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Copy of power point presentation of

lecture taken for MBBS students of


Gandhi Medical College, Bhopal (M.P)
India

by Prof. Sanjay Shrivastava


Regional Institute of Ophthalmology
Gandhi Medical College, Bhopal (M.P.)
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Degenerative Conditions of
Conjunctiva

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Degenerative Conditions of
Conjunctiva
• Concretions
• Pinguecula
• Pterygium

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Concretions (Lithiasis)
• They are minute hard, yellow, projectile
lesions seen in palpabral conjunctiva.
• Concretions are due to collection of
epithelial cells and inspissated mucous in
depressions called Henle’s gland. They
never becomes calcareous, therefore the
term is misnomer. Because of their
hardness, cornea is scratched (corneal
abrasions).

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Concretions …contd.
• They produce foreign body sensation.
Commonly found in elderly patients who
have suffered from Trachoma.
• Treatment: Removal under topical
Anaesthesia with a sharp hypodermic
needle.

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Pinguecula
• It’s a triangular patch on the bulbar
conjunctiva in palpabral aperture in elderly
patients especially those exposed to
strong sunlight, dust ,wind , drying etc
• Its combined expression of changes due
to senility and exposure.
• The pinguecula is due to hyaline infiltration
and elastotic degeneration in sub-mucous
tissue.
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Pinguecula
• Yellow triangular raised lesion with apex away
from cornea are seen in palpabral aperture.
Nasal side is affected first then the temporal.
The patch looks like fat (pinguis = fat). The
lesion is stationary at a moderate size. The
pinguecula becomes more prominent in
congested / inflammed eye.
• No treatment is usually required. If removal is
desired for cosmetic purposes, it may be excised
or destroyed by cautry.
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Pterygium
• Pterygium (A wing) is a triangular
encroachment of bulbar conjunctiva on to
the cornea. It is a degenerative condition
of the sub-conjunctival tissue which
proliferates as vascularized granulation
tissue. The conjunctiva invade the cornea
destroying the superficial layers of the
stroma and bowman membrane , the
corneal tissue is covered by conjunctival
epithelium.
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Etiology
• Commonly seen in dry ,sunny, hot climate
with sandy soil, ultra-violet light also act as
etiological factor. Seen in susceptible
individuals , inheritance is dominant.

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Symptoms
• When small gives rise to no symptoms,
slight irritation , cosmetic disfigurement
and blurring of vision due to induced
astigmatism may be there. Encroachment
in pupillary area leads to restriction of
visual field, and diminution /loss of vision.
Large pterygia may cause diplopia due to
limitation of abduction.

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Signs
• A triangular encroachment of conjunctiva
upon the cornea with numerous small
deep opacities in front of the apex.
Vascularized conjunctiva is drawn on to
the cornea from the canthus. It is loosely
adherent to the deeper structure , the
sclera. The area of adherence is smaller
than its width, resulting in folds in upper
and lower border.
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Signs … contd
• It usually follows pinguecula first develop on
nasal side, in case of double pterygium temporal
side is affected later.
• Progressive pterygium is thick vascular growth
with punctate opacities in front of the apex.
• Atrophic pterygium is thin and pale growth with
few obliterated vessels. It is characterized by
formation of dense fibrous tissue and is
associated with considerable corneal
astigmatism.

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Complications
• Inflammation of pterygium
• Cystic degeneration of pterygium

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Differential Diagnosis
• This condition is to be differentiated from
Pseudo-pterygium, which is a
inflammatory adherence of conjunctiva to
cornea and may occur in any part of
limbus. Chemotic conjunctiva getting
adhered to a marginal corneal ulcer.
Sometimes a probe can be passed behind
pseudo-pterygium; whereas it can not be
passed in case of pterygium.
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Prophylaxis
• UV rays filters, protective glasses
• Artificial tears

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Treatment
• If small and does not cause cosmetic problem, it
be left.
• Subconjunctival resection of pterygium leaving a
bare sclera adjacent to limbus (D’ombrain
technique).
• Sub-conjunctival transplantation of ptrygium.
• Recurrence can be avoided by covering bare
sclera with auto conjunctival graft. Following
subconjunctival resection of pterygium post-
operative therapy with mitomycin-C or thiopepa
(1:2000 solution) given 6 hrly for 6 weeks

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Treatment … contd.
• Recurrent pterygium requires similar
surgery but with a lamellar graft over
affected cornea.

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Dry Eye and Ocular Surface
Disorders

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Xerosis (Xerophthalmia)
• It is defined as a degenerative condition
characterized by changes of the
conjunctiva due to changes in the tissues
themselves (not due to diminution of
lacrimal secretion). If the secretory activity
of mucous membrane is hampered /
decreased by pathological processes
xerosis develops in-spite of normal or
intensified lacrimal secretions.
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Xerosis
It may develop in two forms:
1. As sequel of local ocular diseases:
a. Cicatricial degeneration: as seen in
trachoma, pemphigoid, membranous
conjunctivitis, extensive burns, radiational
injuries. These conditions destroy the mucous
glands of conjunctiva. Conjunctival epithelium
becomes dry, thick, opaque and keratinized.
Tears fail to wet the ocular surface including
cornea. Gradually vision is lost because of
corneal opacities. There are symptoms of
irritation.
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b. Result of exposure (Ectropion and
Proptosis)
2. As a symptom of general nutritional
disturbances: particularly lack of Vitamin
A. Xerosis is usually mild in cases of
deficiency of Vitamin A, found particularly
in children and accompanied by night
blindness.

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Bitot spots – they are small triangular white
patches appears like dried foam, un-wetted by
tears, on the outer/ lateral side of cornea. The
foamy spots are due to gas producing
Corynebacterium Xerosis present on horny
epithelium. These cases occur during summer
months associated with diarrhoea and/or
measles. A similar condition is also associated
with night blindness found in malnourished
children (Marasmic children, associated with
Keratomalacia).
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Treatment
1. Treatment of cause
2. Local symptomatic treatment with
artificial tears and mucomimetic agents
3. Dark glasses
4. Vitamin A deficiency is treated by
adequate doses of Vitamin A and
nutritional supplementation.

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Vitamin A Therapy
• Therapeutic dose: 2 lakh IU orally on two
successive days.
• Prophylactic dose:
– Children <12 months of age- 1 lakh IU once
every 4-6 months
– Children above 12 months of age- 2 lakh IU
every 4-6 months
– Newborn – 50,000 IU at birth

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Vitamin A Therapy
- Women of childbearing age 3 lakh IU
within one month of giving birth
- Pregnant and Lactating women –
5,000 IU everyday or 20,000 IU once a
week

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Keratoconjunctivitis Sicca (KCS)
• Keratoconjunctivitis Sicca (Sjogren’s Syndrome):
it is a condition caused by deficiency of aqueous
component of tear i.e. lacrimal secretion.
• Etiology : it is a autoimmune disorder occurring
in women after menopause and often associated
with Rheumatoid arthritis. Characterized by
dryness of eyes, pathologically lacrimal gland is
fibrotic and infiltrated with lymphocytes. Similar
changes in salivary gland may lead to dry
mouth.
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Keratoconjunctivitis Sicca (KCS)
• Symptoms: Chronic irritation, foreign body
sensation , photophobia, diminution of
vision due to filaments on corneal surface
and mucus strands on corneal surface.
• Signs: Dryness of ocular surface , reduced
Schirmer test reading. Damage to
conjunctival and corneal epithelium
(demonstrated by Rose Bengal staining)

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Treatment
• Artificial tears
• Mucomimetic agents (acetylcystine 5%,
Polyvinylpyrolodone 0.03%)
• Surgical treatment- transplantation of
Stensen’s duct into the conjunctival sac in
the upper fornix has been tried with limited
success.

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Dry Eye
• Disorder of the tear film due to tear
deficiency or excessive evaporation, which
causes damage to the interpalpabral
ocular surface and is associated with
symptoms of discomfort. In this condition
an unstable tear film inadequately support
the health of the ocular surface epithelium,
promotes ocular surface inflammation that
causes pain in eyes.
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• In dry eye tear film becomes chronically
unstable and repeatedly breaks up into dry
spots between blinks, exposing the
conjunctival and corneal epithelium to
evaporation.

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Etiology
1. Deficiency of tears (Sjogren’s syndrome)
2. Deficiency of conjunctival mucous as occurs in
Steven-Johnson Syndrome, Ocular
Pemphigoid, avitaminosis , old trachoma, and
drug induced.
3. Altered ocular surface due to previous
diseases, resulting in poor vetting.
4. Lid deformities, by causing excessive drying /
evaporation or by causing decreased blink rate

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Symptoms
• Irritation, discomfort, itching and diminution of
vision.
Diagnosis:
• History
• For patients with moderate to severe aqueous
tear deficiency, the diagnosis can be made by
using one or more of the following tests: tear
break-up time test, ocular surface dye staining
pattern (rose bengal, fluorescein, or lissamine
green), and the Schirmer test.

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Cycle of Inflammation

Irritation Inflammation

Tear deficiency/ instability

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Diagnosis

• These tests should be performed in this


sequence because the Schirmer test can disrupt
tear film stability. Corneal sensation should be
assessed when trigeminal nerve dysfunction is
suspected. A laboratory and clinical evaluation
for autoimmune disorders should be considered
for patients with significant dry eyes, other signs
and symptoms of an autoimmune disorder (e.g.,
dry mouth), or a family history of an autoimmune
disorder.

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Goals of management
– Establish the diagnosis of dry eye,
differentiating it from other causes of irritation
and redness
– Identify the cause(s) of dry eye
– Establish appropriate therapy
– Relieve discomfort
– Prevent complications, such as loss of visual
function, infection, and structural damage
– Educate and involve the patient in the
management of this disease
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Treatment – Principles
1. Hydrating and lubricating the ocular
surface
2. Suppressing the inflammatory response
of the ocular surface

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Therapy Involves
1. Eliminating exacerbating factors
2. Support of functional unit ( Androgen
hormones)
3. Hydrating, stabilizing and lubricating therapy
Cellulose Esters (Hypermellose,
Hydroxyethylcellulose, Methylcellulose,
Carboxymethylcellulose), Polyvinyl alcohol,
Polyvinyl Pyprolidone, Polyacrylac acid,
Hyaluronic acid, Chondrotin Sulfate

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Treatment
4. Secretogogues
5. Punctal Occlusion
6. Anti-Inflammatory Therapy
7. Use of contact Lens

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Summary
1. Multipronged approach
2. Systemic and environmental stresses should
be minimized
3. Artificial Tears
4. Systemic cholinergic agonists
5. Punctal occlusion
6. Cyclosporin A
7. Topical steroids
8. Environmental correction / counseling

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