b20m02l04 glaucoma edited

GLAUCOMA BLOCK 20

Lecturer: Dr. Enano MODULE 02

Date: March 9 , 2016 LECTURE 4

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OUTLINE Glaucoma

Aqueous Secretion

Aqueous Outflow Pathway

Pathogenenesis of Glaucomatous Damage

Normal IOP Determination Tonometry

Gonioscopy

Perimetry

Glaucoma Classification I.Open Angle Glaucoma

- Primary - Secondary

Pretrabecular

Trabecular

Post trabecular II. Normal Tension Glaucoma (NTG) III. Angle Closure Glaucoma - Primary - Secondary

Glaucoma Drugs

GLAUCOMA

- Includes a complex of eye diseases which have in common an abnormal intraocular pressure that causes organic changes in the optic nerve and produces irreversible blindness through progressive loss of the field of vision

- Many forms are asymptomatic as they destroy the optic nerve.

- Primary angle glaucoma (most common in blacks and whites) causes insidious asymptomatic progressive bilateral visual loss that is not detected until extensive field loss has already occurred.

- If detected and IOP is reduced to normal by medication or surgery, the progression of blindness can be stopped.

- Can only halt progression; cannot return origin state of vision; IRREVERSIBLE

- In the broadest terms, glaucoma involves a study of the following:

1. IOP (intraocular pressure) 2. Optic nerve head damage 3. Visual field loss 4. Drainage angle

- Classical presentation is increased IOP. However, there

are glaucomas with normal IOP but still with destruction of optic nerve.

Glaucoma usually refers to the optic nerve and the

iridocorneal angle. When we talk of glaucoma, we always refer to the iridocorneal angle.

ANATOMIC FEATURES OF THE ANGLE: Schwalbe’s line

- peripheral termination of the Descemet’s membrane and anterior limit of the trabeculum

- most anterior structure of the angle structures, appearing whitish to variably pigmented

- corneal wedge is useful in locating an inconspicuous Schwalbe line

Trabecular meshwork - a sieve-like structure through which the aqueous

leaves the eye Ciliary body band

- stands out just behind the scleral spur as a pink, dull brown or slate grey band

Sclera spur - most anterior projection of the sclera - serves as the attachment for the longitudinal

muscles of the ciliary body - as a general principle, any blood vessel that

crosses the scleral spur onto the trabecular meshwork is abnormal

Schlemm’s canal - a circumferential canal that goes around the eye

and drains the aqueous - may be identified in the angle, especially if non-

pigmented, as a slightly darker line deep to the posterior trabeculum

The trabecular meshwork (trabeculum) is a sieve-like structure at the angle of the anterior chamber through which 90% of aqueous humor leaves the eye. It has three components:

Uveal meshwork - innermost portion, consisting of cord-like

endothelial cell-covered strands arising from the iris and ciliary body stroma

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- intertrabecular spaces are relatively large and offer little resistance to the passage of aqueous

Corneoscleral meshwork - lies external to the uveal meshwork to form the

thickest portion of the trabeculum - composed of layers of connective tissue strands

with overlying endothelial-like cells - intertrabecular spaces are smaller than those of

the uveal meshwork, conferring greater resistance to flow

Juxtacanalicular (cribriform) meshwork - outer part of the trabeculum - links the corneoscleral meshwork with the

endothelium of the inner wall of the canal of Schlemm

- consists of cells embedded in a dense extracellular matrix with narrow intercellular spaces, and offers the major proportion of normal resistance to aqueous outflow

These structures are appreciated using gonioscopy.

AQUEOUS SECRETION

1. ACTIVE SECRETION

80% of aqueous production

Aqueous secreted by the non-pigmented ciliary epithelium via an active metabolic process that is dependent on a number of enzymatic systems

2. PASSIVE SECRETION

20% of aqueous production

Aqueous produced by passive process such as ultrafiltration and diffusion which are dependent on the level of blood pressure in the ciliary capillaries, the plasma oncotic pressure and the level of IOP

Secretion is diminished by:

Drugs - β-blockers, sympathomimetics, carbonic anhydrase

inhibitors

Cyclodestructive Procedures - destruction of ciliary bodies

Ciliary Body Shutdown - detachment of ciliary body (usually in trauma),

inflammation of secretory ciliary epithelium in iridiocyclitis and retinal detachment

AQUEOUS OUTFLOW PATHWAY

A. Conventional (Trabecular) route

90% of aqueous flow

Aqueous produced by the ciliary epithelium is secreted into the posterior chamber anterior chamber passing through the pupil anterior chamber angle fenestrated layers of the trabecular meshwork Schlemm’s canal venous tributaries venous circulation of the eye

This is a bulk flow pressure-sensitive route so that increasing IOP will increase outflow.

B. Unconventional (Uveoscleral) Route

Remaining 10%

Aqueous passes across the ciliary body into the suprachoroidal space and is drained by the venous circulation in the ciliary body, choroid and sclera

Note: some aqueous drains via the iris

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PATHOGENESIS OF GLAUCOMATOUS DAMAGE

A. Ischemic Theory

Compromise of the microvasculature of the axons in the optic nerve head plays a role in the pathogenesis of glaucomatous damage

Possible mechanisms: 1. Loss of capillaries 2. Alteration of capillary blood flow 3. Changes that interfere with the delivery of

nutrients or removal of metabolic products from the axons

4. Failure of regulation of blood flow 5. Delivery of injurious vasoactive substances to

blood vessels of the optic nerve head B. Direct Mechanical Theory

Elevated IOP directly damages the retinal nerve fibers as they pass through the lamina cribrosa

The increase in IOP directly damages the optic nerve head.

DETERMINATION OF NORMAL IOP

1. Rate of aqueous secretion 2. Resistance encountered in outflow channels 3. Level of episcleral venous pressure

The rate of aqueous outflow is proportional to the IOP minus the episcleral venous pressure.

The distribution of IOP within the general population has a range of 10-21 mmHg o Values exceeding 21 mmHg can already be

considered glaucomatous

Normal IOP varies with the time of day, heartbeat, blood pressure level and respiration o IOP has a tendency to be higher in the morning and

lower in the afternoon and evening

o Mean range of diurnal IOP fluctuations in normal eyes is 5 mmHg (>5 suspect glaucoma)

o When suspecting a patient to be glaucomatous, check IOP around the clock (every 2 hrs for 24 hours). We take diurnal pressure.

DIAGNOSTICS

1. Tonometry 2. Gionioscopy 3. Perimetry

TONOMETRY

1. Goldmann Applanation Tonometry

Arrow: yellow green half-moon are called mires- end

point when taking IOP: With the aid of fluorescein dye, one can see 2 half-moons (mires); reading done when the inner lips of the 2 half-moons are touching

Gold standard

Measures the force applied per unit area

IOP is proportional to the pressure applied to the radius of curvature of the globe (cornea) and thickness of the globe

Device attached to a slit-lamp

Needs topical anesthetic

Blue light used in order to see the fluorescein dye

Based on the Imbert–Fick principle, which states that for a dry thin-walled sphere, the pressure (P) inside the sphere equals the force (F) necessary to flatten its surface divided by the area (A) of flattening (P = F/A)

The reading on the dial, multiplied by 10, gives the IOP

Mire thickness should be around 10% of the diameter of its total arc. If too thick or thin, it can be a source of error.

2. Schiotz Tonometry

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Indentation tonometry: a plunger with a preset weight indents the cornea

Handy and cheap

Utilizes pre-set weights

Needs topical anesthetic

Scale is in grams since we use weights; conversion table needed to convert reading to mmHg

3. Perkins Tonometry

Hand-held applanation tonometer which uses a Goldmann prism adapted to a small light source

Same as Goldmann, but prism is attached to a hand held device

Can therefore be used in bed- bound or anaesthetized patients

4. Air-Puff Tonometry

Does not require the use of anesthetic since it does not touch cornea

Noncontact tonometer which uses the Goldmann applanation principle but instead of using a prism, the central part of the cornea is flattened by a jet of air

5. Tono-pen

Handheld , self-contained, battery-powered, miniature

portable tonometer

Correlates with the Goldmann although it slightly overestimates a low IOP and underestimates a high IOP

Can take measurements in an eye with distorted or edematous cornea, as well as through a bandage contact lens

Not very accurate

4. Digital Palpation

using digits to palpate cornea covered by eyelids

lips consistency: soft

tip-of-the-nose: firm

forehead: hard GONIOSCOPY

Diagnostic: to identify abnormal angle structures and to estimate the width of the chamber angle

Surgical: to visualize the angle during procedures such as laser trabeculoplasty and gonitomy

Important in glaucoma screening because it evaluates the angle (visualizes anatomic structures)

Optical principles

The angle of the AC cannot be visualized directly through the intact cornea because light from angle structures undergoes ‘total internal reflection’ at the anterior surface of the precorneal tear film.

Because the refractive index of a goniolens is similar to that of the cornea, it eliminates total internal reflection by replacing the tear film–air interface with a tear film–goniolens interface. Light rays can then be viewed as they exit the contact lens, directly or indirectly.

TYPES OF GONIOLENSES 1. INDIRECT

Provides a mirror image of the opposite angle and can be used only in conjunction with a slitlamp for diagnostic purposes

Uses a mirror to reflect rays from the angle such that they exit the goniolens at much less than the critical angle

a. Goldmann 3-mirror goniolens - Most commonly used - Non-indentation gonioscopy - 12 mm surface area that when placed on

globe stabilizes the globe - Contact surface is steeper than cornea so it

needs a viscous material to make lens stick to the cornea

- Has a thinner curvature compared to the cornea, therefore, a more viscous coupling substance (gel) which has the same refractive power as the cornea is needed to bridge the gap between the cornea and lens

- Utilizes topical anesthetic b. Zeiss 4-mirror goniolens

- Attached to angle compared to Posner which is not

c. Posner 4-mirror goniolens - Both Zeiss and Posner have flatter

curvatures compared to the cornea, therefore, they do not need a coupling substance and can use only tears

- Uses anesthetic - Can view the entire angle of the eye

Zeiss and Posner 4-mirror goniolens

examples of indentation (dynamic, compression) gonioscopy

their lenses do not stabilize the globe and are relatively unsuitable for laser trabeculoplasty

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2. DIRECT

Provides a direct view of the angle and can be used for both diagnostic and surgical purposes

Does not require a slitlamp and used with patient in supine position typically under general anaesthesia in the evaluation and surgical treatment of infantile glaucoma

This approach is called ‘direct’ because light rays from the angle are viewed directly, without reflection inside the lens.

a. Koeppe - Dome-shaped goniolens which comes in

several sizes - Provides a panoramic view of the angle - Can use strong source of light - Usually used during surgery

b. Swan-Jacob - Surgical goniolens which is held on the

cornea by a handle PERIMETRY

A method of evaluating the visual field - At our level, we use confrontation test

Examples: Humphrey perimeter, Octopus o Patient looks at a screen with flashing lights; he

presses a button every time he sees a light. o 2 most commonly used types

Standard automated perimetry (SAP) is the method used routinely in most clinical situations.

Most important defects in glaucoma occur centrally – within a 30° radius from the fixation point – so this is the area most commonly tested.

Other Imaging Procedures

Optical Coherence Tomography (OCT)

Heidelberg Retinal Tomography (HRT)

GDx Nerve Fiber Analyzer Used to view and evaluate the actual status of optic

nerve Not regularly used; those that are commonly used and

often adequate to diagnose glaucoma: tonometry, gonioscopy, and perimetry

The Shaffer system records the angle in degrees between two imaginary lines tangential to the inner surface of the trabeculum and the anterior surface of the iris about one-third of the distance from its periphery.

GRADING OF ANGLE WIDTH

GRADE ANGLE DESCRIPTION

Grade 4 35-45° Widest angle, ciliary body can be visualized with ease characteristic of myopia and pseudophakia

Grade 3 25-35° Open angle in which the scleral spur can be identified

Grade 2 20° Moderately narrow angle in which only the trabeculum can be identified

Grade 1 10° Very narrow angle in which only the Schwalbe line can be identified

Slit Angle No obvious iridocorneal contact but no angle structures can be identified

Grade 0 0° Closed angle due to iridocorneal contact

Wide open angle, Grades 3-4 Moderately narrow angle, Grade 2

Extremely narrow angle, Grade 1 Angle closure, Grade 0

Other Systems

Spaeth system allows formal description of the position of iris insertion, the angular approach and peripheral iris curvature.

Scheie classification refers to the angle structures visible and allocates a Roman numeral accordingly. In contrast to common clinical use, in the original system a higher numeral (e.g. IV) actually signifies a narrower angle.

Van Herick method uses the slit lamp alone to estimate the AC angle width

CHANGES IN GLAUCOMA Glaucomatous damage results in characteristic signs involving (a) the optic nerve head, (b) the peripapillary area and (c) the retinal nerve fibre layer. Subtypes of Glaucomatous Damage

Focal ischemic discs- characterized by localized superior and/or inferior notching and may be associated with localized field defects with early threat to fixation.

Myopic disc with glaucoma - refers to a tilted (obliquely inserted), shallow disc with a temporal crescent of parapapillary atrophy, together with features of glaucomatous damage. Dense superior or inferior scotomas threatening fixation are common. This

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morphology is most common in younger male patients.

Sclerotic discs - characterized by a shallow, saucerized cup and a gently sloping NRR, variable peripapillary atrophy and peripheral visual field loss. Patients are older, of either gender, and there is an association with systemic vascular disease.

Concentrically enlarging discs - characterized by fairly uniform neural retinal rim (NRR) thinning and are frequently associated with diffuse visual field loss.

Other Disc Signs of Glaucomatous Damage:

Disc hemorrhages - often extend from the NRR onto the retina, most commonly inferotemporally. Their presence is a risk factor for the development and progression of glaucoma.

Baring of circumlinear blood vessels - a sign of early thinning of the NRR. It is characterized by a space between the neuroretinal rim and a superficial blood vessel.

Bayoneting - characterized by double angulation of a blood vessel

Collaterals between two veins at the disc, similar to those following central retinal vein occlusion (CRVO), are relatively uncommon.

Loss of nasal NRR - a sign of moderately advanced damage

Laminar dot sign - occurs in advancing glaucoma. Grey dot-like fenestrations in the lamina cribrosa become exposed as the NRR recedes

‘Sharpened edge’ or ‘sharpened rim’ - a sign of advancing damage. As NRR is lost adjacent to the edge of the disc, the disc margin contour assumes a sharper angle backwards

Peripapillary Changes Peripapillary atrophy (PPA) surrounding the optic nerve head may be of significance in glaucoma, and may be a sign of early damage in patients with ocular hypertension.

Alpha (outer) zone - characterized by superficial retinal pigment epithelial changes. It tends to be larger and possibly more common in glaucomatous eyes

Beta (inner) zone - characterized by chorioretinal atrophy. It is larger and more common in glaucoma, and is a risk factor for progression

CLASSIFICATION OF GLAUCOMA

According to manner by which aqueous outflow is impaired Most commonly used classification

o Open-angle o Angle-closure

Presence or absence of associated factors contributing to the rise in IOP

o Primary o Secondary

According to Onset o Congenital o Infantile o Juvenile o Adult

OPEN ANGLE GLAUCOMA

I. PRIMARY OPEN ANGLE GLAUCOMA

Generally bilateral, although not generally symmetrical, characterized in at least one eye by the following:

o Adult-onset o An IOP > 21 mmHg at some point in the course

of the disease o An open angle of normal appearance o Glaucomatous optic nerve head damage o Visual field loss

Normal cup-disc ratio: 0.3-0.4 >/+0.5 – suspect glaucoma

POAG is the most prevalent type of glaucoma in individuals of European and African ethnic origin.

POAG has been associated with at least 20 loci in the human genome, but mutations in only the MYOC gene, coding for the protein myocilin that is found in the trabecular meshwork, and the OPTN gene, which codes for optineurin, are broadly accepted as causing glaucoma.

RISK FACTORS o IOP: The higher the IOP, the greater the likelihood of

glaucoma. Asymmetry of IOP of 4 mmHg or more is also significant.

o Age: older individuals o Race: four times more common, develops at an earlier

age and may be more difficult to control in black individuals than in whites

o Family history of POAG: first-degree relatives of patients o Diabetes Mellitus o Myopia: may be more susceptible to glaucomatous

damage. It is speculated that this may be due to mechanical factors, particularly the region of the optic disc.

o Long-term OCP use o Vascular disease: hypertension, cardiovascular disease,

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diabetes and vasospastic conditions such as migraine o Translaminar pressure gradient: difference in the levels

of IOP and orbital CSF pressure may increase the likelihood of the development and progression of glaucomatous damage, perhaps due to associated deformation of the lamina cribrosa

o Optic disc area: large discs may be more vulnerable to damage

o Ocular perfusion pressure: difference between the arterial BP and IOP

o Steroid responsiveness Pathogenesis of glaucomatous optic neuropathy Retinal ganglion cell death in glaucoma occurs predominantly through apoptosis (programmed cell death) rather than necrosis. One or both of the following mechanisms may be involved: 1) direct mechanical damage to retinal nerve fibres at the optic nerve head, perhaps as they pass through the lamina cribrosa; 2) ischaemic damage, possibly due to compression of blood vessels supplying the optic nerve head; this may relate to ocular perfusion pressure as a possible risk factor for glaucoma; 3) common pathways of damage.

II. SECONDARY OPEN ANGLE GLAUCOMA 1. Pre-Trabecular Glaucoma

- aqueous outflow is obstructed by a membrane covering the trabeculum : o Fibrovascular tissue (e.g. neovascular glaucoma) o Endothelial cellular membranous proliferation (e.g.

iridocorneal endothelial syndrome) o Epithelial cells (e.g. epithelial ingrowth)

2. Trabecular Glaucoma

- obstruction occurs as a result of clogging up of the meshwork and secondary degenerative changes o Pigment particles (e.g. pigmentary glaucoma)

Pigments come from iris o Red blood cells (e.g. red cell glaucoma) o Hemolyzed red cells (e.g. ghost cell glaucoma) o Macrophages (e.g. phacolytic glaucoma) o Proteins (e.g. acute anterior uveitis) o Pseudoexfoliative material (e.g. pseudoexfoliation

glaucoma- white grey fibrogranular structure which deposits in and around the anterior chamber )

Both pre-trabecular and trabecular glaucomas occur in trauma

3. Post-Trabecular Glaucoma

- trabeculum is normal but aqueous outflow is impaired due to elevated episcleral venous pressure o Carotid—cavernous fistula and dural shunts o Sturge-Weber syndrome o Obstruction of the superior vena cava

- Nasalization of vessels – vessels pushed to the nasal side

SYMPTOMS

Asymptomatic until a significant visual field loss has occurred

Initial visual field loss: nasal field - Indicates that temporal part of optic nerve head was

damaged first

Rare: eye pain, headache, halos due to transient corneal epithelial edema-more common in angle closure glaucoma

SIGNS

Raised IOP, fluctuations in IOP

Optic disc changes

Glaucomatous field changes

Open angle on gonioscopy - most important for diagnosis

EVALUATION

History and physical examination

Visual acuity

Slit lamp biomicroscopy

Tonometry: note time of day

Gonioscopy

Ophthalmoscopy: note appearance of the disc

Check visual fields/perimetry MANAGEMENT Medical Therapy

Topical β-blocker

Prostaglandin analogues

Carbonic anhydrase inhibitor

Alpha-agonist

Miotics

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Laser Trabeculoplasty

Application of discrete burns to the trabeculum enhancing aqueous outflow and lowers IOP o For uncontrolled glaucoma o Primary therapy for patients with poor

compliance to medical therapy (drugs are extremely expensive)

o Intolerance of topical medication including allergy

o Failure of medical therapy, as a less aggressive treatment measure than surgery

Trabeculectomy

Conventional filtering (drainage) procedure by creating a new channel (fistula) for aqueous outflow between the anterior chamber and sub-Tenon space without the use of an artificial device

Indications: o Failed medical therapy and laser trabeculoplasty o Lack of stability for laser therapy due to:

Poor patient cooperation

Inability to adequately visualize the trabeculum due to narrow angle or corneal opacification

o Eyes with advanced disease (very low IOP is required)

Trabeculectomy is the surgical procedure most commonly performed for POAG.

Laser Iridotomy

used principally in the treatment of primary angle closure, but may also be indicated in secondary angle closure with pupillary block

Laser Iridoplasty

performed to widen the anterior chamber angle by contraction of the peripheral iris away from the angle recess

can be used to attempt to break an episode of acute angle closure, but is more commonly applied on an elective basis, for example in plateau iris syndrome

NORMAL TENSION GLAUCOMA (NTG)

Low tension glaucoma

Used to describe a type of primary open angle glaucoma (POAG)

Characteristics:

o A mean IOP <21 mmHg on diurnal testing o Glaucomatous optic disc damage and visual field loss o Open angle on gonioscopy o Absence of secondary causes for glaucomatous optic

disc damage o Visual field loss as damage progresses, consistent in

pattern with the nerve appearance Risk factors

o Age: elderly o Gender: females greater risk at 2:1 ratio o Race: more common in Japan than in either Europe

or North America o Family history: mutations in the OPTN gene o Central corneal thickness (CCT): lower in patients

with NTG than POAG. o Abnormal vasoregulation: migraine and Raynaud

phenomenon o Systemic hypotension o Obstructive sleep apnea syndrome o Higher autoantibody levels o Larger translaminar pressure gradient o Myopia: associated with a greater likelihood of

glaucoma and of its progression. o Thyroid disease

Clinical Features o Normal IOP but is usually the high teens (18, 19…) o Optic nerve head is larger in NTG than in POAG and

incidence of splinter hemorrhages at the disc margin is higher in NTG

o Peripapillary atrophic changes may be more prevalent

o Visual field defects are essentially the same as in POAG

o Others

Peripheral vascular spasm

Migraine headaches

Nocturnal systemic hypotension

Overtreated systemic hypertension

Reduced blood flow velocity in the ophthalmic artery when measured with transcranial Doppler ultrasonography

Paraproteinemia and the presence of serum autoantibodies

Management o Take History and PE o Reduction of IOP (indicated only in patients with

documented progressive visual loss with the aim to reduce IOP by at least 30%)

o Systemic calcium channel blockers (considered in younger patients and in those with early disease)

o Monitoring of systemic BP for 24 hrs (if a significant nocturnal drop is detected, medication for hypertension should be avoided)

ANGLE CLOSURE GLAUCOMA

Glaucoma due to obstruction of trabecular meshwork by peripheral iris = iridotrabecular contact (ITC)

May be primary or secondary, with or without pupillary block

May be acute, subacute, intermittent or chronic

Typically associated with greater rapidity of progression and visual morbidity than POAG

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Diagnosed if: o (+) ITC in three or more quadrants, with

glaucomatous optic neuropathy o Optic nerve damage from an episode of severe

IOP elevation, such as acute angle closure, may not appear as typical glaucomatous cupping

MECHANISMS 1. Relative pupillary block

- Failure of physiological aqueous flow through the pupil leads to a pressure differential between the anterior and posterior chambers, with resultant anterior bowing of the iris.

- Usually anatomically relieved by iridotomy, which equalizes anterior and posterior chamber pressure.

- A large lens vault is independently associated with angle closure, though it is not clear whether this is entirely via a pupillary block or non-pupillary block (see next) mechanism, or both.

2. Non-pupillary block - Seen in Far Eastern patients - Associated with a deeper anterior chamber (AC) than

pure pupillary block - Patients with non-pupillary block, particularly those with

plateau iris, tend to be younger than those with pure pupillary block.

- An element of pupillary block is invariably present, but angle closure is not fully relieved by iridotomy.

- Specific anatomical causative factors include plateau iris (anteriorly positioned/rotated ciliary processes), and a thicker or more anteriorly positioned iris; a ‘thick peripheral iris roll’ concept has been introduced by some authorities.

- Plateau iris configuration - characterized by a flat or only slightly convex central iris plane. A characteristic ‘double hump’ sign is seen on indentation gonioscopy.

- Plateau iris syndrome - describes the persistence of gonioscopic angle closure despite a patent iridotomy in a patient with morphological plateau iris.

3. Lens-induced angle-closure - angle closure that is predominantly lens-induced or due

to a retrolenticular cause is often categorized as secondary

4. Retrolenticular - malignant glaucoma (‘ciliolenticular block’) - posterior segment causes of secondary angle closure

5. ‘Combined mechanism’ 6. Reduced aqueous outflow associated with:

o Appositional obstruction by the iris. o Degeneration of the TM itself due to chronic or

intermittent contact with the iris or damage sustained due to elevated IOP.

o Permanent occlusion of the TM by PAS; the

prognosis for IOP control correlates well with the extent of PAS.

RISK FACTORS

Age: relative pupillary block = 60 years at presentation; non-pupillary block = younger age

Gender: F>M

Race: Far Eastern and Indian Asians

Family history

Refraction: eyes with ‘pure’ pupillary block are typically hypermetropic, although this is not as clear-cut with non-pupillary block, which can occur in myopic eyes.

Axial length: short eyes tend to have a shallow AC; eyes with nanophthalmos have a very short eye with a proportionally large lens and are at particular risk.

I- Primary Angle Closure Glaucoma with Pupillary Block

Lens-iris apposition which interferes with aqueous flow and causes the iris to bow forward and occlude the trabecular meshwork

- Imagine the lens sticking to the iris-> aqueous can’t flow from posterior chamber to anterior chamber

II- Primary Angle Closure Glaucoma without Pupillary Block

Plateau-iris syndrome–rare cause of angle closure glaucoma in which iris is attached anteriorly to the ciliary body so when the pupil dilates iris becomes bunched up occluding the trabecular meshwork so when you look at the eye, you can see the anterior chamber is normal but the iris is flatter than convex

- Ciliary body is larger than normal and positioned anteriorly, thereby altering the position of the iris against the cornea; it pushes the iris anteriorly

Vaughan: Plateau iris syndrome is an uncommon condition in which the central anterior chamber depth is normal but the anterior chamber angle is very narrow owing to a congenital high insertion of the iris.

Affected individuals present with acute angle-closure glaucoma at a young age. Long term miotic therapy or laser iridoplasty is required

III- Secondary Angle Closure Glaucoma with Pupillary Block

Lens-induced (e.g. phacomorphic = dislocated lens) - Phacomorphic – lens is swollen iridocorneal

apposition blocks pupils - May be due to lens with water and can

happen to patients with diabetes

Secclusio pupillae – (360° posterior synechiae), usually secondary to recurrent iridocyclitis

Iris bombé - anterior bowing of the peripheral iris from increased pressure in the posterior chamber

Aphakic/pseudophakic pupillary block

Nanophthalmos – small eyeball

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Ciliary block/malignant glaucoma due to retinopathy of prematurity (ROP)

Trauma

Miotic therapy

Secondary angle closure is caused by posterior synechiae extending for 360° (seclusio pupillae), which obstruct aqueous flow from the posterior to the anterior chamber.

IV- Secondary Angle Closure Glaucoma w/o Pupillary Block

Due to posterior pushing mechanisms from: o Tumors, choroidal hemorrhage or effusion o Scleral buckles o Swelling after panretinal photocoagulation (PRP) o Post inflammatory with posterior synechia o Iris bombe– iris is bowing forward o Cilio-choroidal effusion o Capsular block syndrome without iris–capsule

adhesion o Ciliary body/iris cyst or other ciliary body or

posterior segment tumor o Contraction of retrolenticular fibrovascular tissue

such as in proliferative vitreoretinopathy and retinopathy of prematurity

o Malignant glaucoma (cilio-lenticular block)

Anterior pulling mechanism in neovascular glaucoma, post inflammatory peripheral anterior synechiae

Pathogenesis: Chronic anterior uveitis causes the deposition of inflammatory cells and debris in the angle. Subsequent organization and contraction pulls the peripheral iris over the trabeculum, causing gradual and progressive synechial angle closure and eventual elevation of IOP. The eye with a pre-existing narrow angle may be at higher risk.

SYMPTOMS Acute Angle Closure Glaucoma (AACG)

Most patients with angle closure are asymptomatic, including a majority of those with intermittently or chronically elevated IOP.

Presentation can be with intermittent mild symptoms of blurring (‘smoke-filled room’) and haloes (‘rainbow around lights’) due to corneal epithelial edema

Painful red eye, photophobia, decreased/blurred vision, halos around lights, headache, nausea, vomiting

- classic features of AACG

VA is usually 6/60 to HM

IOP is usually very high (50–100 mmHg)

Conjunctival hyperemia with violaceous circumcorneal injection

Corneal epithelial edema Chronic Angle Closure Glaucoma (CACG)

Asymptomatic, may have decreased vision, constricted visual fields (aka tunnel vision)

VA is normal unless damage is advanced

IOP elevation may be only intermittent.

SIGNS

Decreased visual acuity

Increased IOP

Ciliary injection aka eye redness

Corneal edema

Anterior chamber cell/flare - There are floating proteins in anterior chamber

Shallow anterior chamber

Narrow angles on gonioscopy

Mid-dilated nonreactive pupil

Iris bombe

Signs of previous attacks including sector iris atrophy

Anterior subcapsular lens opacities aka glaucomflecken

Dilated irregular pupil

Peripheral anterior synechiae- iris is sticking to the cornea

EVALUATION

History and physical examination

Visual acuity

Slit lamp biomicroscopy

Tonometry: note time of day

Gonioscopy

Ophthalmoscopy: note appearance of the disc

Check visual fields and perimetry

Consider provocative testing (prone test, prone dark-room test and pharmacologic dilation; IOP increase of > 8 mmHg is considered positive)

Prone test – prone position increases IOP. Have you tried bending down? Diba daw ma feel nyo gataas ang pressure sa mata? That’s the rationale behind this test.

Dark room test – pupils dilate in the dark. In a dark room, your pupils dilate and would test then IOP

MANAGEMENT Medical

Topical β-blockers

Topical sympathomimetics (α- and β- adrenergic agonists, topical miotics, topical carbonic anhydrase inhibitor, topical prostaglandin analogue)

Oral carbonic anhydrase inhibitors, oral hyperosmotic agents

- Ask patient to take glycerin with orange juice because patient can’t take glycerin alone

IV hyperosmotic agent (mannitol) Surgical

Argon laser trabeculoplasty, YAG laser iridectomy

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- hole in the iris peripherally to make an outflow passage for aqueous), laser pupilloplasty, laser gonioplasty

- All used to open trabecular meshwork

Trabeculectomy with or without use of anti-metabolites

Artificial filtering shunts - shunt made from anterior going to the

posterior chamber

Cyclodestructive procedures - Cyclocryotherapy - YAG cycloablation

Only done in uncontrollable, very high IOP Ciliary bodies are destroyed (because they

produce aqueous) Only done in patients with almost no vision

Plateau-iris syndrome There is apposition of iris to the cornea, and the iris is flat -> angle is blocked (dotted lines denotes normal configuration of iris)

The most reliable sign in angle-closure glaucoma is the unreactive pupil in the mid-dilation.

Patient w/ glaucoma: ciliary injection(red eye), mid-dilated pupil -> can already suspect glaucoma even before doing tests

Septal iris atrophy. In this eye, gray, thin, depigmented areas of atrophy of the iris, most marked at the arrows, are present around the pupillary margin. Iris atrophy from high intraocular pressure in angle-closure glaucoma usually involves irregular radial sectors of the iris and is most marked near the pupil.

SECONDARY CAUSES OF GLAUCOMA Pseudoexfoliation

Pseudoexfoliative material (PXF), the presence of which in the eye is termed pseudoexfoliation syndrome (PXS), is a common cause of secondary open-angle glaucoma, but is easily overlooked if signs are mild. It is rare before the

age of 50, though after this age its prevalence increases rapidly. It is more common in women than men.

PXF is a grey-white fibrillary amyloid-like material; it may derive from abnormal extracellular matrix metabolism in ocular and other tissues. The material is deposited on various ocular structures including the lens capsule zonular fibres, iris, trabeculum and conjunctiva.

Pigment dispersion syndrome

characterized by the liberation of pigment granules from iris pigment epithelium (IPE), and their deposition throughout the anterior segment

pigment shedding is precipitated by rubbing of the posterior pigment layer of the iris against the zonule as a result of excessive posterior bowing of the mid-peripheral portion of the iris

Characteristic radial spoke-like transillumination defects are seen in lighter, but often not in dark, irides

Pigment is deposited on the endothelium in a vertical spindle shape (Krukenberg spindle)

Neovascular glaucoma

occurs as a result of aggressive iris neovascularization (rubeosis iridis)

common etiological factor is severe, diffuse and chronic retinal ischaemia

Posner–Schlossman syndrome

aka glaucomatocyclitic crisis

a rare condition characterized by recurrent attacks of unilateral acute raised IOP associated with mild anterior uveitis

mechanism is speculated to be acute trabeculitis, and there is evidence that infection, possibly cytomegalovirus (CMV) or H. pylori, may play a role

Iridocorneal endothelial (ICE) syndrome

typically affects one eye of a middle-aged woman

consists of the following three clinical presentations: o Chandler syndrome

- most common clinical presentation and is characterized by an abnormal corneal endothelial appearance said to resemble hammered silver

o progressive or essential iris atrophy o iris nevus (Cogan–Reese) syndrome

due to abnormal corneal endothelial cell layer with a predilection for proliferation and migration across the anterior chamber angle and onto the surface of the iris, with subsequent progression to glaucoma (50%) and corneal decompensation

Lens-related glaucoma o Phacolytic glaucoma - a secondary open-angle

glaucoma occurring in association with a hypermature cataract

o Phacomorphic glaucoma - an acute secondary angle-

of 12

closure glaucoma precipitated by an intumescent cataractous lens

Traumatic glaucoma

IOP elevation may result from trabecular obstruction by red blood cells or occasionally from angle closure due to pupillary occlusion by a blood clot

Ghost cell glaucoma

Generally occurs where there is vitreous hemorrhage and disruption of anterior hyaloid face mechanical obstruction by red cell ghosts in trabeculum

GLAUCOMA DRUGS

β-blockers o decrease aqueous secretion with little effect on

episcleral venous pressure o 10% develop tachyphylaxis o should not be instilled at bedtime as they may

cause a profound drop in blood pressure while the individual is asleep, thus reducing optic disc perfusion and potentially causing visual field deterioration

o preferred in conditions such as ocular inflammation and cystoid macular edema, or where there is a history of herpes simplex keratitis

Sympathomimetics o α- and β- adrenergic agonists; increase aqueous

outflow

Miotics o in POAG, increases aqueous outflow o In ACG, opens the angle which results from the

mechanical contraction of the pupil pulling the peripheral iris away from the trabeculum

Prostaglandin derivatives o Enhances uveoscleral outflow without altering

aqueous outflow through the trabecular meshwork

o now typically preferred to a beta-blocker as first-line treatment for glaucoma due to the latter’s potential for systemic side effects

o Latanoprost may cause fewer ocular adverse events than other PG agents and so is often used first line

Carbonic anhydrase inhibitor o Reduce aqueous secretion through direct

inhibition of carbonic anhydrase. Production of aqueous humor in the ciliary epithelium is a function of the production of bicarbonate

o Carbonic anhydrase – enzyme needed to produce bicarbonate, which is needed in the production of aqueous humor

o relatively contraindicated in patients allergic to sulfonamide antibiotics

Hyperosmotic agents o Increase blood osmolality thereby creating an

osmotic gradient between the blood and vitreous so that water is drawn from the vitreous into the blood

o Used in resistant acute angle-closure glaucoma or when the IOP is very high prior to intraocular surgery

Old notes not in lecture Medical marijuana- no scientific studies proving their benefit in glaucoma Migraine had been associated with glaucoma- vasoconstriction- less blood flow to the optic nerve causes glaucoma (normotension glaucoma, pressure is normal but there is progressive field loss and optic nerve damage) Glaucoma especially open type is hereditary, early detection is the key to prevent progression and blindness. Open angle manifest in late teens thus screening and IOP monitoring should be started. Anti-cataract drugs are indicated only to delay formation of cataract. In cataract, the lens is swollen causing a pupillary block. This causes the iris to bow forward leading to apposition of lens and iris- closed angle glaucoma LUCERO | MIGUEL | NAPALA | PEDREGOSA

b20m02l04 glaucoma edited

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