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Glaucoma

Anatomy:

The trabecular meshwork:

It is a sieve-like structure at the angle of the anterior chamber through which 90% of the aqueous humour leaves the eye.It is made up of the following three portion :
The uveal meshwork is the innermost portion
The corneoscleral meshwork forms the larger middle portion
The juxtacanalicular meshwork is the outer part of the trabeculum and links the corneoscleral meshwork with the endothelium of the inner wall of the Schlem canal .This offers the major proportion of normal resistance to the aqueous outflow .
Schlemm's canal:
Is a circumferential channel in the perilimbal sclera. The inner wall of the canal (which is attached to trabecular meshwork) is lined by endothelial cells, which contain giant vacuoles. The outer wall of the canal lined by flat cells and contains the openings of the collector channels. These collector channels connected either directly or indirectly with episcleral veins.

Physiology

Aqueous humour is produced by :
Active secretion by the non pigmented ciliary epithelium .
Passive secretion by ultrafilteration and diffusion.
Aqueous flows from the posterior chamber via the pupil into the anterior chamber from where it exits the eye by two different routes :
Trabecular (conventional) routes accounts for approximately 90% of aqueous outflow .The aqueous flows through the trabeculum into the Schlemm canal and is then drained by the episcleral vein .
Uveoscleral (unconventional) route account for the remaining 10% in which aqueous passes across the face of the ciliary body into the suprachoroidal space and is drained by the venous circulation in the ciliary body ,choroid and the sclera .


The intraocular pressure (IOP)
Three factors determine the IOP
The rate of aqueous humor production by the ciliary body
Resistance to the aqueous outflow across the trabecular meshwork – Schlemm’s canal system .
The level of episcleral venous pressure .
The accepted range of IOP in the general population is 10-21 mmHg. Normal physiological variations in IOP (1-2 mmHg), varies with :Respiration ,BP, heartbeats ,Time of day (maximum in the morning).
IOP measured by:
-Indentation tonometry: Schiotz tonometry .
-Applanation tonometry: Goldmann tonometry
Glaucoma
The term glaucoma refers to a group of diseases that have in common :
A characteristic optic neuropathy
Associated visual field loss
Intraocular pressure is usually a key modifying factor .
Classification of glaucoma:
1- Congenital (developmental).
2- Acquired: divided into:
a- Open angle: this is either primary (raised IOP not associated with other ocular disorders) or secondary.
b- Angle closure: also either primary or secondary.
* We use gonioscopy to determine whether it is open angle or angle closure glaucoma, so if we see the structures of the angle, then it is open angle glaucoma, while if we do not see some or all of these structures, then the angle is closed or occludable.
* The structures that we can see normally by gonioscopy (using goniolens) in the angle are; (anterio-posteriorly) schwalbe's line, trabecular meshwork, scleral spur and anterior face of ciliary body.
The optic nerve head:
It represents the collection of 1.2 million ganglion cell axons as they pass across the retina to enter the scleral canal to form the optic nerve head (optic disc), there is no photoreceptors (blind spot).
Optic disc:
Anterior end of the optic nerve, about 1.5 mm in diameter. Lies about 3mm from the fovea. All retinal layers except the nerve fiber layer stop at the margin of the optic disc. The nerve fiber layer pass through the lamina cribrosa a sieve like structure, bridge the posterior scleral foramen.
Optic cup; central depression in the optic disc not occupied by neural tissue.
Cup/Disc ratio in most normal eyes is 0.3 or less, asymmetry of 0.2 or more is suspicion. C/D ratio assessed and calculated by:
Clinical fundal examination and fundus photograph. (crude method)
Now a day we use very sophisticated method of imaging technique called Heidelberg retinal tomography (HRT). The imaging technique is used in diagnosis and follows up of patients with glaucoma.
Ocular coherent tomography (OCT) : It give accurate measurement of nerve fibers layer changes and C\D ratio assessment.


Primary Open Angle Glaucoma (POAG)
Definition : is generally bilateral disease (although not nessessarly a symmetrical disease ) of adult onset .
characterized by :
An IOP > 21 mmHg at some stage .
Glaucomatous optic nerve damage .
An open anterior chamber angle .
Characteristic visual field loss as the damage progress
Increase IOP caused by increase resistant to aqueous outflow due to thickening of the trabecular meshwork lamellae, with reduce in the pores size.
Risk factors
1- Age: older people, after age of 65 years due to aging process and sclerosis of trabecular meshwork.
2- Race: more common and amore severe in Blacks.
3- Family history and inheritance.
Myopia: increased incidence of POAG.
D.M and vascular disease .
Diagnosis
History
Visual symptom will usually be absent , unless damage is advanced .
Previous ophthalmic history (Refractive status as myopia and causes of secondary glaucoma such as trauma or surgery or inflammation )
Family history
PMH such as asthma ,heart failure or block
Current medication (steroid and oral B-blocker ) and allergies (sulfonamide) .
Examination
Visual acuity is likely to be normal except in advanced glaucoma .
Pupil exclude relative afferent pupillary defect ,if absent then subsequently develop this indicate substantial progression .
Slit lamp examination exclude causes of secondary glaucoma such as pigmentary glaucoma .
Tonometry noting the time of the day (IOP > 21mmHg is suspicious ,fluctuation in IOP >5 mmHg in glaucoma)
Gonioscopy : Open angle
Optic disc examination : Increase in cup/disc ratio or asymmetry between two eyes of 0.2 or more is suspicion.
Perimetry : Visual field defects :
Paracentral scotoma .
arcuate scotoma .
peripheral field loss with nasal step
generalized visual loss, leaving small central vision which is lost at the end
Optic disc or peripapillary RNFL imaging : such as Heidelberg Retinal Tomography (HRT) or optical coherence tomography (OCT)
Management:
The aim of management is to reduced IOP to the target pressure (safe pressure) at which no further damage occurs.

Continuous follow up with checking IOP, examination of the optic disc and assessment of the visual field is essential.
Initially primary open angle glaucoma is treated medically with topical eye-drops, but if IOP is not reduced to the target pressure then laser therapy or surgery has to be considered .
Treatment:
Medical:
A-Beta adrenergic blocking drugs .
-Mode of action: decrease the aqueous production e.g. Timolol 0.5% eye drops
B-Topical carbonic anhydrase inhibitors;
-Mode of action: decrease the aqueous production e.g. Dorzolmide2% eye drops
C- Cholinergic drug
-Mode of action: increase the aqueous outflow e.g. Pilocarpine 2% eye drops
D- Sympathomimetics drugs;
-Mode of action: decrease the aqueous production and increase uveoscleral aqueous outflow e.g. Brimonidine 0.2% eye drops
E- Prostaglandin derivatives
-Mode of action: increase uveoscleral aqueous outflow e.g. Latanoprost eye drops
2- Laser Trabeculoplasty is a procedure by which the application of discrete burns to the trabeculum meshwork enhance aqueous outflow and lower IOP.
3- Surgical : Trabeculectomy (creating a fistula between the anterior chamber and sub-Tenon space to by pass the trabecular meshwork.
Secondary Open Angle Glaucoma
Angle is open, but the trabecular meshwork blocked by:
Blood (hyphaema) following trauma
Inflammatory cells(iritis)
Pigment from the post pigment epithelium of the iris(pigment dispersion syndrome)
Deposition of amyloid- like substance (pseudoexfoliative syndrome)
Drug induced (steroid induced glaucoma)
Ocular hypertension;
IOP>21 without optic disc cupping and visual field defect.
7% of the general population above 40 have IOP>21 only 1% of them have glaucoma.
Normal tension glaucoma;
patients with IOP= or <21mmHg with optic disc cupping and visual field defect. Treatment as POAG .


Primary angle closure glaucoma (PACG)
Definition : Is a condition in which elevation of IOP occurs as a result of obstruction of the aqueous drainage by closure of the angle with the peripheral iris.
Unlike POAG, the diagnosis is by examination of anterior segment and gonioscopy. Presence of a normal optic disc and absence of visual field loss does not preclude (exclude) diagnosis of PACG (as it is acute so the damage doesn’t occur unless the condition left without treatment and blindness happen within few days or even hours). In addition, there are shallow AC and convex iris-lens diaphragm.
Risk factors:
1- Age: average age 60 years, it does not occur before this age, as the AC is still deep.
2- Gender: ♀/♂ = 4/1.
3- Race: whites 6% of glaucomas, more common in South East Asians, Chinese and Eskimos, uncommon in Blacks.
4- Family history: ocular anatomical features are inherited, 1st degree relatives are at increased risk.
Anatomical predisposing factors:
1- Relative anterior location of iris-lens diaphragm.
2- Shallow anterior chamber (AC).
3- Narrow entrance to anterior chamber angle.

Mechanism of angle closure

In most cases PCAG is initiated by;
a- Pupillary Block : which is increase resistance to aqueous passage between posterior and anterior chamber by the iris lens contact .
b- Iris bombe : increase pressure in the posterior chamber, the peripheral iris will bow forward
c- Irido-corneal contact : obstructing the angle .
If this peripheral irido-corneal contact persist for few days then permanent peripheral anterior synachae (PAS) occurs
Classification of PACG:
1- Latent PACG: the asymptomatic phase of PACG.
Signs: slit-lamp examination:
Shallow anterior chamber.
Convex-shaped iris-lens diaphragm.
Close proximity of iris to cornea.
Normal IOP.
Gonioscopy: shows an occludable angle
Management:
An eye that has latent PACG (which is detected by routine examination ± family history) needs bilateral YAG laser PI (peripheral iridotomy) as prophylactic treatment.
If no treatment done the following may happen:
a- Remain normal for long life.
b- Acute or intermittent PACG.
c- Develop chronic PACG without passing through acute or sub-acute phase.


2- Subacute ( Intermittent) Angle Closure Glaucoma
A transient attack of sudden subtotal closure of the angle results in rapid increase in IOP, followed by spontaneous reopening of the angle with the IOP returns to normal.
Symptoms
The attack may be precipitated by physiological mydriasis (dilation of the pupil) e.g. watching T.V. in dark room
Sudden onset of
1-Blurring of vision
2-Halloes around light due to corneal edema
3- Sometimes eye-ache or headache
The attack may last for 1-2 hours and usually broken by miosis (constriction of the pupil) e.g. exposure to bright light.
Signs
During the attack
Corneal edema
Shallow anterior chamber
Elevated IOP
Between the attacks : The eye looks normal apart from narrow angle
Treatment
Laser iridotomy to create an opening between the posterior chamber and anterior chamber and bypass the pupillary block
Both eyes must be treated with Laser iridotomies
3- Acute Angle Closure Glaucoma
Sudden total closure of the angle with rapid high increase in IOP.
Symptoms
Onset : Sudden
Periocular pain and headache
Bluring of vision
Halloes around light due to corneal edema
Redness of the eye
Sometimes nausea and vomiting
Signs
Cicum-corneal congestion
Corneal edema
Shallow anterior chamber
Mid-dilated ,fixed pupil
IOP elevated (>50 mmHg)
Treatment
Admission to the hospital
Medical treatment :
Systemic Carbonic anhydrase inhibitors, initially Acetazolamide 500mg i.v. followed by 250 mg orally qds.
Topical 2% pilocarpine qds.
Topical 0.5% timolol bds.
Topical steroid: to avoid permanent adhesion between the periphery of iris and the cornea (peripheral anterior synechia)( PAS).
If IOP still high after one hour then hyper osmotic agent is given : 20% mannitol 1-2 gm/kg i.v. over 45 minutes
After reducing IOP medically treatment is essentially by laser iridotomy in early cases without established PAS (to create an opening between the posterior chamber and anterior chamber and by pass the pupillary block).
While in late cases with PAS, treatment is with surgical trabeculotomy to create an opening between the anterior chamber and sub-conjunctival space and by pass the PAS.
The other eye must be prophylactically treated with laser iridotomy.
Secondary Closed Angle Glaucoma
1- Lens-related glaucoma
2- Neovascular glaucoma
3- Inflammatory glaucoma
4- Intra ocular tumor may push iris lens diaphragm forward and closing the angle
1- Lens-related glaucoma:
a- Phacolytic glaucoma (lens protein glaucoma):
Is occur in association with hypermature cataract (leakage of lens materials and shrinkage of lens). Leaked lens material is engulfed by macrophages. The trabecular obstruction is caused by high molecular weight lens proteins which have leaked through the intact capsule into the aqueous humour or by macrophages laden with these proteins.
Treatment: control IOP medically, then surgery (cataract extraction).


b- Phacomorphic (Intumescent) glaucoma:
Is acute secondary angle-closure glaucoma precipitated by an intumescent cataractous lens. Swelling of lens pushes the lens-iris diaphragm forward to occlude the angle of the anterior chamber. Presentation is the same like that of PACG but with cataract.
Treatment: surgery (cataract extraction).
c- Phacoanaphylactic (phacoantigenic) glaucoma:
Is an autoimmune reaction to lens proteins occurring in an eye with a traumatic ruptured anterior capsule (large lens matter passing through a rupture in capsule, this matter is regarded as foreign body and antibodies against it is produced). Therefore, there will be occlusion of the pores of trabecular meshwork by immune complexes and cells.
Treatment: cataract extraction.
2- Neovascular glaucoma (NVG):
Is a relatively common and serious condition, which occurs as a result of iris neovascularization (Rubeosis iridis).
The common aetiopathogenic factor is severe, diffuse and chronic retinal ischaemia.
Retinal ischaemia leads to hypoxic retina which tend to produces vasoproliferative growth factors in an attempt to revascularize hypoxic areas (form new blood vessels to compensate for hypoxia), but unfortunately these blood vessels are very fragile, so they may rupture suddenly and patient get sudden blindness due to retinal or vitreous hemorrhage. These vessels may rupture spontaneously or during valsalva manoeuvre. However, these factors also diffuse in to the anterior segment and initiate Rubeosis iridis (neovascularization of iris) and neovascularization in the angle of the anterior chamber (leading to occlusion of trabecular meshwork).
Causes of retinal ischaemia (causes of NVG):
a- Central retinal vein occlusion. (commonest cause)
b- Diabetes mellitus (proliferative diabetic retinopathy).
c- miscellaneous, e.g.: - Carotid obstructive disease.
- Central retinal artery occlusion.
- Intraocular tumours.
- Long standing retinal detachment.
- Chronic intraocular inflammation.
Treatment:
Medical treatment is initially with topical beta-blockers and acetazolamide. Topical atropine and steroids may decrease inflammation and make the eye more comfortable and less congested, even if IOP remains high.
Panretinal photocoagulation with laser: We destruct retinal tissue in order to decrease O2 consumption and control hypoxia. We photcoagulate the mid periphery and the periphery of retina and we preserve the macula only.
Filteration surgery may be consider if still there is useful vision either by trabeculectomy with anti metabolite or by use artificial filtering shunts.
Cyclodestruction by trans scleral diode laser or trans scleral cyclocryotherapy which lead to destructs part of Ciliary body and decrease aqueous production.
Retrobulbar alcohol injection is useful in relieving pain by destruction of sensory innervation.
Enucleation (evacuation of all intraocular contents and we leave just the sclera) may be considered if all else fails.
3- Inflammatory glaucomas
Glaucomas secondary to intraocular inflammation
In acute anterior uveitis, the IOP is usually normal or subnormal as a result of concomitant ciliary shutdown. Occasionally, however, a trabecular-block open angle glaucoma develops secondary to obstruction of aqueous outflow, most commonly just as the acute inflammation is and ciliary body function returning to normal. The block may be caused by either inflammatory cells and debris or acute trabeculitis. The IOP usually returns to normal once the inflammation has subsided.
Secondary angle closure is caused by 360° iridolenticular adhesions (seclusio pupillae), The pupil block obstructs the passage of aqueous humour from the posterior to the anterior chamber, and the increased pressure in the posterior chamber causes an anterior bowing of the peripheral iris (iris bombé), If severe, iris bombé is associated with a shallowing of the anterior chamber, and apposition of the peripheral iris to the trabeculum and peripheral cornea. If this occurs in an eye with active inflammation, the iris sticks to the trabeculum and the iridocorneal contact becomes permanent with the development of peripheral anterior synechiae (PAS).
Slit lamp examination shows seclusio pupillae, iris bombé and a shallow anterior chamber.
Gonioscopy shows angle closure from iridotrabecular contact.
Treatment involves the following measures:
Prevention of synechial angle closure can be effective by a reduction in the 'stickiness' of the peripheral iris using a combination of intensive topical steroids and anterior sub-Tenon's injection of a long-acting depot steroid preparation.
Lowering of IOP with topical ß-blockers and/or sympathomimetics may be effective in relatively mild cases where the IOP is <30 mmHg. Carbonic anhydrase inhibitors are usually required if the IOP is >30mmHg.
Nd-YAG laser iridotomy may be required if medical therapy fails, It will only eliminate the element of pupil block and will therefore only be effective in lowering IOP, if at least 25% of the angle is still open.
Congenital glaucomas
They are uncommon (not rare), sever and potentially blinding disease.
Types:
1- True congenital glaucoma: represents (40%) of all congenital glaucoma, the IOP is elevated during intra-uterine life.
2- Infantile glaucoma: represents (55%) of congenital glaucomas, the disease is manifested before 3 years age, but the patient was born with normal IOP.
3- Juvenile glaucoma: represents (5%) of congenital glaucomas, least common, present after 3 years but before reaching 16 years (>16 → adult glaucoma).
In general, congenital glaucoma:
- Occurs 1 in 10,000 births.
- Most cases are sporadic, some are inherited as autosomal recessive trait.
- 65% in boys and 35% in girls.
- Bilateral in 75% and 25% unilateral.


Aetiology:
Anterior segment dysgenesis, defect in cleavage during fetal development, so we have abnormal angle and abnormal development of anterior chamber, so there will be no trabecular meshwork and the angle is completely obstructed.
Clinical Features:
The first sign noticed by parents is the corneal haze:
1- Corneal haze (or opacity): caused by epithelial oedema and corneal clouding secondary to elevated IOP.
2- Photophobia, lacrimation and blepharospasm: due to damage of corneal endothelium producing corneal oedema.
3- Buphthalmus: a large eye due to elevated IOP prior to the age of 3 years, so we should expect elevated IOP in every child with large eye below age of 3 years.
- Sclera also enlarges becoming stretched and takes blue appearance due to the enhanced visualization of underlying uvea.
- Corneal enlargement leading to deep AC (Anterior chamber), zonule becomes stretched, rarely lens becomes subluxated.
- Ocular enlargement leads to axial myopia.
4- Breaks in Descemet's membrane (due to stretching).
5-Optic disc cupping, C/D >0.3, it is not a reliable sign, as stretching of sclera will cause enlargement of scleral canal and cupping due to separation of nerve fibers, and as soon as we control IOP, C/D will return to normal.
* The intraocular pressure should be check under general anesthesia by using Perkins hand-held applanation tonometer or Tonopen tonometer.
Management: is always surgical, and surgery should be done as early as possible.
Diagnosis:
Signs.
1- Checking IOP.
2- Corneal diameter: normally, corneal diameter at delivery is ≤ 10 mm, if corneal diameter was > 12mm at age of 1 year, or 13mm at any age, then it is viewed with suspicion. In children, corneal diameter is regarded as visual field assessment in adults to follow patients with glaucoma.
Surgery:
1- Goniotomy. We incised the trabecular meshwork to create a direct communication between the anterior chamber and schlemm's canal bypassing the trabecular meshwork, this operation needs clear cornea to use the instruments and visualized the structures of the angle of the AC. successful rate is 80%.
2- Trabeculotomy. From the limbus, we introduce a probe inside the schlemm's canal and then we open the inner wall of it toward the AC. Also here there is a direct communication between the anterior chamber and schlemm's canal bypassing the trabecular meshwork
3- Trabeculectomy





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