Professional Documents
Culture Documents
1.
Vaughan & Asburys General Ophthalmology 16th Edition 2004 a LANGE medical book
Parsons Diseases of the Eye 19th Edition 2003 Butterworth publication
3.
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
NW Alaska
Beijing, China Hvsgl, Mongolia
40+
40+ 40+
2.65
1.4 1.4
0.24
0.03 0.5
Nil
Not stated 0.3
Nil
Not stated Nil
Affected Congenital 300 000 POAG 13.5 million PACG 6 million Secondary 2.7 million Glaucoma suspects 105 million (IOP>21 mmHg)
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
Race
Chinese European Africans Japanese Asians Refraction ACG POAG ACG POAG POAG<ACG NTG ACG<=POAG
Hypermetopes Myopes
Genetics
Intra-ocular Pressure
Diabetes
Family History Hypertension Vascular Spasm
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 Schlemms 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
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
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
Rate of aqueous humour formation Resistance encountered in out flow channels Level of epi-scleral venous pressure
Membrane
Pupillary Block Synechia Lens Vitreous Trabecular Meshwork block Inflammation Cellular debris Steroids Inflammatory exudates Peripheral Iris bowing Peripheral Anterior Synechia Idiopathic
Hypercarbia
Dysthyroid eye disease Succinyl choline Co-contraction of extra-ocular muscles Decreased by Hypotension Decreased carotid blood flow
Decrease CVP
Bilateral advanced glaucomatous cupping with nasal displacement of the blood vessels
Perimetry Techniques
Advanced Techniques
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.
A- Schiotz tonometer
Gonioscopy
Visualization of the anterior chamber angle is called Gonioscopy
Optical Principal
In normal circumstances the angle of anterior chamber can not be visualized because of the total internal reflection
a b c
Lighter Medium
Denser Medium
d c b a Critical Angle d
Isopter.
Scotoma.
An Isopter is a line in the field of vision exhibiting similar visual acuity 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
4. Ring scotomas
5. Temporal Wedge 6. End Stage fields defects
Isolated paracentral scotomas: superior or inferior scotomas may also be found in early glaucoma
Temporal Wedge
Advanced Techniques
Quantitative Measurements Digitalized photogrammetry Confocal scanning laser ophthalmoscope (HRT) Measurements of ocular blood flow
Digitalized photogrammetry
worldwide blindness.
Early detection and early onset of treatment 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
Presenting
Social
HISTORY
Past
Family
VA Gonio OM
IOP
Exoph
EXAMINATION
Fundus Ocu surf
Lens Pupils AC
Cornea
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
Ocular Examination
Anterior chamber for inflammation, blood, pigment Check for AC depth, central and peripheral
Ocular Examination
Iris for atrophy , rubeosis, trans-illumination defects and pseudoexfoliation
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
Ocular Examination
Gonioscopy: look for width of the angle, configuration of the iris and chamber, PAS, vessels and iris processes
Ocular Examination
Fundoscopy: 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
Investigations
Order for a visual field examination with a standard automated perimeter
Investigations
HRT OCT GDx