Lecture 4 GLAUCOMAS

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Lecture 4
GLAUCOMAS
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• The outflow pathways of aqueous humor
• Main posterior chamber - pupil - anterior
  chamber - trabecular meshwork - Schlemms 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)

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Noncontact pneumatic autotonometry
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• 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, Bjerrums
  scotoma) and specific optic disc changes
  (dislocation of vessels, increased cupping etc.)

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• Congenital glaucoma (or hydrophtalmos) is caused
  by abnormal development of eye drainage system.
  The accumulation of aqueous in the eye due to
  elasticity of babys external coat causes the
  increasing of eye size.
• There are 2 clinical forms
• 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.

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• Methods of diagnostic of congenital glaucoma
• 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

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Classification of primary acquired glaucoma
Clinical form Stage Level of IOP Dynamics of visual functions
Open-angle Close-angle Mixt I early II advanced III far advanced IV - terminal A - compensated B - subcompancated C -decompancated stabile nonstabile
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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
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• Open-angle glaucoma
• Pathogenesis constriction or closing of
  openings in trabeculae Schlemms 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 IOPvisual
  field loss,first of its nasal part optic nerve
  damage).
• Methods of investigation
• Functional visometry, perimetry, campimetry,
  adaptometry.
• B. Objective general examination, focal
  lighting, biomicroscopy, gonioscopy,
  ophthalmoscopy, tonometry.

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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 IOPvisual 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.
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DIFFERENTIAL DIAGNOSIS
Sign CATARACT CHRONIC GLAUCOMA RETINITIS PIGMENTOSA
Visual acuity is decreased progressivly is decreased progressivly is decreased progressivly
Field of vision is not damaged constriction of nasal visual field, Bjerrums scotoma concentric visual field narrowing
Intraocular pressure normal, if increased-secondary phakogenic glaucoma increased normal
Lens opaque transparent, if opaque complicated cataract transparent, if opaque complicated cataract
Fundus if is seen, not damaged. If damaged - complicated cataract optic disc changes nasal dislocation of vessels, glaucomatous cupping mid-peripheral perivascular bone-spicule pigmentation, waxy disc pallor without nasal dislocation of vessels glaucomatous cupping
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• 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
• a, ? adrenomimetics dipinefrini, epinefrini
• Analogs of prostaglandins F 2 a (which stimulate
  the uveo-scleral outflow) latanoprost
  (xalatan), travoprost (travatan)
• II. which reduce production of aqeous
  humour
• Central agonists of a2- 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.

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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

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Nonpenetreting filtration surgeryviscocanalostom
y

• The initial steps of viscocanalostomy are similar
  to those of trabeculectomy. Specifically, the
  surgeon creates a one-half to two-thirdsdepth
  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 Schlemms canal
  is removed. The surgeon then cannulates Schlemms
  canal and injects a bolus of viscoelastic
  material into each of the canals cut ends (as in
  the picture). This viscodissection is intended to
  dilate the canal and facilitate the subsequent
  drainage of aqueous.

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Laser surgery in glaucoma
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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
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• 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
  doesnt disappear during 12-24 hours,
• antiglaucomatous surgery is indicated.
  
  
  
  

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• 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.

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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. Managementsurgery
(enucleation).


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