Transcript Раптова втрата зору. Гострий приступ глаукоми. Емболія

Lecture 4
GLAUCOMAS
The outflow pathways of aqueous humor:
1. Main: posterior chamber - pupil - anterior chamber trabecular meshwork - Schlemm’s canal (scleral sinus)vorticose veins – scleral venous plexus.
Additional:
2. Perivascular spaces of iris.
3. Suprachoroidal space - perivascular spaces – through
sclera into the tenon’ s space.
4. Perivascular spaces of central retinal vessels.
The IOP is maintained by a balance between aqueous
inflow and outflow & usually measures between
16-26 mm Hg (using tonometr of Maklakov) &
10-20 mm Hg (using tonometr of Goldman)
Noncontact pneumatic autotonometry
Not every increasing of IOP is glaucoma. It
may be ocular hypertension, caused, for example, by
using corticosteroids, intoxication or climax. Typical
for ocular hypertension are:
 absence of structural and functional changes;
 lasting existence without complaints;
 symmetrical increasing of IOP.
So, ocular hypertension is a symptom,
glaucoma is a syndrome.
Glaucoma is such increasing of IOP, which
is accompanied by specific visual defects
(constriction of nasal visual field, Bjerrum’s scotoma)
and specific optic disc changes (dislocation of
vessels, increased cupping etc.)
Congenital glaucoma (or hydrophtalmos) is caused by abnormal
development of eye drainage system. The accumulation of aqueous in
the eye due to elasticity of baby’s external coat causes the increasing
of eye size.
There are 2 clinical forms:
I. Hydrophtalmos without stasis (megalocornea, stretching out of
limbus, deep anterior chamber, increased eye, loss of vision, increased
IOP, typical changes of optic nerve).
II. Hydrophtalmos with stasis (all above mentioned signs +
photophobia, blepharospasmus, mixt injection, corneal oedema, which
is reliefed by 40 % glucosae).
There are 4 stages:
I. Early – D of cornea 12,0-12,5 mm, anterior-posterior distance of the
eye is increased on 1,5-2,0 mm, N fundus.
II. Advanced - D of cornea 13,0-14,0 mm, anterior-posterior distance of
the eye is increased on 3,0-4,0, glaucomatous cupping of optic disc
ophthalmoscopically.
III. Far advanced - D of cornea is more then 14,0 mm, anterior-posterior
distance of the eye is more then 30,0 mm, atrophy of optic disc
ophthalmoscopically.
IV. Terminal (or buftalm) – full blidness, scleral staphyloma.
Methods of diagnostic of congenital glaucoma:
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General examination, especially of cornea & limbus
Biomicroscopy or focal lighting
Keratometry
Tonometry
Ultrasound biometry
Ophthalmoscopy
Methods of treatment of congenital glaucoma:
Only surgical. Immediatly!
 Goniotomy
 Sinusotrabeculectomy
 Enucleation in buftalmos
Classification of primary acquired glaucoma
Clinical form
Stage
1. Open-angle I – early
2. Close-angle II – advanced
III – far
3. Mixt
advanced
IV - terminal
Level of IOP
A - compensated
B - subcompancated
C -decompancated
Dynamics of
visual
functions
stabile &
nonstabile
Stages of primary glaucoma (according to visual functions
defects):
I – visual field is consticted less then 10 degrees, physiological
cupping is increased.
II - visual field is consticted more then 10 degrees, edge
excavation.
III – tube visual field (15 degrees from the point of fixation),
edge excavation.
IV – visual field or visual acuity is zero, atrophy of optic disc.
Depending on IOP (using tonometr of Maklakov) glaucoma is
subdivided:
A (compensated) – IOP is less then 27 mm Hg.
B (subcompancated) – IOP is 28-32 mm Hg.
C (decompancated) – IOP is 33 mm Hg and more.
According to dynamics of visual functions during 6 month:
stabile &
nonstabile – constriction of visual field on 10 degree and more;
in tube vision – on 2-3 degrees and more;
increasing of scotomas size;
increasing of size of optic disc cupping
Open-angle glaucoma
Pathogenesis – constriction or closing of openings in trabeculae &
Schlemm’s canal as a result of endocrine, vascular or general
diseases such as atherosclerosis, artery hypertension, diabetus
mellitus etc.
Clinical features: usually asymptomatic until significant loss of
visual field has occured;
the eye looks usual, only dystrophic iris changes may be revealed
biomicroscopically;
open anterior chamber angle on gonioscopy, may be excess
pigmentation of trabeculae;
& typical for glaucoma signs (elevated IOP+visual field loss,first of
its nasal part +optic nerve damage).
Methods of investigation:
A. Functional – visometry, perimetry, campimetry, adaptometry.
B. Objective – general examination, focal lighting, biomicroscopy,
gonioscopy, ophthalmoscopy, tonometry.
Close-angle glaucoma
Pathogenesis –the closing (blockade) of anterior chamber angle by
iris root as a result of excess anterior position of lens or
functional pupil blockade (not organic, i.e. occlusio or seclusio
pupille) due to excess near location of lens & iris.
Clinical features: complaints for clouding of vision, haloes around
lights in the morning, headache, pain in the eye etc.;
frequent change of eye refraction & glasses prescribtion;
sometimes begins from acute attack;
signs of venous stasis – dilated scleral veins;
flat anterior chamber & iris bombee biomicroscopically;
narrow or close anterior chamber angle on gonioscopy;
& typical for glaucoma signs (elevated IOP+visual field loss,first of
its nasal part +optic nerve damage).
Methods of investigation:
A. Functional – visometry, perimetry, campimetry, adaptonetry.
B. Objective – general examination, focal lighting, biomicroscopy,
gonioscopy, ophthalmoscopy, tonometry.
DIFFERENTIAL DIAGNOSIS
CATARACT
Sign
Visual acuity
Field
vision
CHRONIC GLAUCOMA
RETINITIS
PIGMENTOSA
is decreased progressivly
of is not damaged
constriction of nasal concentric visual field
visual field, Bjerrum’s narrowing
scotoma
Intraocular
pressure
normal,
increased
normal
Lens
opaque
transparent,
transparent,
Fundus
if
is
seen,
damaged.
if increased-secondary
phakogenic glaucoma
if opaque– complicated if opaque– complicated
cataract
cataract
not optic disc changes –
nasal dislocation of
If
damaged
- vessels, glaucomatous
complicated cataract
cupping
mid-peripheral
perivascular
“bonespicule” pigmentation,
waxy
disc
pallor
without
nasal
dislocation of vessels &
glaucomatous cupping
Medical treatment of chronic glaucoma:
1. Local hypotensive therapy. The antiglaucomatous drops are divided into
two main groups:
I. which improve outcome of aqeous humour
Cholinomimetics - 1 % pilocarpini, carbachol;
α, Β – adrenomimetics – dipinefrini, epinefrini;
Analogs of prostaglandins F 2 α (which stimulate the uveo-scleral outflow)
– latanoprost (xalatan), travoprost (travatan)
II. which reduce production of aqeous humour
Central agonists of α2- adrenoreceptors - klonidini;
B-adrenoblockers: nonselective - timololi, arutimoli, & selective - betoptic;
Carbonic anhydrase inhibitors – Azopt.
2. Vasodilatators – acidi nicotinici, cavintoni, trentali, halidori etc.
3. Nootrops – piracetami, nootropili, etc.
4. Stimulators of nerve conductivity – proserini.
5. Tissue therapy, vitamins.
Laser treatment of chronic glaucoma:
Laser peripheral iridotomies in primary angle-closure glaucoma;
Laser trabeculoplasty in primary open-angle glaucoma.
Surgery of chronic glaucoma:
Filtration surgery in primary open-angle glaucoma, e.g. trabeculectomy.
In primary angle-closure glaucoma radical surgery – phacoemulsification of
cataract with IOL implantation; palliative surgery – iridectomy.
Nonpenetreting filtration surgery:
canaloplasty
• Figure 1 (left). Introduction of the microcatheter into Schlemm's canal
• Figure 2 (right). A 10-0 polypropylene suture being tied around the end
of the microcatheter
Nonpenetreting filtration surgery:
viscocanalostomy
The initial steps of viscocanalostomy are
similar to those of trabeculectomy.
Specifically, the surgeon creates a
one-half– to two-thirds–depth
superficial scleral flap, within the bed
of which a deep scleral flap is made.
The deep dissection begins 4 to 5 mm
posterior to the limbus and advances
toward the limbus in a tissue plane
just above the suprachoroidal space.
As the dissection advances
anteriorly, the roof of Schlemm’s
canal is removed. The surgeon then
cannulates Schlemm’s canal and
injects a bolus of viscoelastic
material into each of the canal’s cut
ends (as in the picture). This
viscodissection is intended to dilate
the canal and facilitate the
subsequent drainage of aqueous.
Laser surgery in glaucoma
Differential diagnosis of acute close-angle glaucoma
Symptom
acute close-angle
glaucoma
iridocyclitis
haloes around lights
+
-
irradiation of pain
+
-
injection (redness)
mixt
venous stasis
pericorneal
arterial
cornea
oedematous
decreased sensitivity
precipitates on
endothelium
normal sensitivity
anterior chamber
flat
normal
pupil
mydriasis
miosis, posterior
synechia
IOP
increased
normal or decreased
Emergency in acute close-angle glaucoma:
 instillation of miotics (pilocarpini 1 or 2 %)
every 15 minutes during first hour, every 30
minutes during next hour, then 4 times a day;
 analgetics (promedoli 2 % 1,0 ml s/cutaneous);
 diuretics (Diacarbi 0,5 or Hipothiasidi 0,1 per os,
Lasix 1 % 2,0 ml i/m)
If the attack of acute close-angle glaucoma doesn’t
disappear during 12-24 hours,
antiglaucomatous surgery is indicated.
Suspicion of glaucoma may be in such cases:
• IOP is 27 mm Hg and more (using tonometr of Maklakov) and 21
mm and more (using tonometr of Goldman);
• complaints for clouding of vision, haloes around lights in the
morning;
• iris bombee, less depth of anterior chamber;
• typical changes of optic disc;
• the difference in right and left eye IOP is more then
5 mm Hg.
All patients with suspicion of glaucoma must be observed in details in
clinics. This diagnosis can exist only one year.
Methods of investigation:
A. Functional – visometry, perimetry, adaptonetry, campimetry.
B. Objective – general examination, focal lighting, biomicroscopy,
gonioscopy, ophthalmoscopy, tonometry.
C. Necessary additional –
diurnal tonometry, tonography, elastotonometry, provocative test.
Secondary glaucoma is complication or outcome of some
other eye diseases. It may be:
1. Uveal glaucoma – as a result of pupil occlusion.
Management – treatment of uveitis. In deep anterior chamber–
mydriatics. In flat anterior chamber – miotics.
2. Phacogenic – prodused by immature cataract or lens
dislocation into the anterior chamber. Management – cataract
surgery.
3. Phacolytic - prodused by hypermature cataract.
Management – cataract surgery.
4. Vascular glaucoma as a result of central vein occlusion or
neovascularization in diabetus mellitus. Management –
treatment of main disease.
5. Posttraumatic as a result of burns, penetrating or blunt
injury of eyeball. Management – miotics.
6. Neoplastic – as a result of intraocular tumours.
Management–surgery (enucleation).
THANK YOU FOR ATTENTION!