EYELID DISORDERS

An eyelid disorder is any abnormal condition that affects the eyelids.

The eyelids, which consist of

 thin folds of skin,

 muscle,
 connective tissue,

These protect the eyes and spread tears over the front of the eyes.

Some common lid problems include:

i. stye,
ii. blepharitis,
iii. chalazion,
iv. entropion and ectropion,
v. eyelid edema,
vi. eyelid tumors

i. STYE

A stye is an infection of eyelid glands near the lid margins, at the base of the lashes. Styes are usually
caused by bacterial staphylococcal infections. The symptoms are pain and inflammation near the eyelid
margin.

Styes are treated with warm-hot compresses and sometimes topical antibiotics

ii. CHALAZION

A chalazion is an enlargement of a meibomian gland, usually not infectious.

Initially, a chalazion may resemble a stye, but it usually grows larger and may also be located in the
middle of the lid and be internal.

A chalazion is caused by ablockage in the outflow duct of a meibomian gland. Symptoms are
inflammationand painful swelling.

About 25% of chalazia disappears on its own, but hot compresses may speed the process. Medication
may need to be injected or the chalazion may need to be cut out. If a chalazion recurs on the same site,
the possibility of sebaceous gland carcinoma should be investigated
 iii. BLEPHARITIS

Blepharitis is the inflammation of the eyelid margins, often with scales and crust. It can lead to eyelash
loss, chalazia, styes, ectropion, corneal damage, excessive tearing, and chronic conjunctivitis.

Blepharitis can be caused by bacterial infection, headlice, an overproduction of oil by the meibomian
glands, or an unknown cause.It can be a chronic lifelong condition. Symptoms include itching, burning,
afeeling of something in the eye, inflammation, and scales or crusts surrounding the eyelashes.

Blepharitis istreated with hot compresses and antibiotic ointment, and by cleaning the eyelids. If the
blepharitis doesn't clear up with treatment or is a chronic problem, the patient may have acne rosacea
and need to see a dermatologist.

iv. ENTRPION AND ECTROPION

Entropion is a condition where the eyelid margin is turned inward; the eyelashes touch the eye and
irritate the cornea.

Entropion usually results from aging, but is sometimes dueto a congenital defect, a spastic eyelid
muscle, or a scar inside the lid. Symptoms are excessive tearing, redness, and discomfort.

Ectropion is a condition where one or both eyelid margins turn outward, exposing the conjunctiva that
covers the eye and lines the eyelid.

The usual cause of ectropion is aging, but it can also be caused by a spastic eyelid muscle, a scar, or
allergies. Symptoms are excessive tearing and hardening of the eyelid conjunctiva.

Entropion and ectropion can be surgically corrected and treated with lubricating drops to keep the
cornea moist
 v. EYELID EDEMA

Eyelid edema is a condition where the eyelids contain excessive fluid.

Eyelid edema is usually caused by allergic reactions, for example, to eye makeup, eyedrops or other
drugs, or plants. Trichinosis, a disease caused by eating undercooked meat, also causes eyelid edema.
Swelling can also be due to infection and lead to orbital cellulitis which can threaten vision. Symptoms
include swelling, itching, redness, or pain

Patients with swollen eyelids should contact their eye doctor. A severely swollen lid can press on the eye
and increase the intraocular pressure. An infection needs to be ruled out. The best treatment for allergic
eyelid edema is to find and remove the substance causing the allergy. When that isn't possible, cold
compresses and immunosuppresesive drugs such as corticosteroid creams are helpful. For edema
caused by trichinosis, the trichinosis must be treated

vi. EYELID TUMORS

Eyelids are susceptible to the same skin tumors as the skin over the rest of the body, including
noncancerous tumors and cancerous tumors. Eyelid muscles are susceptible to sarcoma.

Eyelid tumors are caused by AIDS (Kaposi's sarcoma) or increased exposure to ultraviolet (UV) rays. They
are usually painless and may or may not be pigmented.

Cancerous tumors should be removed upon discovery, and noncancerous tumors before they grow
enough to interfere with vision or eyelid function. Eyelid reconstruction sometimes accompanies tumor
excision.

Diagnosis of eyelid disorders

To diagnose eyelid disorders, the doctor uses a slit lamp is used to magnify the eyes. He/she may press
on the lid margin to express oil from the meibomian glands or invert the lid to see inside it. Biopsy is
used to diagnose cancerous tumors
BLEPHARITIS

Def: Blepharitis (pronounced /blɛfərˈaɪtɨs/ BLEF-ər-EYE-tis) is an ocular condition characterized by

chronic inflammation of the eyelid, the severity and time course of which can vary. It can onset acutely
resolving without treatment within 2–4 weeks (this can be greatly reduced with lid hygiene) but more
generally is a long standing inflammation varying in severity.

Signs and symptoms

Signs and symptoms that are associated with the chronic inflammation can be;

 Redness of the eyelids.

 Flaking of skin on the lids.
 Crusting at the lid margins, this is generally worst on waking.
 Cysts at the lid margin (hordeolum).
 Red eye.
 Debris in the tear film, seen under magnification (improved contrast with use of fluorescein
drops).
 Gritty sensation of the eye.
 Reduced vision.

Common signs and symptoms of blepharitis also include

 itching,
 irritation and
 burning as well as a foreign body sensation.

Some patients experience eye dryness, which can cause a certain degree of discomfort.

People who wear contact lenses usually have more trouble in coping with their symptoms because
although they need contact-lenses, they cannot wear them. Many such patients complain of being
unable to wear their lenses for long periods of time or that the lenses are causing them even more
irritation of the eye.

Also, the lids may become red and may have ulcerative, non-healing areas which may actually bleed.
Blepharitis does not tend to cause problems with the patient's vision whatsoever, but due to a poor tear
film, one may experience blurred vision.

Eye redness and swelling tend to appear in more advanced cases, and they are rarely primary
symptoms. The symptoms can slightly vary based on the exact cause of the condition. Blepharitis due to
an allergy can cause dark lids, symptom which is known as "allergic shiner" and which tends to be more
frequent in children rather than adults. Infectious blepharitis is accompanied by a yellow- or green-
colored discharge which is more abundant in the morning and which leads to stuck lids. Blepharitis may
also cause eyelid matting or "gluing" of the lashes. Not least, dandruff may occur on the scalp or on the
eyebrows.
Other blepharitis symptoms include sensitivity to light, eyelashes that grow abnormally or even loss of
eyelashes. Also, the tears might seem frothy or bubbly in nature and mild scarring might occur to the
eyelids. The symptoms and signs of blepharitis are often erroneously ascribed by the patient as being
due to "recurrent conjunctivitis".

Blepharitis that localizes in the skin of the eyelids may cause styes or chalazia, which appear like red
bumps, sometimes with a yellow spot if infection is present. Although pain is not common among
blepharitis symptoms, if the condition persists or becomes painful, the individual is recommended to
seek medical attention.

Chronic blepharitis may result in damage of varying severity which may have a negative effect upon
vision and therefore upon the eyeglass prescription.

Infectious blepharitis can cause hard crusts around the eyelashes which leave small ulcers that may
bleed or ooze after cleaning.

As a general rule, blepharitis whose symptoms do not improve despite good hygiene consisting of
proper cleaning and care of the eye area, should be referred to a doctor.

Staphylococcal blepharitis

Staphlycoccal blepharitis is caused by infection of the anterior portion of the eyelid by Staphylococcal
bacteria. As the infection progresses, the sufferer may begin to notice a foreign body sensation, matting
of the lashes, and burning. Usually, the primary care physician will prescribe topical antibiotics for
staphylococcal blepharitis, as this is an acute condition and should heal quickly. The condition can
sometimes lead to a chalazion or a stye.

Staphylococcal blepharitis is a more severe condition which may start in childhood and continue through
adulthood. It is commonly recurrent and it requires special medical care. The prevalence of
Staphylococcus aureus in the conjunctival sac and on the lid margin varies among countries, apparently
according to climate.

In cases of blepharitis caused by Staphylococcus aureus, the presence of a collarette (a ring-like

formation around the lash shaft) can be observed. This is the main sign of this particular condition.
Other specific symptoms include loss of eyelashes or broken eyelashes.

Staphylococcal blepharitis is mainly diagnosed upon the patient's medical history and a bacterial culture.
However, since blepharitis is a condition that is completely understood, diagnosis usually consists of
establishing an accurate medical history of the patient and a proper physical examination. Blepharitis is
diagnosed primarily upon physical examination and rarely further tests are needed. Yet, it is
recommended that older patients or those who are at risk of developing certain skin conditions undergo
biopsy in order to remove the possibility of tumor.

This type of blepharitis is more likely to occur in individuals who are exposed to bacteria. Staphylococcal
blepharitis, unlike the other types of this condition, seems to be seen more frequently in women than in
men.
It is important that this type of blepharitis is properly treated because otherwise the infection may
spread to other parts of the eye or to the scarring of the cornea. Staphylococcal blepharitis is normally
treated with antibiotics such as Chloramphenicol ointment. Fusidic acid is usually the choice of
antibiotics in cases when Chloramphenicol is contraindicated. Antibiotics are given for at least four
weeks and up to six weeks, which is considered enough so the infection is completely cured. Also,
blepharitis treatment includes a short course of topical steroids which are administered to control the
inflammation.

Staphylococcal blepharitis, along with the other types of blepharitis treatment is only effective if given
at the same time with extra cautious eyelid hygiene. This consists of eyelid proper cleaning and
removing crusts and debris and maintaining the hygiene by avoiding expired make up or cosmetics that
are used around the eye. Particularly in blepharitis caused by S. aureus, patients are recommended to
keep the eyelids area clean to avoid spreading the infection when oozing and bleeding occurs.

Posterior blepharitis or rosacea-associated blepharitis

The most common type of blepharitis is often found in people with a Rosacea skin type. The oil glands in
the lid of rosacea sufferers secrete a modified oil which leads to inflammation at the meibomian gland
openings which are found at the edge of the lid.

Treatment and management

The single most important treatment principle is a daily routine of lid margin hygiene, as described
below. Such a routine needs to be convenient enough to be continued for life to avoid relapses as
blepharitis is often a chronic condition. But it can be acute, and one episode does not mean it is a life-
long condition.

A typical lid margin hygiene routine consists of four steps:

1. Softening of lid margin debris and oils: Apply a warm wet compress to the lids - such as a
washcloth with hot water - for about two minutes. New, dry, warm compress masks can be
conveniently warmed in a micro-wave oven and maintain a comfortable 40C temperature for 10
minutes while the waxy oils blocking the glands are cleared.
2. Mechanical removal of lid margin debris: At the end of a shower routine, wash your face with a
wash cloth. Use facial soap or non-burning baby shampoo (make sure to dilute the soap solution
1/10 with water first). Gently and repeatedly rub along the lid margins while eyes are closed.
Too much soap or shampoo may remove the essential oily layer of the eyes' own tear film and
create further problems with dry eye discomfort.
3. Antibiotic reduction of lid margin bacteria (at the discretion of your physician): After lid margin
cleaning, spread small amount of prescription antibiotic ophthalmic ointment with finger tip
along lid fissure while eyes closed. Use prior to bed time as opposed to in the morning to avoid
blurry vision.
4. Avoid the use of eye make-up until symptoms subside.

An alternative after washing is to coat the eyelids with a good quality hair conditioner. Leave in place for
several minutes then rinse. The conditioner seems to break the bacteria / crusting /irritation cycle, and
daily use can eliminate the symptoms.
The following guide is very common but is more challenging to perform by visually disabled or frail
patients as it requires good motor skills and a mirror. Compared with the above, it does not bear any
advantages:

1. Apply hot compresses to both eyes for five minutes once to twice per day. The "hot wet flannel"
treatment is often recommended, however this does not stay hot for long enough, is very messy
& potentially unhygienic. A very effective alternative is a flax filled mask which is heated in a
microwave oven.
2. After hot compresses, in front of a mirror, use a moist Q-tip soaked in a cup of water with a drop
of baby shampoo, or a drop of antibiotic such as Chloramphenicol. Rub along the lid margins
while tilting the lid outward with the other hand.
3. In front of mirror, place small drop of antibiotic ophthalmic ointment (e.g. erythromycin) in
lower conjunctival sac while pulling lid away from eye with other hand.

Often the above is advised together with mild massage to mechanically empty glands located at the lid
margin (Meibomian glands, Zeis glands, Moll glands).

Dermatologists treat blepharitis similarly to seborrhoeic dermatitis by using a safe topical anti-
inflammatory medication like sulfacetamide or brief courses of a mild topical steroid. Although anti-
fungals like ketoconazole (Nizoral) are commonly prescribed for seborrhoeic dermatitis, dermatologists
and optometrists usually do not prescribe anti-fungals for seborrhoeic blepharitis.

If these conventional treatments for blepharitis do not bring relief, patients may consider allergy testing
and ocular antihistamines. Allergic responses to dust mite feces and other allergens can cause lid
inflammation, ocular irritation, and dry eyes. Prescription ocular antihistamines and over-the-counter
ocular antihistamines are very safe and can bring almost immediate relief to patients whose lid
inflammation is caused by allergies.
CHALAZION

Def: A chalazion pronounced /kəˈleɪziən/ (plural chalazia /kəˈleɪziə/), also known as a meibomian gland
lipogranuloma, is a cyst in the eyelid that is caused by inflammation of a blocked meibomian gland,
usually on the upper eyelid.

Chalazia differ from styes (hordeola) in that they are subacute, nontender, and usually painless nodules.
May become acutely inflamed but, unlike a stye, usually point inside the lid rather than on the lid
margin. A chalazion or meibomian cyst could take months to fully heal with treatment and could take
years to heal without any major complications.

Signs and symptoms

 Swelling on the eyelid

 Eyelid tenderness
 Sensitivity to light
 Increased tearing
 Heaviness of the eyelid

A chalazion or meibomian cyst can sometimes be mistaken for a stye.

Treatment

Topical antibiotic eye drops or ointment (e.g. chloramphenicol or fusidic acid) are sometimes used for
the initial acute infection, but are otherwise of little value in treating a chalazion. Chalazia will often
disappear without further treatment within a few months and virtually all will resorb within two years.

If they continue to enlarge or fail to settle within a few months, then smaller lesions may be injected
with a corticosteroid or larger ones may be surgically removed using local anesthesia. This is usually
done from underneath the eyelid to avoid a scar on the skin. If the chalazion is located directly under
the eyelid's outer tissue, however, an excision from above may be more advisable so as not to inflict any
unnecessary damage on the lid itself. Eyelid epidermis usually mends well, without leaving any visible
scar. Depending on the chalazion's texture, the excision procedure varies: while fluid matter can easily
be removed under minimal invasivion, by merely puncturing the chalazion and exerting pressure upon
the surrounding tissue, hardened matter usually necessitates a larger incision, through which it can be
scraped out. Any residual matter should be metabolized in the course of the subsequent healing
process, generally aided by regular appliance of dry heat. The excision of larger chalazia may result in
visible hematoma around the lid, which will wear off within three or four days, whereas the swelling
may persist for longer. Chalazion excision is an ambulant treatment and normally does not take longer
than fifteen minutes. Nevertheless, owing to the risks of infection and severe damage to the eyelid, such
procedures should only be performed by a medical professional.

A home remedy is to have a hot, wet flannel, and rub gently, until the heat has reached the cyst. this
helps to reduce the size, and eventually it will be rid of. It is rare that a chalazion will recur and they will
usually be biopsied to rule out the possibility of a tumour
Complications

A large chalazion can cause astigmatism due to pressure on the cornea.

As laser eye surgery involves shaping the cornea by burning parts of it away, weakening its structure,
post operation patients can be left predisposed to deformation of the cornea from small chalazia.

Complications including, but not limited to hypopigmentation may occur with corticosteroid injection.

Recurring chalazia in the same area may sometimes be a symptom of sebaceous cell carcinoma, albeit
rarely. This is a type of cancer.

Sometimes, as a last resort, surgery is performed. The eyelid is injected with a local anesthetic, a clamp
is put on the eyelid, then the eyelid is turned over, an incision is made on the inside of the eyelid, and
the chalazion is drained and scraped out. A scar on the upper lid can cause discomfort as some patients
feel the scar as they blink. Of course as surgeries are intrusive and damage healthy tissue (e.g. leaving
behind scar tissue or possibly even causing blepharitis), given other options, less intrusive treatment is
always preferable. Similarly, chalazia may recur once the eye is predisposed and surgical intervention
each time is not possible. So surgery should be considered only as a last resort, performed on as few as
5% of all chalazia patients.

Chalazion surgery

Chalazion surgery is normally performed by an ophthalmologist at an eye hospital. This type of surgery is
a simple procedure which is generally performed as a day operation and the patient does not need to
remain in the hospital for further medical care.

Chalazion removal surgery is performed under local or general anesthesia. Commonly, general
anesthesia is administered in children to make sure they stay still and no injury to the eye occurs. Local
anesthesia is used in adults and it is applied with a small injection into the eyelid. The discomfort of the
injection is minimized with the help of an anesthetic cream which is applied locally.

The chalazion may be removed in two ways, depending on the size of cyst. Relatively small chalazia are
removed through a small cut at the back of the eyelid. The surgeon lifts the eyelid so he can have access
to the back of its surface and makes an incision of approximately 3mm just on top of the chalazion. The
lump is then removed and pressure is applied for a few minutes to stop any oozing of blood that may
occur because of the operation. Surgery of small chalazia does not require stitches as the cut is at the
back of the eyelid and therefore the cut cannot be seen and the cosmetic result is excellent.

Larger chalazia are removed through an incision in front of the eyelid. Larger chalazia usually push on
the skin of the eyelid and this is the main reason why doctors prefer removing them this way. The cut is
not larger than 3 mm and it is performed on top of the chalazion. The lump is removed and then
pressure is applied on the incision so oozing is prevented. This type of surgery is closed with very fine
stitches. They are hardly visible and they are usually removed within a week after the surgery has been
performed. Although chalazia are rarely dangerous, every removed chalazion is sent to the laboratory to
be examined under a microscope because very rarely it can harbor cancer.
When surgery for chalazion is considered, patients who take aspirin or any medication that contains
aspirin are advised to stop taking them one week before the procedure as they may cause bleeding.
There are several tests taken prior the surgery to make sure the patient is in good condition for the
operation.

In rare cases, patients are kept overnight in the hospital after chalazion surgery. These include cases in
which complications occurred and the patient needs to be closely monitored. In most cases however,
patients are able to go home after the operation has ended.

The recovery process is easy and quite fast. Most patients experience some very minor discomfort in the
eye which can be easily controlled by taking painkilling medication. Patients are however recommended
to avoid getting water in the eye for up to 10 days after surgery, they may wash, bath or shower but
they must be careful in keeping the area dry and clean. Makeup may be worn after one month after
surgery. Patients who wear contact lenses are recommended to not wear on in the operated side for at
least eight weeks to prevent infection and potential complications.

Commonly, patients receive eye drops to prevent infection and swellings in the eye and pain medication
that will help them cope with the pain and discomfort in the eyelid and eye. One can use paracetamol
rather than aspirin to control the pain. Also, after surgery, a pad and protective plastic shield are used to
apply pressure on the eye in order to prevent leakage of blood after the operation and which may be
removed 6 to 8 hours after the procedure.

People who underwent chalazion surgery are normally asked to check up their operation three to four
weeks after surgery has been performed. They may start driving the day after surgery and they may get
back to work in one or two days.

Chalazion surgery is a safe procedure and complications occur very seldom. Serious complications that
require another operation to be fixed are also very rare. Among potential complications, although rare,
there is infection, bleeding or the recurrence of the chalazion.
ECTROPION & ENTROPION

1. Ectropion is a medical condition in which the lower eyelid turns outwards. It is one of the notable
aspects of newborns exhibiting congenital Harlequin type ichthyosis, but ectropion can occur due to
any weakening of tissue of the lower eyelid. The condition can be repaired surgically. Ectropion is
also found in dogs as a genetic disorder in certain breeds.

Causes

 Congenital
 Aging
 Scarring
 Mechanical
 Allergic
 Facial nerve palsy
 Anti-cancer treatments such as erlotinib, cetuximab, and panitumumab, which block the
function of EGFR (the epidermal growth factor receptor).

2. Entropion is a medical condition in which the eyelid (usually the lower lid) folds inward. It is very
uncomfortable, as the eyelashes constantly rub against the cornea. Entropion is usually caused by
genetic factors and may be congenital. Trachoma infection may cause scarring of the inner eyelid,
which may cause entropion. In human cases this condition is most common to people over 60 years
of age.

Symptoms

Symptoms of entropion include:

 Redness and pain around the eye

 Sensitivity to light and wind
 Sagging skin around the eye
 Excessive tearing
 Decreased vision, especially if the cornea is damaged

Treatment

Treatment is a simple surgery in which excess skin of the outer lids is removed. Prognosis is excellent if
surgery is performed before the cornea is damaged.

Causes

 Congenital
 Ageing
 Scarring
 Spasm
STYE

An external stye (pronounced /ˈstaɪ/) or hordeolum (/hɔrˈdiːələm/) is an infection of the sebaceous

glands of Zeis at the base of the eyelashes, or an infection of the apocrine sweat glands of Moll.

 External styes form on the outside of the lids and can be seen as small red bumps.
 Internal styes are infections of the meibomian sebaceous glands lining the inside of the eyelids.

They also cause a red bump underneath the lid with only generalized redness and swelling visible on the
outside.

Styes are similar to chalazia, but tend to be of smaller size and are more painful and usually produce no
lasting damage. Styes are characterized by an acute onset and usually short in duration (7-10 days
without treatment) compared to chalazia that are chronic and usually do not resolve without
intervention.

Causes

Styes are commonly caused by a Staphylococcus aureus bacterial infection, or by the blocking of an oil
gland at the base of the eyelash. Although they are particularly common in infants, styes are
experienced by people of all ages. Styes can be triggered by poor nutrition, sleep deprivation, lack of
hygiene or rubbing of the eyes. Sharing of washcloths or face towels should be curtailed to avoid
spreading the infection between individuals. Styes can last from 1 to 2 weeks without treatment, or as
little as 4 days if treated properly.

Medical professionals will sometimes lance a particularly persistent or irritating stye with a needle in
order to accelerate its draining. A stye's expansion can also be fought with erythromycin ophthalmic
ointment. Medical professionals may also treat stye with other antibiotics such as chloramphenicol or
Amoxicillin. Chloramphenicol is used successfully in many parts of the world but contains a box warning
in the United States due to concerns about aplastic anemia, which on rare occasions can be fatal.
Erythromycin ointment enjoys widespread usage and may add to comfort and aid in preventing
secondary infections. However, it is poorly absorbed when used topically and usually requires oral
dosing to reach the infection with therapeutic levels inside of a stye. Azasite, a topical eye drop form of
Azithromycin, does appear to penetrate eyelid tissues fairly well and may be a topical treatment for
styes used in the future.

If a stye bursts, care must be taken to cleanse the wound to prevent reinfection.

Signs and Symptoms

The first sign of a stye is a small, yellowish spot at the center of the bump that develops as pus expands
in the area.

Other stye symptoms may include:

 A lump on the top or bottom eyelid

 Localized swelling of the eyelid
  Pain which becomes more intense if the pus ruptures
 Redness
 Tenderness to touch
 Crusting of the eyelid margins
 Burning in the eye
 Droopiness of the eyelid
 Scratchy sensation on the eyeball
 Blurred vision
 Mucous discharge in the eye
 Irritation of the eye
 Light sensitivity
 Tearing
 Discomfort during blinking
 Sensation of a foreign body in the eye.

Treatment

As styes usually go away within a week, most patients do not require medical treatment. The first steps
in treating styes include applying warm compresses on the affected eye, four to six times a day, for
approximately 15 minutes. This helps the drainage and hastens the curing process.

As a part of self-care at home, patients may cleanse the affected eyelid with tap water or with a mild,
nonirritating soap or shampoo (such as baby shampoo) to help clean crusted discharge. Cleansing must
be done gently and while the eyes are closed to prevent eye injuries.

Patients are highly advised to not squeeze or puncture the stye as serious infection can occur as a result.
The infection could spread to the surrounding tissues and areas.

Eye stye sufferers should avoid eye makeup (e.g., eyeliner), lotions and wearing contact lenses since
these can aggravate and spread the infection (sometimes to the cornea).

Medical treatment can also be provided by a doctor and it is aimed on relieving the symptoms. Pain
relievers such as acetaminophen may be prescribed and in some cases, antibiotics may be needed.
Antibiotics are normally given to patients with multiple styes or with styes that do not seem to cure and
to patients who also suffer from blepharitis or rosacea. Commonly, the ophthalmologist prescribes oral
or IV antibiotics only when the infection has spread. Antibiotics that are usually given include
Vibramycin, Oracea, Atridox and Adoxa. Topical antibiotic ointments or antibiotic/steroid ointment
combination can also be administered in stye treatment.

Surgery is the last resort in stye treatment. Styes that do not respond to any type of therapies are
usually surgically removed. Stye surgery is performed by an ophthalmologist in his office, and generally
under local anesthesia. The procedure consists in making a small incision on the inner or outer surface
of the eyelid depending if the stye is pointing externally or not. After the incision is made, the pus is
drained out of the gland and very small and unnoticeable sutures are used to close the lesion. It is
common that the removed stye is biopsied to rule out the possibility of skin cancer.
Complications

Stye complications occur in very rare cases. However, the most frequent complication of styes is
progression to a chalazion that causes

 cosmetic deformity,
 corneal irritation, and
 often require surgical removal.

Complications may also arise from the improper surgical lancing and mainly consist of disruption of lash
growth, lid deformity or lid fistula. Styes that are too large may interfere with one's vision.

Eyelid cellulitis is another potential complication of eye styes, which is a generalized infection of the
eyelid. Progression of a stye to a systemic infection (spreading throughout the body) is extremely rare,
and only a few instances of such spread have been recorded.

Prognosis

Although styes are harmless in most cases and complications are very rare, styes often recur. They do
not cause intraocular damage, meaning that they do not affect the eye. Styes normally heal on their
own by rupturing within few days to a week, causing the relief of symptoms. Few people require surgery
as part of stye treatment.With adequate treatment, styes tend to heal quickly and without arising any
type of complications.

The prognosis is better if one does not attempt to squeeze or puncture the stye as infection may spread
to adjacent tissues. Styes usually heal within few days to a week, but if it does not improve or it worsens
within two weeks, a doctor's opinion should be sought. Also, patients are recommended to call a doctor
if they encounter problems with vision, the eyelid bumps becomes very painful, the stye bleeds,
recurrent styes or the eyelid or eye becomes red.

Prevention

Stye prevention is closely related to proper hygiene. Proper hand washing can not only reduce the risks
of developing styes, but all other types of infections.

Upon awakening, application of a warm washcloth to the eyelids for one to two minutes may be
beneficial in decreasing the occurrence of styes by liquefying the contents of the oil glands of the eyelid
and thereby preventing blockage. Some studies suggest oral flaxseed supplementation to prevent the
occurrence of styes.

In order to prevent developing styes it is recommended to never share cosmetics or cosmetic eye tools
with other people. People should also keep their eye tools clean and generally having proper eye
hygiene. Women are recommended to remove makeup every night before going to sleep and discard
old or contaminated eye makeup.
CATARACT

Def: A cataract is a clouding that develops in the crystalline lens of the eye or in its envelope, varying in
degree from slight to complete opacity and obstructing the passage of light.

Early in the development of age-related cataract the power of the lens may be increased, causing near-
sightedness (myopia), and the gradual yellowing and opacification of the lens may reduce the
perception of blue colours. Cataracts typically progress slowly to cause vision loss and are potentially
blinding if untreated. The condition usually affects both the eyes, but almost always one eye is affected
earlier than the other.

A senile cataract, occurring in the elderly, is characterized by

 An initial opacity in the lens,

 Subsequent swelling of the lens and
 Final shrinkage with complete loss of transparency.

Moreover, with time the cataract cortex liquefies to form a milky white fluid in a Morgagnian cataract,
which can cause severe inflammation if the lens capsule ruptures and leaks. Untreated, the cataract can
cause phacomorphic glaucoma. Very advanced cataracts with weak zonules are liable to dislocation
anteriorly or posteriorly. Such spontaneous posterior dislocations (akin to the historical surgical
procedure of couching) in ancient times were regarded as a blessing from the heavens, because some
perception of light was restored in the cataractous patients.

Cataract derives from the Latin cataracta meaning "waterfall" and the Greek kataraktes and
katarrhaktes, from katarassein meaning "to dash down" (kata-, "down"; arassein, "to strike, dash"). As
rapidly running water turns white, the term may later have been used metaphorically to describe the
similar appearance of mature ocular opacities. In Latin, cataracta had the alternate meaning "portcullis",
so it is also possible that the name came about through the sense of "obstruction". Early Persian
physicians called the term nazul-i-ah, or "descent of the water"—vulgarised into waterfall disease or
cataract—believing such blindness to be caused by an outpouring of corrupt humour into the eye. In
dialect English a cataract is called a pearl, as in "pearl eye" and "pearl-eyed".

Age-related cataract is responsible for 48% of world blindness, which represents about 18 million
people, according to the World Health Organization (WHO). In many countries surgical services are
inadequate, and cataracts remain the leading cause of blindness. As populations age, the number of
people with cataracts is growing. Cataracts are also an important cause of low vision in both developed
and developing countries. Even where surgical services are available, low vision associated with
cataracts may still be prevalent, as a result of long waits for operations and barriers to surgical uptake,
such as cost, lack of information and transportation problems.

The increase in ultraviolet radiation resulting from depletion of the ozone layer is expected to increase
the incidence of cataracts.
classification of the various types of cataracts.

 Classified by etiology

 Age-related cataract

 Cortical Senile Cataract

 Immature senile cataract (IMSC): partially opaque lens, disc view hazy
 Mature senile cataract (MSC): Completely opaque lens, no disc view
 Hypermature senile cataract (HMSC): Liquefied cortical matter: Morgagnian
cataract

 Senile Nuclear Cataract

 Cataracta brunescens
 cataracta nigra
 cataracta rubra

 Congenital cataract

 Sutural cataract
 Lamellar cataract
 Zonular cataract
 Total cataract

 Secondary cataract

 Drug-induced cataract (e.g. corticosteroids)

 Traumatic cataract

 Blunt trauma (capsule usually intact)

 Penetrating trauma (capsular rupture & leakage of lens material—calls for an
emergency surgery for extraction of lens and leaked material to minimize further
damage)

 Classified by opacities, cataract can be classified by using Lens Opacities Classification System III
(LOCS III: Nuclear NC1-5, Cortical C1-5 and Posterior P1-5. By application planning in procedures of
phacoemulsification, LCOS III can be converted in newer cataract grading system. Gede Pardianto
(2009) introduced Optical Biometry Based Cataract Grading System (OBBCGS) that so helpful in
cataract grading due to phacoemulsification planning. LOCS III's NC0, C0 and P0 acan be converted
as OBBCGS' No cataract (NC), LOCS III's NC1-3, C1-3, P1-4 can be converted to OBBCGS' Optical
Biometry Examined Cataract (OBEC) and LOCS III's NC4-5, C4-5, P4-5 can be converted to OBBCGS's
Optical Biometry Un-examined Cataract (OBUC); that need examination by Applanation Ultrasound
Biometry.
  Classified by location of opacity within lens structure (However, mixed morphology is quite
commonly seen, e.g. PSC with nuclear changes & cortical spokes of cataract)

 Anterior cortical cataract

 Anterior polar cataract
 Anterior subcapsular cataract
 Nuclear cataract—Grading correlates with hardness & difficulty of surgical removal

 1: Grey
 2: Yellow
 3: Amber
 4: Brown/Black (Note: "black cataract" translated in some languages (like Hindi) refers to
glaucoma, not the color of the lens nucleus)

 Posterior cortical cataract

 Posterior polar cataract (importance lies in higher risk of complication—posterior capsular tears
during surgery)
 Posterior subcapsular cataract (PSC) (clinically common)
 After-cataract: posterior capsular opacification (PCO) subsequent to a successful extracapsular
cataract surgery (usually within three months to two years) with or without IOL implantation.
Requires a quick & painless office procedure with Nd:YAG laser capsulotomy to restore optical
clarity.

Signs and symptoms

As a cataract becomes more opaque, clear vision is compromised. A loss of visual acuity is noted.
Contrast sensitivity is also lost, so that contours, shadows and color vision are less vivid. Veiling glare can
be a problem as light is scattered by the cataract into the eye. The affected eye will have an absent red
reflex. A contrast sensitivity test should be performed and if a loss in contrast sensitivity is
demonstrated an eye specialist consultation is recommended.

In the developed world, particularly in high-risk groups such as diabetics, it may be advisable to seek
medical opinion if a 'halo' is observed around street lights at night, especially if this phenomenon
appears to be confined to one eye only.

The symptoms of cataracts are very similar to the symptoms of ocular citrosis.
Causes

1. Cataracts develop for a variety of reasons, including long-term exposure to ultraviolet light,
exposure to radiation, secondary effects of diseases such as

 diabetes,
 hypertension and
 advanced age, or trauma (possibly much earlier);
 they are usually a result of denaturation of lens protein.

2. Genetic factors are often a cause of congenital cataracts and positive family history may also
play a role in predisposing someone to cataracts at an earlier age, a phenomenon of
"anticipation" in pre-senile cataracts.
3. Cataracts may also be produced by eye injury or physical trauma.
4. A study among Icelandair pilots showed commercial airline pilots are three times more likely to
develop cataracts than people with non-flying jobs. This is thought to be caused by excessive
exposure to radiation coming from outer space.
5. Cataracts are also unusually common in persons exposed to infrared radiation, such as
glassblowers who suffer from "exfoliation syndrome".
6. Exposure to microwave radiation can cause cataracts. Atopic or allergic conditions are also
known to quicken the progression of cataracts, especially in children.
7. Cataracts can also be caused by iodine deficiency
8. Cataracts may be partial or complete, stationary or progressive, hard or soft.
9. Some drugs can induce cataract development, such as corticosteroids and Seroquel.

There are various types of cataracts, e.g. nuclear, cortical, mature, and hypermature. Cataracts are also
classified by their location, e.g. posterior (classically due to steroid use) and anterior (common (senile)
cataract related to aging).

Associations with systemic conditions

 Chromosomal disorders

 Alport's syndrome
 Cri-du-chat syndrome
 Conradi's syndrome
 Myotonic dystrophy
 Patau's syndrome
 Trisomy 18 (Edward's syndrome)
 Turner's syndrome

 Disease of the skin and mucous membranes

 Atopic dermatitis
 Basal-cell nevus syndrome
  Ichthyosis
 Pemphigus

 Metabolic and nutrition diseases

 Aminoaciduria (Lowe's syndrome)

 Diabetes mellitus
 Galactosemia / galactosemic cataract
 Homocystinuria
 Hyperparathyroidism
 Hypervitaminosis D
 Hypothyroidism
 Mucopolysaccharidoses
 Wilson's disease

 Infectious diseases

 Congenital

 Congenital herpes simplex

 Congenital syphilis
 Cytomegalic inclusion disease
 Rubella

 Others

 Cysticercosis
 Leprosy
 Onchocerciasis
 Toxoplasmosis

 Toxic substances introduced systemically

 Corticosteroids
 Haloperidol
 Miotics
 Triparanol

Prevention

Although cataracts have no scientifically proven prevention, it is sometimes said that wearing
ultraviolet-protecting sunglasses may slow the development of cataracts.

Regular intake of antioxidants (such as vitamin A, C and E) is theoretically helpful, but taking them as a
supplement has been shown to have no benefit. The less well known antioxidant N-acetylcarnosine has
been shown in randomized controlled clinical trials to treat cataracts, and can be expected to prevent
their formation by similar mechanisms. N-acetylcarnosine is a proposed treatment for other ocular
disorders that are instigated, or exacerbated by oxidative stress including glaucoma, retinal
degeneration, corneal disordes, and ocular inflammation.

Treatment

When a cataract is sufficiently developed to be removed by surgery, the most effective and common
treatment is to make an incision (capsulotomy) into the capsule of the cloudy lens in order to surgically
remove the lens. There are two types of eye surgery that can be used to remove cataracts:

 extra-capsular (extracapsular cataract extraction, or ECCE) and

 intra-capsular (intracapsular cataract extraction, or ICCE).

Extra-capsular (ECCE) surgery consists of removing the lens but leaving the majority of the lens capsule
intact. High frequency sound waves (phacoemulsification) are sometimes used to break up the lens
before extraction.

Intra-capsular (ICCE) surgery involves removing the entire lens of the eye, including the lens capsule, but
it is rarely performed in modern practice.

In either extra-capsular surgery or intra-capsular surgery, the cataractous lens is removed and replaced
with a plastic lens (an intraocular lens implant) which stays in the eye permanently.

Cataract operations are usually performed using a local anaesthetic and the patient is allowed to go
home the same day. Recent improvements in intraocular technology now allow cataract patients to
choose a multifocal lens to create a visual environment in which they are less dependent on glasses.
Under some medical systems multifocal lenses cost extra. Traditional intraocular lenses are monofocal.

Complications are possible after cataract surgery, including

 endophthalmitis,
 posterior capsular opacification and
 retinal detachment.

Investigational Treatments

In the past few years, eye drops containing acetyl-carnosine have been used by several thousands
cataract patients across the world. The drops are believed to work by reducing oxidation and glycation
damage in the lens, particularly reducing crystallin cross-linking. Randomized controlled trials indicate
the drops may be especially appropriate for seniors, or others where surgery is not advised.
Investigational preventives

Although statins are known for their ability to lower lipids, they are also believed to have antioxidant
qualities. It is believed that oxidative stress plays a role in the development of nuclear cataracts, which
are the most common type of age-related cataract. To explore the relationship between nuclear
cataracts and statin use, a group of researchers took a group of 1299 patients who were at risk of
developing nuclear cataracts and gave some of them statins. Their results suggest that statin use in an
at-risk population may be associated with a lower risk of developing nuclear cataract disease.

Long term (avg 5 year) observation showed that systematic application of azapentacene sodium
polysulfonate (Quinax) slows down the progress of the disease.
CONJUNCTIVITIS

Def: Conjunctivitis (also called "madras eye"or "pink eye") is an acute inflammation of the conjunctiva
(the outermost layer of the eye and the inner surface of the eyelids), most commonly due to an allergic
reaction or an infection (usually viral, but sometimes bacterial)

Classification

Classification can be either by cause or by extent of the inflamed area.

By cause

 Allergic Conjunctivitis
 Bacterial conjunctivitis
 Viral conjunctivitis
 Chemical conjunctivitis
 Neonatal conjunctivitis is often defined separately due to different organisms

By extent of involvement

 Blepharoconjunctivitis is the dual combination of conjunctivitis with blepharitis (inflammation of

the eyelids).
 Keratoconjunctivitis is the combination of conjunctivitis and keratitis ( corneal inflammation).
 Episcleritis is an inflammatory condition that produces a similar appearance to conjunctivitis,
but without discharge or tearing

Signs and symptoms

 Redness (hyperaemia),
 Irritation (chemosis)
 Watering (epiphora) of the eyes

are symptoms common to all forms of conjunctivitis.

Acute Conjunctivitis

Acute conjunctivitis is typically caused by either an allergy, virus, or bacteria. Typically, it is associated
with a red eye and discharge.

Allergic

Allergic conjunctivitis is typically itchy, sometimes distressingly so, and often involves some eye swelling.
Chronic allergy often causes just itching or irritation.

Allergic conjunctivitis shows pale watery swelling or edema of the conjunctiva and sometimes the whole
eyelid, often with a ropy, non-purulent mucoid discharge. There is variable redness.
  Itching must be a primary symptom to make this diagnosis.

Viral

Viral conjunctivitis is often associated with an infection of the upper respiratory tract, a common cold,
and/or sore throat . Its symptoms include watery discharge and variable itch. The infection usually
begins with one eye, but may spread easily to the other.

Viral conjunctivitis, commonly known as "pink eye," shows a fine diffuse pinkness of the conjunctiva
which is easily mistaken for the 'ciliary injection' of iritis, but there are usually corroborative signs on
microscopy, particularly numerous lymphoid follicles on the tarsal conjunctiva, and sometimes a
punctate keratitis.

Bacterial

Bacterial conjunctivitis due to the common pyogenic (pus-producing) bacteria causes

 Marked grittiness/irritation
 A stringy, opaque, grey or yellowish mucopurulent discharge (mucus, gowl, goop, gunk, googies,
eye crust, or other regional names, officially known as 'gound') that may cause the lids to stick
together (matting), especially after sleeping.
 Another symptom that could be caused by bacterial conjunctivitis is severe crusting of the
infected eye and the surrounding skin. However discharge is not essential to the diagnosis,
contrary to popular belief.

Bacteria such as

 Chlamydia trachomatis or
 Moraxella

Can cause a non-exudative but persistent conjunctivitis without much redness. The gritty and/or
scratchy feeling is sometimes localized enough for patients to insist they must have a foreign body in the
eye. The more acute pyogenic infections can be painful. Like viral conjunctivitis, it usually affects only
one eye but may spread easily to the other eye. However, it is dormant in the eye for three days before
the patient shows signs of symptoms.

Pyogenic bacterial conjunctivitis

i. shows an opaque purulent discharge,

ii. a very red eye, and
iii. On bio microscopy there are numerous white cells and desquamated epithelial cells seen in the
tear duct along the lid margin.
iv. The tarsal conjunctiva is a velvety red and not particularly follicular.
Non-pyogenic infections

 Can show just mild infection and be difficult to diagnose.

Scarring of the tarsal conjunctiva is occasionally seen in chronic infections, especially in trachoma.

Chemical

Irritant or toxic conjunctivitis symptoms

 Is irritable or painful when the infected eye is pointed far down or far up.
 Discharge and itch are usually absent.
 This is the only group in which severe pain and unconfort may occur.

Irritant or toxic conjunctivitis signs

 show primarily marked redness.

 If due to splash injury, it is often present only in the lower conjunctival sac.
 With some chemicals—above all with caustic alkalis such as sodium hydroxide—there may be
necrosis of the conjunctiva with a deceptively white eye due to vascular closure, followed by
sloughing of the dead epithelium. This is likely to be associated with slit-lamp evidence of
anterior uveitis.

Other

Inclusion conjunctivitis of the newborn (ICN) is a conjunctivitis that may be caused by the bacteria
Chlamydia trachomatis, and may lead to acute, purulent conjunctivitis. However, it is usually self-
healing.

Conjunctivitis is identified by irritation and redness of the conjunctiva. Except in obvious pyogenic or
toxic/chemical conjunctivitis, a slit lamp (biomicroscope) is needed to have any confidence in the
diagnosis. Examination of the tarsal conjunctiva is usually more diagnostic than the bulbar conjunctiva.

Causes

Conjunctivitis is most commonly caused by viral infection, but bacterial infections, allergies, other
irritants and dryness are also common etiologies for its occurrence. Both bacterial and viral infections
are contagious. Commonly, conjunctival infections are passed from person-to-person, but can also
spread through contaminated objects or water.

 The most common cause of viral conjunctivitis is adenoviruses.

 .Herpetic keratoconjunctivitis (caused by herpes simplex viruses) can be serious and requires
treatment with acyclovir.
 Acute Hemorrhagic Conjunctivitis is a highly contagious disease caused by two enteroviruses,
Enterovirus 70 and Coxsackievirus A24.
Differential diagnosis

Conjunctivitis symptoms and signs are relatively non-specific. Even after bio microscopy, laboratory tests
are often necessary if proof of etiology is needed.

A purulent discharge (a whitish-yellow, yellow or yellow-brown substance more commonly known as

pus) strongly suggests a cause from fecal matter, unless there is known exposure to toxins. It can also be
caused by bacteria from faeces, pet hair, or by smoke or other fumes. Infection with Neisseria
gonorrhoeae should be suspected if the discharge is particularly thick and copious.

Itching (rubbing eyes) is the hallmark symptom of allergic conjunctivitis. Other symptoms include past
history of eczema, or asthma.

A diffuse, less "injected" conjunctivitis (looking pink rather than red) suggests a viral cause, especially if
numerous follicles are present on the lower tarsal conjunctiva on bio microscopy.

Scarring of the tarsal conjunctiva suggests trachoma, especially if seen in endemic areas, if the scarring is
linear (von Arlt's line), or if there is also corneal vascularisation.

Clinical tests for lagophthalmos, dry eye (Schirmer test) and unstable tear film may help distinguish the
various types of conjunctivitis.

Other symptoms including pain, blurring of vision and photophobia should not be prominent in
conjunctivitis. Fluctuating blurring is common, due to tearing and mucoid discharge. Mild photophobia is
common. However, if any of these symptoms are prominent, it is important to exclude other diseases
such as glaucoma, uveitis, keratitis and even meningitis or caroticocavernous fistula.

Many people who have conjunctivitis have trouble opening their eyes in the morning because of the
dried mucus on their eyelids. There is often excess mucus over the eye after sleeping for an extended
period.

Diagnosis

These are done infrequently because most cases of conjunctivitis are treated empirically and
(eventually) successfully, but often only after running the gamut of the common possibilities.

1) Swabs for bacterial culture are necessary if the history and signs suggest bacterial conjunctivitis,
but there is no response to topical antibiotics. Research studies indicate that many bacteria
implicated in low-grade conjunctivitis are not detected by the usual culture methods of medical
microbiology labs, so negative results are common. Viral culture may be appropriate in epidemic
case clusters.
2) Conjunctival scrapes for cytology can be useful in detecting chlamydial and fungal infections,
allergy and dysplasia, but are rarely done because of the cost and the general lack of laboratory
staff experienced in handling ocular specimens.
3) Conjunctival incisional biopsy is occasionally done when granulomatous diseases (e.g.,
sarcoidosis) or dysplasia are suspected.
Management

Conjunctivitis resolves in 65% of cases without treatment, within 2 – 5 days. The prescribing of
antibiotics to most cases is not necessary.

Allergic

For the allergic type, cool water poured over the face with the head inclined downward constricts
capillaries, and artificial tears sometimes relieve discomfort in mild cases. In more severe cases, non-
steroidal anti-inflammatory medications and antihistamines may be prescribed. Persistent allergic
conjunctivitis may also require topical steroid drops.

Bacterial

Bacterial conjunctivitis usually resolves without treatment. Antibiotics, eye drops, or ointment are thus
only needed if no improvement is observed after 3 days. In patients receiving no antibiotics recovery
was in 4.8 days, immediate antibiotics 3.3 days, delayed antibiotics 3.9 days. No serious effects were
noted either with or without treatment.

Viral

Although there is no specific treatment for viral conjunctivitis, symptomatic relief may be achieved with
cold compresses and artificial tears. People are often advised to avoid touching their eyes or sharing
towels and washcloths.

Chemical

Conjunctivitis due to chemicals is treated via irrigation with Ringer's lactate or saline solution. Chemical
injuries (particularly alkali burns) are medical emergencies as they can lead to severe scarring, and
intraocular damage.
CORNEAL ULCER

Def: A corneal ulcer, or ulcerative keratitis, or eyesore is an inflammatory or more seriously, infective
condition of the cornea involving disruption of its epithelial layer with involvement of the corneal
stroma.

It is a common condition in humans particularly in the tropics and the agrarian societies. In developing
countries, Children afflicted by Vitamin A deficiency are at high risk for corneal ulcer and may become
blind in both eyes, which may persist lifelong.

Corneal anatomy of the human

The cornea is a transparent structure that is part of the outer layer of the eye. It refracts light and
protects the contents of the eye. The corneal thickness ranges from 450 to 610 micrometres and on an
average 550 µm thick in caucasian eyes. In Indian eyes, the average thickness is slightly less at 510 µm.
The trigeminal nerve supplies the cornea via the long ciliary nerves. There are pain receptors in the
outer layers and pressure receptors are deeper.

Transparency is achieved through a lack of blood vessels, pigmentation, and keratin, and through tight
layered organization of the collagen fibers. The collagen fibers cross the full diameter of the cornea in a
strictly parallel fashion and allow 99 percent of the light to pass through without scattering.

There are five layers in the human cornea, from outer to inner:

 Epithelium
 Bowman's layer
 Stroma
 Descemet's membrane
 Endothelium

The outer layer is the epithelium, which is 25 to 40 µm and five to seven cell layers thick. The epithelium
holds the tear film in place and also prevents water from invading the cornea and disrupting the
collagen fibers. This prevents corneal edema, which gives it a cloudy appearance. It is also a barrier to
infectious agents. The epithelium sticks to the basement membrane, which also separates the
epithelium from the stroma. The corneal stroma comprises 90 percent of the thickness of the cornea. It
contains the collagen fibers organized into lamellae. The lamellae are in sheets which separate easily.
Posterior to the stroma is Descemet's membrane, which is a basement membrane for the corneal
endothelium. The endothelium is a single cell layer that separates the cornea from the aqueous humor.
Corneal healing

An ulcer of the cornea heals by two methods:

1) migration of surrounding epithelial cells followed by mitosis (dividing) of the cells, and
introduction of blood vessels from the conjunctiva. Superficial small ulcers heal rapidly by the
first method.
2) However, larger or deeper ulcers often require the presence of blood vessels to supply
inflammatory cells. White blood cells and fibroblasts produce granulation tissue and then scar
tissue, effectively healing the cornea. The ulcer heals by the fourth day

1. Superficial and deep corneal ulcers

Corneal ulcers are a common human eye disease. They are caused by

 Trauma, particularly with vegetable matter, as also

 Chemical injury,
 Contact lenses and
 Infections.

Other eye conditions can cause corneal ulcers, such as

i. entropion,
ii. distichiae,
iii. corneal dystrophy, and
iv. keratoconjunctivitis sicca (dry eye).

Many micro-organisms cause infective corneal ulcer. Among them are

 bacteria,
 fungi,
 viruses,
 protozoa, and
 chlamydia.

Bacterial keratitis is caused by

1) Staphylococcus aureus,
2) Streptococcus viridans,
3) Escherichia coli,
4) Enterococci,
5) Pseudomonas,
6) Nocardia

and many other bacteria.

Fungal keratitis causes deep and severe corneal ulcer. It is caused by

1) Aspergillus sp.,
2) Fusarium sp.,
3) Candida sp., as also
4) Rhizopus,
5) Mucor, and other fungi.

The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more
than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and
hypopyon is usually seen.

Viral keratitis causes corneal ulceration. It is caused most commonly by

1) Herpes simplex,
2) Herpes Zoster
3) Adenoviruses.
4) coronaviruses & many other viruses.

Herpes virus cause a dendritic ulcer, which can recur and relapse over the lifetime of an individual.

Protozoa infection like Acanthamoeba keratitis is characterized by severe pain and is associated with
contact lens users swimming in pools. Chlamydia trachomatis can also contribute to development of
corneal ulcer.

Superficial ulcers involve a loss of part of the epithelium.

Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation.

Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially
dangerous and can rapidly result in corneal perforation, if not treated in time.

The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by

1) trauma,
2) dry eye, or
3) exposure from facial nerve paralysis or exophthalmos.

 Entropion,
 severe dry eye and
 trichiasis (inturning of eye lashes)

may cause ulceration of the peripheral cornea.

Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include

 Rheumatoid arthritis,
 rosacea,
 systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a
circumferential crater like depression of the cornea, just inside the limbus, usually with an
overhanging edge.

Symptoms

Corneal ulcers are extremely painful due to nerve exposure, and can cause

 tearing,
 squinting, and
 vision loss of the eye.

There may also be signs of anterior uveitis, such as

 miosis (small pupil),

 aqueous flare (protein in the aqueous humour), and
 redness of the eye.

An axon reflex may be responsible for uveitis formation — stimulation of pain receptors in the cornea
results in release inflammatory mediators such as

 prostaglandins,
 histamine, and
 acetylcholine.

Diagnosis/investigations

1) Diagnosis is done by direct observation under magnified view of slit lamp revealing the ulcer on the
cornea.
2) The use of fluorescein stain, which is taken up by exposed corneal stroma and appears green, helps
in defining the margins of the corneal ulcer, and can reveal additional details of the surrounding
epithelium. Herpes simplex ulcers show a typical dendritic pattern of staining.
3) Rose-Bengal dye is also used for supra-vital staining purposes, but it may be very irritating to the
eyes. In descemetoceles, the Descemet's membrane will bulge forward and after staining will
appear as a dark circle with a green boundary, because it does not absorb the stain.
4) Doing a corneal scraping and examining under the microscope with stains like Gram's and KOH
preparation may reveal the bacteria and fungi respectively.
5) Microbiological culture tests may be necessary to isolate the causative organisms for some cases.
6) Other tests that may be necessary include a

 Schirmer's test for keratoconjunctivitis sicca and

 an analysis of facial nerve function for facial nerve paralysis.
Treatment

 Proper diagnosis is essential for optimal treatment. Bacterial corneal ulcer require intensive
fortified antibiotic therapy to treat the infection.
 Fungal corneal ulcers require intensive application of topical anti-fungal agents.
 Viral corneal ulceration caused by herpes virus may respond to antivirals like topical acyclovir
ointment instilled at least five times a day.
 Alongside, supportive therapy like pain medications are given, including topical cycloplegics like

 atropine or
 homatropine

To dilate the pupil and thereby stop spasms of the ciliary muscle.

Superficial ulcers may heal in less than a week.

Deep ulcers and descemetoceles may require

 conjunctival grafts or conjunctival flaps,

 soft contact lenses, or corneal transplant.

 Proper nutrition, including protein intake and Vitamin C are usually advised. In cases of
Keratomalacia, where the corneal ulceration is due to a deficiency of Vitamin A, supplementation of
the Vitamin A by oral or intramuscular route is given.
 Drugs that are usually contraindicated in corneal ulcer are topical

 corticosteroids and
 anesthetics

- These should not be used on any type of corneal ulcer because they prevent healing, may lead to
superinfection with fungi and other bacteria and will often make the condition much worse.

2. Refractory corneal ulcers

Refractory corneal ulcers are superficial ulcers that heal poorly and tend to recur. They are also known
as indolent ulcers or Boxer ulcers. They are believed to be caused by a defect in the basement
membrane and a lack of hemidesmosomal attachments. They are recognized by undermined epithelium
that surrounds the ulcer and easily peels back. Refractory corneal ulcers are most commonly seen in
diabetics and often occur in the other eye later. They are similar to Cogan's cystic dystrophy.
Treatment

Topical fortified antibiotics are used at hourly intervals to treat infectious corneal ulcers. Cycloplegic eye
drops are applied to give rest to the eye. Pain medications are given as needed. Loose epithelium and
ulcer base can be scraped off and sent for culture sensitivity studies to find out the pathogenic
organism. This helps in choosing appropriate antibiotics. Complete healing takes anywhere from about a
few weeks to several months.

Refractory corneal ulcers can take a long time to heal, sometimes months. In case of progressive or non-
healing ulcers, surgical intervention by an ophthalmologist with corneal transplantation may be required
to save the eye. In all corneal ulcers it is important to rule out predisposing factors like diabetes mellitus
and immunodeficiency.

3. Melting ulcers

Melting ulcers are a type of corneal ulcer involving progressive loss of stroma in a dissolving fashion.
This is most commonly seen in Pseudomonas infection, but it can be caused by other types of bacteria or
fungi. These infectious agents produce proteases and collagenases which break down the corneal
stroma. Complete loss of the stroma can occur within 24 hours. Treatment includes antibiotics and
collagenase inhibitors such as acetylcysteine. Surgery in the form of corneal transplantation (penetrating
keratoplasty) is usually necessary to save the eye.
GLAUCOMA

Def: Glaucoma is a disease in which the optic nerve is damaged, leading to progressive, irreversible loss
of vision. It is often, but not always, associated with increased pressure of the fluid in the eye.

The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. There are many
different sub-types of glaucoma but they can all be considered a type of optic neuropathy. Raised
intraocular pressure is a significant risk factor for developing glaucoma (above 21 mmHg or 2.8 kPa).
Normal pressure is 10mmhg – 20mmhg.

Glaucoma can be divided roughly into two main categories, "open angle" and "closed angle" glaucoma

 Closed angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly
but the discomfort often leads patients to seek medical attention before permanent damage
occurs.
 Open angle, chronic glaucoma tends to progress at a slower rate and the patient may not notice
that they have lost vision until the disease has progressed significantly.

Epidemiology

Glaucoma has been nicknamed the "silent thief of sight" because the loss of vision normally occurs
gradually over a long period of time and is often only recognized when the disease is quite advanced.
Once lost, this damaged visual field cannot be recovered. Worldwide, it is the second leading cause of
blindness. Glaucoma affects 1 in 200 people aged fifty and younger, and 1 in 10 over the age of eighty. If
the condition is detected early enough it is possible to arrest the development or slow the progression
with medical and surgical means.

Signs and symptoms

 Open-angle Glaucoma: It is painless and does not have acute attacks. The only signs are
gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio on
fundoscopic examination).
 Closed-angle Glaucoma: About 10% of patients with closed angles present with acute angle
closure crises characterized by sudden ocular pain, seeing halos around lights, red eye, very high
intraocular pressure (>30 mmHg), nausea and vomiting, sudden decreased vision, and a fixed,
mid-dilated pupil. Acute angle closure is an ocular emergency.

Pathophasiology

The major risk factor for most glaucomas and focus of treatment is increased intraocular pressure.
Intraocular pressure is a function of production of liquid aqueous humor by the ciliary processes of the
eye and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes
into the posterior chamber, bounded posteriorly by the lens and the zonules of Zinn and anteriorly by
the iris.
 It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and
anteriorly by the cornea. From here the trabecular meshwork drains aqueous humor via Schlemm's
canal into scleral plexuses and general blood circulation.

 In open angle glaucoma there is reduced flow through the trabecular meshwork
 In angle closure glaucoma, the iris is pushed forward against the trabecular meshwork, blocking
fluid from escaping.

Risk factors

1) Ocular hypertension (increased pressure within the eye) is the largest risk factor in most
glaucomas, but in some populations only 50% of patients with primary open angle glaucoma
actually have elevated ocular pressure.
2) Those of African descent are three times more likely to develop primary open angle glaucoma.
3) People who are older have thinner corneal thickness and often suffer from hypermetropia. They
are also at higher risk for primary open angle glaucoma.
4) People with a family history of glaucoma have about six percent chance of developing glaucoma.
5) Many East Asia groups are prone to developing angle closure glaucoma due to their shallower
anterior chamber depth, with the majority of cases of glaucoma in this population consisting of
some form of angle closure.
6) Women are three times more likely than men to develop acute angle-closure glaucoma due to
their shallower anterior chambers. Normal depth of anterior chamber is about 3mm
7) Other factors can cause glaucoma, known as "secondary glaucomas," including
 prolonged use of steroids (steroid-induced glaucoma);
 conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy
and central retinal vein occlusion (neovascular glaucoma);
 ocular trauma (angle recession glaucoma); and uveitis (uveitic glaucoma).
8) Primary open angle glaucoma (POAG) has been found to be associated with mutations in genes
at several loci. Normal tension glaucoma, which comprises one third of POAG, is associated with
genetic mutations.
9) There is increasing evidence that ocular blood flow is involved in the pathogenesis of glaucoma.
Current data indicate that fluctuations in blood flow are more harmful in glaucomatous optic
neuropathy than steady reductions. Unstable blood pressure and dips are linked to optic nerve
head damage and correlate with visual field deterioration.
10) A number of studies also suggest a possible correlation between hypertension and the
development of glaucoma. In normal tension glaucoma, nocturnal hypotension may play a
significant role.

There is no clear evidence that vitamin deficiencies cause glaucoma in humans. It follows then that oral
vitamin supplementation is probably not useful in glaucoma treatment.
 11) Various rare congenital/genetic eye malformations are associated with glaucoma. Occasionally,
failure of the normal third trimester gestational atrophy of the hyaloid canal and the tunica
vasculosa lentis is associated with other anomalies.

Those at risk for glaucoma are advised to have a dilated eye examination at least once a year.

Diagnosis

 Screening for glaucoma is usually performed as part of a standard eye examination performed
by ophthalmologists, orthoptists and optometrists.
 Testing for glaucoma should include measurements of the intraocular pressure via tonometry,
changes in size or shape of the eye, anterior chamber angle examination or genioscopy, 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 formal visual field test should be
performed.
 The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence
tomography (OCT), scanning laser polarimetry (GDx), and/or scanning laser ophthalmoscopy
also known as Heidelberg Retina Tomography (HRT3).
 Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as
Goldmann tonometry should be augmented with pachymetry to measure central corneal
thickness (CCT). A thicker-than-average cornea can result in a pressure reading higher than the
'true' pressure, whereas a thinner-than-average cornea can produce a pressure reading lower
than the 'true' pressure. Because pressure measurement error can be caused by more than just
CCT (i.e., corneal hydration, elastic properties, etc.), it is impossible to 'adjust' pressure
measurements based only on CCT measurements.
 The Frequency Doubling Illusion can also be used to detect glaucoma with the use of a
Frequency Doubling Technology (FDT) perimeter.
 Examination for glaucoma also could be assessed with more attention given to sex, race, history
of drug use, refraction, inheritance and family history.

Management

The modern goals of glaucoma management are

 To avoid glaucomatous damage and nerve damage,

 To preserve visual field and total quality of life for patients with minimal side effects.

This requires appropriate diagnostic techniques and follow up examinations and judicious selection of
treatments for the individual patient. Although intraocular pressure is only one of the major risk factors
for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the
mainstay of glaucoma treatment.
Medication

Intraocular pressure can be lowered with medication, usually eye drops. There are several different
classes of medications to treat glaucoma with several different medications in each class.

Each of these medicines may have local and systemic side effects. Adherence to medication protocol can
be confusing and expensive; if side effects occur, the patient must be willing either to tolerate these, or
to communicate with the treating physician to improve the drug regimen. Initially, glaucoma drops may
reasonably be started in either one or in both eyes.

Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma
patients. Patient education and communication must be ongoing to sustain successful treatment plans
for this lifelong disease with no early symptoms.

 Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost

(Travatan) increase uveoscleral outflow of aqueous humor. Bimatoprost also increases
trabecular outflow
 Topical beta-adrenergic receptor antagonists such as timolol, levobunolol (Betagan), and
betaxolol decrease aqueous humor production by the ciliary body
 Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a dual mechanism,
decreasing aqueous production and increasing trabecular outflow.
 Less-selective Sympathomimetics such as epinephrine decrease aqueous humor production
through vasoconstriction of ciliary body blood vessels.
 Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary
muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous
humour. Ecothiopate is used in chronic glaucoma.
 Carbon anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide
(Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.
 Physostigmine is also used to treat glaucoma and delayed gastric emptying.

Surgery

Both laser and conventional surgeries are performed to treat glaucoma.

Surgery is the primary therapy for those with congenital glaucoma.

Generally, these operations are a temporary solution, as there is not yet a cure for glaucom
 I. Canaloplasty

Canaloplasty is a nonpenetrating procedure utilizing microcatheter technology. To perform a

canaloplasty, an incision is made into the eye to gain access to Schlemm's canal in a similar fashion to a
viscocanalostomy. A microcatheter will circumnavigate the canal around the iris, enlarging the main
drainage channel and its smaller collector channels through the injection of a sterile, gel-like material
called viscoelastic. The catheter is then removed and a suture is placed within the canal and tightened.
By opening the canal, the pressure inside the eye may be relieved, although the reason is unclear since
the canal (of Schlemm) does not have any significant fluid resistance in glaucoma or healthy eyes. Long-
term results are not available.

II. Laser surgery

Laser trabeculoplasty may be used to treat open angle glaucoma. It is a temporary solution, not a cure.
A 50 μm argon laser spot is aimed at the trabecular meshwork to stimulate opening of the mesh to allow
more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser
trabeculoplasty utilizes a thermal argon laser. The procedure is called Argon Laser Trabeculoplasty or
ALT. A newer type of laser trabeculoplasty exists that uses a "cold" (non-thermal) laser to stimulate
drainage in the trabecular meshwork. This newer procedure which uses a 532 nm frequency-doubled, Q-
switched Nd:YAG laser which selectively targets melanin pigment in the trabecular meshwork cells,
called Selective Laser Trabeculoplasty or SLT. Studies show that SLT is as effective as ALT at lowering eye
pressure. In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated
only once.

Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle
closure glaucoma or pigment dispersion syndrome. During laser iridotomy, laser energy is used to make
a small full-thickness opening in the iris. This opening equalizes the pressure between the front and back
of the iris correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover the
trabecular meshwork. In some cases of intermittent or short-term angle closure this may lower the eye
pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases
it also reduces the risk of developing chronic angle closure or of adhesions of the iris to the trabecular
meshwork.

Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary
epithelium.
 III. Trabeculectomy

The most common conventional surgery performed for glaucoma is the trabeculectomy. Here, a partial
thickness flap is made in the scleral wall of the eye, and a window opening made under the flap to
remove a portion of the trabecular meshwork. The scleral flap is then sutured loosely back in place. This
allows fluid to flow out of the eye through this opening, resulting in lowered intraocular pressure and
the formation of a bleb or fluid bubble on the surface of the eye. Scarring can occur around or over the
flap opening, causing it to become less effective or lose effectiveness altogether. One person can have
multiple surgical procedures of the same or different types.

IV. Glaucoma drainage implants

There are also several different glaucoma drainage implants. These include the original Molteno implant
(1966), the Baerveldt tube shunt, or the valved implants, such as the Ahmed glaucoma valve implant or
the ExPress Mini Shunt and the later generation pressure ridge Molteno implants. These are indicated
for glaucoma patients not responding to maximal medical therapy, with previous failed guarded filtering
surgery (trabeculectomy). The flow tube is inserted into the anterior chamber of the eye and the plate is
implanted underneath the conjunctiva to allow flow of aqueous fluid out of the eye into a chamber
called a bleb.

 The first-generation Molteno and other non-valved implants sometimes require the ligation of
the tube until the bleb formed is mildly fibrosed and water-tight.This is done to reduce
postoperative hypotony—sudden drops in postoperative intraocular pressure (IOP).
 Valved implants such as the Ahmed glaucoma valve attempt to control postoperative hypotony
by using a mechanical valve.

The ongoing scarring over the conjunctival dissipation segment of the shunt may become too thick for
the aqueous humor to filter through. This may require preventive measures using anti-fibrotic
medication like 5-fluorouracil (5-FU) or mitomycin-C (during the procedure), or additional surgery. And
for Glaucomatous painful Blind Eye and some cases of Glaucoma, Cyclocryotherapy for ciliary body
ablation could be considered to be performed.[

V. Laser assisted non-penetrating deep sclerectomy

The most common surgical approach currently used for the treatment of glaucoma, is trabeculectomy,
in which the sclera is punctured to alleviate inner eye pressure (IOP). Non-penetrating deep sclerectomy
(NPDS) surgery is a similar but modified procedure, in which instead of puncturing the scleral wall, a
patch of the sclera is skimmed to a level, upon which, percolation of liquid from the inner eye is
achieved and thus alleviating IOP, without penetrating the eye. NPDS is demonstrated to cause a
significantly less side effects than trabeculectomy. However, NPDS is performed manually and requires
great skill to achieve a lengthy learning curve.
Laser assisted NPDS is the performance of NPDS with the use of a CO2 laser system. The laser-based
system is self-terminating once the required scleral thickness and adequate drainage of the intra ocular
fluid have been achieved. This self-regulation effect is achieved as the CO2 laser essentially stops
ablating as soon as it comes in contact with the intra-ocular percolated liquid, which occurs as soon as
the laser reaches the optimal residual intact layer thickness.

Classification of glaucoma

1. Primary glaucoma and its variants (H40.1-H40.2)

 Primary glaucoma

i. Primary angle-closure glaucoma, also known as primary closed-angle glaucoma, narrow-angle

glaucoma, pupil-block glaucoma, acute congestive glaucoma

a) Acute angle-closure glaucoma

b) Chronic angle-closure glaucoma
c) Intermittent angle-closure glaucoma
d) Superimposed on chronic open-angle closure glaucoma ("combined mechanism" - uncommon)

ii. Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple
glaucoma, glaucoma simplex

a) High-tension glaucoma
b) Low-tension glaucoma

 Variants of primary glaucoma

i. Pigmentary glaucoma
ii. Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare

Primary angle-closure glaucoma - This is caused by contact between the iris and trabecular meshwork,
which in turn obstructs outflow of the aqueous humor from the eye. This contact between iris and
trabecular meshwork (TM) may gradually damage the function of the meshwork until it fails to keep
pace with aqueous production, and the pressure rises. In over half of all cases, prolonged contact
between iris and TM causes the formation of synechiae (effectively "scars"). These cause permanent
obstruction of aqueous outflow. In some cases, pressure may rapidly build up in the eye causing pain
and redness (symptomatic, or so called "acute" angle-closure). In this situation the vision may become
blurred, and halos may be seen around bright lights. Accompanying symptoms may include headache
and vomiting. Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive
to light, cornea edematous (cloudy), reduced vision, redness, pain. However, the majority of cases are
asymptomatic. Prior to very severe loss of vision, these cases can only be identified by examination,
generally by an eye care professional.
 Once any symptoms have been controlled, the first line (and often definitive) treatment is laser
iridotomy. This may be performed using either Nd:YAG or argon lasers, or in some cases by conventional
incisional surgery. The goal of treatment is to reverse, and prevent, contact between iris and trabecular
meshwork. In early to moderately advanced cases, iridotomy is successful in opening the angle in
around 75% of cases. In the other 25% laser iridoplasty, medication (pilocarpine) or incisional surgery
may be required.

Primary open-angle glaucoma - Optic nerve damage resulting in progressive visual field loss. This is
associated with increased pressure in the eye. Not all people with primary open-angle glaucoma have
eye pressure that is elevated beyond normal, but decreasing the eye pressure further has been shown
to stop progression even in these cases. The increased pressure is caused by trabecular blockage which
is where the aqueous humor in the eye drains out. Because the microscopic passage ways are blocked,
the pressure builds up in the eye and causes imperceptible very gradual vision loss. Peripheral vision is
affected first but eventually the entire vision will be lost if not treated. Diagnosis is made by looking for
cupping of the optic nerve. Prostaglandin agonists work by opening uveoscleral passageways. Beta
blockers such as timolol, work by decreasing aqueous formation. Carbonic anhydrase inhibitors decrease
bicarbonate formation from ciliary processes in the eye, thus decreasing formation of Aqueous humor.
Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway
and constricting the pupil. Alpha 2 agonists (brimonidine, apraclonidine) both decrease fluid production
(via. inhibition of AC) and increase drainage.

2. Secondary glaucoma (H40.3-H40.6)

 Secondary glaucoma

i. Inflammatory glaucoma

a) Uveitis of all types

b) Fuchs heterochromic iridocyclitis

ii. Phacogenic glaucoma

a) Angle-closure glaucoma with mature cataract

b) Phacoanaphylactic glaucoma secondary to rupture of lens capsule
c) Phacolytic glaucoma due to phacotoxic meshwork blockage
d) Subluxation of lens

iii. Glaucoma secondary to intraocular hemorrhage

a) Hyphema
b) Hemolytic glaucoma, also known as erythroclastic glaucoma
 iv. Traumatic glaucoma

a) Angle recession glaucoma: Traumatic recession on anterior chamber angle

b) Postsurgical glaucoma

 Aphakic pupillary block

 Ciliary block glaucoma

v. Neovascular glaucoma (see below for more details)

vi. Drug-induced glaucoma

a) Corticosteroid induced glaucoma

b) Alpha-chymotrypsin glaucoma. Postoperative ocular hypertension from use of alpha
chymotrypsin.

vii. Glaucoma of miscellaneous origin

a) Associated with intraocular tumors

b) Associated with retinal detachments
c) Secondary to severe chemical burns of the eye
d) Associated with essential iris atrophy
e) Toxic Glaucoma

Neovascular glaucoma is an uncommon type of glaucoma that is difficult or nearly impossible to treat.
This condition is often caused by proliferative diabetic retinopathy (PDR) or central retinal vein occlusion
(CRVO). It may also be triggered by other conditions that result in ischemia of the retina or ciliary body.
Individuals with poor blood flow to the eye are highly at risk for this condition.

Neovascular glaucoma results when new, abnormal vessels begin developing in the angle of the eye that
begin blocking the drainage. Patients with such condition begin to rapidly lose their eyesight.
Sometimes, the disease appears very rapidly, specially after cataract surgery procedure. A new
treatment for this disease, as first reported by Kahook and colleagues, involves use of a novel group of
medications known as Anti-VEGF agents. These injectable medications can lead to a dramatic decrease
in new vessel formation and, if injected early enough in the disease process, may lead to normalization
of intraocular pressure.

Toxic glaucoma is open angle glaucoma with an unexplained significant rise of intraocular pressure
following unknown pathogenesis. Intraocular pressure can sometimes reach 80 mmHg (11 kPa). It
characteristically manifests as ciliary body inflammation and massive trabecular oedema that sometimes
extends to Schlemm's Canal.
This condition is differentiated from malignant glaucoma by the presence of a deep and clear anterior
chamber and a lack of aqueous misdirection. Also, the corneal appearance is not as hazy. A reduction in
visual acuity can occur following neuroretinal breakdown. Associated factors include inflammation,
drugs, trauma and intraocular surgery, including cataract surgery and vitrectomy procedures. Gede
Pardianto (2005) reports on four patients who had toxic glaucoma. One of them underwent
phaecoemulsification with small particle nucleus drops. Some cases can be resolved with some
medication, vitrectomy procedures or trabeculectomy. Valving procedures can give some relief but
further research is required.

3. Developmental glaucoma (Q15.0)

 Developmental glaucoma

i. Primary congenital glaucoma

ii. Infantile glaucoma
iii. Glaucoma associated with hereditary of familial diseases

4. Absolute glaucoma (H44.5)

 Absolute glaucoma is the end stage of all types of glaucoma. The eye has no vision, abscence of
PL and PR, and has a stony hard in appearance. Severe pain is present in eye. The treatment of
absolute glaucoma is a destructive procedure like cyclocryo application, cyclophotocoagulation,
or injection of 100% alcohol
HYPHEMA

Def: Hyphema (or hyphaema, see spelling differences) is blood in the front (anterior) chamber of the
eye. It may appear as a reddish tinge, or it may appear as a small pool of blood at the bottom of the iris
or in the cornea

Causes

Hyphemas are frequently caused by injury (blunt trauma) and may partially or completely block vision.

Presentation and prognosis

Hyphemas may resolve by themselves, they may require medical treatment, or they may result in
permanent visual impairment.

A long-standing hyphema may result in

 hemosiderosis and
 heterochromia.

Blood accumulation may also cause an elevation of the intraocular pressure

Treatment

Treatment of hyphema consists of 4 major tenets:

1. Light activity or even bedrest (to prevent a rebleed into the anterior chamber, which may cause
obstruction of vision, or a painful rise in pressure)

2. Elevation of the head of the bed by approximately 45 degrees (so that the hyphema can settle out
inferiorly and avoid obstruction of vision, as well as to facilitate resolution)

3. Wearing of an eye shield at night time (to prevent accidental rubbing of the eyes during sleep, which
can precipitate a rebleed)

4. Avoidance of pain medications such as aspirin or ibuprofen (which thin the blood and increase the risk
of a rebleed - instead, acetaminophen can be used for pain control).

It is controversial among ophthalmologists whether a steroid medication or a dilating drop should be

used in treatment of hyphema. Steroids aim to reduce the amount of inflammation, but are not without
side effects. Dilating drops aim to increase comfort from the traumatized iris as well as reduce bleeding,
but can also cause the pupil to be fixed in a dilated state via posterior synechiae.

The vast majority of hyphemas resolve on their own without complication.

Some cases of non-resolving hyphemas, or hyphemas that are associated with high pressure, may
require surgery to clean out the anterior chamber and prevent corneal blood staining.
HYPOPYON

Def: Hypopyon is pus in the eye.

It is a leukocytic exudate, seen in the anterior chamber, usually accompanied by redness of the
conjunctiva and the underlying episclera. It is a sign of inflammation of the anterior uvea and iris, i.e.
iritis, which is a form of anterior uveitis. The exudate settles at the bottom due to gravity.

Differential diagnosis

Hypopyon can also be present in a corneal ulcer, particularly of fungal etiology like Aspergillus and
Fusarium sp., Behcet's disease, endophthalmitis, and panuveitis/panophthalmitis. Hypopyon is also
known as sterile pus, as it occurs due to the release of toxins and not by the actual invasion of
pathogens. The toxins secreted by the pathogens mediate the outpouring of leukocytes that settle down
in the anterior chamber of the eye. Hypopyon is the only pus in the body that does not require any
specific treatment as treatment of the underlying cause results in its resolution. An inverse hypopyon
needs to be differentiated from a standard hypopyon. Inverse hypopyon is seen sometimes after a pars
plana vitrectomy with insertion of silicon oil (as a replacement of the vitreous humour that has been
removed in the operation; the silicon oil maintains internal tamponade). When the silicon oil emulsifies,
it seeps into the anterior chamber and settles at the top of the anterior chamber. Compare from the
hypopyon resulting due to the toxins where the leukocytes settle at the bottom of the anterior
chamber. This is due to the effect of gravity, hence the name inverse hypopyon.

STAPHYLOMA

Def: A staphyloma is an abnormal protrusion of the uveal tissue through a weak point in the eyeball.
The protrusion is generally black in colour, due to the inner layers of the eye. It occurs due to weakening
of outer layer of eye (cornea or sclera) by an inflammatory or degenerative condition. It may be of 5
types, depending on the location on the eye ball (bulbus oculi).

Intercalary staphyloma

It is the name given to the localised bulge in limbal area, lined by the root of the iris. It results due to
ectasia of weak scar tissue formed at the limbus, following healing of a perforating injury or a peripheral
corneal ulcer. There may be associated secondary angle closure glaucoma, which may cause progression
of the bulge if not treated. Defective vision occurs due to marked corneal astigmatism. Treatment
consists of localised staphylectomy under heavy doses of oral steroids.

Ciliary staphyloma

As the name implies, it is the bulge of weak sclera lined by ciliary body, which occurs about 2-3 mm
away from the limbus. Its common causes are thinning of sclera following perforating injury, scleritis &
absolute glaucoma.
Equatorial staphyloma

On the equator of the eye (region circumferencing the largest diameter orthogonal to the visual axis). Its
causes are scleritis & degeneration of sclera in pathological myopia. It occurs more commonly in the
regions of sclera which are perforated by vortex veins.

Posterior staphyloma

In the posterior segment of the eye, typically diagnosed at the region of the macula, deforming the eye
in a way that the eye-length is extended associated with myopia (nearsightedness). It is diagnosed by
ophthalmoscopy, which shows an area of retinal excavation in the region of the staphyloma.

MACULAR EDEMA

Macular edema occurs when fluid and protein deposits collect on or under the macula of the eye, a
yellow central area of the retina, causing it to thicken and swell. The swelling may distort a person's
central vision, as the macula is near the center of the retina at the back of the eyeball. This area holds
tightly packed cones that provide sharp, clear central vision to enable a person to see form, color, and
detail that is directly in the line of sight.

Macular edema is sometimes a complication appearing a few days or weeks after cataract surgery, but
most such cases can be successfully treated with NSAID or cortisone eye drops.

Until recently there were no good treatments for macular edema caused by central retinal vein
occlusion (CRVO). Laser photocoagulation has been used for macular edema caused by branch retinal
vein occlusion (BRVO).

Classification

Cystoid macular edema (CME) is any type of macular edema that involves cyst formation, including
Irvine-Gass syndrome and others.

Diabetic macular edema is classified into focal and diffuse types. Each can be treated by types of laser
photocoagulation
OPHTHALMIA NEONATORUM

Neonatal conjunctivitis, also known as ophthalmia neonatorum, is a form of bacterial conjunctivitis

contracted by newborns during delivery. The baby's eyes are contaminated during passage through the
birth canal from a mother infected with either Neisseria gonorrhoeae or Chlamydia trachomatis.
Eyedrops containing erythromycin are typically used to prevent the condition. If left untreated it can
cause blindness.

Def: Neonatal conjunctivitis by definition presents during the first month of life. It may be infectious or
non infectious

Cause

Non infectious

Chemical irritants such as silver nitrate can cause chemical conjunctivitis, usually lasting 2–4 days. Thus,
silver nitrate is no longer in common use. In most countries neomycin and chloramphenicol eye drops
are used instead.

Infectious

Many different bacteria and viruses can cause conjunctivitis in the neonate. The two most feared causes
are

 N. gonorrheae and
 Chlamydia

acquired from the birth canal during delivery.

Ophthalmia neonatorum due to gonococci (Neisseria gonorrhoeae) typically manifests in the first 5 days
of life and is associated with marked bilateral purulent discharge and local inflammation.

In contrast, conjunctivitis secondary to infection with chlamydia (Chlamydia trachomatis) produces

conjunctivitis after day 3 of life, but may occur up to 2 weeks after delivery. The discharge is usually
more watery in nature (mucopurulent) and less inflammed. Babies infected with chlamydia may develop
pneumonitis (chest infection) at a later stage (range 2 weeks – 19 weeks after delivery). Infants with
chlamydia pneumonitis should be treated with oral erythromycin for 10–14 days.

Other agents causing Opthalmia neonatorum include

1. Herpes simplex virus (HSV 2),

2. Staphylococcus aureus,
3. Streptococcus haemolyticus,
4. Streptococcus pneumoniae
Signs & symptoms

1. Pain and tenderness in eyeball

2. Conjunctival discharge:purulent, mucoid or mucopurulent depending on the cause.
3. Conjunctiva shows hyperaemia and chemosis. Eye lids are usually swollen.
4. Corneal involvement (rare) may occur in herpes simplex opthalmia neonatorum.

Complications

Untreated cases may develop corneal ulceration, which may perforate resulting in corneal opacification
and Staphyloma formation.

Treatment

A. Prophylaxis needs antenatal, natal and post natal care.

1. Antenatal measures include thorough care of mother and treatment of genital infections when
suspected.
2. Natal measures are of utmost importance as mostly infection occurs during childbirth. Deliveries
should be conducted under hygienic conditions taking all asceptic measures. The newborn baby's
closed lids should be thoroughly cleansed and dried.
3. Postnatal measures include:

a) Use of 1% tetracycline ointment or 0.5% erythromycin ointment or 1% silver nitrate solution

(crede's method) into the eyes of babies immediately after birth
b) Single injection of ceftriaxone 50 mg/kg IM or IV should be given to infants born to mothers with
untreated gonococcal infection. B. Curative treatment as a rule, conjunctival cytology samples
and culture sensitivity swabs should be taken before starting treatment

 Chemical ophthalmia neonatorum is a self-limiting condition and does not require any treatment.
 Gonococcal ophthalmia neonatorum needs prompt treatment to prevent complications. Topical
therapy should include

1. Saline levarage hourly till the discharge is eliminated

2. Bacitracin eye ointment four times per day (Because of resistant strains topical penicillin therapy is
not reliable. However in cases with proved penicillin susceptibility, penicillin drops 5000 to 10000 units
per ml should be instilled every minute for half an hour, every five minutes for next half an hour and
then half-hourly till infection is controlled)
 3. If the cornea is involved then atropine sulphate ointment should be applied. Systemic therapy:
Neonates with gonococcal ophthalmia neonatorum should be treated for seven days with one of the
following regimens

Ceftriaxone 75–100 mg/kg/day IV or IM, QID

Cefotaxime 100–150 mg/kg/day IV or IM, 12 hourly
Ciprofloxacin 10–20 mg/kg/day or Norfloxacin 10 mg/kg/day
Crystalline benzyl penicillin G 50,000 units (for full-term normal weight babies) or 20,000 units (for
premature or low weight babies) IM twice daily for three days (if penicillin is susceptible)

 Other bacterial ophthalmia neonatorum should be treated by broad spectrum antibiotics drops
and ointment for two weeks.
 Neonatal inclusion conjunctivitis caused by Chlamydia trachomatis responds well to topical
tetracycline 1% or erythromycin 0.5% eye ointment QID for three weeks. However systemic
erythromycin should also be given since the presence of chlamydia agents in conjunctiva implies
colonization of upper respiratory tract as well. Both parents should also be treated with
systemic erythromycin.
 Herpes simplex conjunctivitis is usually a self-limiting disease. Topical antiviral drugs control the
infection more effectively and may prevent recurrence.
REFRACTIVE ERROR

Def: A refractive error, or refraction error, is an error in the focusing of light by the eye and a frequent
reason for reduced visual acuity.

Classification

An eye that has no refractive error when viewing a distant object is said to have emmetropia or be
emmetropic.

An eye that has a refractive error when viewing a distant object is said to have ametropia or be
ametropic.

Refractive errors are frequently categorized as spherical errors and cylindrical errors:

 Spherical errors occur when the optical power of the eye is either too large or too small to focus
light on the retina. People with refraction error frequently have blurry vision.
o When the optics are too powerful for the length of the eyeball (this can arise from a
cornea with too much curvature or an eyeball that is too long), one has myopia.
o When the optics are too weak for the length of the eyeball (this can arise from a cornea
with not enough curvature or an eyeball that is too short), one has hyperopia.

 Cylindrical errors occur when the optical power of the eye is too powerful or too weak across
one meridian. It is as if the overall lens tends towards a cylindrical shape along that meridian.
The angle along which the cylinder is placed is known as the axis of the cylinder, while 90
degrees away from the axis is known as the meridian of the cylinder. People with a simple
astigmatic refractive error see contours of a particular orientation as blurred, but see contours
with orientations at right angles as clear. When one has a cylindrical error, one has astigmatism.

Causes

Refractive errors are thought to occur due to a combination of genetic and environmental factors.
Trauma or ocular disorders such as keratoconus may induce refractive errors.

Diagnosis

Blurry vision may result from any number of conditions not necessarily related to refractive errors. The
diagnosis of a refractive error is usually confirmed by an eye care professional during an eye
examination using an instrument called a phoropter which contains a large number of lenses of varying
optical power. In combination with a retinoscope (a procedure entitled retinoscopy), the doctor instructs
the patient to view an eye chart while he or she changes the lenses within the phoropter to objectively
estimate the amount of refractive error the patient may possess. Once the doctor arrives at an estimate,
he or she typically shows the patient lenses of progressively higher or weaker powers in a process
known as refraction or refractometry. Cycloplegic agents are frequently used to more accurately
determine the amount of refractive error, particularly in children
An automated refractor is an instrument that is sometimes used in place of retinoscopy to objectively
estimate a person's refractive error.

Vision defects caused by refractive error can be distinguished from other problems using a pinhole
occluder, which will improve vision only in the case of refractive error.

Management

How refractive errors are treated or managed depends upon the amount and severity of the condition.
Those who possess mild amounts of refractive error may elect to leave the condition uncorrected,
particular if the patient is asymptomatic. For those who are symptomatic, glasses, contact lenses,
refractive surgery, or a combination of the three are typically used.

In the case of myopia, however, some believe that such treatments may also have the long-term effect
of exacerbating that refractive error — i.e., making the patient even more nearsighted. This would be
due to the very same prescription that is tailored for use at a 12-to-20-foot distance also commonly
being used for close-up work as well, thus artificially amplifying the focusing stress that would normally
be presented to the accommodation mechanisms of the eye at that distance.

However, this exacerbating effect is not generally believed to exist in the general case, although in cases
where the myopia is due to accommodative spasm, removing the corrective lenses for a time may lead
to improvement.

Epidemiology

The global prevalence of refractive errors has been estimated from 800 million to 2.3 billion.
RETINOBLASTOMA

Def: Retinoblastoma (Rb) is a rapidly developing cancer which develops in the cells of retina, the light
detecting tissue of the eye

Classification

There are two forms of the disease;

 A genetic, heritable form and

 A non-genetic, non-heritable form.

Approximately 55% of children with Rb have the non-genetic form. If there is no history of the disease
within the family, the disease is labelled "sporadic", but this does not necessarily indicate that it is the
non-genetic form.

 In about two thirds of cases, only one eye is affected (unilateral retinoblastoma);
 In the other third, tumours develop in both eyes (bilateral retinoblastoma). The number and size
of tumours on each eye may vary.
 In certain cases, the pineal gland is also affected (trilateral retinoblastoma). The position, size
and quantity of tumours are considered when choosing the type of treatment for the disease.

Signs and symptoms

The most common and obvious sign of retinoblastoma is an abnormal appearance of the pupil,
leukocoria. Other less common and less specific signs and symptoms are:

 deterioration of vision,
 a red and irritated eye,
 faltering growth or delayed development.

Some children with retinoblastoma can develop a squint commonly referred to as "cross-eyed" or "wall-
eyed" (strabismus). However, retinoblastoma presence with advanced disease in developing countries
and eye enlargement is a common finding.

Depending on the position of the tumors, they may be visible during a simple eye exam using an
ophthalmoscope to look through the pupil. A positive diagnosis is usually made only with an
examination under anesthetic (EUA). A white eye reflection is not always a positive indication of
retinoblastoma and can be caused by light being reflected badly or by other conditions such as Coats's
Disease.

In a photograph, the photographic fault red eye may be a sign of retinoblastoma, if in the photograph it
is in one eye and not in the other eye
Epidemiology

 Retinoblastoma is rare and affects approximately 1 in 15,000 live births

 Most children are diagnosed before the age of five years old
 Bilateral cases usually present within the first year with the average age at diagnosis being 9
months. Diagnosis of unilateral cases peaks between 24 and 30 months.

Cause of retinoblastoma

In children with the heritable genetic form of retinoblastoma there is a mutation on chromosome 13,
called the RB1 gene. The genetic codes found in chromosomes control the way in which cells grow and
develop within the body. If a portion of the code is missing or altered (mutation) a cancer may develop.

The defective RB1 gene can be inherited from either parent; in some children, however, the mutation
occurs in the early stages of fetal development. It is unknown what causes the gene abnormality; it is
most likely to be a random mistake during the copy process which occurs when a cell divides.

Genetic forms of retinoblastomas are more likely to be bilateral; in addition, they may be associated
with pinealoblastoma (also known as trilateral retinoblastoma) with a dismal outcome. The genetic
codes found in chromosomes control the way in which cells grow and develop within the body

Diagnosis

Screening for retinoblastoma should be part of a "well baby" screening for newborns during the first
three months of life, to include:

o The Red reflex: checking for a normal reddish-orange reflection from the eye's retina
with an ophthalmoscope or retinoscope from approximately 30 cm / 1 foot, usually
done in a dimly lit or dark room.
o The Corneal light reflex: checking for symmetrical reflection of beam of light in the same
spot on each eye when a light is shined into each cornea, to help determine whether the
eyes are crossed.
o Eye examination: checking for any structural abnormalities.

Differential diagnosis
1. Persistent hyperplastic primary vitreous (PHPV): congenital developmental anomaly of the
eye resulting from failure of the embryological, primary vitreous and hyaloid vasculature to
regress, whereby the eye is shorter, develops a cataract, and may present with whitening of the
pupil.

2. Coat's disease: a typically unilateral disease characterised by abnormal development of blood

vessels behind the retina, leading to blood vessel abnormalities in the retina and retinal
detachment to mimic retinoblastoma.

3. Toxocara canis: an infectious disease of the eye associated with exposure to infected puppies,
which causes a retinal lesion leading to retinal detachment.
 4. Retinopathy of prematurity (ROP): associated with low birth weight infants who receive
supplemental oxygen in the period immediately after birth, it involves damage to the retinal
tissue and may lead to retinal detachment.

If the eye examination is abnormal, further testing may include imaging studies, such as Computerized
Tomography (CT), Magnetic Resonance Imaging (MRI), and Ultrasound. CT and MRI can help define the
structure abnormalities and reveal any calcium depositions. Ultrasound can help define the height and
thickness of the tumor. Bone marrow examination or lumbar puncture may also be done to determine
any metastases to bones or the brain.

Morphology

Gross and microscopic appearances of retinoblastoma are identical in both hereditary and sporadic
types. Macroscopically, viable tumor cells are found near blood vessels, while zones of necrosis are
found in relatively avascular areas. Microscopically, both undifferentiated and differentiated elements
may be present. Undifferentiated elements appear as collections of small, round cells with
hyperchromatic nuclei; differentiated elements include Flexner-Wintersteiner rosettes and fluerettes
from photoreceptor differentiation.

Treatment

Treatment of retinoblastoma varies from country to country. The first priority is to preserve the life of
the child, then to preserve the vision and thirdly to minimize any complications or side effects of the
treatment. The exact course of treatment will depend on the individual case and will be decided by the
Ophthalmologist in discussion with the Paediatric Oncologist.

Options for treatment include:

1. chemotherapy (which can be administered locally through a thin catheter that is threaded
through the groin through the aorta and the neck into the optic vessels),
2. cryotherapy,
3. radioactive plaques,
4. laser therapy,
5. external beam radiotherapy and
6. surgery.

Any combinations of these treatments may be adopted.

In recent years, there has been an effort to find alternatives to enucleation and radiation therapy.
TRACHOMA

Trachoma (Ancient Greek: "rough eye") is an infectious eye disease, and the leading cause of the world's
infectious blindness. Globally, 84 million people suffer from active infection and nearly 8 million people
are visually impaired as a result of this disease. Globally this disease results in considerable disability.

Causes

Trachoma is caused by Chlamydia trachomatis and it is spread by direct contact with eye, nose, and
throat secretions from affected individuals, or contact with fomites (inanimate objects), such as towels
and/or washcloths, that have had similar contact with these secretions. Flies can also be a route of
mechanical transmission. Untreated, repeated trachoma infections result in entropion—a painful form
of permanent blindness when the eyelids turn inward, causing the eyelashes to scratch the cornea.
Children are the most susceptible to infection due to their tendency to easily get dirty, but the blinding
effects or more severe symptoms are often not felt until adulthood.

Blinding endemic trachoma occurs in areas with poor personal and family hygiene. Many factors are
indirectly linked to the presence of trachoma including

 lack of water,
 absence of latrines or toilets,
 poverty in general,
 flies,
 close proximity to cattle,
 crowding and so forth.

However, the final common pathway seems to be the presence of dirty faces in children that facilitates
the frequent exchange of infected ocular discharge from one child’s face to another. Most transmission
of trachoma occurs within the family.

Signs and symptoms

The bacterium has an incubation period of 5 to 12 days, after which the affected individual experiences
symptoms of conjunctivitis, or irritation similar to "pink eye." Blinding endemic trachoma results from
multiple episodes of reinfection that maintains the intense inflammation in the conjunctiva. Without
reinfection, the inflammation will gradually subside.

The conjunctival inflammation is called “active trachoma” and usually is seen in children, especially pre
school children. It is characterized by white lumps in the undersurface of the upper eye lid (conjunctival
follicles or lymphoid germinal centres) and by non-specific inflammation and thickening often associated
with papillae. Follicles may also appear at the junction of the cornea and the sclera (limbal follicles).
Active trachoma will often be irritating and have a watery discharge. Bacterial secondary infection may
occur and cause a purulent discharge.
The later structural changes of trachoma are referred to as “cicatricial trachoma”. These include scarring
in the eye lid (tarsal conjunctiva) that leads to distortion of the eye lid with buckling of the lid (tarsus) so
the lashes rub on the eye (trichiasis). These lashes will lead to corneal opacities and scarring and then to
blindness. Linear scar present in the Sulcus subtarsalis is called Arlt's line(named after Carl Ferdinand
von Arlt). In addition, blood vessels and scar tissue can invade the upper cornea (pannus). Resolved
limbal follicles may leave small gaps in pannus (Herbert’s Pits).

Most commonly children with active trachoma will not present with any symptoms as the low grade
irritation and ocular discharge is just accepted as normal. However, further symptoms may include:

 Eye discharge
 Swollen eyelids
 Trichiasis (turned-in eyelashes)
 Swelling of lymph nodes in front of the ears
 Corneal scarring
 Further ear, nose and throat complications.

The major complication or the most important one is corneal ulcer occurring due to rubbing by
concentrations, or trichiasis with superimposed bacterial infection.

Grading of trachoma

1. McCallan's classification-McCallan in 1908 divided the clinical course of trachoma into 4 stages

Stage 1 (Incipient Stage 2 (Established Stage 3 (Cicatrising Stage 4 (Healed

trachoma) trachoma) trachoma) trachoma)
Hyperaemia of Appearance of mature Scarring of palpebral Disease is cured or is not
palpebral conjunctiva follicle & papillae conjunctiva markable
Progressive corneal Scars are easily visible Sequelae to cicatrisation
Immature follicle
pannus as white bands cause symptoms

2. WHO classification-The World Health Organization recommends a simplified grading system for
trachoma. The Simplified WHO Grading System is summarized below:

• Trachomatous inflammation, follicular (TF) – Five or more follicles of >0.5 mm on the upper tarsal
conjunctiva

• Trachomatous inflammation, intense (TI) – Papillary hypertrophy and inflammatory thickening of the
upper tarsal conjunctiva obscuring more than half the deep tarsal vessels

• Trachomatous scarring (TS) - Presence of scarring in tarsal conjunctiva.

• Trachomatous trichiasis (TT) – At least one ingrown eyelash touching the globe, or evidence of
epilation (eyelash removal)

• Corneal opacity (CO) – Corneal opacity blurring part of the pupil margin
Prevention

Although trachoma was eliminated from much of the developed world in the last century, this disease
persists in many parts of the developing world particularly in communities without adequate access to
water and sanitation. In many of these communities, women are three times more likely than men to be
blinded by the disease, due to their roles as caretakers in the family.

Without intervention, trachoma keeps families shackled within a cycle of poverty, as the disease and its
long-term effects are passed from one generation to the next.

National governments in collaboration with numerous non-profit organizations implement trachoma

control programs using the WHO-recommended SAFE strategy, which includes:

 Surgery to correct advanced stages of the disease;

 Antibiotics to treat active infection, using Zithromax (azithromycin) donated by Pfizer Inc
through the International Trachoma Initiative;
 Facial cleanliness to reduce disease transmission;
 Environmental change to increase access to clean water and improved sanitation.

Surgery: For individuals with trichiasis, a bilamellar tarsal rotation procedure is warranted to direct the
lashes away from the globe. Early intervention is beneficial as the rate of recurrence is higher in more
advanced disease.

Antibiotic therapy: WHO Guidelines recommend that a region should receive community-based, mass
antibiotic treatment when the prevalence of active trachoma among one to nine year-old children is
greater than 10 percent. Subsequent annual treatment should be administered for three years, at which
time the prevalence should be reassessed. Annual treatment should continue until the prevalence drops
below five percent. At lower prevalences, antibiotic treatment should be family-based.

Antibiotic selection: (single oral dose of 20 mg/kg) or topical tetracycline (one percent eye ointment
twice a day for six weeks). Azithromycin is preferred because it is used as a single oral dose. Although it
is expensive, it is generally used as part of the international donation program organized by Pfizer
through the International Trachoma Initiative. Azithromycin can be used in children from the age of six
months and in pregnancy.

Facial cleanliness: Children with grossly visible nasal discharge, ocular discharge, or flies on their faces
are at least twice as likely to have active trachoma as children with clean faces. Intensive community-
based health education programs to promote face-washing can significantly reduce the prevalence of
active trachoma, especially intense trachoma (TI). . If somebody is already infected washing one’s face is
strongly encouraged, especially a child, in order to prevent re-infection. ((Prevention-Trachoma. 18 July
2008. 24 March 2009 Environmental improvement: Modifications in water use, fly control, latrine use,
health education and proximity to domesticated animals have all been proposed to reduce transmission
of C. trachomatis. These changes pose numerous challenges for implementation. It seems likely that
these environmental changes ultimately impact on the transmission of ocular infection by means of lack
of facial cleanliness. Particular attention is required for environmental factors that limit clean faces.
Prognosis

If not treated properly with oral antibiotics, the symptoms may escalate and cause blindness, which is
the result of ulceration and consequent scarring of the cornea. Surgery may also be necessary to fix
eyelid deformities.
UVEITIS

Def: Uveitis specifically refers to inflammation of the middle layer of the eye, termed the "uvea" but in
common usage may refer to any inflammatory process involving the interior of the eye.

Anatomical Classification

Uveitis may be classified anatomically into anterior, intermediate, posterior and panuveitic forms, based
on which part of the eye is primarily affected by the inflammation.

1. Anywhere from two-thirds to 90% of uveitis cases are anterior in location (anterior uveitis),
frequently termed iritis - or inflammation of the iris and anterior chamber. This condition can
occur as a single episode and subside with proper treatment or may take on a recurrent or
chronic nature.

Symptoms include

 red eye,
 injected conjunctiva,
 pain and
 decreased vision.

Signs include

 dilated ciliary vessels,

 presence of cells and flare in the anterior chamber, and
 keratic precipitates ("KP") on the posterior surface of the cornea.

2. Intermediate uveitis (pars planitis) consists of vitritis - inflammatory cells in the vitreous cavity,
sometimes with snowbanking, or deposition of inflammatory material on the pars plana.
3. Posterior uveitis is the inflammation of the retina and choroid.
4. Pan-uveitis is the inflammation of all the layers of the uvea.

Conditions associated with uveitis and uveitis syndromes

Myriad conditions can be associated with uveitis, including diseases with major extra-ocular
involvement, as well as syndromes confined to the eye. In anterior uveitis, no associated condition or
syndrome is found in approximately one-half of cases. However, anterior uveitis is often one of the
syndromes associated with HLA-B27. Presence this type of HLA allele has a relative risk of evolving this
disease by approximately 15%.
 1. Systemic disorders associated with uveitis

Systemic disorders that can be associated with uveitis include:

 Ankylosing spondylitis
 Chronic granulomatous disease
 Inflammatory bowel disease
 Juvenile rheumatoid arthritis
 Kawasaki's disease
 Multiple sclerosis
 Polyarteritis nodosa
 Sarcoidosis
 Systemic lupus erythematosus
 Whipple's disease
 Lyme disease
 A wide range of autoimmune and autoinflammatory disease

2. Infectious causes

Uveitis may be a (normal) immune response to fight an infection inside the eye. While representing the
minority of patients with uveitis, such possible infections include:

 Brucellosis
 Herpes simplex
 Herpes zoster
 Leptospirosis
 Lyme disease
 Presumed ocular histoplasmosis syndrome
 Syphilis
 Toxocariasis
 Toxoplasmosis
 Tuberculosis

3. Uveitis Syndromes

In many cases, uveitis is not associated with a systemic (i.e. extraocular) condition: the inflammation is
confined to the eye. In some of these cases, the presentation in the eye is characteristic of a described
syndrome, and include the following diagnoses:

 Acute posterior multifocal placoid pigment epitheliopathy (APMPPE)

 Birdshot retinochoroidopathy
  Fuchs Heterochromic Iridocyclitis
 Multifocal Choroiditis and Panuveitis Syndrome
 Multiple Evanescent White Dot Syndrome (MEWDS)
 Punctate Inner Choroidopathy (PIC)
 Serpiginous Choroiditis

4. Masquerade syndromes

Masquerade syndromes are ophthalmic disorders that clinically present as either an anterior or
posterior uveitis, but are not primarily inflammatory. The following are some of the most common:

 Anterior segment

 Intraocular foreign body

 Juvenile xanthogranuloma
 Leukemia
 Malignant melanoma
 Retinal detachment
 Retinoblastoma

 Posterior segment

 Lymphoma
 Malignant melanoma
 Multiple sclerosis
 Reticulum cell sarcoma
 Retinitis pigmentosa
 Retinoblastoma

Symptoms

 Redness of the eye

 Blurred vision
 Sensitivity to light (photophobia)
 Dark, floating spots along the visual field
 Eye pain
Treatment

The prognosis is generally good for those who receive prompt diagnosis and treatment, but serious
complication (including

 cataracts,
 glaucoma,
 band keratopathy,
 retinal edema and
 permanent vision loss)

may result if left untreated.

The type of uveitis, as well as its severity, duration, and responsiveness to treatment or any associated
illnesses, all factor in to the outlook.

Uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (prednisolone
acetate) or oral therapy with corticosteroids. But before giving corticosteroids, rule out corneal ulcers by
Florescence Dye test. In addition to corticosteroids, topical cycloplegics, such as atropine or
homatropine, may be used. In some cases an injection of PSTTA (posterior subtenon triamcinolone
acetate) can also be given to reduce the swelling of the eye.

Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive
cases of uveitis. Experimental treatment with Infliximab or other anti-TNFs' infusions may prove helpful.
VITAMIN A DEFICIENCY

“Vitamin A deficiency is one of the common causes of blindness in the world.”

Role of Vitamin A
 Precursor of photosensitive visual pigment
 Outer segment turnover
 Maintain conjunctival mucosa and corneal stroma

Clinical featuresMlH0 classification

 XN: night blindness
 x1
 X1A: conjunctiva xerosis
 X1B: bitot's spots
 X2: corneal xerosis
 x3
 X3A: corneal ulcerationkeratomalacia < 1/3 corneal surface
 X3B: corneal ulcerationkeratomalacia > 1/3 corneal surface
 XS: corneal scarring
 XF: xerophthalmic fundus

DIABETIC RETINOPATHY:

1. Background: microaneurysms (dots), microhaemorrhages (blots), and hard exudates

2. Pre-proliferative retinopathy: cotton-wool spots (infarcts); microhaemorrhages
3. Proliferative retinopathy: New vessels form
4. Maculopathy: visual acuity 

HYPERTENSIVE RETINOPATHY

I. Tortuous arteries with thick shiny walls (silver or copper wiring)

II. A-V nipping (narrowing were arteries cross veins)
III. Flame haemorrhages and cotton wool spots
IV. Papilloedema.