Download ppt - Conjunctiva 6

Pinguecula• Common, innocuous, bilateral, asymptomatic condition• Usually seen in elderly people, especially those exposed to

strong sunlight, dust & wind.• Though yellow in color and looks like fat (hence the name,

penguis meaning fat), it is due to hyaline infiltration and elastotic degeneration of the submucous connective tissue.

• Signs : • Yellowish triangular patch of bulbar conjunctiva, near the

limbus in the palpebral aperture, the apex of the traingle being away from the cornea.

• Usually nasal side affected first, then temporal• Treatment : usually unnecessary because growth is very slow

or absent. If acutely inflammed (pingueculitis) – short course of weak steroids (flourometholone)

Pinguecula

Pterygium • A pterygium is a triangular, wing shaped, fibrovascular

subepithelial ingrowth of degenerative bulbar conjunctival tissue over the limbus onto the cornea (pterygos - “wing”)

• It is a degenerative condition of subconjunctival tissues which proliferate as a vascularized granulation tissue to invade the cornea, destroying the superficial layers of the stroma and Bowman’s membrane, the whole being covered by conjunctival epithelium

• It is loosely adherent in its whole length to the underlying sclera, the area of adherence being always smaller than its breadth, so that there are folds at the upper and lower borders .

Pterygium Etiology : • 1. Usually develop in patients who live in hot dry climates,

high winds and abundance of dust. • 2. Exposure to ultraviolet light (UV type B)in solar radiation is

most significant environmental factor.

- Involuntary partial closure of the interpalpebral fissure, mostly confined to the temporal side, to avoid glare from bright sunlight, may explain the predominance of pterygia on the nasal side.

• 3. Genetic predisposition• 4. Pinguecula as a precursor of pterygium

Pterygium Histopathologically : - it is a fibrovascular proliferation of conj tissue onto cornea - it is hyperplasia, not dysplasia - stains with elastic tissue stains, but unlike elastic tissue, it is not

digested by elastase, hence termed elastotic degeneration. - body of pterygium incorporates the underlying Tenon’s capsule, but not

the episclera, hence it can be easily mobilized over the sclera - at the limbus – no Tenon’s – hence adherent to episclera - Head of the pterygium grows in a plane between Bowman’s layer and

the basement membrane of corneal epithelium – Bowman’s membrane initially pushed posteriorly – later gets destroyed and pterygium tissue grows into stroma – pterygium becomes firmly adherent.

- primary pterygium are histopathologically different from recurrent pterygium : Recurrent pterygium is composed of only fibrovascular tissue, no elastotic degeneration, involves underlying episclera, sclera, rectus muscle sheath and corneal stroma and is firmly adherent to underlying structures throughout its extent, is highly vascularized.

Pterygium Clinical Features :• A small, grey, corneal opacity develops, near the nasal limbus.• The conjunctiva overgrows the opacity and progressively encroaches

onto the cornea in a triangular fashion.• Anatomically divided into : head, neck and tail.

Head – part on the cornea

Neck – at the limbus

Tail – part on the sclera• A deposit of iron (Stocker line) may be seen in the corneal epithelium

anterior to the advancing head of the pterygium in slow growing pterygiums, due to pooling of tears at the leading edge of pterygium

• A probe can be slipped under the upper and lower folded borders of the body of the pterygium for a short extent and not across the entire breadth.

Pterygium Classification of pterygium :1. Progressive Pterygium : actively growing, fleshy, vascular and

inflamed – looking pterygium with no Stocker’s line2. Stationary Pterygium : pterygium still looks vascular, but the

head of the pterygium looks pale and sparsely vascularized and stops growing, develops a Stocker’s line

3. Regressive pterygium : pale, thin, papery, gray, anemic and membranous pterygium appears to be regressing, has a gray apex resembling corneal opacity

Nasal TemporalDouble pterygia (both nasal and temporal)Bilateral pterygia (both eyes)

Primary / Recurrent pterygium (regowth after excision)

Pterygium • Treatment : surgical treatment is the only effective treatment

for pterygium. However, none of the surgical procedures is perfect and universally accepted because of high recurrence rates.

• Indications for surgery:

- primary indication is decreased visual acuity because of encroachment of the pterygium into visual axis or the irregular astigmatism induced by the growth.

- restricted ocular motility

- binocular diplopia

- ocular irritation and discomfort unresponsive to lubrication

- where pterygium restricts wearing of contact lenses

- difficulty in performing corneal refractive surgery

- cosmetic reasons

Pterygium

Pterygium• Current surgical procedures for pterygium treatment

1. Bare Sclera excision

2. Adjunctive use of Beta irradiation

3. Adjunctive use of Thiotepa

4. Adjunctive use of Mitomycin – C

5. Conjunctival transplantation / autograft

6. Limbal stem cell transplantation

7. Amniotic membrane allograft transplantation

Pterygium

• Bare sclera excision :

- surgical dissection of the pterygium starting from the head of the pterygium with lamellar keratectomy and extending to remove the body of the pterygium. The head, neck and body of pterygium are removed in one piece, leaving behind bare scleral area slightly more than the body of the removed pterygium. Hemostasis achieved using thermal cautery

- high rate of recurrence (23 – 75%)

Pterygium

• Beta irradiation :

- Standard Sr-90 applicator (dose : 1500 – 2500 reps) with shield

- expend most of their energy within superficial 2 mm of tissue

- irradiation induces obliterative endarteritis and arrest of fibroblast proliferation due to ionization changes in nucleus and cytoplasm of cells

- applied immediately after surgical excision of pterygium

- reduces recurrence rates to 0.5 – 16%

- limitations : requires trained radiologists / radiotherapists

- complications : cataract formation (dose related), dry eyes, corneal/ scleral thinning and ulceration

-

Pterygium

• Thiotepa :

- rarely used now

- nitrogen mustard family

- inhibits capillary endothelial proliferation, thereby inhibiting pterygium recurrence

- applied as topical drops

- poliosis, periorbital skin depigmentation, chronic conjunctivitis, scleral ulceration

Pterygium

• Mitomycin C

- antimetabolite agent

- selectively inhibits DNA replication, non-cell specific, action during late G1 and S phases of cell division

- intraoperative use of 0.02 – 0.05% (0.2 – 0.5 mg/dl) Mitomycin C for 30 sec – 3 min to bare sclera after pterygium excision

- reduces recurrence rate to 4 – 23 %

- postoperative use of mitomycin C topical drops (0.02%)

- complications : scleral thinning and perforation, corneal perforation, iritis, secondary glaucoma, cataract

Pterygium

• Conjunctival transplantation (conj autograft):

- conjunctival tissue taken from another site of same eye or other eye and grafted to pterygium excision site and sutured using vicryl/ nylon

- reduces recurrence rate to 5 – 7 %

- can be combined with intraoperative Mitomycin C application

Pterygium

• Limbal stem cell transplantation (autologous):

- healthy limbal epithelium acts as a junctional barrier to conjunctival cells migrating onto corneal surface.

- 0.5 mm of limbal/ peripheral corneal tissue is taken along with conjunctival autograft (Limbal conjunctival graft)

- graft placed with correct orientation on scleral recipient bed (corneal side towards cornea) and sutured using vicryl/nylon.

- recurrence rate 0 – 15%

- limitations : technically demanding, time consuming.

Pterygium

• Amniotic membrane transplantation :

- amnion innermost layer of the placenta

- amniotic membrane separated from chorion, washed with antibiotics, and cut into small pieces and stored in Eagle’ medium at – 80o C

- stroma of amniotic membrane suppresses proliferation and differentiation of fibroblasts

- recurrence rate of 10-16%

Pterygium

Pseudopterygium

• Clinical features: – Adhesion of the conjunctiva to the peripheral cornea due to

inflammatory causes, always stationary.– May occur on any quadrant of the cornea, at any age– Lacks firm adhesion throughout the underlying structures, and

occasionally has a broad leading edge on the corneal surface, a probe can be passed under the neck

– These findings differentiate it from true pterygium.

• Pseudopterygium may result from a peripheral corneal ulcer and ocular surface inflammation such as cicatrizing conjunctivitis, chemical burns, or may also occur secondary to chronic mechanical irritation from contact lens movement associated with inadequate lubrication of the corneal surface.

Dermoid, dermolipoma

• Choristoma : congenital overgrowth of normal tissue in an abnormal location

• They are not true neoplasms• Two main types : dermoid , dermolipoma

Dermoid, dermolipoma• Dermoid :- May occur in isolation or often in patients with Goldenhar

syndrome, Treacher Collins syndromes- Contain a variety of tissues such as cartilage, fat, muscle, hair

follicles, sebaceous glands- Present in early childhood- Signs: smooth, soft, yellowish, subconjunctival masses most

frequently located at inferotemporal limbus- Occasionally the lesion may encircle the limbus- Treatment : for cosmetic deformity, extends to visual axis,

astigmatism – small lesions excised with or without lamellar corneal / scleral grafting

Dermoid

Dermoid, dermolipoma

• Dermolipoma:

- fibrofatty tumours are congenital tumors consisting of fibrous tissue and fat, are not encapsulated

- more common in children

- signs : soft, movable, subconjunctival mass most commonly located at outer canthus

- treatment : should be avoided as surgery may be complicated by scarring, ptosis, dry eye and ocular motility problems. However, if they are particularly unsightly, then debulking the anterior portion.

Dermolipoma

Epithelioma (conj squamous cell carcinoma)• Rare, slow growing tumour of low-grade malignancy• May arise de novo or from preexisting carcinoma-in-situ• Seen with increased frequency in patients with xeroderma

pigmentosum and AIDS• C/F: presents in late adult life with ocular irritation or mass• Signs : a fleshy pink, papillomatous or gelatinous mass, often

associated with feeder vessels• Tumour most frequently juxtalimbal, seldom arising from fornices• May involve adjacent cornea, but deep scleral invasion is uncommon• Treatment : - surgical excision with adjunctive chemotherapy

- topical chemotherapy with mitomycin C or 5-FU for recurrences

- Enucleation if intraocular invasion

- Exenteration if orbital invasion

Epithelioma (conj squamous cell carcinoma)

Vitamin A Deficiency (xerophthalmia)• Vitamin A : fat soluble, ingested in the form of retinol• Found in foods such as milk, eggs, fish, meat and liver• also obtained as its precursor Carotene - found in yellow fruits,

green leafy vegetables, red palm oils• In small intestine – metabolized to retinol and absorbed• Retinol esterified to palmitic acid (retinyl palmitate) that travels

to liver through lymphatics• When required – retinyl palmitate in liver converted to retinol

and released with retinol-binding protein• Vit A required for conj cell RNA and glycoprotein synthesis,

necessary for maintaining the integrity of conj epithelium and corneal stroma, Retina - rhodopsin synthesis in rods.

• Cause for deficiency : measles or other RTI, severe diarhhoea

Vitamin A Deficiency (xerophthalmia)

• Xerophthalmia : abnormalities involving the ocular surface secondary to Vitamin A deficiency are referred to as xerophthalmia

• WHO classification of xerophthalmia :

X1A : Conjunctival xerosis

X1B : Bitot’s spots with conj xerosis

X2 : Corneal xerosis

X3A : Corneal ulceration with xerosis

X3B : Keratomalacia

XN : Night Blindness

XS : Corneal scars

Biochemical criterion : plasma vitamin A 0.35 µmol/L or less



• X1A : conjunctival xerosis :

- dryness, loss of transparency, thickening, wrinkling, pigmentation

- dry patches stand out “like sandbanks at receding tide”, stain with rose bengal

- bulbar conj esp the temporal interpalpebral area involved.

- histologically, conj epithelium changes from normal columnar to stratified squamous appearance.

- loss of goblet cells

- keratinized epithelium


• X1B : Bitot’s spot with Conj xerosis :

- A Bitot’s spot is a small, triangular, white plaque with a foamy surface that appears on the bulbar conj in the temporal or nasal quadrants, frequently bilateral

- Histologically, Bitot’s spot is a mixture of keratin, bacteria (often Corynebacterium xerosis), inflammatory subepithelial infiltrate and mucus


• X2 : Corneal xerosis :

- lustreless, dull appearance of cornea, with keratinization and stromal edema.

- Vitamin A supplements can reverse corneal xerosis without permanent damage to the corneal or conjunctival surface


• X3A : Corneal Ulceration with Xerosis

- corneal ulcers less than one third of the corneal surface

- due to colliquative necrosis

- characteristically circular, steep margins, sharply demarcated.

- superficial ulcers heal with small scars, deeper ulcers may perforate

- vitamin A therapy cannot reverse stromal ulceration


• X3B : Keratomalacia :

- Corneal ulceration involving more than one third of the cornea is classified as X3B.

- usually associated with stromal necrosis and dissolution of cornea

- with minimal inflammatory reaction, the cornea can very easily melt away in part or entirely.

- associated with prolapse of intraocular contents, with loss of vision

- usually seen in young children (6 mths to 3 yrs) with chronic severe malnutrition

- untreated : mortality rate 50 – 90% due to diarhhoea, dehydration


• XN: Night Blindness :

- retinol is necessary for the production of rhodopsin by rod photoreceptors

- early sign of vitamin A deficiency

- rapidly responds to systemic vitamin A supplementation

- used as a sensitive and specific screening tool for vitamin A deficiency


• XF : Xerophthalmic fundus :

- characteristic appearance of the fundus associated with chronic night blindness

- whitish – yellow changes in pigment epithelium of retina

- both eyes affected

- respond to vitamin A therapy

- not used as a survey parameter or for severity of deficiency


• XS : Corneal scars :

- scars left after healed ulcers


• Treatment :

1.Local ocular therapy :

- artificial tears for conj xerosis

- for corneal ulcers : full fledged treatment as for bacterial corneal ulcer

2. Vitamin A therapy :

- treatment applies to all stages of active xerophthalmia

- oral administration recommended

- intramuscular injections of water-miscible prearation if severe vomiting or diarhhoea

3. Treatment of underlying conditions : PEM, diarrhoea, infections


• Diagnosis of xerophthalmia is considered a medical emergency and therapy instituted

• Treatment* :

AGE PREPARATION DOSE

< 6 months Retinyl palmitate orally 50,000 IU

6 – 12 months Retinyl palmitate orally 1,00,000 IU

(or weight < 8 kg)

>12 months or Retinyl palmitate orally 2,00,000 IU

(or weight > 8 kg) except women of child bearing age

Women of child bearing age, pregnant or not : daily dose of 10,000 IU orally for 2 weeks

* A total of 3 doses are administered on days 0,1 and after 4 weeks.


• Prophylactic therapy: in areas with endemic vitamin A deficiency

1. Short-term therapy :- 2,00,000 IU vitamin A orally every 6 months to children 1-

6 years of age or > 8 kg of weight- Infants 6 -12 months : 1,00,000 IU every 3-6 months- Lactating mothers (vitamin A can be teratogenic in high

doses en early pregnancy) – 20,000 IU given at delivery or within 2 months of giving birth

- Infants <6 months, not on breastfeeding : 50,000 IU vitamin A orally as a single dose


• Revised schedule of vitamin A supplements : being followed in India , under “child survival and safe motherhood” programme

• First dose (1 lakh IU) – at 9 mths along with measles vaccine• Second dose (2 lakh IU) – at 18 mths along with booster dose

of DPT/OPV• Third dose (2 lakh IU) – at 2 years of age


2. Medium term approach:

- vitamin A fortification of foods : cereals, fats and oils

3. Long term approach : Action at primary levels :

- health education

- dietary advice

- regular administration of prophylactic vitamin A in endemic areas

- Provitamin A rich foods such as carrot, mango, papaya, dark green leafy vegetables

- foods rich in preformed vitamin A : egg, fish, milk