Conj Degeneration

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.)

29th October 2006

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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). 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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 postoperative therapy with mitomycin-C or thiopepa (1:2000 solution) given 6 hrly for 6 weeks 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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). 29th October 2006

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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. 29th October 2006

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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 29th October 2006

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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. 29th October 2006

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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) 29th October 2006

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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. 29th October 2006

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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 29th October 2006

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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. 29th October 2006

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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. 29th October 2006

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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 29th October 2006

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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 29th October 2006

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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 29th October 2006

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