6
4/2/2008
• Corneal oedema may occur as a secondary
response to expansion
t i
• detectable by the irregular reflection of light
from the corneal surface and stromal haze
• photophobia and epiphoria are important
signs
Ocular signs ‐ Lids
• Ptosis and overhanging folds of excessive eyelid
skin (dermatochalasis) are important to note not
skin (dermatochalasis) are important to note, not
to aid the diagnosis of glaucoma, but because
they are often responsible for superior edge
artefacts on visual field testing
• For these to occur, the pupil edge does not need
to be visibly obstructed
• Similarly, non‐pathological visual field loss may
result from deep orbits or a prominent nose
7
4/2/2008
• Similarly, non‐pathological visual field loss
may result from deep orbits or a prominent
nose
• Eyelid retraction and proptosis in adults suggest
thyroid eye disease
thyroid eye disease
• As a result of orbital congestion this condition can
obstruct venous drainage, elevating episcleral
venous pressure, and lead to a rise in IOP by
impairing the post‐trabecular flow of aqueous
humour.
• Lid retraction can also occur with therapeutic
adrenergic agents, owing to stimulation of their
sympathetically innervated musculature
8
4/2/2008
Ocular signs ‐ conjunctiva
• Conjunctival hyperaemia may have a number of
causes related to glaucoma
– direct consequence of an acute rise in IOP
– or secondary to uveitis, scleritis, or raised episcleral
venous pressure
– allergic reaction to glaucoma eye‐drops, particularly
topical α2‐agonists and carbonic anhydrase inhibitors,
the topical prostaglandin analogues
– This redness typically abates in the first few weeks of
use. Excessive conjunctival hyperaemia persisting
beyond six weeks may warrant a change in therapy, as
it is unlikely to resolve.
– allergic reaction to glaucoma eye‐drops,
particularly topical α2‐agonists and carbonic
particularly topical α agonists and carbonic
anhydrase inhibitors, the topical prostaglandin
analogues
– This redness typically abates in the first few weeks
of use
– Excessive conjunctival hyperaemia persisting
Excessive conjunctival hyperaemia persisting
beyond six weeks may warrant a change in
therapy, as it is unlikely to resolve.
9
4/2/2008
Ocular Signs ‐ Irides
• Iris heterochromia may be caused by
asymmetric iris atrophy e.g.,
ti ii t h
– Fuch's heterochromic iridocylitis
– pigment dispersion syndrome (PDS)
– following iris ischaemia secondary to primary
angle‐closure glaucoma
• brown eyes usually become less brown and
blue eyes assume a more saturated blue
colour
• However, enhanced visibility of the posterior
pigmented layer can lead to hyperchromia
10
4/2/2008
• iris heterochromia may be caused by
– benign iris naevi, which must be differentiated
from a melanoma,
– or iatrogenically by the unilateral use of
prostaglandin analogues that darken iris colour
– response to prostaglandin agents most marked in
green‐brown and yellow‐brown irides, and
generally does not resolve following their
termination
11
4/2/2008
Ocular Signs ‐ Cornea
• Large corneal diameter ‐ buphthalmos
• Small cornea is also of clinical relevance.
Microcornea is indicative of a crowded
anterior chamber angle – increased risk of
angle‐closure
Ocular Signs ‐ Pupils
• Glaucoma, either directly or through an
association with a shared aetiology, can
i ti ith h d ti l
influence the size, shape, and reactivity of
pupils
• The detection of subtle pupil abnormalities or
differences between the eyes is often missed
y
if examination is solely conducted through the
eyepieces of a slit‐lamp.
12
4/2/2008
Slit Lamp Examination – Eye Lids
• Blepharitis ( & tear film anomalies) must not
b
be neglected by the glaucoma specialist
l t d b th l i li t
• The glaucoma specialist may be the only eye
practitioner the patient is seeing
• Treatment may improve tolerance of
glaucoma medication
glaucoma medication
• topical prostaglandin analogues (e.g.,
latanoprost)
• lengthening and thickening of lashes, and
even the development of a second row
(distichiasis) may occur with their use.
13
4/2/2008
Examination of the conjunctiva and
related structures
• Anterior uveitis, either as a primary event or
secondary to very high IOP results in a
secondary to very high IOP, results in a
circumcorneal flush, due to the injection of blood
vessels overlying the inflamed ciliary body.
• In scleritis the affected area is violaceous red,
often with a bluish hue, and the irregular criss‐
cross pattern of the involved deep vascular‐
plexus, distinct from the radial orientation of
episcleral blood vessels, can be visualized.
• Diffuse congestion of the conjunctival and
episcleral
i l l vasculature, characterized by
l t h t i db
marked dilation and tortuosity, with an
absence of inflammation, identifies raised
episcleral venous pressure
14
4/2/2008
Congestion of conjunctival and episcleral vessels due to
raised episcleral venous pressure
• Peculiar to the use of topical α1‐agonists are
bl k d
black deposits within crypts of the palpebral
it ithi t f th l b l
conjunctiva.
• Resemble flakes mascara, and are known as
adrenochrome deposits
• Result from drug photo‐oxidation, and can be
Result from drug photo‐oxidation and can be
a source of irritation.
15
4/2/2008
Bleb assessment
• A trabeculectomy creates an alternative
drainage pathway for aqueous humour,
through the sclera so it subsequently collects
through the sclera, so it subsequently collects
under the superior conjunctiva where it forms
an externally visible smooth mound, known as
a bleb.
16
4/2/2008
• Eventually this pooled aqueous dissipates
through absorption into venous vasculature
• The patency of a drain is inferred from the
elevation of its bleb and IOP measurements, with
a flat bleb indicating poor drainage
a flat bleb indicating poor drainage
• Bleb integrity is evaluated with the Seidel test
• In this assessment, fluorescein is applied directly
onto the bleb, and if present, aqueous leakage is
revealed where the fluorescent tear film is
displaced
• This is important as bleb leakage is associated
Thi i i t t bl b l k i i t d
with a significant risk of ocular infection, and may
cause a very low IOP (hypotony) with its
attendant complications
• An improved variant of the classic Seidel test
uses highly concentrated 2% fluorescein. This
does not fluoresce when first instilled into the
eye due to quenching
• Dilution of fluorescein solution by leaked
aqueous results in easily detectable
fluorescent rivulets
17
4/2/2008
Examination of the cornea
• The cornea provides valuable diagnostic
information in glaucoma
• It can be directly affected by abnormal IOP,
It b di tl ff t d b b l IOP
and may be the site of developmental or
acquired signs particular to specific aetiologies
• Optimal viewing is usually achieved by
forming a parallelepiped section, maximizing
g p pp , g
illumination, and directing attention to the
side of this beam
18
4/2/2008
Influence of intraocular pressure
• Very high IOP causes epithelial and stromal
oedema of the cornea by forcing water into its
d f th b f i t i t it
structure and impairing the endothelial pump,
although corneal swelling may be absent if the
rise in pressure is gradual, as in chronic angle‐
closure glaucoma
• Such IOP elevations are most commonly
caused by acute primary angle‐closure
glaucoma (PACG)
• But may also occur following secondary angle‐
But may also occur following secondary angle
closure and aetiologies that choke the
trabecular‐meshwork with debris
• At particular risk of developing corneal
oedema are individuals with pre‐existing
endothelial cell loss or dysfunction, e.g.,
Fuch’s endothelial dystrophy, iridocorneal
endothelial syndrome, or a corneal graft
19
4/2/2008
• At particular risk of developing corneal
oedema are individuals with pre existing
oedema are individuals with pre‐existing
endothelial cell loss or dysfunction, e.g.,
Fuch’s endothelial dystrophy, iridocorneal
endothelial syndrome, or a corneal graft
• In these circumstances, swelling may occur
when the IOP is only minimally elevated
when the IOP is only minimally elevated,
owing to a reduced corneal detumescent
capability
• Paradoxically, hypotony may be encountered
in patients with glaucoma.
• Most commonly occurs immediately after
trabeculectomy due to excessive filtration or
trabeculectomy, due to excessive filtration or
bleb leakage
• The absence of posterior corneal support
leads to development of folds in Descemet’s
membrane
20
4/2/2008
• Moreover, a reduction in the tension of
B
Bowman’s layer permit its contortion under
’ l it it t ti d
the pull of inserting stromal lamellae, resulting
in faint, subepithelial, polygonal shagreen‐like
opacities
21
4/2/2008
Keratoplasty
• A corneal graft increases the risk of glaucoma,
particularly when the graft was necessitated
ti l l h th ft it t d
by
– congenital corneal anomalies
– in aphakes or
– when there is a history of graft rejection
y g j
• Mechanisms by which IOP may become
elevated following keratoplasty include
– the collapse of the trabecular‐meshwork, caused
by tight suturing and loss of anterior pulling forces
by tight suturing and loss of anterior pulling forces
by Descemet’s membrane;
– blockage of outflow by viscoelastics retained from
surgery;
– and ocular inflammation and the corticosteroids
used in its treatment
used in its treatment.
22
4/2/2008
Refractive corneal surgery
• History of refractive surgery is often not volunteered by
patients, possibly because these procedures are not
patients, possibly because these procedures are not
necessitated by medical condition, and thus may
erroneously be considered of no medical significance
• These procedures act on cornea and unintentionally
weaken biomechanical resistance to deformation
• Leads to an unpredictable underestimation of IOP with
conventional techniques
conventional techniques.
• In these patients IOP measurements are less
important in, and may confuse, the diagnosis of
glaucoma
Corneal endothelium
• Corneal endothelium must be examined for
– deposited pigment (PDS)
– pseudoexfoliative (PXF) material
– and keratic precipitates (KPs)
23
4/2/2008
• Aqueous convention currents, driven by the
temperature differential between the iris and
cornea, typically cause pigment granules to be
deposited in a spindle pattern (Krukenberg’s
spindle), orientated with its long‐axis vertical
Kruckenberg spindle in pigment dispersion syndrome
24
4/2/2008
• This sign intimates pigmentary dispersion
syndrome, but masquerading entities must be
excluded.
• These include
– PXF syndrome
PXF syndrome
– Uveitis
– pigmented neoplasia
– iris and ciliary body cysts
– trauma
– p
previous ocular surgery In PXF syndrome, the quantity
g y y , q y
of pigment on the endothelium is less than in PDS,
and the pattern of deposition tends to be more
scattered and limited to the inferior cornea.
• PXF syndrome, the quantity of pigment on the
endothelium is less than in PDS and the pattern of
endothelium is less than in PDS, and the pattern of
deposition tends to be more scattered and limited to
the inferior cornea
25
4/2/2008
Keratic precipitates (KP)
• Accumulations of inflammatory cells that settle
on corneal endothelium during episodes of
uveitis
• Ocular inflammation is generally associated with
Ocular inflammation is generally associated with
a decrease in IOP, because ciliary body
involvement reduces aqueous humour
production
• However, it can elevate pressure, directly by
involving the trabecular‐meshwork (trabeculitis),
obstructing trabecular outflow with leaked
obstructing trabecular outflow with leaked
viscous protein and leukocytes, and encouraging
the formation of peripheral anterior synechiae
(PAS); and indirectly, by its management with
corticosteroids
• Glaucoma is more commonly associated with
uveitis
iti when the inflammation is recurrent or
h th i fl ti i t
chronic, and in the special case of Fuch’s
heterochromic iridocyclitis.
26
4/2/2008
• KPs usually settle on the middle and lower
cornea in a diffuse or triangular pattern, due
to the interplay between aqueous convection
currents and gravity
g y
• When fresh, they normally appear as fine,
white, spheroidal bumps
• Larger, waxy “mutton fat” deposits indicate
granulomatous uveitis
• In Fuch’s heterochromic iridocyclitis the KPs
are very small, stellate, with interconnecting
feathery fibrin filaments, and involve the
superior cornea.
• With time KPs flatten and accumulate
pigment, but remain of clinical interest; they
may explain non‐progressive glaucomatous
damage in normotensives.
27
4/2/2008
Posterior embryotoxon
• prominent and anteriorly displaced
t
termination of Descemet’s
i ti fD t’ membrane
b
(Schwalbe’s line)
• On slitlamp examination it appears as a thin
white line at the level of the endothelium,
encircling the cornea, just in from the limbus
I i
It is usually most prominent nasally and
ll i ll d
temporally
28
4/2/2008
• Posterior embryotoxon as an isolated finding
is both common, affecting 15% of a normal
population, and benign
• However, the attachment of peripheral
However the attachment of peripheral
strands of iris to Schwalbe’s line identifies
Axenfeld‐Rieger syndrome, which is linked
with glaucoma
Endothelial dysfunction
• Less common anomalies of corneal
endothelium include those associated with
endothelium include those associated with
the proliferation, migration, and contraction
of endothelial cells over the anterior chamber
angle, that consequently lead to synechial
angle‐closure
• These include
These include
– posterior polymorphous dystrophy
– iridocorneal endothelial (ICE) syndromes
29
4/2/2008
• Posterior polymorphous dystrophy is a bilateral
condition vesicles and striae
condition – vesicles and striae
• In all of the ICE syndromes, particularly Chandler’s
syndrome, the endothelium resembles hammered
silver, and specular reflection reveals polymegathism
and polymorphism
• In addition to dysfunctional endothelial cells,
epithelial cells may migrate through a wound
and extend over the corneal endothelium,
anterior chamber angle, and iris
• This epithelial ingrowth typically leads to
recalcitrant glaucoma
• In these cases, examination detects a
scalloped grey‐white translucent sheet of cells
contiguous with the back of the cornea, with
overlying oedema, and invariably a history of
wound leakage
• With advent of microsurgical techniques,
epithelial ingrowth is now rare
30
4/2/2008
Examination of the iris
• Iris abnormalities are common to many of the
glaucoma subtypes
l bt
• The most obvious are those that change the
size and shape of the pupils
• When IOP approaches 50 mmHg, segmental
ischaemia of the iris occurs, and spiralling
• Pupil mid‐dilated, irregular, and unresponsive
• The pupil is often elongated vertically
The pupil is often elongated vertically
31
4/2/2008
• Following such an event the iris frequently
does not return to normal, but may remain
whirled and develop atrophy and, less
commonly, iridoschisis
Iris transillumination
• R
Retro‐illumination is useful technique for
t ill i ti i f lt h i f
assessing subtle abnormalities of iris integrity,
particularly that of its pigmented epithelium.
• The technique involves aligning the
observation and illumination systems of the
slitlamp, and shining light through the pupil;
litl d hi i li ht th h th il
or alternatively, directing the probe of a fibre
optic transilluminator onto the sclera
32
4/2/2008
• Intact iris prevents the visibility of orange light
reflected by the fundus
• Areas with deficient iris tissue are seen to
transilluminate
• To enhance contrast view ambient use
maximum light intensity and slit lamp beam
size adjusted so that it just fits through the
pupil; dim room lights
• Diffuse iris transillumination occurs in iris
hypoplasia and diffuse iris atrophy e.g.,
aniridia; Fuch’s heterochromic iridocyclitis
33
4/2/2008
• In PXF syndrome, the rubbing of PXF material
on the anterior lens capsule against the inner
border of the iris leads to a moth‐eaten
appearance of the peripupillary iris that
appearance of the peripupillary iris that
transilluminates when retro‐illuminated
• Other causes of localized
transillumination defects include
– iridotomies
– atrophy resulting from previous iris
ischaemia
– chaffing of the iris by the haptic portion of a
posterior chamber intraocular lens implant
– and damage by implements used during
dd b i l t dd i
intraocular surgery
34
4/2/2008
Peripheral iridotomy at 11 o’clock. Ease with which
fundus reflection can be sees intimates its patency
Iris neovascularization
• New, abnormal blood vessel formation on the
iris (iris rubeosis) and in the anterior chamber
g
angle identifies individuals at risk of
developing neovascular glaucoma
• If advanced has a poor prognosis
• Early detection improves treatment response,
and thus patients considered at risk,
principally those with previous retinal vascular
principally those with previous retinal vascular
occlusions or diabetic retinopathy, must be
examined carefully for subtle signs of mild
disease
35
4/2/2008
• Vasoproliferation occurs in response to
angiogenic factors originating from ischaemic
factors originating from ischaemic
retina, and is first seen at the pupil margin and
later in the trabecular‐meshwork
• New blood vessels are initially wisp‐like, and
spread irregularly over the iris surface, in
contrast to well formed normal iris vasculature
contrast to well formed normal iris vasculature
that is strictly limited to radial or
circumferential orientations
36
4/2/2008
Developmental iris anomalies
• Aniridia
– iris hypolasia
– glaucoma in 75%
37
4/2/2008
• Peter’s anomaly
– mutation of same PAX6 gene
– Iridocorneal adhesions
– Central corneal opacification
p
• Less significant iris hypoplasia may feature in
primary congenital glaucoma and Axenfeld‐
Rieger syndrome
• Absence of iris crypts
yp
• Enhanced visibility of the sphincter pupillae
and iris vasculature, and diffuse iris
transillumination defects secondary to stromal
thinning
38
4/2/2008
Enhanced visibility of the sphincter pupillae in iris
hypoplasia iris
• Pupil displacement (corectopia) is most marked when
it is pulled towards the anterior chamber angle by a
contractile membrane that extends onto the iris
surface
– Rieger anomaly and syndrome
– iridocorneal endothelial syndrome
– neovascular glaucoma
– posterior polymorphous dystrophy,
– and epithelial ingrowth.
• Frequently,
Frequently, the posterior, pigmented epithelium of the
the posterior, pigmented epithelium of the
iris is dragged around the pupil margin (ectropion
uveae) and gonioscopy reveals PAS corresponding to
the direction of pupil displacement
39
4/2/2008
• Tractional forces may create secondary pupils
(pseudopolycoria) in the Rieger and
(pseudopolycoria) in the Rieger and
progressive iris atrophy variants of Axenfeld‐
Rieger syndrome and iridocorneal endothelial
syndrome, respectively
• In addition to these stretch holes, full‐
thickness iris defects may develop in
thickness iris defects may develop in
progressive iris atrophy in the absence of
traction due to ischaemia = melt holes
Progressive iris atrophy – melt hole
40
4/2/2008
Examination of the crystalline lens
‐ anterior lens
• Pigment granules, liberated by PDS, PXF syndrome, or
other causes may settle on any structure in the AC,
other causes may settle on any structure in the AC,
including anterior lens capsule
• In PXF syndrome, epithelium of lens, pigmented
epithelium of iris, non‐pigmented epithelium of ciliary
body, and possibly zonules of lens, produce PXF
material
• Histologically, PXF material consists of fibrillar
Histologically PXF material consists of fibrillar
proteoglycosaminoglycans that tend to aggregate
linearly‐ appear as white‐translucent granular material
• PXF material on anterior lens surface, deposited
classically has bull’s eye configuration, because the
mid‐peripheral region is rubbed clear by the
movement of the touching inner border of the iris
41
4/2/2008
• Bright slit‐lamp → pupil constriction = <
visibility of scalloped edge of these zones
• ∴ often requires mydriasis
• PXF syndrome is an ocular manifestation of a
systemic disorder
• In affected individuals, PXF material can be
detected in visceral organs and the skin, but it
is only in the eye that it is known to be of
is only in the eye that it is known to be of
consequence
• Irregular, grey‐white, anterior subcapsular
opacities (glaukomflecken) represent necrosis
iti ( l k fl k ) t i
of the tips of lens fibres (Figure 24)
• These arise from localized ischaemia, and are
pathognomonic for previous acute or
subacute attacks of angle‐closure
g
42
4/2/2008
‐ Cataract
• Crystalline lens is capable of causing glaucoma by
various primary mechanisms
• Swelling of the lens promotes relative pupil‐block
that can lead to angle closure (phacomorphic
that can lead to angle‐closure (phacomorphic
glaucoma)
• Increase in lens thickness increases with age as
new lens fibres are laid down
• Changes accelerated and exaggerated by cataract
formation, often following trauma in a blind eye
• Bilateral occurrences have been reported as
idiosyncratic response to systemic
sulphonamides, carbonic anhydrase inhibitors,
and thiazide diuretics
43
4/2/2008
• In mature (complete lens opacification) or
hypermature (free‐floating nucleus in liquefied
cortex) cataracts, high molecular weight soluble
proteins accumulate and may leak through
grossly intact lens capsule
grossly intact lens capsule
• Initiates an immune response
• Proteins and protein‐engorged macrophages
overwhelm the outflow system, causing
phacolytic glaucoma.
• Macrophages laden with protein can be detected
Macrophages laden with protein can be detected
as messy white clumps on the anterior lens
capsule and in the anterior chamber
Macrophages laden with protein can be detected as
messy white clumps on the anterior lens capsule and
in the anterior chamber – phacolytic glaucoma
44
4/2/2008
• Lens particle glaucoma ‐ rupture of the lens
capsule
l from penetrating trauma or surgery
f t ti t
• Lens material released into the anterior
chamber obstructs the trabecular‐meshwork
and incites an inflammatory reaction, typically
more virulent than that occurring with
g
phacolytic glaucoma
45
4/2/2008
Ectopia lentis
• Subluxation and dislocation of the lens
(ectopia lentis) may cause pupillary block,
directly by iridolenticular contact; or indirectly,
directly by iridolenticular contact; or indirectly
by enabling the vitreous to prolapse forward
and form iridovitreal block
– Isolated congenital anomaly; or
– part of a generalized systemic disease, for
example, Marfan syndrome, Homocystinuria, and
PXF syndrome; or
– following trauma
Examination of the anterior chamber
• Both the depth and contents of the anterior
chamber are relevant to assessment of the
h b l tt t f th
glaucoma patient and glaucoma suspect
46
4/2/2008
Central anterior chamber depth
• Along its inner edge the iris rests against anterior
surface of crystalline lens
• Iridolenticular contact is accentuated in eyes with
shallow central anterior chambers, which
h ll t l t i h b hi h
increases risk of iris bombé and vulnerability
PACG
• Central anterior chamber depth of less than 1.8
mm is considered a significant risk for the
development of PACG
• The condition is rare when it exceeds 2.5 mm
• Crude estimation of anterior chamber depth may
be made by setting up an optical section with slit‐
lamp and comparing its width with that of cornea
The Smith method of central anterior
chamber depth estimation
• Greater accuracy is achievable using the Smith
method
• Slitlamp
Slitl microscope to be directed forward and
i t b di t d f d d
illumination system at 60° temporally
• Slit narrowed and rotated so that orientated
horizontally
• With the slit beam focused on the central cornea,
one may observe a second posterior image
one may observe a second posterior image
formed by reflection from anterior surface of the
crystalline lens
47
4/2/2008
• Slit length is then adjusted until the inner
edges of these two images just touch
• At this point, the length of the slit is read off
the scale on the slitlamp and multiplied by 1.4
the scale on the slitlamp and multiplied by 1 4
to give the central anterior chamber depth.
Smith method: Length of horizontal beam adjusted until
reflection from cornea and anterior lens surface just touch in
middle of pupil (x 1.4 = AC depth)
48
4/2/2008
49
4/2/2008
• A shallow anterior chamber is most commonly
encountered in small eyes ‐ crowded internal
structures.
• It may also occur as a result of lens
intumescence, ectopia lentis,
microspherophakia, hypotony, or pushing
forces posterior to the iris – as may occur in
aqueous misdirection syndrome and from
intraocular neoplasia
intraocular neoplasia
• The shallowing of the anterior chamber in
hypotony and aqueous misdirection syndrome
differs to that resulting from pupil block
mechanisms, in that it is often extreme and
th
there is no mid‐peripheral bowing of the iris
i id i h lb i f th i i
• In these conditions the iris may lie in
apposition with the cornea, both centrally and
periphery.
50
4/2/2008
AC is flattened in aqueous misdirection syndrome.
Absence of midperipheral bowing excludes pupil block
Anterior chamber activity
• Normal AC is optically empty
• Situation is disturbed in many secondary
causes of glaucoma
f l
• To detect cells in AC, magnification and light
intensity of the slitlamp should be high
• Dark room
• Direct obliquely a small conical beam, approx
Direct obliquely a small conical beam approx
3 mm high and 1 mm wide, with the
microscope positioned straight ahead
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• First focus on the inferior cornea with small
portion over the iris and rest over the pupil
• Adjust focus from the posterior corneal
surface to the anterior lens capsule a few
surface to the anterior lens capsule a few
times to get a feel of the distance
• Then adjust joystick of the slitlamp to focus
midway i.e., AC
• Detection may enhanced by agitating cells by
asking the patient to look up, down, and then
straight ahead – Tyndall phenomenon
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• Protein in aqueous humour through
immature dilated or damaged blood vessels
immature, dilated, or damaged blood vessels
is aqueous flare
• Appears as a hazy streak in the anterior
chamber, like a torch beam in fog iris detail
• Dense flare is easy to detect and may be
graded by its obscuration of iris detail
d d b it b ti f i i d t il
• When faint in unilateral disease, comparison
with the other eye helps detection
• Trauma may cause erythrocytes to be released
into AC
• Gravitate inferiorly, forming a hyphaema
• Erythrocytes can normally traverse the
trabecular‐meshwork, but this ability is impaired
b l h k b h bl d
in the presence of fibrinous aqueous and other
aqueous debris.
• The prognosis of a hyphaema is largely
dependent on its size, pre‐existing outflow
compromise and the presence of sickle cell
compromise, and the presence of sickle cell
disease.
• Small hyphaemas infrequently raise IOP, whereas
those that involve more than half the anterior
chamber usually do.
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• 1‐3 weeks after vitreous haemorrhage
haemoglobin leaks out of erythrocytes
haemoglobin leaks out of erythrocytes.
• This degeneration changes erythrocytes from
red, biconvex, pliable cells to tan‐brown,
spherical, inflexible cells.
• These “ghost cells” may pass into the anterior
chamber and become entrapped within the
h b db t d ithi th
trabecular‐meshwork, resulting in ghost cell
glaucoma.
Assessment of the anterior chamber
angle
• The anterior chamber angle of great
i
importance in glaucoma patients
t i l ti t
• Main aim of clinicians is to determine if angle
is open, closed, or has a high risk of closure
• However, its examination may also assist the
diagnosis of a secondary glaucoma and reveal
diagnosis of a secondary glaucoma and reveal
signs of other ocular diseases
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• Angle recess cannot be visualized in most eyes
because light emerging from the angle is
internally reflected where the pre‐ocular tear film
contacts air
• This occurs because the angle of incidence of
This occurs because the angle of incidence of
these light rays, the angle formed with a line
dropped perpendicular to the corneal surface,
exceeds the critical angle of the tear‐air interface
• This problem is overcome by placing lens in
optical continuity with cornea and tear film that,
by means of steep anterior surface or tilted
by means of steep anterior surface or tilted
mirror, reduces the incidence angle formed at the
surface contacting air, permitting a direct or
indirect view of the angle structures, respectively.
• Non‐gonioscopic methods can also be used to
rapidly estimate peripheral anterior chamber
angle width.
• These are considered inferior because, in
h d d f b
comparison, they have a greater propensity
for erroneous interpretation and may
potentially miss pertinent angle signs and
p
pathology
gy
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Shadow test
• Illuminate AC from side with pentorch
• Dim room lights; patient look straight ahead
• Illuminate from temporal side and look how
much nasal iris is in shadow
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The Van Herick method of angle
width estimation
• Most commonly used non‐gonioscopic technique
of assessing the width of the anterior chamber
of assessing the width of the anterior chamber
angle
• Microscope is positioned straight ahead and the
illumination system is set at 60° to the side
• The patient is asked to look forward
• Narrow slit beam is traversed from the sclera
onto the cornea, stopping just past the limbus
when an optical section of the cornea is first seen
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• At this point, the separation distance between
th
the posterior corneal surface and iris is
t i l f di i i
compared to the corneal width
• This observation can be made on both the
temporal and nasal sides
Van Herrick grading system for angle width
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Gonioscopy
• Why needed ?
• Cannot visualise angle with Slit Lamp because:
– Total internal reflection
– Scleral overhang
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Gonioscopy
The technique of gonioscopy
• Indirect more commonly used than direct
• Anaesthetise corneas
• Goldmann style gonioscopes require gel
• Zeiss (Posner) have flatter surfaces ‐ contact
gel not required
l d
• Inferior angle generally widest
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Normal angle structures
Normal wide open angle
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Show video
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Angle grading systems for gonioscopy
• Numerous systems for grading the anterior
chamber angle, each with their virtues and
proponents
• Limitations of reducing complex anatomical
relationships to a single variable must be
appreciated.
• Angles with the same grade do not necessarily
have an equal probability of closure
• All grading systems assume that the angle viewed
during gonioscopy is essentially as it was before
the goniolens contacted the eye
• This assertion may not be valid, particularly when
gonioscopic technique is poor
Shaffer method
• Sh
Shaffer method simply estimates the angle
ff th d i l ti t th l
that the iris makes with the trabecular‐
meshwork and posterior corneal surface in
four quadrants
• Practically, the angle width is usually
d t
determined by the ease at which the various
i d b th t hi h th i
angle structures can be seen, or conversely, by
the structures obscured by the iris
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Schaffer grading system
Shaffer grading system for angle width
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Schaffer grading system
Spaeth system
More elaborate
1) Level of iris insertion (A
Level of iris insertion (A‐E)
E)
2) Geometric angle of iris contact in degrees (as
with the Shaffer system)
3) Peripheral iris contour (r, s, or q)
4)) Trabecular p pigmentation (TMP 1 minimal to 4
g (
very heavy)
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Example
• Spaeth grading of B20.r.TMP‐2 refers to an iris
th t i
that inserts just behind Schwalbe’s
t j t b hi d S h lb ’ line at an
li t
angle of 20°, with a regular contour, and
moderate trabecular pigmentation
• Such a grading would be typical for a
hypermetropic
yp p eye with a narrow angle.
y g
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Spaeth grading classification
Iris Insertion Peripheral Iris Contour
A Anterior to trabecular s Steep
meshwork
B Behind Schwalbe’s line
C At scleral spur r Regular
D Deep – ciliary body visible
E Very deep q Queer
Angle anatomy and gonioscopic
examination
Iris contour
• When performing gonioscopy, the contour of the
iris plane and its surface should be assessed
• A slight convexity of the iris is common
• This occurs due to relative pupil block, and as
such, tends to be greater in hypermetropic eyes
with shallow anterior chambers
• This forward bowing is grossly exaggerated when
pupil block is absolute, caused either by primary
or secondary mechanisms.
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• Conversely, flat or minimally concave irides
may occur in myopia pseudophakia and
may occur in myopia, pseudophakia, and
aphakia
• Pronounced concavity is often encountered in
PDS, where in anatomically predisposed eyes,
reverse pupillary block is created when
aqueous humour is forced from the posterior
aqueous humour is forced from the posterior
chamber into the anterior chamber by the
action of blinking
Angle of approach
• After surveying the general iris contour,
g
attention should be directed to its angle of
approach and the position at which it appears
to insert into the ciliary body or other angle
structures
• Normally, the angle is narrowest superiorly
y, p y
and widest inferiorly, possibly due to a
combination of eyelid forces and gravity
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• As a general rule, anterior chamber depth, iris
convexity, and anterior chamber angle width
are correlated
• However, exceptions do occur, e.g., iris
However exceptions do occur e g iris
plateau configuration and iris plateau
syndrome, which are both characterized by a
normal anterior chamber depth and an iris
that remains relatively flat until its periphery,
whereupon it sharply turns anteriorly
h it h l t t i l to t
create a narrow angle recess
Angle structures Clinical appearance
(Posterior to Anterior)
Ciliary body Dull‐brown band. Possibly slate‐grey or
pink in lighter eyes
Scleral spur Narrow white band. Slightly shiny.
Yellows with age.
ll ih
Trabecular meshwork Semi‐transparent blue‐grey band with
textural depth in young. Less
translucent and darker colour with age
Canal of Schlemm Not usually visible. Pink/red line in
trabecular meshwork when filled with
meshwork when filled with
blood
Schwalbe’s line Fine white protruberance, often with
some pigment. Located at apex of
corneal wedge
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Peripheral anterior synechiae
Iris neovascularisation
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Trabecular hyperpigmentation
Further reading
• Stamper, R.L., Lieberman M.F., Drake, M.V., 1999.
Becker‐Shaffer’s Diagnosis and Therapy of the
g py
Glaucomas. Mosby
• Kanski, J., 2003. Clinical Ophthalmology.
Butterworth Heinemann
• Wallace, L., Alward, M., 2000. Color Atlas of
Gonioscopy. American Academy of
Ophthalmology
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Angle structures Clinical appearance
(Posterior to Anterior)
Ciliary body Dull‐brown band. Possibly slate‐grey or
pink in lighter eyes
Scleral spur Narrow white band. Slightly shiny.
Yellows with age.
ll ih
Trabecular meshwork Semi‐transparent blue‐grey band with
textural depth in young. Less
translucent and darker colour with age
Canal of Schlemm Not usually visible. Pink/red line in
trabecular meshwork when filled with
meshwork when filled with
blood
Schwalbe’s line Fine white protruberance, often with
some pigment. Located at apex of
corneal wedge
Visante
• Visualise
Visualise Anterior
Anterior
Segment
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Corneal Surgeons
Penetrating Keratoplasty (PKP) with sutures
Phakic IOL
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Glaucoma
Pathologies
Anterior Synechiae
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Thanks to
Michael E. Johnson BSc(Hons) MCOptom & the
I tit t f O t
Institute of Optometry, London
t L d
Carl Zeiss Medical
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