1.

All about glaucoma

Glaucoma

Glaucoma is a group of eye disorders that lead to progressive damage to the nerve that
connects the eye to the brain called the optic nerve. People with glaucoma can lose
nerve tissue, resulting in vision loss.

The optic nerve is a bundle of about 1 million individual nerve fibers that transmits
the visual signals from the eye to the brain. In the most common form of glaucoma,
primary open-angle glaucoma, the fluid pressure inside the eye increases. This
increase in pressure may cause progressive damage to the optic nerve and loss of
nerve fibers. Advanced glaucoma may even lead to blindness.

Not everyone with high eye pressure will develop glaucoma, and some people with
normal eye pressure will develop glaucoma. When the pressure inside a person's eye
is too high for a particular optic nerve, whatever that pressure measurement may be,
glaucoma will develop.

Glaucoma is the second-leading cause of blindness in the U.S. It most often occurs in
people over age 40, although an infant (congenital) form of glaucoma exists. People
with a family history of glaucoma, African Americans over the age of 40 and
Hispanics over the age of 60 have an increased risk of developing glaucoma. Other
risk factors include thinner corneas, chronic eye inflammation and taking medications
that increase the pressure in the eyes.

The most common form of glaucoma, primary open-angle glaucoma, develops

slowly and usually without any symptoms. Many people are not aware they have the
condition until they have significant vision loss. Initially, glaucoma affects peripheral
or side vision, but it can advance to central vision loss. If left untreated, glaucoma can
lead to significant vision loss in both eyes, and may even lead to blindness.

A less common type of glaucoma, acute angle-closure glaucoma, usually occurs

abruptly due to a rapid increase of pressure in the eye. Its symptoms may include
severe eye pain, nausea, redness in the eye, seeing halos or colored rings around lights
and blurred vision. This is an emergency condition in which severe vision loss can
occur quickly; see your optometrist immediately.

Glaucoma cannot currently be prevented. But if it is diagnosed and treated early, it

can usually be controlled. Medication or surgery can slow or prevent further vision
loss.

However, vision already lost to glaucoma cannot be restored. That is why the
American Optometric Association recommends an annual dilated eye examination for
people at risk for glaucoma. Depending on your specific condition, your doctor may
recommend more frequent examinations.
What causes glaucoma?

There are many theories about the causes of glaucoma, but the exact cause is
unknown. Although the disease is usually associated with an increase in the fluid
pressure inside the eye, other theories include lack of adequate blood supply to the
nerve. Following are the different types of glaucoma and their potential causes.

 Primary open-angle glaucoma. This is the most common form of glaucoma.

Damage to the optic nerve is slow and painless. Those affected can lose a large
portion of vision before they notice any vision problems.

One theory about its development is that the eye's drainage system becomes
inefficient over time. This leads to an increased amount of fluid and a gradual
buildup of pressure within the eye. Another theory about the cause of this type of
glaucoma is that there is poor blood flow (perfusion) to the optic nerve. Other
theories also exist.

 Angle-closure glaucoma. This type of glaucoma, also called closed-angle

glaucoma or narrow-angle glaucoma, is a less common form of the disease. It is
a medical emergency that can cause vision loss within a day of its onset.

It occurs when the drainage angle in the eye (formed by the cornea and the iris)
closes or becomes blocked. Many people who develop this type of glaucoma
have a very narrow drainage angle. With age, the lens in the eye becomes larger,
pushing the iris forward and narrowing the space between the iris and the
cornea. As this angle narrows, the fluid in the eye is blocked from the drainage
system. Therefore the fluid builds up and eye pressure increases.

Angle-closure glaucoma can be chronic (progressing gradually) or acute

(appearing suddenly). The acute form occurs when the iris completely blocks
fluid drainage. When people with a narrow drainage angle have their pupils
dilated, the angle may close and cause a sudden increase in eye pressure.
Although an acute attack often affects only one eye, the other eye may be at risk
of an attack as well.

 Secondary glaucoma. This type of glaucoma results from an injury or other

eye disease. It may be caused by a variety of medical conditions, medications,
physical injuries and eye abnormalities. Infrequently, eye surgery can lead to
secondary glaucoma.

 Normal-tension or low-tension glaucoma. In this form of glaucoma, eye

pressure remains within the "normal" range, but the optic nerve is damaged
nevertheless. It is not known why this happens.

Possibly, people with low-tension glaucoma have an abnormally sensitive optic

nerve. Or they may have a reduced blood supply to the optic nerve caused by a
 condition such as atherosclerosis, a hardening of the arteries. Under these
circumstances even normal pressure on the optic nerve can cause damage.
Risk factors

The following factors can increase the risk for developing glaucoma:

 Age. People over age 60 are at increased risk for the disease. African
Americans, however, are at increased risk after age 40. The risk of developing
glaucoma increases slightly with each year of age.
 Race. African Americans are significantly more likely to get glaucoma than
Caucasians, and they are much more likely to suffer permanent vision loss.
People of Asian descent and Native Alaskans are at higher risk of angle-closure
glaucoma. People of Japanese descent are more likely to develop low-tension
glaucoma.
 Family history of glaucoma. Having a family history of glaucoma increases
the risk of developing glaucoma.
 Medical conditions. Some studies indicate that diabetes, high blood pressure
and heart disease may increase the risk of developing glaucoma.
 Physical injuries to the eye. Severe trauma, such as being hit in the eye, can
result in immediate increased eye pressure. Internal damage from such a trauma
can also cause future increases in pressure. Injury can also dislocate the lens,
closing the drainage angle and increasing pressure.
 Other eye-related risk factors. Certain features of eye anatomy, namely
thinner corneas and optic nerve sensitivity, indicate an increased risk for
developing glaucoma. Conditions such as retinal detachment, eye tumors and
eye inflammations may also trigger glaucoma. Some studies suggest that high
amounts of nearsightedness may also be a risk factor for glaucoma.
 Corticosteroid use. Using corticosteroids (including cortisone, hydrocortisone
and prednisone) for prolonged periods of time appears to put some people at risk
of getting secondary glaucoma.
How is glaucoma diagnosed?

Glaucoma is diagnosed through a comprehensive eye examination. Because glaucoma

is a progressive disease, meaning it worsens over time, a change in the appearance of
the optic nerve, a loss of nerve tissue, and a corresponding loss of vision confirm the
diagnosis. Some optic nerves may resemble nerves with glaucoma, but the patients
may have no other risk factors or signs of glaucoma. These patients should have
routine comprehensive exams to monitor any changes.
Glaucoma testing includes:

 Patient history to determine any symptoms the patient is experiencing and if

there are any general health problems and family history that may be
contributing to the problem.
 Visual acuity measurements to determine if vision is being affected.
 Tonometry to measure the pressure inside the eye to detect increased risk
factors for glaucoma.
 Pachymetry to measure corneal thickness. People with thinner corneas are at
an increased risk of developing glaucoma.
 Visual field testing, also called perimetry, to check if the field of vision has
been affected by glaucoma. This test measures your side (peripheral) vision and
central vision by either determining the dimmest amount of light that can be
detected in various locations of vision, or by determining sensitivity to targets
other than light.
 Evaluation of the retina of the eye, which may include photographs or scans
of the optic nerve, to monitor any changes over time.
 Supplemental testing, which may include gonioscopy. This procedure offers
a view of the angle anatomy, which is where eye fluid drainage occurs. Serial
tonometry is another possible test. This procedure acquires several pressure
measurements over time, looking for changes in the eye pressure throughout the
day. In addition, devices can be used to measure nerve fiber thickness and to
look for tissue loss on specific areas of the nerve fiber layer .
[back to top]
How is glaucoma treated?
Glaucoma treatment is aimed at reducing pressure in the eye. Regular use of
prescription eye drops are the most common and often the first treatment. Some cases
may require systemic medications, laser treatment or other surgery. While there is not
yet a cure for glaucoma, early diagnosis and continuing treatment can preserve
eyesight.

 Medications. A number of medications are currently available to treat

glaucoma. Typically, medications reduce elevated pressure in the eye. A single
medication or a combination of medications may be prescribed. The type of
medication may change if it is not reducing pressure enough or if the patient is
experiencing side effects.
 Surgery. Procedures include laser treatment, making a drainage flap in the
eye, inserting a drainage valve, or destroying the tissue that creates the fluid in
the eye. All procedures aim to reduce the pressure inside the eye when
medication is not sufficient. Surgery cannot reverse vision loss.
o Laser surgery. Laser trabeculoplasty helps fluid drain out of the eye.
A high-energy laser beam stimulates the structure that drains fluid from the
eye (the trabecular meshwork) so that fluid drains more efficiently. The
results may be somewhat temporary, and the procedure may need to be
repeated in the future.
o Conventional surgery. If eye drops and laser surgery aren't
controlling eye pressure, you may need a trabeculectomy. This filtering
microsurgery creates a drainage flap. Fluid can then percolate into the flap
and later drain into the vascular system.
o Drainage implants. Drainage valve implant surgery may be an option
for adults with uncontrolled glaucoma or secondary glaucoma or for
children with glaucoma. A small silicone tube is inserted in the eye to help
drain fluid.

Treatment for acute angle-closure glaucoma

Acute angle-closure glaucoma is a medical emergency. Those affected can take

medication to reduce eye pressure as quickly as possible. They will also likely
undergo a laser procedure called laser peripheral iridotomy. In this procedure, a
laser beam creates a small hole in the iris to allow fluid to flow more freely into
the front chamber of the eye where it then can drain.

Lifelong treatment

There is no cure for glaucoma. Patients with glaucoma need to continue

treatment for the rest of their lives. Because the disease can progress or change
without warning, compliance with eye medications and undergoing eye
examinations are essential; treatment may need to be adjusted periodically.
 Keeping eye pressure under control can slow or stop damage to the optic nerve
and continued loss of vision. Your optometrist may focus on lowering the eye
pressure to a level that is least likely to cause further optic nerve damage. This
level is often referred to as the target pressure and is likely a range rather than a
single number. Target pressure differs for each person, depending on the extent
of the damage and other factors. Target pressure may change over time. New
medications to help fight glaucoma are always being developed.

Early detection, prompt treatment and regular monitoring can help to control
glaucoma and reduce the chances for vision loss.

2. T2 P4 masing-masing obat fungsinya apa, dosagenya, berapa lama, MOA

obatnya & 3. T2 P4 indikasi surgery

TIMOPTIC®
0.25% AND 0.5%
(TIMOLOL MALEATE OPHTHALMIC SOLUTION)
in OCUDOSE® (DISPENSER)
PRESERVATIVE-FREE STERILE OPHTHALMIC SOLUTION
in a Sterile Ophthalmic Unit Dose Dispenser
DESCRIPTION
Timolol maleate is a non-selective beta-adrenergic receptor blocking agent. Its
chemical name is(-)-1-(tert-butylamino)-3-[(4-morpholino-1,2,5-thiadiazol-3-yl)oxy]-
2-propanol maleate (1:1)(salt). Timolol maleate possesses an asymmetric carbon atom
in its structure and is provided asthe levo-isomer. The optical rotation of timolol
maleate is:25° [α] in 1.0N HCl (C = 5%) = –12.2° (–11.7° to –12.5°). 405 nm
Its molecular formula is C13H24N4O3S•C4H4O4

Timolol maleate has a molecular weight of 432.50. It is a white, odorless, crystalline

powder which is soluble in water, methanol, and alcohol. Timolol maleate is stable at
room temperature. Timolol maleate ophthalmic solution is supplied in two
formulations: Ophthalmic Solution TIMOPTIC* (timolol maleate ophthalmic
solution), which contains the preservative benzalkonium chloride; and Ophthalmic
Solution TIMOPTIC* (timolol maleate ophthalmic
solution), the preservative-free formulation. Preservative-free Ophthalmic Solution
TIMOPTIC is supplied in OCUDOSE*, a unit dose container, as a sterile, isotonic,
buffered, aqueous solution of timolol maleate in two dosage
strengths: Each mL of Preservative-free TIMOPTIC in OCUDOSE 0.25% contains
2.5 mg of timolol (3.4 mg of timolol maleate). The pH of the solution is
approximately 7.0, and the osmolarity is 252-328 mOsm. Each mL of Preservative-
free TIMOPTIC in OCUDOSE 0.5% contains 5 mg of timolol (6.8 mg of timolol
maleate). Inactive ingredients: monobasic and dibasic sodium phosphate, sodium
hydroxide to adjust pH, and water for injection.
CLINICAL PHARMACOLOGY
Mechanism of Action
Timolol maleate is a beta1 and beta2 (non-selective) adrenergic receptor blocking
agent that does not have significant intrinsic sympathomimetic, direct myocardial
depressant, or local anesthetic (membrane-stabilizing) activity.
Beta-adrenergic receptor blockade reduces cardiac output in both healthy subjects and
patients with heart disease. In patients with severe impairment of myocardial function,
beta-adrenergic receptor blockade may inhibit the stimulatory effect of the
sympathetic nervous system necessary to maintain adequate cardiac function. Beta-
adrenergic receptor blockade in the bronchi and bronchioles results in increased
airway resistance from unopposed parasympathetic activity. Such an effect in patients
with asthma orother bronchospastic conditions is potentially dangerous.
TIMOPTIC (timolol maleate ophthalmic solution), when applied topically on the eye,
has the action of reducing elevated as well as normal intraocular pressure, whether or
not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in
the pathogenesis of glaucomatous visual field loss. The higher the level of intraocular
pressure, the greater the likelihood of glaucomatous visual field loss and optic nerve
damage.
The onset of reduction in intraocular pressure following administration of TIMOPTIC
(timololmaleate ophthalmic solution) can usually be detected within one-half hour
after a single dose.
The maximum effect usually occurs in one to two hours and significant lowering of
intraocular pressure can be maintained for periods as long as 24 hours with a single
dose. Repeated observations over a period of one year indicate that the intraocular
pressure-lowering effect of TIMOPTIC (timolol maleate ophthalmic solution) is well
maintained.
The precise mechanism of the ocular hypotensive action of TIMOPTIC (timolol
maleate ophthalmic solution) is not clearly established at this time. Tonography and
fluorophotometry studies in man suggest that its predominant action may be related to
reduced aqueous formation.
However, in some studies a slight increase in outflow facility was also observed.
Pharmacokinetics
In a study of plasma drug concentration in six subjects, the systemic exposure to
timolol was determined following twice daily administration of TIMOPTIC 0.5%.
The mean peak plasma concentration following morning dosing was 0.46 ng/mL and
following afternoon dosing was 0.35 ng/mL.
Clinical Studies
In controlled multiclinic studies in patients with untreated intraocular pressures of 22
mmHg or greater, TIMOPTIC (timolol maleate ophthalmic solution) 0.25 percent or
0.5 percent administered twice a day produced a greater reduction in intraocular
pressure than 1, 2, 3, or 4 percent pilocarpine solution administered four times a day
or 0.5, 1, or 2 percent epinephrine hydrochloride solution administered twice a day.
In these studies, TIMOPTIC (timolol maleate ophthalmic solution) was generally well
tolerated and produced fewer and less severe side effects than either pilocarpine or
epinephrine. A slight reduction of resting heart rate in some patients receiving
TIMOPTIC (timolol maleate ophthalmic solution) (mean reduction 2.9 beats/minute
standard deviation 10.2) was observed.
INDICATIONS AND USAGE
Preservative-free TIMOPTIC in OCUDOSE is indicated in the treatment of elevated
intraocular pressure in patients with ocular hypertension or open-angle glaucoma.
Preservative-free TIMOPTIC in OCUDOSE may be used when a patient is sensitive
to the preservative in TIMOPTIC (timolol maleate ophthalmic solution),
benzalkonium chloride, or when use of a preservative-free topical medication is
advisable.
CONTRAINDICATIONS
Preservative-free TIMOPTIC in OCUDOSE is contraindicated in patients with (1)
bronchial asthma; (2) a history of bronchial asthma; (3) severe chronic obstructive
pulmonary disease (4) sinus bradycardia; (5) second or third degree atrioventricular
block; (6) overtcardiac failure (7) cardiogenic shock; or (8) hypersensitivity to any
component of this product.
WARNINGS
As with many topically applied ophthalmic drugs, this drug is absorbed systemically.
The same adverse reactions found with systemic administration of beta-adrenergic
blocking agents may occur with topical administration. For example, severe
respiratory reactions and cardiac reactions, including death due to bronchospasm in
patients with asthma, and rarely death in association with cardiac failure, have been
reported following systemic or ophthalmic administration of timolol maleate (see
CONTRAINDICATIONS).
Cardiac Failure
Sympathetic stimulation may be essential for support of the circulation in individuals
with diminished myocardial contractility, and its inhibition by beta-adrenergic
receptor blockade may precipitate more severe failure.
In Patients Without a History of Cardiac Failure continued depression of the
myocardium with beta-blocking agents over a period of time can, in some cases, lead
to cardiac failure. At the first sign or symptom of cardiac failure, Preservative-free
TIMOPTIC in OCUDOSE should be discontinued.
Obstructive Pulmonary Disease
Patients with chronic obstructive pulmonary disease (e.g., chronic bronchitis,
emphysema) of mild or moderate severity, bronchospastic disease, or a history of
bronchospastic disease (other than bronchial asthma or a history of bronchial asthma,
in which TIMOPTIC in OCUDOSE is contraindicated [see
CONTRAINDICATIONS]) should, in general, not receive beta-blockers,
including Preservative-free TIMOPTIC in OCUDOSE.
Major Surgery
The necessity or desirability of withdrawal of beta-adrenergic blocking agents prior to
major
surgery is controversial. Beta-adrenergic receptor blockade impairs the ability of the
heart to respond to beta-adrenergically mediated reflex stimuli. This may augment the
risk of general anesthesia in surgical procedures. Some patients receiving beta-
adrenergic receptor blocking agents have experienced protracted severe hypotension
during anesthesia. Difficulty in restarting and maintaining the heartbeat has also been
reported. For these reasons, in patients undergoing
elective surgery, some authorities recommend gradual withdrawal of beta-adrenergic
receptor
blocking agents.
If necessary during surgery, the effects of beta-adrenergic blocking agents may be
reversed by
sufficient doses of adrenergic agonists.
Diabetes Mellitus
Beta-adrenergic blocking agents should be administered with caution in patients
subject to
spontaneous hypoglycemia or to diabetic patients (especially those with labile
diabetes) who are
receiving insulin or oral hypoglycemic agents. Beta-adrenergic receptor blocking
agents may
mask the signs and symptoms of acute hypoglycemia.
Thyrotoxicosis
Beta-adrenergic blocking agents may mask certain clinical signs (e.g., tachycardia) of
hyperthyroidism. Patients suspected of developing thyrotoxicosis should be managed
carefully to
avoid abrupt withdrawal of beta-adrenergic blocking agents that might precipitate a
thyroid
storm.
PRECAUTIONS
General
Because of potential effects of beta-adrenergic blocking agents on blood pressure and
pulse,
these agents should be used with caution in patients with cerebrovascular
insufficiency. If signs
or symptoms suggesting reduced cerebral blood flow develop following initiation of
therapy with
Preservative-free TIMOPTIC in OCUDOSE, alternative therapy should be
considered.
Choroidal detachment after filtration procedures has been reported with the
administration of
aqueous suppressant therapy (e.g. timolol).
Angle-closure glaucoma
In patients with angle-closure glaucoma, the immediate objective of treatment is to
reopen the
angle. This requires constricting the pupil. Timolol maleate has little or no effect on
the pupil.
TIMOPTIC in OCUDOSE should not be used alone in the treatment of angle-closure
glaucoma.
Anaphylaxis
While taking beta-blockers, patients with a history of atopy or a history of severe
anaphylactic
reactions to a variety of allergens may be more reactive to repeated accidental,
diagnostic, or
therapeutic challenge with such allergens. Such patients may be unresponsive to the
usual doses
of epinephrine used to treat anaphylactic reactions.
Muscle Weakness
Beta-adrenergic blockade has been reported to potentiate muscle weakness consistent
with
certain myasthenic symptoms (e.g., diplopia, ptosis, and generalized weakness).
Timolol has
been reported rarely to increase muscle weakness in some patients with myasthenia
gravis or
myasthenic symptoms.
Information for Patients
Patients should be instructed about the use of Preservative-free TIMOPTIC in
OCUDOSE.
Since sterility cannot be maintained after the individual unit is opened, patients should
be
instructed to use the product immediately after opening, and to discard the individual
unit and
any remaining contents immediately after use.
Patients with bronchial asthma, a history of bronchial asthma, severe chronic
obstructive
pulmonary disease, sinus bradycardia, second or third degree atrioventricular block,
or cardiac
failure should be advised not to take this product. (See CONTRAINDICATIONS.)
Drug Interactions
Although TIMOPTIC (timolol maleate ophthalmic solution) used alone has little or
no effect on
pupil size, mydriasis resulting from concomitant therapy with TIMOPTIC (timolol
maleate
ophthalmic solution) and epinephrine has been reported occasionally.
Beta-adrenergic blocking agents:
Patients who are receiving a beta-adrenergic blocking agent orally and Preservative-
free TIMOPTIC in OCUDOSE should be observed for potential additive effects of
beta-blockade,
both systemic and on intraocular pressure. The concomitant use of two topical beta-
adrenergic blocking agents is not recommended.
Calcium antagonists:
Caution should be used in the coadministration of beta-adrenergic blocking agents,
such as
Preservative-free TIMOPTIC in OCUDOSE, and oral or intravenous calcium
antagonists,
because of possible atrioventricular conduction disturbances, left ventricular failure,
and
hypotension. In patients with impaired cardiac function, coadministration should be
avoided.

PILOCARPINE HCL 2% , 3% , 4% EYE DROPS

CLASS: Ophthalmic Agent, Antiglaucoma; Ophthalmic Agent, Miotic
INDICATIONS: Management of chronic simple glaucoma, chronic and acute angle-
closure
glaucoma
AVAILABLE DOSAGE FROM THE HOSPITAL:
PILOCARPINE HCL 2% EYE DROPS, PILOCARPINE HCL 3% EYE DROPS,
PILOCARPINE HCL 4% EYE DROPS
DOSAGE:
-Glaucoma: Ophthalmic:
-Solution: Instill 1-2 drops up to 6 times/day; adjust the concentration and frequency
as
required to control elevated intraocular pressure.
-Gel: Instill 0.5” ribbon into lower conjunctival sac once daily at bedtime.
-To counteract the mydriatic effects of sympathomimetic agents (unlabeled use):
Ophthalmic: Solution: Instill 1 drop of a 1% solution in the affected eye.
Geriatric
Refer to adult dosing.

COMMON SIDE EFFECT: Frequency not defined.

Cardiovascular: Hypertension, tachycardia
Gastrointestinal: Diarrhea, nausea, salivation, vomiting
Ocular: Burning, ciliary spasm, conjunctival vascular congestion, corneal granularity
(gel
10%), lacrimation, lens opacity, myopia, retinal detachment, supraorbital or temporal
headache, visual acuity decreased
Respiratory: Bronchial spasm, pulmonary edema
Miscellaneous: Diaphoresis

4. All about katarak

A cataract is a clouding of the lens of the eye which leads to a decrease in
vision.[1] Cataracts often develop slowly and can affect one or both eyes.
[1]
 Symptoms may include faded colors, blurry or double vision, halos around
light, trouble with bright lights, and trouble seeing at night.[1] This may result
in trouble driving, reading, or recognizing faces.[7] Poor vision caused by
cataracts may also result in an increased risk of falling and depression.
[2]
 Cataracts cause half of all cases of blindness and 33% of visual
impairment worldwide.[3][8]
Cataracts are most commonly due to aging but may also occur due
to trauma or radiation exposure, be present from birth, or occur following eye
surgery for other problems.[1][4] Risk factors include diabetes, smoking
tobacco, prolonged exposure to sunlight, and alcohol.[1] 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.[1] Diagnosis is by an eye examination.[1]
Prevention includes wearing sunglasses, a wide brimmed hat, eating leafy
vegetables and fruits, and avoiding smoking.[1][9] Early on the symptoms may
be improved with glasses.[1] If this does not help, surgery to remove the cloudy
lens and replace it with an artificial lens is the only effective treatment.
[1]
 Surgery is needed only if the cataracts are causing problems and generally
results in an improved quality of life.[1][10] Cataract surgery is not readily
available in many countries, which is especially true for women, those living
in rural areas, and those who do not know how to read

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.
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.
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.[37] 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.
Cortical cataracts are due to the lens cortex (outer layer) becoming opaque. They
occur when changes in the fluid contained in the periphery of the lens causes
fissuring. When these cataracts are viewed through an ophthalmoscope, or other
magnification system, the appearance is similar to white spokes of a wheel.
Symptoms often include problems with glare and light scatter at night.[37]
Posterior subcapsular cataracts are cloudy at the back of the lens adjacent to the
capsule (or bag) in which the lens sits. Because light becomes more focused toward
the back of the lens, they can cause disproportionate symptoms for their size.
An immature cataract has some transparent protein, but with a mature cataract, all the
lens protein is opaque. In a hypermature or Morgagnian cataract, the lens proteins
have become liquid. Congenital cataract, which may be detected in adulthood, has a
different classification and includes lamellar, polar, and sutural cataracts.[38][39]
Cataracts can be classified by using the lens opacities classification system LOCS III.
In this system, cataracts are classified based on type as nuclear, cortical, or posterior.
The cataracts are further classified based on severity on a scale from 1 to 5. The
LOCS III system is highly reproducible
Treatment
The appropriateness of surgery depends on a person's particular functional and visual
needs and other risk factors.[47] Cataract removal can be performed at any stage and no
longer requires ripening of the lens. Surgery is usually "outpatient" and usually
performed using local anesthesia. About 9 of 10 patients can achieve a corrected
vision of 20/40 or better after surgery.[37]
Several recent evaluations found that cataract surgery can meet expectations only
when significant functional impairment due to cataracts exists before surgery. Visual
function estimates such as VF-14 have been found to give more realistic estimates
than visual acuity testing alone.[37][48] In some developed countries, a trend to overuse
cataract surgery has been noted, which may lead to disappointing results.[49]
Phacoemulsification is the most widely used cataract surgery in the developed world.
[50][51]
 This procedure uses ultrasonic energy to emulsify the cataract lens.
Phacoemulsification typically comprises six steps:

 Anaesthetic – The eye is numbed with either a subtenon injection around the
eye (see: retrobulbar block) or topical anesthetic eye drops. The former also
provides paralysis of the eye muscles.
 Corneal incision – Two cuts are made at the margin of the clear cornea to
allow insertion of instruments into the eye.
 Capsulorhexis – A needle or small pair of forceps is used to create a circular
hole in the capsule in which the lens sits.
 Phacoemulsification – A handheld ultrasonic probe is used to break up and
emulsify the lens into liquid using the energy of ultrasound waves. The resulting
'emulsion' is sucked away.
 Irrigation and aspiration – The cortex, which is the soft outer layer of the
cataract, is aspirated or sucked away. Fluid removed is continually replaced with a
saline solution to prevent collapse of the structure of the anterior chamber (the
front part of the eye).
 Lens insertion – A plastic, foldable lens is inserted into the capsular bag that
formerly contained the natural lens. Some surgeons also inject an antibiotic into
the eye to reduce the risk of infection. The final step is to inject salt water into the
corneal wounds to cause the area to swell and seal the incision.
A Cochrane review found little to no difference in visual acuity as a function of the
size of incisions made for phacoemulsification in the range from ≤ 1.5 mm to 3.0 mm.
[52]

Extracapsular cataract extraction (ECCE) consists of removing the lens manually, but
leaving the majority of the capsule intact.[53] The lens is expressed through a 10- to 12-
mm incision which is closed with sutures at the end of surgery. ECCE is less
frequently performed than phacoemulsification, but can be useful when dealing with
very hard cataracts or other situations where emulsification is problematic. Manual
small incision cataract surgery (MSICS) has evolved from ECCE. In MSICS, the lens
is removed through a self-sealing scleral tunnel wound in the sclera which, ideally, is
watertight and does not require suturing. Although "small", the incision is still
markedly larger than the portal in phacoemulsion. This surgery is increasingly popular
in the developing world where access to phacoemulsification is still limited.
Intracapsular cataract extraction (ICCE) is rarely performed.[54] The lens and
surrounding capsule are removed in one piece through a large incision while pressure
is applied to the vitreous membrane. The surgery has a high rate of complications