Presentation on theme: "Glaucoma."— Presentation transcript:
1 Glaucoma
2 Glaucoma
Glaucomas are group of diseases causing damage to the optic nerve by the effect of raised ocular pressure on the optic nerve head
The intraocular pressure depends on the balance btw production and removal of aqueous humour
3 Pathophysiology
Aqueous is produced from ciliary processes in the posterior chamber (by active transport and ultrafiltration)
Aqueous leaves the eye through tubercular meshwork (iridocorneal angle)*, Schlemm’s canal and then episceral veins “the conventional pathway”
4% of the aqueous is drained into the supra-choroidal space and via the venous circulation across the sclera “uveoscleral pathway”
4 Pathophysiology
5 4%
6 the mechanism by which an elevated intraocular pressure damages nerve fibers:
Raised IO pressure causes “mechanical” damage to the optic nerve axon
Raised IO pressure causes “ischemia” of the nerve axon by reducing blood flow to it
7 Classification:
8 Primary glaucoma: This classification depends on: The iris doesn’t
cover the trabecular
meshwork (open angle)
the iris covers
the trabecular
meshwork (closed angle)
.
9 Primary open angle glaucoma
Pathogenesis:
The structure of trabecular meshwork appears normal but there is an increased resistance to the outflow, this happened due to:
Thinking of the trabecular lamellae which reduces the pore size
Reduction in the number of lining trabecular cells
Increased extracellular material in the meshwork spaces
10 Chronic open angle glaucoma
Epidemiology:
Affects of population over the age of 50
Males equally affected as females
May be a family hx, although the exact mode of inheritance is not clear
Genetic factors play a rule in developing open angle glucoma: mutation in the myocillin gene (GLC1A) om chromosome 1, optineurin (GLC1E)……..
11 History: -Symptoms depends on the rate of IO pressure rises
History: -Symptoms depends on the rate of IO pressure rises. -Associated with slow rise in pressure and it’s symptomless until
pt becomes aware of visual deficit. -Many pts diagnosed via an optometrist.
12 Chronic open angle glaucoma
On examination:
The eyes are mainly white and the corneas are clear
Perimetry….(for visual field loss)
On slit lamp:
1- Measure the ocular pressure using the tonometer (NL pressure is15.5 mmHg); mean(11-21 mmHg)
In chronic open angle glaucoma: pressure mmHg
In angle closure glaucoma >60 mmHg
2- Exclude other ocular disease that may be 2ry cause for the glaucoma
3- Measure the thinkness of the cornea with
a pachymeter*, to adjust the value of IO
pressure.
13 4- Examin the iridocorneal angle by Gonioscopy to confirm that an open angle glucoma is present
14 5- Examine the optic disc: Glaucomatous optic disc demonstrating:
1-Increased cupping and central pallor with baring of circumlinear vessel
2-Splinter optic disc hemorrhages
3-Nasalization of the vessels
4-Localized notching of the neural rim between
5. Primary Angle Closure
drainage angle occludable from primary
mechanism (iris trabecular meshwork contact
in three or more quadrants), with either raised
IOP and/or primary peripheral anterior
synechiae
and if optic nerve damage = glaucoma
12. Acute Angle Closure
Crisis
Examination: VA, IOP, slit-lamp examination,
gonioscopy, undilated optic disc viewing,
fellow eye assessment
think about and look for the mechanism of
closure during the examination
13. Acute Angle Closure
Crisis
Medical management
Eyedrops: beta blockers, alpha agonists,
carbonic anhydrase inhibitors and
pilocarpine
oral or intravenous acetazolamide
oral hyperosmotic agent (glycerol) if safe for
patient
14. Acute Angle Closure
Crisis
Medical Management
Intravenous hyperosmotic agents (mannitol)
it safe for patient
topical glycerin/glycerol eyedrops to
improve the view
topical steroids
15. Acute Angle Closure
Crisis
Surgical treatment
peripheral iridoplasty early if IOP not
lowering
AC paracentesis for temporary IOP
lowering - usually reserved for cases where
other treatment has failed
Laser peripheral iridotomy: YAG,
argon/diode. Treat fellow eye also!
16. Acute Angle Closure
Crisis
Surgical treatment
Lens extraction - often effective in refractory
cases and/or if significant cataract present
trabeculectomy not usually performed (50%
failure rate)
17. Acute Angle Closure
Crisis
if you are sure of a secondary non pupil block
mechanism (especially if it is atypical and
asymmetric) then use atropine
18.
19. Case NM
91 yr old frail woman (double
amputee)referred from rest-home with three
week history of red aching eyes and reduced
vision bilaterally
seen at local private practice: VA HM, 3/60;
IOP 68, 53 mmHg, hazy corneae and shallow
ACs
diagnosed with acute angle closure crisis:
topical timolol, brimonidine, pred forte and oral
diamox 250mg administered
20. Case NM
arrived at GCC A&E: IOP 54, 48.
Bilateral YAG Laser peripheral iridotomy
performed
IOPs one hour later were 18, 14
discharged home on combigan BD and pred
forte Q2hrly OU
21. Case NM
returned for review 2 days later: IOP 46,23
corneae a little clearer, difficult view of disc as
very dense cataracts
drainage angle closed synechially in 3/4
quadrants OD
22. Case NM
phaco/PCIOL OD 2 days later, subTenon’s
anaesthesia
generalised zonule weakness noted
intraoperatively so capsular tension ring
inserted
corneal oedema gradually settled and UAVA
6/9
optic nerve OD 0.9
23. Case NM
IOPs 17, 14 on Latanoprost nocte, Combigan
BD OU
planning phaco/PCIOL OD in the next month
or two - VA 6/18, angle very narrow but open
in 2 quadrants, hazy view of disc 0.3
24. Open Angle Glaucoma
Emergencies
If IOP > 40mmHg
Primary: not common, but possible (younger)
Secondary: trauma-related, steroid response,
hyphaema, pigment dispersion syndrome,
pseudoexfoliation, Posner-Schlossman
syndrome, phacolytic glaucoma, ghost cell
glaucoma
