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Glaucoma

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Glaucoma Glaucoma is a name given to a group of diseases in which the intraocular pressure (IOP) is sufficiently elevated to induce pathological changes in the eye. These changes primarily affect the optic nerve head and the nerve fibre layer of the retina leading to progressive visual field changes.

The aqueous humor : Is a watery fluid secreted by the ciliary processes. This processes passes through two steps; first by processes of filtration from the blood vessels of the ciliary processes into stroma and then by secretions by the ciliary epithelium into the posterior chamber then circulates through the pupil and fills the anterior chamber. New aqueous is formed all the time. The process of aqueous production is controlled by both alpha and beta receptors, and modulated through the action of carbonic anhydrase enzyme present in the ciliary epithelial cells. Aqueous humor has the same composition of plasma except its protein content which is very low. (During iritis, the protein content of aqueous is increased and aqueous becomes like plasma and is called plasmoid aqueous.) Aqueous is saturated with oxygen and nutrients. . it is essential for the Nutrition and removal of waste product of the avascular cornea and cystallin lens. Aquoeus is drained out of the eye at the angle of the anterior chamber.

Fig.1 : aqueous humor supply nutrients and remove waste products of metabolism of the crystalline lens and the cornea.

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Anatomy of the angle of the anterior chamber : It is the most peripheral portion of the anterior chamber. The angle is a

360° region corresponding externally to the limbus It can be seen

clinicaly using a goniolens. The patient is seated on the slit lamp and after application of local anaesthesia, a special lens (gniolens) is applied to the cornea. This techique is calles gonioscopy. The angle of the Anterior chamber consists of five structures from before backwards :

1. Schwalbe line : is the peripheral thickened end of Descemet's membrane

2. Trabecular meshwork : This tissue is partially scleral and partially uveal. it is triangular in cut section with its apex at the Schwalbe's line and its base at the scleral spur. It is formed of layers and has many perforations through which aqueous pass from the A C to the canal of schlemm. The perforations in each layer alternate with those in the next layer creating some resistance to aqueous outflow. During gonioscopy, the trabecular meshwork appears grayish and semi transluscent but it may become pigmented especially in dark races, old age or in certain types of glaucoma. 3. Scleral spur : it is an inward projection of the inner surface of the sclera at its most anterior part. It gives attachment to the longitudinal fibres of the ciliary muscle posteriorly and the trabecular band anteriorly it appears as a dark white band or line during gonioscopy.

4. Part of the anterior surface of the ciliary body which is the darkest part of the angle.

5. Root of the iris as it is inserted in the anterior surface of C.B.

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Fig.2. The angle of the anterior chamber extends 360

o

Fig.3 : aqueous passes through the trabcular meshwork to reach the canal of Schlemm then passes through the collector channels to reach veins on surface of the globe.

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Fig.4 : Gonioscope is a special lens that is applied to the surface of the eye to visualize the angle of the anterior chamber where aqueous is drained out of the eye.

Fig.5 : when the trabecular meshwork is seen the angle is said to be opened, and when the iris obscure

seeing the trabecular meshork then the angle is described as closed.

Aqueous drainage : 1. conventional outflow (90% of aqueous) Aqueous is filtered through the trabecular meshwork (TM) it inters The canal of Schlemm, which is a venous like channel situated at the corneo-scleral junction, on the outer aspect of the posterior 2/3 of the trabecular meshwork. The canal receives aqueous from its inner surface through the perforations present within the layers of the trabecular meshwork. From the external surface of the canal of Schlemm a group of channels comes out, called the collecting channels. These,

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take aqueous out to the aqueous veins present on the external surface of the eye, which in turn take the aqueous to the episcleral veins.

2. uveoscleral outfolw : About 10% of aqueous humor in normal human eyes traverses the ciliary muscle to reach the suprachoroidal space and leaves the eye through the sclera or blood vessels.

Fig.6 : most of aqueous finds its way through the trabecular meshork. Only small part is drained through the uveo-scleral path. This pathway is markedly enhanced by the action of topocal prostaglandins eye drops .

Functions of aqueous humor : 1. Nutrition and removal of waste product of the avascular cornea and lens

2. Maintain the intra ocular pressure 10-21 mm Hg above the atmospheric pressure. As any closed container, the pressure inside the eye depends on the volume of its contents. All the ocular contents are almost static from the volume point of view (e.g. lens, retina, vitreous body and uveal tract) except the aqueous humor which is in a dynamic state, it is always produced and always drained to maintain a normal level of the IOP. Hence it is the rate of aqueous production and aqueous drainage that affect the control of the IOP. What is the value of having an IOP higher than the astospheric pressure? This is important to keep the shape of eye globe regular, against the forces exerted on it by the lids and extraocular muscles. Thus keep the corneal curvature even and keep the retina smoothly spread over the regularly stretched globe wall. This is essential obrain a good quality of the image formed by the eye.

Glaucoma


N.B. Marked variation of IOP out of the normal range can affects the eye. An average pressure regulates the perfusion of ocular tissues from the capillaries.

If the IOP is markedly lowered (hypotony), tissue edema (e.g. optic disc edema- macular edema ) may occur.

On the other hand, a high IOP may impede tissue perfusion (ischaemia) leading to pathological changes particularly in the optic nerve (glaucoma).

Fig. 7 : A. postmortum eyeball to show the effect of zero pressue inside the globe. B. Diagram of a nicely

streched outer wall of a globe with pressure higher than the atmospheric pressure.

The average IOP (intra ocular pressure): The normal IOP ranges between 10 - 21 mm/Hg above the atmospheric pressure. It has a normal diurnal variation of about 2 -4 mm/Hg being highest at 6 am and lowest at 6 pm.

Measurement of IOP: The IOP can be measured by one of the following methods : 1. Schiotz tonometer : it measures the amount of indentation produced by a known weight placed on the cornea. This is shown on the scale of the instrument. The IOP is obtained from special tables showing the pressue in mmHg the corrosponds to the different scale readings. 2. Applanation tonometer : This is the most accurate method. During applanation tonometry, patient is set on the slit lamp. Tonomter is attached to the slit lamp, and the observer uses the slit lamp to see a magnified image of the tip of the cone of the tonometer (see image). The tip of the cone is applied directly against the anesthetized cornea.The tip of the cone is gradually

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pushed against the cornea by moving a knob on the side of the instrument. When force at the tip of the cone is enough to flatten an area of the cornea with a dimater of 3.06 mm; as seen by the observer, that force is equal to the IOP and the pressure can be obtained directlyfrom scale on the knob.

Fig . 8 : Applanation tonometer is more accurate tool to measure IOP compared to Schoitz tonometer.

Glaucoma When IOP is sufficiently elevated it will induce pathological changes in the eye. These changes primarily affect the optic nerve head and the nerve fibre layer of the retina leading to progressive visual field changes. The average IOP ranges from 10 - 21 mm Hg. The level of IOP at which glaucomatous changes appear vary from one subject to another. Ocular hypertension : An eye with IOP higher than average IOP but does not have field changes nor disc changes of glaucoma. Low tension glaucoma : An eye with IOP looks to be normal (within average range) but shows the characteristics field changes and disc changes of glaucoma

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Fig. 9 : in normal tension glaucoma IOP is within the normal range of the population and there is

glaucomatous damage, while in ocular hypertension IOP is higher than normal range of the population and there is no glaucomatous damage of the eye.

The changes of glaucoma : In order to understand these changes, the following points should be considered. 1. Factors affecting blood vessels inside the eyeball: Any blood vessel in the body is subjected to the following factors : - Blood pressure : which press on the vessel walls from inside, directed

outwords. - Interstitial pressure: (i.e.pressure in tissues outside the BV) Which press on

the vessel wall from outside into inward direction. It resists passage of fluids from inside the blood vessel into the tissues. In case of the eyeball, blood vessels inside the eye are subjected to an interstitial pressure higher than other blood vessels of the body by the value of the IOP (10-21 mm/Hg)

- Osmotic pressures along both sides of vessel wall (inside-outside) The difference between systolic and diastolic BP is essential for perfusion of tissues. When systemic BP is low or when intrastitial pressure is high, perfusion of tissues will be affected. 2. Arrangement of nerve fibres of the retina : - Fibres coming from the macula pass directly into the disc ( forming what is know as the papillo macular bundle). When these fibres reach optic disc, they occupy an extended areas of the disc that these fibres are the least crowded of all neural rim of the optic disc. - There is a horizontal line that divides the retina into upper and lower halves.

Fibres from the upper temporal quadrant and those from the lower temporal quadrant arcuate above and below the papillo macular bundle respectively to reach the optic disc. On reaching the optic disc to form the corrosponding

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upper temporal and lower temporal parts of the neural rim, these are the most crowded all neural rim of the optic disc.

- - - Fibres from the upper and lower nasal quadrants of the retina pass directly

into the disc’s upper and nasal quadrants. On reaching the optic disc to form the corrosponding upper temporal and lower nasal parts of the neural rim, these are the least crowded all neural rim of the optic disc.

Fig. 10 : arrangement of the retinal nerve fibres as they pass toward the lamina cribrosa to form the optic

nerve.

3. Anatomy of the optic nerve head :

Nerve fibres of the retina occupy the whole surface of the optic disc except a small area in the centre which is known as the physiological cup. The area

occupied by the neurons is know as the neural rim. Capillaries found on the optic disc supply the nerve fibres as they pass from the retina into the optic nerve

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. Fig.11 : the central part of the disc is devoid of neural rim and is known as the optic cup while the

peripheral part is formed of neurons and is known as the neural rim.

In Glaucoma, as the IOP rises, this will result in more pressure on the capillaries that supply the optic disc (ischemia). The first fibres to suffer are the upper and lower temporal fibres (most crowded) then the nasal and the last to suffer is the papillo macular bundle. With destruction of nerve fibres, progressive parts of optic disc will not be occupied by nerve fibres and the surface of area of the cup will gradually increase in size (glaucomatous cupping)

Fig. 12 : when damage affects a focal area at the level of the disc, impulses carred by these bundles of

fibres are not transmitted so there will a corrosponding scotoma. As time passes, these axons will die and diappear thus leading to notching of the neural rim and widening of the cup.

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Field changes in Glaucoma: Damage to NFL (nerve fiber layer) of the retina in glaucoma tends to involve bundles of fibers resulting in corresponding defects in field of vision Field defects in glaucoma usually start as relative defects and then become absolute in advanced cases. Scotomas are usually negative (patient is not aware of them) Evaluation of the field is done by 1. static perimeters : (e.g. Humphery, Octopus, etc.) which evaluate the

sensitivity numerically in each point of the field examined 2. Kinetic perimeters : like Goldmann perimeter or Bjerrum screen (which

magnifies the central field)

A. Changes in the field: a. Scotomata develop in the Bjerrum area (area lying between 10-20

o around

the point of fixation. Later these scotoma enlarge fuse together and with the blind spot forming Siedel scotoma.

1. Seidle scotoma : a small wing-shaped upper or lower extension from the blind spot is detected.

2. Bjerrum scotoma : it is a arcuate scotoma continuous with the blind spot and is concentric with the point of fixation, and stops at the horizontal raphe.

3. Double arcuate scotomata : It results from the fusion of two Bjerrrum scotomata. When the two arcuate scotmata meet in the nasal field at the horizontal meridian, they may form a sharp right angle defect with a sharply defined horizontal border. This step is called Roenne's nasal step. Sometiems (temporal wedge is formed) Rarely, the two arcuate scotomata appear symmetrically given rise to a ring scotoma or annular scotoma.

b. Isolated paracentral nasal scotoma may be detected in early glaucoma. c. Field defects enlarge peripherally and centrally that may end in a

tubular field - Still at this stage the visual acuity might be near normal although the field

defect makes the patient visually handicapped. We notice that vision of

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patient with tubular field could be still 6/6 therefore, the visual acuity is not a measure of the gravity of the disease

- A temporal island of vision might be retained at late stages. d. Later both central and temporal islands disappear resulting in total blindness

(absolute glaucoma)

Fig. 13: Different scotoma in cases of glaucomatou damage. For details, check the text.

Fig 14: para central area as well as the central area still functioning normally

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Fig 15:

upper left (1)is the blind sopt and (2)is Seidle scotoma enlarging into Bjerrum scotoma. There is also

contraction of the peripheral field.

Upper right : (3) damage in upper area with no corrosponding damage of the lower area is step.

(characteristic of glaucoma) (4) complete Bjerrum scotoma : notice horizotal meridian is respected , a

charactesitic of glaucomatous damage.

Lower left : more damage of the field and an arcute damage is seen in lower Bjerrum area (7)

Lower right : only paracentral(9) and central (8) islands of vision are what is left.

Glaucomatous optic atrophy: Changes could be detected stereoscopically by binocular ophthaloscopy or slit lamp biomicroscopy. Typically it has three features: 1. Large cup : this might reach the edge of the disc. The degree of cupping is expressed by the cup/disc ratio where we compare the diameter of the cup to the diameter of the disc. It is a ratio that could have any value between 0.1 to 0.9

2. Deep cup: 3. The edge is undermined: this is evidenced by the apparent interruption of the blood vessels. Glaucomatous cupping could be due to: 1. Effect of the raised IOP that leads to bowing of the lamina cribrosa.

(mechanical) 2. Effect of the raised IOP on the blood supply to the disc (ishaemia) Or both.

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Glaucomatous damage can be detected as the disc will show progressive cupping and the field of vision will exhibitth progressive deterioration.

Fig 16: showing progressive atrophy of neural rim with progressive widening of the cup starting from the

normal in the upper lt corner and ending in marked atrophy in the lower right corner.

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NERVE FIBER LAYER (NFL) of retina : By examining the nerve fiber layer of the retina using red-free illumination, defects in the NFL could be detected even before visible changes in the optic disc. Defects in NFL appear as a wedge shaped defects, running towards or touching the optic disc

Fig 17 : the Red free light helps demonstrating the wedge shape atrophic area of the retinal nerve fiber layer seen at the upper temporal pole of the optic disc

.

Glaucoma could be due to either 1. increase in production of aqueous (rare) 2. diminished drainage of aqueous (main )

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Classification of Glaucoma Glaucoma can be classified in many ways. I. According to the age : 1 congenital and infantile glaucoma 2 adult type glaucoma: II. According to etiology :

Primary glaucoma : Where the aetiology is not definitely known.

Secondary glaucoma : Where the glaucoma is of a known aetiology and

results from another disease

III According to Angle of Anterior chamber :

- Open angle glaucoma : where the angle looks anatomically normal but does not function properly

- Angle closure glaucoma : where the aqueous outflow is obstructed by peripheral anterior synechaie "PAS"

It is noticed that the three classifications can be applied to any case of glaucoma e.g. primary glaucoma may be an open angle or closed angle and may occur in ad adult or in an infant and the same is case for secondary glaucoma.

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Congenital or Developmental or Infantile Glaucoma “Buphthalmos" "Hydrophthalmos”

it is a glaucoma occurring at birth or during the first 1-3 years of life.

- At this stage, the outer coat of the eye is elastic and so it distends under the effect of high IOP.

- The cornea and the globe enlarge resembling the appearance of bull or cow's eye and hence the name "Buphthalmos".

Etiology : Most of cases are primary (due to congenital angle anomaly), however any cause of secondary glaucoma that may occur in adults can also occur in infants thus result in secondary buphthalmos. . Primary Buphthalmos : due to angle anomaly. Various types of angle anomalies were described in association with congenital glaucoma:

- the presence of abnormal mesodermal tissue in the angle of AC.(Brakan's membrane)

- anterior insertion of the ciliary muscle to the trabecular meshwork instead of the scleral spur

- Absence or malformations of Schlemm's canal. The disease is usually limited to the eye. Primary buphthalmos : The disease is bilateral in 75% of cases. It may be manifest at birth or shortly after. Secondary Buphthalmos :

- all causes of secondary adult glaucoma may affect infant's eye leading to secondary buphthalmos e.g. uveitic glaucoma .

- Some conditions are uniques for young age e.g. - Retinoblastoma : malig tumours of young - Anaridia : congential imcomplete absence of iris with some

remanate of iris tissue that may be associated with extensive PAS (peripheral anterior synechiae)

Symptoms “given by the mother “

- -Early cases : lacrimation, photophobia, blepharospasm. These symptoms are due to access of aqueous into the cornea through tears in Descemet’s membrane, causing corneal irriation.

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- later, parents notice change in colour of eyes (Hazy cornea:due to edema - and blue sclera) - large size, and poor vision

- In unilateral cases, discrepancy in size of both eyes attacks attention

very early.

Signs : As the outer coat of the eye of the infant contains much elastic tissue, the eye ball will increase in size under the effect of raised IOP. This will result in : Cornea : - becomes large in diameter. Normal horizontal corneal diameter in the new

born is 9.5 - 10 mm. The advanced the glaucoma, the larger the corneal diameter. It may reach up to 15 mm. (N.B. The axial length of the eye (measured by ultrasonography) also increases. )

- Corneal edema (haziness) first appear (reversible). Later on, corneal scarring (permanent) may result if Bowman's membrane is ruptured. Horizontal corneal striae may be present.

Sclera : - becomes thin & bluish is colour (uveal tissue apparent through the thinned

sclera) Anterior Chamber : deep Iris : may be atrophic and may be tremulous (iridodenesis) lack of support of the crystalline lens being subluxated in advanced cases Lens: may become subluxated in advanced cases because of tear in part of the zonule as a result of increase size of the eye ball. IOP is high. It is measured under general anesthesia . Fundus : cupping of the optic disc is partly due to atrophy of nerve fibers and partly due to stretch and widening of scleral canal. The latter part improves after surgery partly (reversible cupping unlike in adults) Gonioscopy : (Examination of the angle ) shows a mesodermal membrane closing the angle

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Fig. 19: Photophobia because of corneal edema.

Fig 20 : right cornea looks larger and hazy.

Fig 21 : lt cornea looks larger.

Fig 22: bilateral hazy large corneas

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Fig. 23 : IOP is measured with hand held applanation tonometer and corneal diamter is meaured under general anaesthesia

Differential diagnosis : 1. lacrimation, photophobia, blepharospasm can occur in the following

conditions : - distichiasis - ophthalmia neonatorum - dacyrocystitis in infants

2. Big cornea may occur in : - Megalocornea : here cornea is clear, tension is normal and fundus is

normal.

Fig.24 : Distichiasis (congenital rubbing lashes) An extra row of lashes in place of meibobian glands

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Fig 25 : ophthalmia neonatorum (infective

conjunctivitis of infants)

Fig. 26 : Congential dacryocystitis (inflammation of lacrimal sac) will result in wetting of th eye

Fig. 27 : Megalocornea : is a normal but large sized cornea.

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Management: Treatment . Surgery should be done as early as possible. The better eye is usually operated upon first.

1.Early cases are treated by goniotomy

- corneal diameter less than 13 mm - clear cornea permitting visualization of the angle

A surgical gonioscope is used to visualize the angle. 1/3 to 1/2 of the angle is incised using a special knife so as to communicate the AC directly to the canal of Schlemm. The operation may be repeated in another part of the angle if needed.

Fig. 28 : a knife is used to cut the abnormal mesodermal tissue in the angle of the Anterior chamber

(goniotomy operation)

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Fig 29. Goniotomy operation : 1. Lamillar incision of the cornea. 2. A needle is used as a knife is introduced into the anterior chamber. 4. A surgical goniolens is applied to visualize the angle of AC. 5. The abnormal mesodermal tissue is cut. 6. Closure of corneal wound.

2. Late cases : ( corneal diameter larger than 13 mm with cornea not clear

enough to permit visualization of the angle with the gonioscope) These cases can be treated by :

A. Trabeculotomy B. Subscleral traculectomy (SST) with intra operative application of

5-FU or Mitomycin on surface of sclera C. Glaucoma device

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a. Trabeculotomy :

- lamellar scleral flap is prepared as in subscleral trabeculectomy - at the limbus, radial incision is applied and gradually deepened till canal

of Schlemm is identified

- A traculotome (a metal probe) is introduced into canal of Schlemm and is swept into the AC to through the trabeculum and connect the canal to the AC.

Fig. 30: (1) After dissecting the conjunctiva and creating a supferical lamellar scleral flap, radial incision is done to expose the canal of Schlemm. (2) Canal of Schlemm is opened. (3)and (4) A trabeculotome is introduced into the canal of Schlemm. (5) A swep movement is done so that that trabeculotome is now in the AC thus the corrosponding part of canal of schlemm inner wall and trabecular meshork and the abnormal mesodermal tissue in the angle are cut.

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b. Fistulizing operation e.g. subscleral trabeculoectomy (SST) is done in advanced cases or if goniotomy and trabeculotomy fail to control IOP.

Same steps are in adult glaucoma. for details see section of glaucoma surgery.

NB. In children, there is a great tendency for closure of the fistula due to excessive conjunctival scarring. This may be controlled by the local use of antimetabolies (5 fluorouracil (5-FU) or Mictomycin) at the time of surgery. In cases of failure of repeated trabeculotomies and SST , a glaucoma device (shunt tube) may be used. For details see section of glaucoma surgery.

Fig 31: Ahmed glaucoma implant is a valved device that allows aqueous to escape from AC to be drainged in the sub Tenon’s space at the back of the globe.

Glaucoma


Primary angle closure glaucoma (PACG) (narrow angle, decompensated, congestive glaucoma)

it is a primary glaucoma in which the IOP is elevated (usually in an acute manner) as a result of partial or complete occlusion of the angle of the AC.

- is a bilateral disease that may affect one eye before the other. - Age : above 45 yrs - Females are more affected than males - More in anxious personalities, with sympathetic over stimulation - It is more common in eyes with axial hypermetropia (shallow AC and

narrow angle) Predisposing Factors and pathogenesis :

- Eyes with axial hypermetropia, the whole globe is small and the lens is relatively big pushing the iris and causing further shallowing of the Anterior chamber (AC) and narrowing of the angle. The most common local factor is the presence of a narrow (shallow) angle of AC.

- Normally the iris moves on the anterior surface of the lens during miosis and mydriasis. The aqueous is secreted in the posterior chamber and has to push the iris slightly forwards in order to pass through the pupil to the anterior chamber. This causes slight forward convexity of the iris mid periphery called physiological iris bombé.

Precipitating factors : 1. Pupillary dilatation : due to prolonged stay in dark, emotions or mydriatic

application, This may precipitate acute attack by one of two mechanisms : - Crowding of the root of the iris in the angle that is already narrow may

close it (Angle block) - Pupillary block and iris bombé : In eyes with shallow angles, the

pupil tightly opposed the lens capsule. This produces a relative pupillary block and the aqueous has to push its way with difficulty. When the pupil is semi-dilated, the block is maximum and the aqueous will accumulate between the iris and lens, pushing the iris forward leading to iris bombé. This will close the angle

2. Congestion of the ciliary body: which pushes the iris root producing further

narrowing of the angle. (emotions, prone position)

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Fig. 32 : mechanisms of rise of IOP in cases of angle closure glaucoma

Fig.33: pupillary block is maximum when pupil is mid dilated, resulting in iris bombe and appositional

closure of the angle of AC, With miosis,the mechanism is reversed and the angle will open again provided no synechia were formed

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Fig 34: closed angle can be due to just appostion between iris and trabecular meshwrok, is is reverisble when iris is pulled away from trabecular meshwork with narrowing of the pupil. The other angle closure is synechial where actual adhesions develop between iris and cornea and this type does not breakdown with dilatation of pupil. When such peripheral anterior synechae extend more than 180o persistant rise of IOP will occur.

Fig 35 : Extensive peripheral anterior synechia

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Clinical picture : PACG can be divided into four overlapping phases. However, the disease may not progress from one stage to the next in an orderly manner.

1. prodromal stage : this stage occurs a result of rapid partial closure and reopening of the angle. The level of IOP during that stage depends on the extend of angle closure but usually does not exceed 45 mm Hg.

Symptoms : This stage is characterized by the occurrence of transient attacks of elevated IOP that may follow excitement or stay in dark place (cinema). The patient notice during the attack :

- frontal headache, eye ache or sense of tightness - transient blurring of vision (foggy vision) due to corneal edema - The patient usually complains of seeing rainbow coloured halos

around light because water droplets collected in the cornea act as a prism analyzing the white light into its component wave lengths

- attacks are usually recurrent and resolve spontaneously in one - two hours as miosis occurs the iris root is pulled away from the trabecular meshwork and angle reopens.

Signs: If patient is examined during the attack a high IOP and corneal edema will be found, and signs will disappear with the end of the attack. Patients are usually examined in between the attacks, where the eye looks normal and history may simulate cases of migraine. Diagnosis can be suspected by finding hyperopia, shallow AC, iris bombé and narrow angle(gonioscopy).

Provocative tests : As tension is normal in between the attacks, a normal tension does not mean the patient is free and diagnosis depends on ; Provocation tests : depends on pupillary dilatation

- Mydriatic test : tension is measured before and after instillation of a short acting mydriatic (mydiacyl eye drops). A rise of 8 mm Hg or more is diagnostic. Should be done only using weak mydriatic, in selected cases and the patient should be kept under observation till the pupil is narrow again. This test is dangerous and may precipitate an acute attack.

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Prognosis : Eyes with prodromal attacks may develop acute attacks or pass directly into chronic angle closure. The other eye of the patient is said to be in a latent phase. If untreated, 50% of these eyes develop acute attack within 5 years.

Management : During the attack : Miotics (2% pilocarpine) are given to abort the attack Prophylactic weak miotic (1% pilocarpine) is also given to the other eye. After the attack :

Bilateral laser iridotomy should be done as early as possible. This allows aqueous to pass directly from the posterior chamber to the AC bypassing the relative pupillary block. (Laser iridotomy means creation of a hole in the peripheral iris by the use of laser energy either Argon or YAG (Yetrium. Aluminum garnet) laser. It largely replaced surgical iridectomy.)

Fig 36: Laser peripheral iridotomy has replaced the surgical peripheral iridectomy as it is an out patient procedure with marked less incidence of complications

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2. Acute stage (acute congestive glaucoma )

pathogenesis : - It results from sudden total angle closure.

Or it may follow previous prodromal attacks which usually result in formation of some PAS, added to some precipitating factors , sudden

total angle closure occurs. 50% or more of patients give a history of

previous prodromal attacks.

- IOP level may rise to 50 mm Hg or more, a level that causes temporary

paralysis of sphincter pupillae muscle (ischemia). This interferes with physiological miosis and thus the attack is not self-limited (unlike prodromal attack)

Symptoms : usually present as an emergency. - Sudden severe periocular pain and headache, referred along the branches of

the ophthalmic division of trigeminal nerve to temple giving rise to temporal headache. Pain is due to pressure on the ciliary nerves

- Rapid severe visual impairment due to corneal edema. May be

nausea and vomiting from the severe pain . Signs : 1. Very poor VA : HM or finger counting. 2. Ciliary injection seen around the limbus 3. Corneal edema : hazy (cannot see through it). Bullae may be formed under

the epithelium. Edema is due to loss of the endothelial function of sodium pump which keeps the cornea detergescent (relatively dehydrated)

4. Very shallow AC with iridocorneal touch at the periphery as seen by slit lamp. (this type of glaucoma is commoner in hypermetropic eyes with short anteroposterior diameter) Iris bombé may be present

5. Pupil is vertically oval, semidilated, irreactive to light (due to paresis of sphincter pupillae) . It appears bluish in colour (hence the name blue water). This is an optical illusion caused by edema of the cornea, turbid AC. These multiple interfaces cause scattering of incident light and short wave lenths (blue) are the mostly scattered and thus they return to the examiner who sees the pupil bluish. (the same way the sky and the sea looks blue)

6. Tension is high (up to 60-70 mm Hg) 7. Fundus can not be seen because of the corneal edema, if fundus is visible,

we may detect pulsations of the central retinal artery and venous congestion.

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Fig 37: ciliary injection is arround the limbus, pink in colour and diffuse no individual vessels seen. On other hand conjunctival injection usually extend to the fornix and is park red in colour with individual vessels seen

Fig. 38: Hazy cornea with dilated oval pupil and some redness around the limbus

Fig 39: Corneal endothelium is imporant to keep the water content of cornea low. Edematous cornea is hazy.

Fig 40. Section of cornea seen on slit lamp, notice thickening of the cornea (normally it is thin in the centre compared to the periphery which is not the case here) Cornea is bluish because of scatter of the blue light

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Fig 41 Hazy cornea with with dilated pupil and some redness around the limbus

Fig 42 : Slit lamp of anterior segment of the eye. Notice the shallow AC and that cornea is edematous you can see a hazy appearnce of light coming from the iris.

Fig 43 : cornea is clear as IOP is back to normal but pupil is dilated and there are areas of iris atrophy (depigmented parts). This is the result of ischemia during the acute attack.

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Fig 44 : following the acute attack, some areas of cataract are seen due to disturbance of lens metabolism during the attack

Fig 45 : two patches of iris atrophy are seen with irregular pupil because of ischemia during the attack. Iris has a segmental blood supply that is why only segments were affected by the ischemia. Notice surgical iridectomy was done at 12 o’clock.

Fate : 1 . If the raised tension is not relieved, complete visual loss will result due to atrophy of the optic nerve fibers at the level of the disc (absolute glaucoma) 2. If the raised IOP is controlled by medication or surgery, the attack will

subside. Some defects in the field of vision could be found after the attack depending on the duration and severity of rise of the IOP and the state of health of the optic nerve head. A healthy disc can withstand rise of IOP more than already damaged disc.

3. If IOP is not controlled properly, the tIOP will gradually comes down and patient will pass into chronic stage of glaucoma. This will occur even without treatment as a result of the effect of the raised IOP on the ciliary body causing ischema and decreased aqueous production.

Glaucoma


DD : 1. From other causes of ciliary injection :Acute iritis-corneal ulcers (keratitis) 2. secondary angle closure glaucoma.

Cornel ulcer Acute iritis Acute congestive

glaucoma

Pupil : constricted constricted dilated

+ve fluorescein stain Aqueous flare High IOP

Management : - The treatment of PACG is essentially surgical. IOP must be controlled

medically before surgery to avoid the risk of intraocular hemorrhage - Medical treatment is tried for 24-48 hours to lower the IOP. By the end of this

period one of two situations might be reached. a. IOP is controlled : pain will diminish, vision will improve, congestion becomes less and pupil becomes constricted, Now gonioscopy should be done. :

- : peripheral iridectomy or laser iridotomy :if angle is opened (no or minimal P.A.S.) and IOP is controlled.

- subscleral trabeculectomy (SST) if angle is closed ( extensive PAS 50% or more of circumference) or the IOP is not controlled medically.

b. IOP still high: here we must prepare the patient of a rapid operation (SST)

- Prophylactic peripheral iridotomy should be done in the other eye

Medical treatment for acute attack: 1. Hypersomotic agents : are the most effective drugs in acute attacks. They

raise the osmotic pressure of the plasma and thus they draw water out of the

Glaucoma


eye by dehydrating the vitreous so decreasing the size of ocular contents. Problem is effect is temporary and is followed by rebound rise of IOP.

- 250 ml of mannitol 20% given rapidly (intravenous drip) dose (1-2 g/kg body wt) is the most commonly used agent.

- glycerine by mouth 1.5 cc / kg body weight - urea Intravenously 30%

2. Carbonic anhydrase inhibitors : e.g, acetazolamide :decrease IOP by

reducing aqueous secretion at the CB. Two tables (500 mg) are given initially followed by one tablet (250 mg) / 6 hours

3. miotics :Are essential for treatment. Miotics constrict the pupil so can relieve

the pupillary block and may open the angle of the AC. However they start to act only when IOP is lowered so that the temporary sphincter paralysis is relieved. Pilocarpine 2% is the drug of choice. Higher concentrations (3 or 4%) may increase congestion and vascular permeability particularly if given very frequently.

4. Beta blockers: e.g. timolol maleate 0.5% eye drops given twice daily help

lowering IOP by decreasing aqueous secretion.

3. Chronic stage ( Chronic congestive glaucoma) Here the IOP is moderately elevated. This may follow acute rise of IOP (acute attack) or may start de novo. Here the process of ischemia and damage of field of vision and optic nerve is slow but steadily going on. Symptoms : 1. mild pain, comfort and headache.

Glaucoma


2. Some blurring of vision because of corneal edema and affection of accommodation (ischemia of CB)

3. Changes in the field of vision Signs : 1. mild ciliary injection 2. mild corneal edema 3. patches of iris atrophy (ischemia of iris BV) 4. lens opacities 5. pupil dilated with sluggish reaction 6. IOP raised 7. Gonioscope : P.A.S (peripheral anterior synechiae) 8. Fundus : glaucomatous cupping 9. Field of vision : changes of glaucoma NB. Sometimes an angle closure occurs very quitely with no symptoms nor signs at all (i.e. similar to chronic simple glaucoma). In such a case, condition can only be diagnosed when patient had disc and field changes of glaucoma and on doing gonioscopy the angle is closed) Treatment Here P.A.S. are present and the treatment is SST with prophylactic iridotomy for the other eye.

Fig 46 : mild corneal edema- some redness of the eye – moderate rise of IOP if there is some vision then it is chronic congestive glaucoma and if vision is no PL then it is absolute glaucoma

4. Absolute stage : This is the end stage of neglected glaucoma where total optic atrophy occurs with complete and irreversible loss of vision. The eye is blind and vision is no PL (no perception of light )

Glaucoma


Examination of an eye with absolute glaucoma following closed angle glaucoma shows the following:

1. ciliary injection 2. Edematous cornea, appear hazy and even may show bullae . If these bullae

rupture patient suffers severe pain. Degenerative pannus may be present. It is seen superficial vascularization and cellular infitaration all round the periphery of the cornea. Vessels can get into the cornea when there is a persistant prolonged edema of the cornea that result of loss of the normal compact arrangment of the laminae of the cornea.

3. shallow A.C 4. Patches of Iris atrophy and pupil dilated irreactive (may be oval in shape

with its long axis vertical or rounded) : due to ischemai of iris and its sphincter pupillae muscle

5. Complicated cataract due to disturbance of lens metabolism as aqueous circulation is impaired

6. Advanced glaucomatous optic disc cupping. 7. Staphyloma may occur :

a. Ciliary staphyloma : in the ciliary region. Here sclera is bulged and is lined with CB. Bulging is posterior to site of entry of anterior ciliary vessels.

b. Inter-calary staphyloma : present at the limbus, anterior the site of entry of the anterior ciliary arteries. Sclera is bulging and is lined by root of the iris

c. Equatorial staphyloma : in the region of equator, at the site of perforation of vortex veins. Here sclera is bulging and is line by choroid and retina.

Glaucoma


Fig. 47: cilary staphyloma is posterior the site of entery of the anterior ciliary vessels

Fig. 48: intercalary staphyloma is anterior to the site of entery of the anterior ciliary vessels

Fig 49 : vision is no PL and pupil is dilated irreactive to light and there is hazzy cornea and mature cataract and IOP is high. This is an eye with absolute glaucoma as an end stage of Closed angle glacuoma

N.B. Absolute glaucoma may pass into Atrophic phase : atrophy of the ciliary

body occurs. The IOP drops and the eye may shrink (atrophia bulbi). Treatment : as this type of absolute glaucoma, that follows closed angle glaucoma, is a blind painful eye, the treatment is only indicated for pain. Treatment include medical treatment, cyclodestructive procedures, retrobulbar injection of alcohol or even enucleation (being blind painful) .

Glaucoma


Fig 50: if eye is blind and painful, enucleation (removal of the whole globe) is one of the available options.

Glaucoma


Primary open angle glaucoma (POAG) Chronic simple, compensated, glaucoma simplex)

It is a primary glaucoma resulting form decreased facility to outflow of aqueous through the trabecular meshwork although the angle is opened and looks normal. There is slowly progressive elevation of the IOP leading to progressive damage to the optic nerve (either directly "mechanical theory" or by interfering with perfusion for capillaries " ischemia theory" ). Atrophy of nerve fibers result in progressive deterioration of the field of vision.

It is a bilateral disease though one eye may be affected before the other.

No sex predilection

It has an incidence of 2% of the population

Slightly more common in high myopia (or may say difficult to diagnose in high myopia)

Heredity plays an important role in the pathogenesis. So with a positive family history of glaucoma should rise the suspicion of condition among other members of the family.

More common is steroid resonders

Etiology : the rise of IOP is not due to angle closure which is seen opened with gonioscopy. There is obstruction of outflow of aqueous. No definite pathogenesis is known. Site of pathology may be at part of tabacular meshwork adjacent to the canal of Schlemm ( the juxta canalicular layer of tissue).

Normal tension glaucoma (NTG) or Low tension glaucoma : Is a type of open angle glaucoma when the IOP is within the normal range of IOP of the population. This type of glaucoma could be due to shortage of the blood circulation affecting the optic disc while the IOP is within normal. Sometimes patients with POAG with wide flaucation of the IOP over the day may be mistaken for NTG when IOP is measured during the trough peroids.

Symptoms : POAG is essentially symptomless because of the following :

1. Sensory nerves are adapted to the slowly rising IOP and thus there is no pain or headache.

2. Field defects are usually of the negative type (not felt by the patient) and visual acuity remains normal until very late stages (macular fibres are the last to suffer)

The condition could be discovered after one eye is already lost. Occasionally the patient may complain of :

- Prolonged dark adaptation from lowered retinal senstivity due to

chemical changes in the rods.

Glaucoma


- Decreased sensitivity to light : patient notices that he now needs stronger illumination to see around satisfactorily.

- pathological presbyopia : frequent change of reading glasses at short intervals. This is due to ischemia to the ciliary muscle.

- Vague inconstant symptoms e.g. headaches and blurring of vision N.B. It is commonly discovered accidentally in patients attending ophthalmic clinics for other reasons e.g. for changing of glasses.

Signs : no visible signs as in congestive glaucoma. The only positive sign is increase of IOP. For diagnosis we have to carry out the following 1. check the IOP 2. check the field of vision 3. Fundus examination for glaucomatous cupping of disc.

a. IOP Patients with typical POAG have IOP higher than 21 mm Hg. High tension in the presence of an open angle is diagnostic. A normal tension does not exclude chronic simple glaucoma because of fluctuation in tension that normally may occur. For this reason the following methods could be done :

1. The presence of difference in IOP between the two eyes. Normally it should not exceed 4 mm Hg. A high difference is suggestive of glaucoma.

2. Diurnal variation : normally the IOP is highest in the early morning and goes to a minimum in the evening. The variation is never more than 4 mm Hg. A high difference is suggestive of glaucoma.

3. Provocation test : These tests do not depend on pupillary dilation as in closed angle glaucoma but they aim at increase the formation of aqueous. Because the drainage of aqueous is not normal the tension will rise

Water drinking test : Tension is measured and patient drinks one liter of water. Tension is measured after one hour. A rise of 5 mm Hg or more is diagnostic.

B. Changes in the optic disc : By examination of nerve fiber layer of the retina using red-free illumination, defects in NFL can be detected even before visible changes in optic disc appear.

The normal cup / disc ratio (C/D ratio) varies from 0.0 to 0.3 and depends on the volume of nerve fibres in relation to the size of the scleral foramen.

In glaucoma due to atrophy of the fibers, cupping of the disc occurs in the form of increase in C/D ratio accompanied by deepening of the cup.

Glaucoma


detected stereoscopically by binocular ophthalmoscopy:

When the disease advances the cup disc ratio widens with

limping of the central retinal vessels.

By the end the cup disc ratio reaches more than 0.9

C. Changes in the field of vision : Damage to the nerve fiber layer (NFL) of the retina in glaucoma tends to involve bundles of fibres resulting in corresponding defects in visual field.

The clinically significant field changes are:

Scotomata that develop in Bjerrum area (area lying between 10-20° around fixation point e,g Siedel scotoma, arcuate (Bjerrum) scotoma , double arcuate scotoma

Isolated nasal scotoma may be detected in early glaucoma, with

nasal step (unequal scotomatous areas above versus below the horizontal

meridian of the field)

Concentric contraction of the peripheral field.

Field defects enlarge peripherally and centrally that may end in a tubular field .

Still at this stage the visual acuity might be near normal although the field defect makes the patient visually handicapped.

A temporal island of vision might be retained to late stages.

Later on both central and temporal islands disappear resulting in total blindness (absolute glaucoma).

NB. If POAG is not controlled and disc and field changes were allowed to continue, glaucoma will reach to stage where the whole field of vision is lost and vision is no PL i.e. : absolute glaucoma. In contrast to absolute glaucoma following PACG, the eye with absolute glaucoma following POAG looks normal in every way except :

Vision in no PL

Pupillary light reflex is lost when this eye is stimulated by light (no PL)

Fundus shows advanced glaucomatous optic atrophy

Glaucoma


Fig 51 : eye looks completely normal yet fundus examination is shown in next figure

Fig 52 : marked cupping of the right eye and moderate cupping of the left eye IF IOP is higher than average (> 21 mmHg) then the diagnosis is POAG. IF IOP is within average (between 14-20 mmHg ) the diagnosis is normal tension glaucoma.

Fig. 53 : patient did not receive treatment till the whole field of vision was completely lost and vision is now no PL. So the patient reach to the stage of absolute glaucoma. As you notice the looks completely normal with normal pupil size. The only +ve finding are high IOP and marked cupping and no PL. (Eye with absolute glaucoma following open angle type looks normal)

Treatment : The treatment of chronic simple glaucoma is essentially medical unlike closed angle glaucoma, which is treated surgically.

1. Medical treatment : As there is no emergency, we start by one drug in one eye and test the eye response. If suitable we use the drug in both eyes. We always can add a second or a third drug to obtain the desired effect. Our goal is to stop the damage to nerve fibers (as determined by field of vision and fundus examination)

Glaucoma


The principle is to use the least possible and safest drugs to control IOP Success of medical treatment means that the IOP is lowered to a level which prevents any further deterioration in the appearance of the fundus or in the field of vision. Regular follow up is essential step for the treatment and should continue for life. A glaucoma controlled by medical treatment may later on become out of control.

1. Beta blockers - Decrease aqueous production through blocking the beta receptors of

the ciliary epithelium - Do not affect pupillary size nor affect the ciliary muscle. - Suitable for all types of glaucoma. - Example Timolol maleate 0.25-0.5 % eye drops/12 hours - Side effects are due to blocking the beta receptors in heart and

bronchial tree : - Bradycardia, decrease myocardial contractility and may precipitate

heart failure and hypotension in cardiac patient - May precipitate attacks of bronchial asthma in asthmatic patients.

In those patients, selective 1 blockers can be used ( e.g. betaxolol 0.5% eye drops)

- Contraindications

- Due to systemic absorption, undesirable Beta-blocker effects e.g.,

bradycardia, decrease myocardial contractility and bronchospasm

might occur. The drugs are better avoided in patients with heart

failure, heart block and bronchial asthma. 2. Prostaglandin analoges :

( e.g. Latanoprost, travoprost and bimatoprost eye drops) they increase the uveo-scleral outflow of aqueous humor. It is used once daily by night . Once a day use allows better compliance to medication. Drug is expensive. Its side effect include increased pigmentation of iris and skin of lids, elongation of lashes, may help development of iridocyclitis and CME (cystoid macular edema) especially in aphakic persons. 3. Topical Carbonic andydrase inhibitors (TCAI) :

Topical CAI in the form of eye drops (dorzolamide, brinzolamide eye drops) it topical CA inhibitor used as eye drops every 12 hours. It decreases aqueous production via inhibition of carbonic andydrase enzyme of the inner layer of ciliary epithelium.

Glaucoma


Side effects : burning sensation – stinging

4. Miotics eye drops :

Pilocarpine 1-4 % eye drops :

Oldest, cheapest and most effective drugs

Mechanism of action - Induces contraction of the longitudinal muscle fibers of CM, thus

pulls on the scleral spur leading to opening of the trabecular meshwork and increasing aqueous out flow

- Contraction of ciliary muscle squeezes of the ciliary vessels leading to decrease aqueous production - Stretch of iris and open iris crypts, increasing the surface area for

aqueous absorption. - Contraction of the pupil that open the angle (most important in closed

angle glaucoma)

Drawbacks and side effects: - Used 6-8 hours/day (difficult to comply with)

- conjunctival congestion - miosis : dimness of vision especially a night and especially if there is central corneal or lens opacity. - Ciliary body spasm : headache and transient myopia especially in

young patients. - Cysts might form at the pupillary border (miotic cysts)

5. Alphagan eye drops (0.2% brimonidine) twice daily

is a selective 2 adrengergic agonists : it decreases aqueous formation and increases uveo-scleral outflow. Side effects allergy and dry month Should not be ued in first year of life as may cause fatal systemic hypertension and also CNS affection

Oral CAI acetazolamide tablets : 250 mg 1-4 tab/day it is reserved only for cases which are not adequately controlled by local treatment. Side effects : tingling and numbness of hands and feet GIT upset Renal stones Generalized malaise, anorexia and depression. Hypokalemia so that potassium syrup must be add to the treatment

Glaucoma


It is related chemically to suflonamides so that it can cause drug rash, aplastic anemia or agranulocytosis. It should be used for long time because of these side effects. Its use is largerly replaced by the topical form (TCAI).

Observation : Patients under medical treatment for POAG must be examined at regular intervals, checking the IOP, field of vision and disc changes. Treatment may be modified to keep glaucoma under control, as demonstrated by having no glaucomatous changes in field of vision nor in the optic disc. Alternative lines of treatment "surgery or laser trabeculoplasty" are indicated when 1. medical treatment failed to control IOP : e.g. drugs are not effective any

more or patient is irregular in applying the drugs 2. field deteriorates or optic disc deteriorates even though tension looks within

average 3. lack of facilities for proper follow up. e.g. patient coming from far locations

and cannot come back regularly

2. Laser trabeculoplasty: it was found that application of scattered laser burns to the trabecular meshwork improves aqueous drainage through the non treated areas of the meshwork. Laser is applied to the angle of AC using a goinoscopic lens under topical anesthesia on the slit lamp. It lowers the IOP 8-10 mm Hg. So can be used for patients on maximum tolerable medications and their IOP not higher than 26-28 mm Hg. The effect of laser may decrease or even totally lost within couple of years so again follow up is essential in all cases of glaucoma.

Fig 54: Argon laser applied to the trabecular meshwork can lower IOP by 6-8 mmHg but the effect will be lost within 5-10 years

Glaucoma


3. Surgery :

subscleral trabeculectomy : Where a guarded fistula is created between the AC and the subconjunctival space so aqueous can be drained by the conjunctival blood vessels.

Secondary glaucomas It is glaucoma secondary to another disease whether systemic or local, i.e. the etiology of glaucoma is known.

Systemic causes : these are rare causes and usually results form diseases

which raise the pressure in the episcleral veins, superior vena cava obstruction.

Local causes : 1. Corneal causes :

hypopyon ulcer : secondary iridocyclitis with plasomoid aqueous and cells obstructing the angle of AC and impairing drainage or the cyclitis is accompanied by increased aqueous production Perforated corneal ulcer : lost AC if for sufficient time will result of formation of PAS (peripheral anterior synechia). If PAS are extensive glaucoma will appear. If peroration is big and total anterior staphyloma is formed, the angle will be closed and glaucoma will appear .

Fig 55: hypopyon or severe aqueous flare can block the aqueous drainage and IOP will go up

Glaucoma


Fig 56 : leucoma adherence can affect the angle of AC and aqueous circulation might be affected and glaucoam may develop

Fig 57 : Total anterior staphyloma will definitely affect aquous passage and secondary glaucoma will definitly appear.

2. Anterior chamber : The normal aqueous has a low protein content (2:10000) and contains no cells or solid particles so it can flow easily through the trabecular meshwork. Any abnormal contents in the aqueous will increase its viscosity and block the meshwork pores .

- abnormal contents e.g. plasmoid aqueous, hypopyon, hyphema, lens matter, tumor cells.

Fig 58: hypopyon or flare and cells can affect aqueous drainage

Glaucoma


Fig 59 : limited hyphema is not likely affect drainage of aqueous

Fig 60 : the risk of secondary glaucoma is quite high with total hyphema when not managed properly

3. Iris and CB : iridocycitis :

- Active stage : excess aqueous production or plasmoid aqueous with high contents of proteinceous material and inflammatory cells.

- Chronic stage : - Ring posterior synechiae - Total posterior synechiae - Occluso pupillae - Extensive PAS

N.B. The treatment of glaucoma secondary to active iridocylclitis is directed to the cause so we give atropine and steroids This will control the inflammation. Pilocarpine is contraindicated in iridocyclitis. Aqueous production could be reduced using tilolol and CA inhibitors.

Glaucoma


Fig 61 : showing possible mechanisms that chronic iridocyclitis may cause secondary glaucoma

Fig 62 : hypopyon may obstruct the angle of AC.

Fig 63 : ring synechia will cause iris bombe and pupilary block glaucoma

Glaucoma


Fig 64 : Occluso pupillae and iris bombe are seen

4. Rubeosis iris : Is characterized by the formation of abnormal BVs and fibrous tissue on the surface of the iris and the angle of the AC This abnormal neovascular membrane will close the angle of the AC. Condition could be seen in

- chronic recurrent iridocyclitis (local ischemia of the iris tissue)

- Proliferative Diabetic retinopathy - Central Retinal Vein occlusion : 100 days glaucoma as it usually

occurs 3 months following CRVO. In the last two conditions, if there is a wide area of ischemia affecting large area of retina, these areas will produce vasoformative substances that stimulate the development of abnormal vessels. These new vessels occur on the surface of the disc (NVD: new vessels disc), surface of the retina (NVE : new vessels else where) and iris and angle of AC (rubeosis iridis)

Neovascular glaucoma, rubeotic glaucoma, thrombotic glaucoma, hemorrhagic glaucoma.

Treatment : Prophylactic : Condition is prevented by photocoagulation of the ischemic areas in the retina changing them into infarcted areas which are not capable of producing vasoformative substances. Curative : If neovascular glaucoma is developed, it is difficult to treat.

Ordinary fistulizing operations usually fails because the neovascular membrane usually grows and occludes the fistula. Application of 5FU or Mitomycin during surgery may help.

Treatment could be achieved by inserting a valve (special device that connect the AC with the suprascleral space It is special plastic tubes that

Glaucoma


open when IOP is high and closed as IOP drops so acts like a valve : e.g. Ahmed's valve an example of glaucoma devices )

A second way of treatment is defunctioning operations.

Fig 65 : Rubeosis iridis is commonly associated with a fibrovascular membrane that occlude the angle of the AC

Fig 66: Rubeosis iridis is common following proliferative diabetic retinopathy

Fig 67 : Rubeosis iridis may follow CRVO Central retianal vein occlusion

Glaucoma


5. Lens (lens induced glaucoma) a. Displacement of the lens :

- Anterior displacement : the lens will block the pupil so prevents the circulation of aqueous. This type is known as glaucoma inversus (inverted glaucoma) because miotics will increase the glaucoma.

- Posterior dislocation : continuous hitting to iris and CB will lead to iridocyclitis and secondary glaucoma.

b. Increased size of the lens (swollen lens) : Phacomorphic glaucoma

- Intumescent type of cataract - Morganian cataract - Traumatic cataract

c. Glaucoma capsulare : (pseudo exfoliation syndrome) This is a specific type of glaucoma that occurs in some susceptible races in which small flakes of material is deposited on the lens capsule, CB epithelium and angle of AC. It was thought to be parts of lens capsule desquamated as a result of rubbing of iris against the lens but it was found to be abnormal material secreted by the epithelium of CB. These flacks may block the angle of AC resulting if glaucoma d. Phacolytic glaucoma : This occurs in hypermature cataract where the degenerated lens matter escapes though microscopic opening of the lens capsule into the AC These will act as Foreign protein which will be engulfed by phagocytes. (lens proteins are encapsulated by lens capsule long before the development of the immune system so they are not recognized as being self-proteins) If the lens matter are of huge amounts the angle of AC will be blocked and IOP will go up. Clinically we have a patient of long history of drop of vision in the eye and white pupil who suddenly develop pain redness of the eye and on examining him we find the

signs of acute glaucoma together with milky material in the AC.

Treatment is removal of the lens.

Glaucoma


Fig 68: Speudo exfoliation of lens capsule. Sometimes the tiny exfoliative material blocks opening of trabvecular meshwork thus aqueous drainage is affected and IOP rises. It is an open angle glaucoma.

Glaucoma


Fig 69: Morganian cataract may be associated with pupillary block and hence rise of IOP

Fig 70 intumscent cataract is a lens with minimal immature cataract that absorbs water from aqueous and swell and become mature in few days. This increase in size of lens may result in pupillary block and secondary glaucoma.

Fig 71 : patient known to have mature cataract and suddenly developed pain, redness and rise of IOP and on examination there is flare in AC and even may develop hypopyon. This is the typical presenation of phacolytic glaucoma

Fig 72: a lens in the AC may be associated with rise of the IOP

Glaucoma


6. Haemorrhagic glaucoma : Hyphema blocking the angle Vitreous hemorrhage pushing iris lens diaphragm forwards blocking angle.

Fig 73 : Blood in AC may occlude the angle and IOP will rise.

7. Tumours : The rise of tension could be due to

Direct invasion of the angle in cases of tumors of iris or ciliary body.

For tumors of posterior segment (retinoblastoma or malig. Melanoma) glaucoma may occur a result of :

- tumor is space occupying lesion, closure of angle by pushing of iris lens diaphragm forward

- block of angle by tumor cells - intra ocular hemorrhage - a rapidly growing tumour might consume most of the blood supply

creating a state of ischemia, rubeosis iridis and neovascular glaucoma - extensive tumour necrosis might lead to toxic iridocyclitis and 2ry

glaucoma

Orbital tumors may press on vortex veins leading to vascular engorgement.

Glaucoma


Fig 74 : Retinoblastoma may cause secondary buphthalmos

Glaucoma


Treatment of secondary glaucoma is that of the cause

Operations for Glaucoma

1. Peripheral iridectomy 2. fistulizing operations The idea of external fistulizing operations is to create a passage (fistula) for the aqueous to pass to the subconjunctival space to be absorbed by blood vessels of the conjunctiva and episclera. This passage is usually created at the limbus superiorly. SST (Subscleral trabeculectomy ) -conjunctiva is opened to expose the sclera lamellar dissection of scleral flap is done (50% depth) about 4x4mm ending into the limbal area trabeculectomy is done 1x2 mm peripheral iridectomy (work as an alternative pathway for aqueous if postoperative pupillary block occurs closure of scleral flap then closure of conjunctiva

Glaucoma


the aqueous coming through the fistula passes first under a partial thickness scleral flap before reaching the subconjunctival sapce, thus the filtration is more gradual and the wall of the filtering bleb is guarded by a layer of sclera in addition to the conjunctiva.

Fig. 75 : Subscleral trabeculectomy. (1)Conjunctival incision (2) lamellar scleral flap is outlined (3)and (4) sponge soaked in MMC in applied under the Tenon’s capsule for 1-3 minutes. (5) Wash to remove excess

MMC (6) scleral flap is dissected, 1/3 depth of sclera.

Glaucoma


Fig 77: SST-Continue. (7) and (8) two sutures are pre placed at corners of scleral flap. (9) and (10) small area of trabecular meshwork is removed. (11) peripheral iridectomy (12) clousre of scleral flap. (13) tight closure of conjunctival wound.

Glaucoma


Shunt operations:

These are done in advanced cases, or after failure of more than one filtering surgery or as primary procedure in some cases of secondary glaucoma e.g neovascular glaucoma and aphakic glaucoma.

This is achieved by inserting tubes with or without valves, made of synthetic material connecting the anterior chamber to the

subconjunctival space.

Antifibrotic angents : Whed doing fistulizing operation in cases where there is a great tendency for closure of the fistula due to excessive conjunctival scarring e.g. neovascular glaucoma or pt with POAG on medical treatment for years . This may be controlled by the local use of antimetabolies (5 fluorouracil (5-FU) or Mictomycin) at the time of surgery or in the post operative peroid.

4. Defunctioning operations These surgeries aim to reduce IOP by the amount of aqueous production by destroying part of the CB.(cyclodestructive procedures) This could be achieved by : heat (cyclodiathermy), cooling (cyclocryotherapy) or laser (diode cycloablation) . The first two proceduces are less used these days as the diode cycloablation has marked less incidence of complications. Severe iridocyoclytis and over effect resulting in marked decrease of aqueus secretion and trophy of the eye were most unpleasant complication that could occur with cyclodiathermy or cylcocryotherapy. Such complications are quite rare with the diode cyclo ablation. In the past defuctioning operation was reserved to late stages of glaucoma or absolute stage but nowadays the diode cycloablation is a proceduce that can be done in seeing eye in special cases of glaucoma e.g. rubeotic glaucoma and aphakic glaucoma. and also in cases with failure of SST.

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