anatomy of the angle structure (glaucoma)
DESCRIPTION
This presentation is orginaly uploaded to http://kpkmedicalcolleges.tk by Dr.SulemanTRANSCRIPT
Recommended Books for Ophthalmology
1. Vaughan & Asbury’s
General Ophthalmology
16th Edition 2004 a LANGE medical book
2. Parsons’ Diseases of the Eye
19th Edition 2003 Butterworth publication
3. Clinical Ophthalmology by Jack J. Kanski
5th Edition 2003 Butterworth publication
GLAUCOMA
Patho-physiology & Detection
Dr. Nasir Saeed
Epidemiology of Glaucoma
Glaucoma is not a single disease entity,but the result of a
group of different mechanisms which cause a loss of retinal
ganglion cells. This loss may be acute or episodic, or slowly
and relentlessly progressive. Some authors therefore refer to
‘the glaucomas’. The common, connecting feature used to be
regarded as the height of the intraocular pressure (IOP), which
dominated the understanding of the clinical manifestations to a
greater or lesser extent. Although intraocular pressure is
frequently raised, it is now regarded as a risk factor, and no
longer considered a defining characteristic.
Location Age PACG (%) POAG (%) Secondary glaucoma
Congenital/
Developmental
European
Origin
Baltimore, Md. 40+ 0.31 1.29 0.68 No available
Beaver Dam, Wisc. 43-84 0.04 2.1 Not stated Not stated
Blue Mountains, Australia
49+ 0.27 3.0 0.15 Nil
African
Origin
Jamaica 35-74 Nil 1.4 0.35 Nil
Baltimore, Md. 40+ 0.67 4.74 1.42 Not available
Asian
Origin
Umanaq area, Greenland
>40 4.8 1.26 1.00 Nil
NW Alaska 40+ 2.65 0.24 Nil Nil
Beijing, China 40+ 1.4 0.03 Not stated Not stated
Hövsgöl, Mongolia 40+ 1.4 0.5 0.3 Nil
Glaucoma prevalence surveys, by racial groups
Affected Blind
Congenital 300 000 200 000
POAG 13.5 million 3 million
PACG 6 million 2 million
Secondary 2.7 million ?
Glaucoma suspects
(IOP>21 mmHg)
105 million
World estimates of glaucoma prevalence
RISK FACTORS
Age:
The prevalence and incidence of PACG
increase with age. Although a peak has been
claimed, the best evidence suggests that
incidence rises continually with age. Attacks
of ACG are rare before age 45.
GENDER
• POAG Equal• PACG Females > Males
Race• Chinese ACG• European POAG• Africans POAG<ACG• Japanese NTG• Asians ACG<=POAG
Refraction• ACG Hypermetopes • POAG Myopes
Genetics
• Intra-ocular Pressure
• Diabetes
• Family History
• Hypertension
• Vascular Spasm
ANATOMY OF THE ANGLE STRUCTURES
Aqueous Humour
Produced by the ciliary processes into the posterior chamber
• Through the pupil it circulates into the anterior chamber
• 90% of it is drained through the trabecular meshwork into the Schlemm’s canal and the epi-scleral venous system (conventional pathway)
• 10% of it leave the eye through the uveo-scleral route (un-conventional pathway) into the suprachoroidal space and chained by venous circulation of the ciliary body and sclera
Functions of Aqueous humour
It maintains the shape and internal structure of the eye by
sustaining an intraocular pressure higher then atmospheric pressure
and helps in maintaining the optical structure.
It carries oxygen and nutrients to the lens and cornea
It carries waste products away from the lens and cornea
Aqueous humour production
• Produced by the ciliary processes of the ciliary body.
Two Mechanisms
I- Active secretion
• 80% of aqueous is produced by the non pigmented ciliary epithelium as a result of active metabolic process
• Involves several enzymatic systems i.e. Na+ - K + ATPase / Carbonic
Anhydrase
• Na+, K+, Ascrobate, HCO3
• Transported into the posterior chamber
• Secretion diminishes by factors which will inhibit active metabolism
like drugs, hypoxia, hypothermia
• Independent of IOP
Aqueous humour production
II- Passive Secretions
• 20%
• Diffusion to maintain equilibrium between the osmotic pressure and electrical balance on the two sides of the ciliary processes
• Ultra-filtration
• When the diffusion of water and salt is accelerated by blood pressure (hydrostatic pressure) in the ciliary body
The passive secretion is dependent on level of blood pressure in the ciliary body, plasma oncotic pressure and intraocular pressure
• Blood Aqueous Barrier
• Large molecules such as plasma proteins and cells do not get into the aqueous chambers even when the plasma concentration is very high
•Sites of the barrier is tight junctions between the non-pigment ciliary epithelium and their basement membrane
Intra-ocular pressure (IOP)
• The circulation of aqueous humour in the eye maintains the IOP
• The equilibrium of aqueous formation and outflow rate is of crucial
importance
• Normally aqueous humour is secreted at a rate of 0.02µl / minute and
same amount is drained
•The distribution of IOP in general population : 11-21 mm of Hg
•Average = 15 mm of Hg
• Diurnal variation – High in morning
Low in evening by 5 mm of Hg
• No sex difference
Determinants of Intraocular Pressure
• Rate of aqueous humour formation
• Resistance encountered in out flow channels
• Level of epi-scleral venous pressure
Factors influencing Intra-Ocular Pressure
I- Rate of Aqueous Humour formation
Increased by
a. Inflammation
b. Blood Pressure
c. Hypo-osmolarity of plasma
Decreased by
a. Retinal / Choroidal / Ciliary body detachments
b. Drugs
c. Anaesthesia
B-Blocker
Carbonic Anhydrase hulibitors
II- Out flow Resistance
Increased by
Age
Membrane
• Pupillary Block Synechia
Lens
Vitreous
• Trabecular Meshwork block
Inflammation
Cellular debris
Steroids
Inflammatory exudates
Peripheral Iris bowing
Peripheral Anterior Synechia
Idiopathic
• Outflow Resistance Decreased by
• Accommodation
• Drugs
• Miotics
• Prostaglandins
• Adrenaline
III- Episcleral Venous Pressure
Increased by
• Increased CVP
• Valsalva
• Carotid Cavernous fistula
• Hypercarbia
•Dysthyroid eye disease
•Succinyl – choline
• Co-contraction of extra-ocular muscles
Decreased by
• Hypotension
• Decreased carotid blood flow
• Decrease CVP
Applied Anatomy of the optic n. head
Retinal Nerve fibre layers
Relative positions of nerve fibre layer
Cross Section of the Optic N. Head
Optic Cup & Neuro-retinal rim
Physiological Cup & Neuro-retinal rim
Glaucomatous Damage Retinal Nerve fibre layers Normal
Glaucomatous Damage Abnormal Nerve fibre layers
Abnormal nerve fibre layers
Glaucomatous Damage
Optic disc cupping
Bilateral glaucomatous cupping with inferior notching and ‘bayonetting’
Bilateral advanced glaucomatous cupping with nasal displacement of the blood vessels
End – Stage glaucomatous cupping
Clinical Methods for detection and evaluation of glaucoma
• IOP Measurements
• Gonioscopy
• Perimetry Techniques
• Advanced Techniques
Measurement of Intraocular Pressure Tonometry
Principal
• The pressure inside a sphere may be measured directly by canulating
it and connecting it to a measuring device. This is called manometry. It
is the most accurate method but not practical for routine clinical
measurement.
• It can also be measured by the
• Imbert – Fick Law – Pressure = Force /Area.
• The pressure can be measured by measuring the force necessary to
flatten a fixed area or by measuring the area flattened by a fixed force.
• Also a known force will indent a sphere. In low pressure the
indentation will be more and in high pressure the indentation will be
less.
Goldmann Applanation Tonometer
• Applanation tonometry measures the force applied per unit area. The
Goldmann tonometry is a variable force tonometer consisting of a
double prism with a diameter of 3.06 mm. It is the most popular and
accurate tonometer.
Goldmann applanation tonometer
Fluorescein-stained semicircles seen during tonometry
A- Schiotz tonometer
B- Principles of indentation tonometry
• Checking for diurnal changes= phasing
• Demonstrating elevation of IOP after pupillary
dilation, water drinking
• IOP checking in different direction of gaze
• Checking for steroid responsiveness
• IOP-measurement digitally
Gonioscopy
• Visualization of the anterior chamber angle is called Gonioscopy
Purposes
1. Diagnostic: to identify abnormal angle structures and to
estimate the width of the anterior chamber angle. This is
particularly important to classify the open angle and angle
closer glaucoma
2. Surgical: to visualize the angle during the procedures
such as laser trabeculopasty and goniotomy
Optical Principal
• In normal circumstances the angle of anterior chamber can not be visualized because of the total internal reflection
Critical Angle
Lighter Medium
Denser Medium
a
c
d
b
a
c
d
b
Optical Principal of Gonioscopy
Single Mirror goniolens & Zeiss four mirror goniolens
Swan-Jacob surgical goniolens & Koeppe goniolenses
Normal Anatomy of Angle structure
Schaffer’s Grading System
Abnormal Anterior Chamber Angle
Perimetry
• Visual fields ;
• An island of vision surrounded
by a sea of darkness
• Isopter. An Isopter is a line in the field of vision exhibiting similar visual acuity
• Scotoma. Is a defect in the visual field
• Absolute
• Relative
• Positive
• Negative
• Visible threshold. Is the luminance of the stimulus measured in dB at
which it is perceived 50% of times when it is
presented statically
Perimetric Principals
• Perimetry is a method of evaluating the visual fields
• Qualitative Perimetry is a method of detecting a visual field defect
and is the first screening phases of glaucoma suspects
• Quantitative Perimetry
Visual Fields defects in glaucoma1. Arcuate scotomas : develop between 100 and 200 of
fixation in areas that constitute downward or more
commonly, upward extensions from the blind spot
(Bjeerrum area)2. Isolated paracentral scotomas: superior or inferior
scotomas may also be found in early glaucoma.
3. A nasal (Roenne) step
4. Ring scotomas
5. Temporal Wedge
6. End Stage fields defects
1. Arcuate scotomas : develop between 100 and 200 of fixation in
areas that constitute downward or more commonly, upward
extensions from the blind spot (Bjeerrum area)
Isolated paracentral scotomas: superior or inferior scotomas may also be found in early glaucoma
A nasal (Roenne) step
Temporal Wedge
End Stage fields defects
Advanced Techniques
Quantitative Measurements
• Digitalized photogrammetry
• Confocal scanning laser ophthalmoscope (HRT)
• Measurements of ocular blood flow
Digitalized photogrammetry
Confocal scanning laser
ophthalmoscope (HRT)
Glaucoma is the second leading cause of
worldwide blindness.
Early detection and early onset of treatment are
the most important factors for preventing
progressive glaucoma damage.
A comprehensive evaluation of a glaucoma
suspect is the key to diagnosis and management.
The aims of assessment are:
• To assess the risk factors to determine whether
glaucoma is present or likely to develop
• To exclude or confirm the alternative diagnosis
• To identify the underlying mechanism of
damage; so as to select best choice for
management
• To plan a strategy for management
ASSESSMENT
HISTORYSocial
Family
Presenting
Past
Gonio
IOP
Fundus
Lens
Pupils AC
Cornea
Ocu surf
Exoph
OM
VA
EXAMINATION
Ocular Examination
• Record visual functions
• Ocular motility
• Exclude any proptosis/exophthalmos
• Ocular surface for episcleral blood vessels
• Conjunctiva for papillae and follicles
• Cornea for size, shape and transparency
• Check for corneal thickness
Ocular Examination
• Anterior chamber for inflammation, blood, pigment
• Check for AC depth, central and peripheral
• Convex iris-lens diaphragm
• Shallow anterior chamber
• Narrow entrance to chamber angle
Ocular Examination
Iris for atrophy , rubeosis, trans-illumination defects and pseudoexfoliation
Stromal iris atrophy with spiral-like configuration
Mid-peripheral iris atrophy
Central disc with peripheral band
Ocular Examination
• Pupil for size, shape and reaction
• Lens for presence, transparency,
thickness, position and shape
Ocular Examination
• Record intraocular pressure, look for diurnal variations
• Evaluate IOP for 24 hours if in doubt• Use a Goldmann-style applanation
tonometer
Trabecular hyperpigmentation - may extend anteriorly
(Sampaolesi line)
Open angle of normal appearance
Synechial angle closure
Irregular widening of ciliary body band
Ocular ExaminationGonioscopy: look for width of the angle, configuration of the iris and chamber, PAS, vessels and iris processes
Schaffer’s grading of angle
Ocular ExaminationFundoscopy: evaluate optic nerve head and retinal nerve fibre layer
use slit lamp indirect lenses and a dilated pupil
Look for optic disc size, colour, neuro-retinal rim, disc haemorrhage, vascular pattern, peri-papillary atrophy and cup disc ratio
Small dimple central cup Larger and deeperpunched-out central cup
Cup with sloping temporal wall
Optic disc evaluation
Retinal nerve fibre layer analysis
InvestigationsOrder for a visual field examination with a standard automated perimeter
Investigations
HRT
OCT
GDx
Systemic investigation includeImaging of CNSEvaluation of CVSHaematological profile