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Hasan Arafat
Glaucoma ‫األسود‬ ‫الماء‬ ‫أو‬ ‫األزرق‬ ‫الماء‬ ،‫رق‬َّ‫الز‬
Introduction
• Glaucomas are a group of disease;
• All of these diseases cause damage to the optic nerve
head;
• Axon loss results in visual field defects and decreased
visual acuity.
Anatomy & Physiology
• IOP is determined by a balance between
production and removal of aqueous
humor
• Aqueous is actively secreted into the
posterior chamber by the ciliary
processes
• It then passes through the pupil into the
anterior chamber and leaves the eye
• Aqueous drains through two pathways
Glaucoma and Blindness
• Glaucoma is the second most common cause of
blindness, two theories exist:
 Raised intraocular pressure causes mechanical damage to the
axons
 Raised intraocular pressure causes ischemia of the nerve axons by
reducing blood flow at the nerve head
Classification: Primary Glaucoma
• The mechanism by which aqueous
drainage is reduced provides a
means to classify the glaucoma:
 clear of the trabecular meshwork
(open angle glaucoma);
 covering the meshwork (closed angle
glaucoma).
Open-Angle Glaucoma
• The trabecular meshwork is normal structurally
• Functionally, the meshwork shows increased resistance
to aqueous outflow
• Causes:
 Thickening in the trabecular lamellae (reduced pore size);
 reduction in the number of lining trabecular cells;
 increased extracellular material in the trabecular meshwork spaces.
• Normal tension/low tension glaucoma
• Ocular hypertension
Open Angle Glaucoma
History
 Symptoms depend on the rate in
which IOP rises
 Usually symptomless
 The patient might present after they
notice a visual deficit
 Usually discovered by chance by an
optometrist
Examination
 White eye, clear cornea
 Measure the IOP using a tonometer
 Measure the corneal thickness using
a pachymeter
 Examine the iridocorneal canal using
a gonioscopy
 Examine the optic disc and identify
pathologic cupping
 Exclude secondary causes
• Goldman Tonometer • Pachymeter
Gonioscope
Open-Angle Glaucoma
Medical Treatment
• Topical Agents
 β-blockers
 Parasympathomimetics
 Sympathomimetic
 α-2 agonists
 Carbonic Anhydrase Inhibitors
 Prostaglandin Analogues
• Systemic Agents
 Carbonic Anhydrase Inhibitors
Surgical Treatment
• Trabeculectomy
• Laser Trabeculoplasty
Open-Angle Glaucoma
Trabeculectomy Procedure Trabeculectomy Bleb
Closed-Angle Glaucoma
• Occurs in small eyes (hypermetropes/Asians) due to
their shallow anterior chamber
• Increased resistance to aqueous flow increases the pre
ssure in the posterior chamber
• Pressure pushes the iris forward, obstructing aqueous
outflow
• Long standing contact between the iris and the
drainage angle leads to peripheral anterior synechiae
Closed-Angle Glaucoma
• Impaired drainage increases IOP
• Increased pressure deprives the entire cornea of
nutrition and the posterior cornea from oxygen
• This leads to clouding of the cornea and pressure on
the optic nerve, leading to decreased vision
• Usually preceded by subacute attacks, in which the
patient experiences increased IOP, headache and
colored halos around light
Closed-angle glaucoma affects Asians because of their naturally
small eyes
Closed-Angle Glaucoma
History
 Photophobic, very painful eye
 Watering of the eye
 Loss of vision
 N/V, referred abdominal pain
Examination
 Visual acuity is reduced
 Red eye
 Cloudy cornea
 Oval, dilated, fixed pupil
Closed-Angle Glaucoma
Treatment
• Combined medical and surgical, must be urgent
 Acetazolmide (IV & oral)
 Topical pilocarpine and β-blockers
 Iridotomy/ iridectomy
 +/- a procedure to relieve PAS
Secondary Glaucoma
• Caused by obstruction of the trabecular meshwork
Meshwork abnormalities
Hyphema
Uveitis
Pigment dispersion syndrome
Pseudoexfoliative glaucoma
Steroid-induced glaucoma
Angle abnormalities
 Angle recession (trauma)
 Uveitis
 Large choroidal melanoma
 Cataract
 Rubeosis iridis
Secondary Glaucoma
Treatment
• Depends on the primary cause
• In refractory cases, ablation of the ciliary processes
might be required, this is performed using laser or
cryoprobe to the sclera overlying the area of choice
Congenital Glaucoma
• The cause of congenital glaucoma remains uncertain
• One view is that the iridocorneal angle is
developmentally abnormal and covered with a
membrane which increases the outflow resistance
Congenital Glaucoma
• S/Sx
 excessive tearing, photophobia and blepharospasm;
 an increased corneal diameter and enlargement of the globe (buphthalmos),
 resulting in progressive myopia;
 a cloudy cornea due to epithelial and stromal edema;
 splits in Descemet’s membrane.
Congenital Glaucoma
Treatment
• Surgical treatment
 Goniotomy
 Trabeculotomy
A child with congenital glaucoma
Prognosis of Glaucoma

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Glaucoma

  • 1. Hasan Arafat Glaucoma ‫األسود‬ ‫الماء‬ ‫أو‬ ‫األزرق‬ ‫الماء‬ ،‫رق‬َّ‫الز‬
  • 2. Introduction • Glaucomas are a group of disease; • All of these diseases cause damage to the optic nerve head; • Axon loss results in visual field defects and decreased visual acuity.
  • 3. Anatomy & Physiology • IOP is determined by a balance between production and removal of aqueous humor • Aqueous is actively secreted into the posterior chamber by the ciliary processes • It then passes through the pupil into the anterior chamber and leaves the eye • Aqueous drains through two pathways
  • 4. Glaucoma and Blindness • Glaucoma is the second most common cause of blindness, two theories exist:  Raised intraocular pressure causes mechanical damage to the axons  Raised intraocular pressure causes ischemia of the nerve axons by reducing blood flow at the nerve head
  • 5. Classification: Primary Glaucoma • The mechanism by which aqueous drainage is reduced provides a means to classify the glaucoma:  clear of the trabecular meshwork (open angle glaucoma);  covering the meshwork (closed angle glaucoma).
  • 6. Open-Angle Glaucoma • The trabecular meshwork is normal structurally • Functionally, the meshwork shows increased resistance to aqueous outflow • Causes:  Thickening in the trabecular lamellae (reduced pore size);  reduction in the number of lining trabecular cells;  increased extracellular material in the trabecular meshwork spaces. • Normal tension/low tension glaucoma • Ocular hypertension
  • 7. Open Angle Glaucoma History  Symptoms depend on the rate in which IOP rises  Usually symptomless  The patient might present after they notice a visual deficit  Usually discovered by chance by an optometrist Examination  White eye, clear cornea  Measure the IOP using a tonometer  Measure the corneal thickness using a pachymeter  Examine the iridocorneal canal using a gonioscopy  Examine the optic disc and identify pathologic cupping  Exclude secondary causes
  • 8. • Goldman Tonometer • Pachymeter
  • 10. Open-Angle Glaucoma Medical Treatment • Topical Agents  β-blockers  Parasympathomimetics  Sympathomimetic  α-2 agonists  Carbonic Anhydrase Inhibitors  Prostaglandin Analogues • Systemic Agents  Carbonic Anhydrase Inhibitors Surgical Treatment • Trabeculectomy • Laser Trabeculoplasty
  • 12. Closed-Angle Glaucoma • Occurs in small eyes (hypermetropes/Asians) due to their shallow anterior chamber • Increased resistance to aqueous flow increases the pre ssure in the posterior chamber • Pressure pushes the iris forward, obstructing aqueous outflow • Long standing contact between the iris and the drainage angle leads to peripheral anterior synechiae
  • 13. Closed-Angle Glaucoma • Impaired drainage increases IOP • Increased pressure deprives the entire cornea of nutrition and the posterior cornea from oxygen • This leads to clouding of the cornea and pressure on the optic nerve, leading to decreased vision • Usually preceded by subacute attacks, in which the patient experiences increased IOP, headache and colored halos around light
  • 14. Closed-angle glaucoma affects Asians because of their naturally small eyes
  • 15. Closed-Angle Glaucoma History  Photophobic, very painful eye  Watering of the eye  Loss of vision  N/V, referred abdominal pain Examination  Visual acuity is reduced  Red eye  Cloudy cornea  Oval, dilated, fixed pupil
  • 16. Closed-Angle Glaucoma Treatment • Combined medical and surgical, must be urgent  Acetazolmide (IV & oral)  Topical pilocarpine and β-blockers  Iridotomy/ iridectomy  +/- a procedure to relieve PAS
  • 17. Secondary Glaucoma • Caused by obstruction of the trabecular meshwork Meshwork abnormalities Hyphema Uveitis Pigment dispersion syndrome Pseudoexfoliative glaucoma Steroid-induced glaucoma Angle abnormalities  Angle recession (trauma)  Uveitis  Large choroidal melanoma  Cataract  Rubeosis iridis
  • 18. Secondary Glaucoma Treatment • Depends on the primary cause • In refractory cases, ablation of the ciliary processes might be required, this is performed using laser or cryoprobe to the sclera overlying the area of choice
  • 19. Congenital Glaucoma • The cause of congenital glaucoma remains uncertain • One view is that the iridocorneal angle is developmentally abnormal and covered with a membrane which increases the outflow resistance
  • 20. Congenital Glaucoma • S/Sx  excessive tearing, photophobia and blepharospasm;  an increased corneal diameter and enlargement of the globe (buphthalmos),  resulting in progressive myopia;  a cloudy cornea due to epithelial and stromal edema;  splits in Descemet’s membrane.
  • 21. Congenital Glaucoma Treatment • Surgical treatment  Goniotomy  Trabeculotomy
  • 22. A child with congenital glaucoma

Editor's Notes

  1. It then passes through the pupil into the anterior chamber and leaves the eye, predominantly, via the trabecular meshwork, Schlemm ’ s canal and the episcleral veins to reach the bloodstream ( the conventional pathway ). A small but important proportion of the aqueous (4%) drains across the ciliary body into the supra - choroidal space and is absorbed into the venous circulation ( the uveoscleral pathway ).
  2. Second to cataract
  3. A form of glaucoma also exists in which glaucomatous field loss and cupping of the optic disc occurs even though the intraocular pressure is not raised ( normal tension or low tension glaucoma ). It is thought that the optic nerve head in these patients is unusually susceptible to the intraocular pressure and/or has an intrinsically low blood flow. Conversely, intraocular pressure may be raised without evidence of visual damage or pathological optic disc cupping ( ocular hypertension ). These subjects may represent the extreme end of the normal range of intraocular pressure; however, a small proportion (about 1% per year) will subsequently develop glaucoma.
  4. β-blockers: timolol, cateolol, levobunolol, metipranolol. They decrease secretion but exacerbate asthma and chronic airway disease, hypotension and bradycardia Parasympathomimetics: pilocarpine, increase outflow but cause visual blurring, pupillary constriction thus darkening of the visual world and headache due to visual spasm Sympathomimetics: adrenaline, increase outflow and decrease secretion, cause redness of the eye and headache α-2 agonists: apraclonidine, increase outflow through the uveoscleral pathway, cause redness of the eye, fatigue and drowsiness Carbonic anhydrase: decrease secretion with stinging, unpleasant taste and headache Prostaglandine analogues: increase outflow but increased pigmentation of the iris and periocular skin with lengthening and darkening of the lashes Systemic carbonic anhydrase: decrease secretion with tingling of the limbs, depression, sleepiness, renal stones and SJS
  5. Procedue aims at creating a bleb in the subconjunctival space forming a fistula between the anterior chamber and the subconjunctival space Laser burns the trabecular meshwork serially to improve aqueous outflow
  6. Normally, there is some sort of resistance to aqueous flow caused by the iris partially blocking the ciliary processes In closed angle glaucoma this resistance is increased
  7. These rainbows are due to presence of mild corneal epithelial oedema which separates the regularly arranged basal epithelial cells so that they act as a diffraction grating. Any patient presenting with a history of headaches should be asked about the presence of rainbows around lights , which are a key symptom of such prodromal attacks.