Course no.7.I.

THE LENS
(7.II- GLAUCOMA)

Anatomy:
The lens : is a unique transparent, biconvex, avascular , noninervated, intraocular structure.
The lens is part of the anterior segment of the human eye.
In front of the lens is the iris, which regulates the amount of light entering into the eye.

The lens is suspended in place by the suspensory ligament of the lens or Zonula , a ring of fibrous tissue that
attaches to the lens at its equator and connects it to the ciliary body.
The lens is an encapsulated body composed entirely of epithelial cells and fibers.
The 3 layers of the lens are :
1.the nucleus,
2.cortex,
3.capsule.

Accommodation= phenomenon that The eye has the capacity to adjust its focus
from distance to near objects because of the ability of the lens to change shape,.
accommodation picture:

*ciliary muscles: The inherent elastic property of the lens allows it to become more or less spherical depending
on the amount of tension exerted by the zonular fibers on the lens capsule. Zonular tension is controlled by the
action of the parasympathetically innervated ciliary muscle. When cilliary muscles contracts, relaxation of
zonular tension occurs.
The lens then assumes a more spherical shape, resulting in increased dioptric power which helps to bring nearer
objects into focus.
Ciliary muscle relaxation causes the zonular tension to increase. As a result, lens flattens, which helps in bringing
more distant objects into view.

Pathology:
1. Ectopia lentis is the dislocation or displacement of the natural crystalline lens. The lens is defined as
luxated (dislocated) when it lies completely outside of the hyaloid fossa, is free-floating in the vitreous, is in the
anterior chamber, or lies directly on the retina. The lens is considered subluxed when it is partially displaced but

remains within the lens space.  

Causes:
1. Ectopia lentis may occur after trauma or may be associated with ocular or systemic disease. As ectopia lentis
may be the first sign of a more serious systemic disease.
2.Marfan syndrome is the most common cause of heritable ectopia lentis, and ectopia lentis is the most frequent
ocular manifestation of Marfan syndrome, occurring in approximately 75% of patients Lens dislocation in
Marfan syndrome is usually bilateral and occurs most often in the superotemporal direction, though other
directions are not uncommon.
-Individuals with Marfan syndrome are usually tall and slender, have elongated fingers and toes
(arachnodactyly), loose joints, and have an arm span that exceeds their body height.
- Other common features include a long and narrow face, crowded teeth, an abnormal curvature of the spine,
stretch marks (striae) not related to weight gain or loss, and either a sunken chest .
- Some individuals develop an abnormal accumulation of air in the chest cavity that can result in the collapse
of a lung (spontaneous pneumothorax).
- The dura, which surrounds the brain and spinal cord, can be abnormally enlarged (dural ectasia) and can
cause pain in the back, abdomen, legs, or head.  
- Most individuals with Marfan syndrome have some degree of nearsightedness (myopia).
-Cataract may occur in mid-adulthood, glaucoma occurs more frequently in people with Marfan syndrome
than in those without the condition.
- Stretching of the aorta may cause the aortic valve to leak, which can lead to a sudden tearing of the layers in
the aorta wall (aortic dissection). Aortic aneurysm and dissection can be life threatening.

2. Acquired Cataract
A cataract is an opacification of the lens of the eye which leads to a decrease in vision.
-Cataracts often develop slowly and can affect one or both eyes.
Symptoms may include faded colors, blurry or double vision, halos around light, trouble with bright lights, and
trouble seeing at night.
-For people who have cataracts, seeing through cloudy lenses is a bit like looking through a frosty or fogged-
up window This may result in trouble driving, reading, or recognizing faces.
- Poor vision caused by cataracts may also result in an increased risk of falling and depression.
- Cataracts cause half of all cases of blindness and 33% of visual impairment worldwide.

cause: Cataracts are most commonly due to aging but may also occur due to trauma or radiation exposure, or
occur following eye surgery for other problems.

Risk factors include diabetes, longstanding use of corticosteroid medication, smoking tobacco, prolonged
exposure to sunlight, and alcohol. The underlying mechanism involves accumulation of clumps of protein or
yellow-brown pigment in the lens that reduces transmission of light to the retina at the back of the eye.
Diagnosis is by an eye examination.
Cataracts may be partial or complete, stationary or progressive, or hard or soft.
The main types of age-related cataracts are nuclear sclerosis, cortical, and posterior subcapsular.

  Aquired cataractsymptoms: : can make images appear dull or yellow, blurry

and distortion as ghost image,
 
2.I Nuclear Sclerotic Cataracts
This is the most common type of age-related cataract, caused primarily by the hardening and yellowing
of the lens over time.
-“Nuclear” refers to the gradual clouding of the central portion of the lens, called the nucleus;
-“sclerotic” refers to the hardening, or sclerosis, of the lens nucleus.
Nuclear sclerosis is the most common type of cataract, and involves the central or 'nuclear' part of the
lens. This eventually becomes hard, or 'sclerotic', due to condensation on the lens nucleus and the
deposition of brown pigment within the lens.
Evolution: In its advanced stages it is called a brunescent cataract. In early stages, an increase in
sclerosis may cause an increase in refractive index of the lens. This causes a myopic shift (lenticular shift) that
decreases hyperopia and enables presbyopic patients to see at near without reading glasses. This is only
tempororary and is called second sight.  

2.II. Cortical cataracts are due to the lens cortex (outer layer) becoming opaque.
At the slit lamp, the appearance is similar to white spokes of a wheel.
Wedge-shaped opacity with clear areas of lens matter mostly present at the periphery (incipient  cortical
cataract)
Well-developed wedge-shaped opacity (progressive cortical cataract)

Stages of cortical cataract

- Advanced opacity with a greyish lens, clear cortex, and an iris shadow (immature cortical cataract)
-Findings of the immature stage but with a swollen lens due to the accumulation of fluid making anterior

chamber shallow (intumescent cortical cataract)  

-The entire opaque cortex with the absence of iris shadow (mature cortical cataract)  
-Milky fluid bag with lens nucleus present at the bottom due to liquefaction of the cortex without an iris shadow

and a shallow anterior chamber (hypermature cortical cataract)  

Ophthalmic examination
 1. Visual acuity: can be assessed by Snellen chart to identify the severity of the disease and limitations in
routine activities of life
2. Refraction: Important factor to plan management
3.Cover test: poor vision caused by cataract can be a reason for a divergent squint
4. Slit-lamp examination
5. Pupillary responses: to check the shape of the pupil and photomotor reflex
6. Adnexal examination: a thorough examination is needed to exclude any adnexal pathology, i.e.,
dacryocystitis, blepharitis, chronic conjunctivitis, lagophthalmos, ectropion, entropion, and tear film
abnormalities - these conditions may predispose to endophthalmitis, so their diagnosis and optimization are
necessary to treat cataract.
7. Cornea: important to asses whether cornea will able to handle operative trauma - arcus senilis is an
important finding because it can obstruct the operative field clarity.
8. Anterior Chamber: a shallow anterior chamber can make cataract surgery extremely difficult.
9. Lens: part of the lens involved can be an important factor to plan our surgical technique - nuclear cataract is
harder while cortical cataract is softer in consistency
10. Fundus Examination: any pathology in the fundus, i.e., age-related macular degeneration can be an
important factor to determine visual outcome after surgery.

Investigations
The following investigations can help diagnose and plan the management of the disease:
1.Intraocular pressure: to rule out glaucoma
2. Ophthalmoscopy to rule out any vitreous or retinal pathology
3. Biometry: for intraocular lens (IOL) placement during surgery
4. Systemic diseases: Blood glucose levels, electrocardiography
5. Baseline tests: Complete blood count, liver function test, renal function test.

Treatment
Treatment options are the following:
1. Medical: No medical treatment is effective once the cataract has become mature.
2. Surgical: Mature cataract has a very hard nucleus, and one of the following methods are used to
3. extract lens:picture:

Extracapsular cataract extraction: a procedure of choice.  

Intracapsular cataract extraction: an old technique not used frequently due to complications.
4. Phaco-emulsification: a modification of extracapsular cataract extraction (ECCE) with less astigmatism and
early visual recovery.
5. Laser phacolysis: a recent advancement under trial
6. Phacoemulsification cataract surgery, or phaco, as surgeons refer to it, is a procedure in which an
ultrasonic device is used to break up and then remove a cloudy lens, or cataract, from the eye to improve vision.
The insertion of an intraocular lens (IOL) usually immediately follows phacoemulsification:pic:.

 
Proper anesthesia is essential for ocular surgery. Topical anesthesia is most commonly employed, typically by
the instillation of a local anesthetic such as tetracaine or lidocaine.
Before the phacoemulsification can be performed, more incisions are made in the eye to allow the introduction
of surgical instruments.

7. Capsulorhexis or capsulorrhexis,([picture) also known as continuous curvilinear capsulorhexis (CCC), is a

technique used to remove the capsule of the lens from the eye. It generally refers to removal of a part of the

anterior lens capsule.  

Then the cataract is usually broken into two or four pieces and each piece is emulsified and aspirated out with
suction. The nucleus emulsification makes it easier to aspirate the particles. After removing all hard central lens
nucleus with phacoemulsification, the softer outer lens cortex is removed with suction only.
 In order to remove a cataract with modern techniques, the capsule of the lens must be opened.
In older style surgery (intracapsular cataract extraction), the whole lens and capsule was removed.
In most cases, surgery restores vision very effectively. Recent studies reveal that in most of the cases, the
prognosis is excellent after surgery almost 70 to 80%.
Most patients show excellent results after surgery if they strictly follow postoperative instructions and
medication regimens advised by their ophthalmologist.
A routine eye examination is advisable, which will detect any cataract development in the other eye.

Many patients with a monofocal IOL :  may require refractive glasses to achieve their
best visual acuity after surgical cataract removal. Gradual opacification of the posterior capsule can develop in a
large number of patients that can affect the patient's vision (secondary cataract).

Complications
Cataract cause multiple complications discussed as follows:
These can be A. disease-related or B. surgery related:
A. Disease-related complications:
1.Intumescent stage: acute congestive glaucoma,
2. Hypermature stage: phacolytic glaucoma, iritis, subluxation of the lens, secondary glaucoma,
 3. Blindness
B. Surgery-related complications: these are classified as follows:
1. During surgery: posterior capsular rupture, hyphaema, expulsive hemorrhage, corneal burn, nucleus
drop in vitreous.
Expulsive hemorrhage or Suprachoroidal hemorrhage (SCH) is a rare, but potentially vision threatening
pathology that may manifest as a consequence of intraocular surgery. It occurs when blood from the long or short
ciliary arteries fills within the space between the choroid and the sclera.
2. Post surgery: iris prolapse, delayed anterior chamber formation, infections like endophthalmitis or
panophthalmitis, striate keratitis, malpositioning of IOL, pseudophakic glaucoma, cystoid macular edema, ptosis,
retinal detachment, posterior capsular thickening, and opacifications.

*Secondary cataract(picture) or after-cataract is an opacification of the posterior capsule of the lens that may
appear after a few months or years of having undergone a cataract extraction. This prevents the passage of light

to the retina and leads to loss of vision  

Nd:YAG laser (picture) capsulotomy is accepted as standard treatment for secondary cataract.

Prevention of cataract includes wearing sunglasses, a wide brimmed hat, eating leafy vegetables and fruits, and
avoiding smoking.
Early on the symptoms may be improved with glasses. If this does not help, surgery to remove the cloudy lens
and replace it with an artificial lens is the only effective treatment.
Cataract surgery is not readily available in many countries, and surgery is needed only if the cataracts are causing
problems and generally results in an improved quality of life

Course no.7.II. GLAUCOMA

Glaucoma=group of eye diseases result in damage to the optic nerve & cause vision loss.
Anterior chamber angle

It is located between iris, cornea and sclera

This is the area in which the trabecular

meshwork lies and is therefore the part of the eye t
hat is responsible for aqueous outflow.

Diagnosis: Gonioscopy consists in the biomicroscopic exam

of the topography of the anterior chamber angle (camerular sinus),
where the aqueous fluid has access to drainage pathways. This is the most important exam for the classification
of glaucoma, and it is used as a reference for the evaluation of the anterior chamber angle configuration. The
identification of all anatomical details of the camerular sinus allows the assessment of crucial aspects for
diagnosis of several types of glaucoma

1.Congenital glaucoma
1.I.Primary congenital glaucoma (PCG) is a rare disease due to genetically-determined abnormalities in the
trabecular meshwork and anterior chamber angle resulting in elevated intraocular pressure (IOP), without other
ocular or systemic developemental anomalies.

Evolution: PCG commonly presents between the ages of 3-9 months, but the most severe form is the newborn
onset. Elevated IOP is associated with the classic “triad” of symptoms (photophobia, epiphora and
blepharospasm), which occurs due to rapid expansion of the child’s eye causing buphthalmos , corneal
enlargement, horizontal or oblique breaks in Descemet membrane (Haab striae) and subsequent corneal edema
and opacification.

Due to the elasticity of the eye in young children, the 2013 International Classification System for Childhood
Glaucoma defined childhood glaucoma as: A. irreversible or B.reversible damage to the whole eye (not just the
optic nerve as glaucoma is defined for adults).
Thus, additional important clinical signs in PCG, besides elevated IOP and optic nerve cupping, are corneal
enlargement and clouding, Haab striae, and buphthalmos. Not all signs are always present, however, and other
parts of the eye also stretch with elevated IOP.

Diagnosis of PCG can be delayed if corneas remain clear, despite being enlarged, and bilateral PCG can be
missed if signs and symptoms are mild in one eye.
A. Irreversible vision loss results if elevated IOP is untreated or uncontrolled in PCG. Optic nerve damage
occurs, and focal corneal edema overlying Haab striae, which can be single or multiple, can lead to permanent
corneal scarring and opacification. This corneal scarring can obscure the visual axis or cause astigmatism with or
without refractive amblyopia. Amblyopia may also develop due to optic nerve damage, anisometropia,
strabismus or a combination.

Symptoms
Patients with PCG experience one or more of the "clinical triad" of symptoms including epiphora, photophobia
and blepharospasm. This triad of symptoms is classically associated with PCG due to the corneal edema that
results from the elevated IOP, and causes irritation. Reduced vision can also occur from corneal
edema/opacification or progressive myopia and/or astigmatism. Amblyopia can further worsen vision.    

Signs
The main clinical signs of PCG include elevated IOP >21 mmHg, corneal edema and/or enlargement of the eye
with buphthalmos, and Haab striae. The IOP at presentation is usually between 30-40 mmHg, though it can be
outside this range. With IOP in the 30-40s mmHg, the cornea becomes cloudy due to diffuse and/or focal edema.

A newborn’s cornea is typically 9.5-10.5 mm in diameter and increases to 10.0-11.5 mm by age. Any diameter
above 12.0 mm before 1 year of age suggests an abnormality, especially if there is asymmetry between the two
eyes. If the diameter is greater than 13 mm at any age, glaucoma suspicion should be high.

Treatment: surgery

2. Acquired glaucoma
There are several types of glaucoma.
The two main types are
A. open-angle (most common form of glaucoma, accounting for at least 90% of all glaucoma cases and Is
caused by the slow clogging of the drainage canals, resulting in increased eye pressure
B. angle-closure. These are marked by an increase of intraocular pressure (IOP).

A. open-angle GLAUCOMA
Features:
Has a wide and open angle between the iris and cornea
Develops slowly and is a lifelong condition
Has symptoms and damage that are not noticed.
“Open-angle” means that the angle where the iris meets the cornea is as wide and open as it should be. Open-
angle glaucoma is also called primary or chronic glaucoma.
Open-angle glaucoma develops slowly over time and there is no pain. Peripheral vision may begin to decrease,
followed by central vision, resulting in blindness if not treated.
- About 70 million people have glaucoma globally
 - It occurs more commonly among older people. Glaucoma has been called the "silent thief of sight", because
the loss of vision usually occurs slowly over a long period of time

Risk factors for primary open-angle glaucoma include

- Older age
- Positive family history
- African ethnicity
- Thinner central corneal thickness
- Systemic hypertension
- Diabetes
- Myopia (one can see near objects but cannot see far objects clearly)

The mechanism of open-angle glaucoma is believed to be slow exit of aqueous humor through the trabecular
meshwork.

Signs and symptoms

Open-angle glaucoma is usually painless with no symptoms early in the disease process, thus screening via
regular eye check-ups important.
*The only signs are gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio
on fundoscopic examination)
*The cup-to-disc ratio ( notated CDR) is a measurement used in ophthalmology to assess the progression of
glaucoma. The optic disc is the anatomical location of the eye's "blind spot", the area where the optic nerve and
blood vessels enter the retina. The optic disc can be flat or it can have a certain amount of normal cupping. But
glaucoma, which is in most cases associated with an increase in intraocular pressure, often produces additional
pathological cupping of the optic disc.
- The pink rim of disc contains nerve fibers. The white cup is a pit with no nerve fibers. As glaucoma
advances, the cup enlarges until it occupies most of the disc area.

Characteristic optic nerve changes include

-Increased cup:disk ratio (particularly an increasing ratio over time)
-Thinning of the neurosensory rim
-Pitting or notching of the rim
-Nerve fiber layer hemorrhage that crosses the disk margin (ie, Drance hemorrhage or splinter hemorrhages)
-Vertical elongation of the cup
-Quick angulations in the course of the exiting blood vessels (called bayoneting)
- Thinning of the retinal nerve fiber layer over time alone can be diagnostic of glaucoma regardless of the
IOP or visual field and is the initial sign of damage in up to 80% of cases.

Visual field defects caused by lesions of the optic nerve include

-Nasal step defects (which do not cross the horizontal meridian—an imaginary horizontal line between the
upper and lower parts of the visual field)
-Arcuate (arc-shaped) scotomata extending nasally from the blind spot
-Temporal wedge defects
-Paracentral scotomata

Diagnosis of Optic nerve in advanced glaucoma disease

Screening for glaucoma is usually performed as part of a standard eye examination performed by optometrists
and ophthalmologists.
-Testing for glaucoma should include measurements of the intraocular pressure via tonometry, anterior chamber
angle examination or gonioscopy, and examination of the optic nerve to look for any visible damage to it, or
change in the cup-to-disc ratio and also rim appearance and vascular change.
-A visual field test should be performed.
-The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence tomography,
scanning laser polarimetry, and/or scanning laser ophthalmoscopy (Heidelberg retinal tomogram).
Visual field loss is the most specific sign of the condition; however, it occurs later in the condition.

Treatment=Decreasing intraocular pressure (IOP)

*Initially, drugs (eg, prostaglandin analogs such as latanoprost or tafluprost, beta-blockers such as timolol)
*Sometimes surgery, such as laser trabeculoplasty or guarded filtration procedure
* Vision lost by glaucoma cannot be recovered. The goal is to prevent further optic nerve and visual field
damage by lowering IOP. The target level is 20 to 40% below pretreatment readings or the IOP at which damage
is known to have occurred.
* In general, the greater the damage caused by glaucoma, the lower the IOP must be to prevent further damage.
If damage progresses, the IOP goal is lowered further and additional therapy is initiated.
1. Initial treatment is usually drug therapy, proceeding to laser therapy and then incisional surgery if the target
IOP is not met. Surgery may be the initial treatment if IOP is extremely high, the patient does not wish to use or
has trouble adhering to drug therapy, or if there is significant visual field damage at presentation.

II. B. angle-closure GLAUCOMA. is more common in women and in hypermetropia(=nearby objects

look blurred, while the distant objects are more clearly visible.) .
eyes with angle-closure glaucoma have a drainage angle that is blocked. This leads to elevated eye pressure,
which causes damage to the optic nerve.

II.B.1. Primary angle-closure glaucoma

Narrow angles are not present in young people. As people age, the lens of the eye continues to grow. In some but
not all people, this growth pushes the iris forward, narrowing the angle.

Risk factors for developing narrow angles include:

- family history,
-advanced age, and
-ethnicity; r
**risk is higher among people of Asian ethnicity and lower among people of
European and African ethnicity.
-In people with narrow angles, the distance between the iris at the pupil and the
lens is also very narrow.  

Pathophysiologic mechanisms of angle closure glaucoma

- Pupillary block due to pupil dilatation is the most common mechanism of
angle closure. It occurs when the pupil comes into contact with the lens and obstructs the aqueous flow from the
posterior chamber to the anterior chamber. This causes an elevation in pressure within the posterior chamber,
resulting in bowing of the peripheral iris anteriorly and apposition of the peripheral iris to the trabecular
meshwork. Consequently, the aqueous cannot drain out and IOP rises

primary acute angle-closure glaucoma: mechanism

1. Pressure from the continued secretion of aqueous into the posterior chamber by the ciliary body pushes the
peripheral iris anteriorly (causing a forward-bowing iris called iris bombe), closing the angle.
2. This closure blocks aqueous outflow, resulting in rapid (within hours) and severe (> 40 mm Hg) elevation of
intraocular pressure (IOP).
3. Because of the rapid onset, this condition is called primary acute angle-closure glaucoma and is an ophthalmic
emergency requiring immediate treatment.
Pupillary dilation (mydriasis) can push the iris into the angle and precipitate acute angle-closure glaucoma in
any person with narrow angles. This development is of particular concern when applying topical agents to dilate
the eye for examination

Signs and symptoms of an angle closure attack.

Red painful eye
Sudden blurring or loss of vision
Severe headache
Excessive tearing or watering
Sudden nausea or vomiting
Signs of angle closure attac
A very high intraocular pressure (>30 mmHg) ,a fixed, mid-dilated pupil and a red eye.
It is also associated with an oval pupil, in fixed semimydriasis.
Acute angle closure is an emergency.

Non-pupillary block mechanism:

1. include plateau iris syndrome in which the central anterior chamber is deep, but the peripheral anterior
chamber is made shallow by a ciliary body that is displaced forward.
Signs of intermittent angle closure:
Blurry or unfocused field of vision
Difficulty adjusting to dark rooms
Recurring mild pain around or in eyes
Recurrent headaches
Seeing colorful rings or halos around lights

Intermittent angle-closure glaucoma occurs if the episode of pupillary block resolves spontaneously after
several hours, usually after sleeping supine.

Chronic angle-closure glaucoma occurs if the angle narrows slowly, allowing scarring between the peripheral
iris and trabecular meshwork; IOP elevation is slow.

Drugs that have the potential to precipitate acute angle closure glaucoma(cause closure).
1.Adrenergic agonists-
Alpha-adrenergic agonists can precipitate acute angle closure glaucoma by pupillary block due to pupil dilatation
in individuals with innately narrow iridocorneal angles. Phenylephrine (alpha-adrenergic agonist) eye drops are
often administered.
Systemic ephedrine is often administered to manage hypotension, particularly in the setting of general
anaesthesia.

2.Non-catecholamine adrenergic agonists-

Cases of acute angle closure glaucoma have been reported following administration of nasal ephedrine and
naphazoline to treat epistaxis.

3.Anticholinergic agents-

Tropicamide drops are commonly administered for the purpose of ocular fundus examination and have been
associated with acute angle closure glaucoma. Other longer acting anticholinergic eye drops such as atropine and
cyclopentolate, administered for ciliary muscle relaxation and pupil dilatation, are also known to precipitate
angle closure.

4. Antihistamines- (H1 and H2 receptor blockers) can also induce acute angle closure glaucoma due to their
anticholinergic properties. Promethazine has been reported to cause swelling of the lens that can in turn result in
pupillary block. Ranitidine and cimetidine used in the treatment of gastroesophageal reflux and peptic ulcers
have also been shown to increase intraocular pressure in individuals known to have glaucoma.

Botulinum toxin:This subsequently results in inhibition of the pupillary sphincter that causes pupil dilatation and
pupillary block.

5.Antidepressants-
Tricyclic antidepressants e.g., clomipramine, imipramine, amitryptyline and selective serotonin reuptake
inhibitors (SSRI) e.g., venlafaxine, citalopram, escitalopram, fluoxetine and paroxetine have been reported to
precipitate acute angle closure glaucoma. The underlying mechanism is pupillary block caused by pupil
dilatation

6. Sulfa-based agents-

Sulfa-based agents such as topiramate, acetazolamide and hydrochlorothiazide are among the few drugs that can
induce “non-pupillary block” acute angle closure glaucoma. The typical presentation is blurred vision due to
forward displacement of the lens-iris diaphragm (myopia). The exact mechanism by which sulfa-based agents
cause acute angle closure glaucoma is unknown. Ciliary body swelling and anterior choroidal effusion can both
cause forward displacement of the iris-lens diaphragm resulting in obstruction to aqueous flow and subsequent
acute angle closure glaucoma.

Topiramate is commonly used for migraines and weight loss. More than 100 previously published cases of
topiramate-induced angle closure described bilateral non-pupillary block acute angle closure glaucoma (only
three cases of unilateral involvement) after taking the first doses of the medication. The attacks typically
occurred between days 1 and 49 and resolved after discontinuing the causative agent.2 It is important to
emphasize that topiramate induces mostly bilateral attack of angle closure glaucoma that occurs simultaneously
in both eyes. The element of bilaterality is a clear sign that the acute attack is drug-induced.

The management of sulfa drug-induced acute angle closure glaucoma involves stopping the medication and
controlling the intraocular pressure with topical or systemic steroid and cycloplegics. Topical miotics should be
avoided as they have the potential of causing pupillary block. Moreover, laser iridotomy is of no benefit in these
cases.

Acetazolamide is routinely used in ophthalmic and neurologic practice to reduce intraocular and intracranial
pressure. Incidentally, oral acetazolamide is commonly administered for one day following cataract surgery to
prevent excessive intraocular pressure increases. A few case reports have described acute bilateral angle-closure
glaucoma and choroidal effusion associated with acetazolamide administration following cataract surgery

**The presenting symptoms of patients with acute angle-closure glaucoma can be misleading because
headache, blurred vision, abdominal pain, nausea and vomiting are non-specific symptoms.

However, sudden onset of visual disturbance and a mid-dilated pupil are suggestive of acute angle-closure
glaucoma. Hyperopic glasses are a telltale sign for acute angle-closure glaucoma in patients presenting with
these symptoms. It is not possible for clinicians prescribing these drugs to refer all patients for ophthalmic
investigations. Moreover, it is difficult to identify all patients at risk of acute angle-closure glaucoma, as the
majority of these patients are asymptomatic and unaware of the increased risk associated with innately narrow
iridocorneal angles.

Patients known to have angle closure glaucoma are typically treated with laser iridotomy, filtering surgery or
cataract extraction to prevent attacks of acute angle-closure glaucoma. These patients who have undergone laser
iridotomy should be able to safely take medications that have the potential to induce acute angle-closure
glaucoma only by pupillary block. This educational review illustrates the importance for clinicians to be mindful
of medications that can potentially precipitate acute angle-closure glaucoma.

A careful history taking and obtaining a detailed list of both prescribed and non-prescribed medications–
including discontinued ones–in patients presenting with acute angle-closure glaucoma can help identify the
causative drug(s). Once the diagnosis is suspected, urgent medical intervention is required as appropriate and
prompt management potentially can be sight saving.

3. Secondary glaucoma refers to any form of glaucoma in which there is an identifiable cause of increased
eye pressure, resulting in optic nerve damage and vision loss.
As with primary glaucoma, secondary glaucoma can be of the open-angle or angle-closure type and it can occur
in one or both eyes.

Secondary glaucoma may be caused by an eye injury, inflammation, certain drugs such as steroids and advanced
cases of cataract or diabetes. The type of treatment will depend on the underlying cause, but usually includes
medications, laser surgery, or conventional surgery.

Exfoliative Glaucoma occurs when a flaky, dandruff-like material peels off the outer layer of the lens within the
eye. The material collects in the angle between the cornea and iris and can clog the drainage system of the eye,
causing eye pressure to rise. It is also called pseudoexfoliative glaucoma.

4. Neovascular Glaucoma is caused by the abnormal formation of new blood vessels on the iris and over
the eye's drainage channels. Neovascular glaucoma is always associated with other abnormalities, most often
diabetes. It never occurs on its own. The new blood vessels block the eye’s fluid from exiting through the
trabecular meshwork (the eye’s drainage canals), causing an increase in eye pressure.

Pigmentary Glaucoma occurs when the pigment granules that are in the back of the iris (the colored part of the
eye) break into the clear fluid produced inside the eye. These tiny pigment granules flow toward the drainage
canals in the eye and slowly clog them, causing eye pressure to rise.

5. Lens-induced glaucoma is a secondary glaucoma in which the crystalline lens is involved in the mechanism
of intraocular pressure (IOP) increase.

6. Traumatic Glaucoma — Injury to the eye may cause traumatic glaucoma. This form of open-angle glaucoma
can occur immediately after the injury or develop years later. It can be caused by blunt injuries that bruise the eye
(called blunt trauma) or by injuries that penetrate the eye.

7. Uveitic Glaucoma — Uveitis is swelling and inflammation of the uvea, the middle layer of the eye. The uvea
provides most of the blood supply to the retina. Increased eye pressure in uveitis can result from the
inflammatory process itself or the medication (steroids) used to treat it.

8. Lens damage – subluxation or dislocation

Partial zonular rupture results in lens subluxation and complete rupture in lens dislocation, either anteriorly into
the AC or posteriorly into the vitreous. These ruptures result from blunt or penetrating injuries and suggest a
significant injury. However, in children with underlying zonular fragility (such as Marfan syndrome and
homocystinuria, or in buphthalmic eyes) a simple trauma can dislocate the lens.
Mechanism of glaucoma
A subluxed lens leads to angle-closure glaucoma by forward displacement of the lens-iris diaphragm narrowing
the angle, and/or by a secondary pupillary block mechanism. Anterior dislocation can result in the lens becoming
trapped in the pupil, causing acute angle closure from secondary pupillary block or, if completely dislocated into
the AC, may cause raised IOP by reverse pupil block. Posterior dislocation is less likely to lead to glaucoma.
 Corneal abrasions typically resolve within 24-72 hours. They are most commonly caused by
ocular trauma or an ocular foreign body. Corneal abrasions are treated with a topical
antibiotic such as erythromycin or ciprofloxacin. Tetanus vaccination should be given to
patients who are not up to date.
Exacerbation ַ‫חרפָ ה‬
ָ

violaceous coloration ‫צבעוניות אלימה‬

septic ‫רקוב‬

accentuate ‫מּודגָׁש‬

Tenacious ִ‫תעַ קֵ ׁש‬

clover shape ‫צורת תלתן‬

Course no.10. cranial nerves