Glaucoma presentation for ophthalmology course, presented as a student seminar. Class location: ophthalmology unit, An-Najah National University Hospital.
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
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
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.
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 ).
Second to cataract
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.
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
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
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
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.