Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

perfusion.69 Management consists of intensive local steroids and use of cycloplegic. It is presumed that if only two muscles are disinserted at a time, the condition can be avoided.

Endophthalmitis

Endophthalmitis is one of the most dreaded catastrophes in ophthalmology. It is defined as inflammation of intraocular tissues due to infection by bacteria, fungi and parasite (toxocara). Immune reaction, physical or chemical reaction, vasculitis or neoplasm can also cause it. The lens is not capable of inflammation hence it is spared.70 It is generally acute that can become chronic or may have chronic onset.

Clinical presentation depends upon—1. Virulence of the causative organism, 2. Chemical composition of the offending causative factor, 3. Treatment received. It is generally unilateral but can be bilateral in endogenous type. No age, sex or race is immune, however, endogenous endophthalmitis is more common in children in developing countries due to prevailing malnutrition, xerophthalmia and systemic pyogenic disease and unattended or poorly managed trauma. Clinically there are two main types of endophathalmitis,

1.Endogeneous (metastatic) end opthalmitis—This is caused by micro organism. Bacteria or fungi reach the eye from a primary site due to hematogenous spread. Viruses are not known to cause endophthalmitis.

2.Exogenous endophthalmitis is caused due to direct entry of bacteria or fungi inside the eye following trauma or spread from neighbouring structure i.e perforated corneal ulcer. The trauma can be (1) accidental with or without retained foreign body,

(2) Surgical.

Surgical

Commonest surgery that results in endophthalmitis is lens extraction of any type with or without IOL. Other surgeries include all intraocular surgeries i.e. paracentesis, iridectomy, trabeculectomy, iris inclusion procedures, mechanical capsulotomy, penetrating keratoplasty, vitrectomy. Rarely extra ocular surgeries may produce endophthalmitis, this happens following inadvertent perforation of globe during squint and retinal surgery, periocular or peribulbar injection. The basic pathology is lodgement of the offfending organism and multiplication of it, in case of micro organism or setting an immune reaction or release of chemicals. It may start in the uvea and spread to the vitreous involving the retina in between or it may start in the vitreous and spread to the uvea and retina. While the first route is generally seen in endogenous endophthalmitis. The second path is commonly seen in exogenous endophthalmitis. In all the cases, the vitreous is severely inflamed as it acts as a good growing medium for microbia to proliferate resulting in formation of a pocket of pus in the vitreous commonly referred to as vitreous abscess. According to the site of its commencement it can be anterior vitreous abscess seen following intraocular surgeries of anterior segment or posterior abscess as in endogenous endophamitis, vitrectomy, fluid gas exchange, retained intraocular foreign body. Ultimately whole of the vitreous is involved in abscess formation. The inflammatory process from choroid spreads to ciliary body and iris resulting in purulent pan uveitis.

Endogenous endophthalmitis in children

Endogenous endophthalmitis in children is due to spread of micro organism from primary site that can be abdomen, lung, para nasal sinus, infected teeth, middle ear, bones and joints,

heart, skin, lacrimal sac etc. Causative organisms can either be bacteria or fungus or parasite. Presenting features of bacterial endophthalmitis differ from fungal in many ways. Endogenous endophthalmitis generally has an indolent course that may be initially masked by more serious systemic condition. frequently it can be bilateral. As the infection is hematogenous it starts in posterior uvea. The anterior uveal inflammation lags behind in contrast to exogenous endophthalmitis where anterior segment inflammation is more pronounced than posterior. Endogenous endophthalmitis is more common in children who are malnourished, chronically ill, have under gone extensive abdominal surgery, have been on systemic antibiotic or steroids for long time, under radiation therapy or have immuno compromised status. Fungi are considered to be more common causative organism than bacteria. However, in developing countries bacterial metastatic endophthalmitis is equally common if not more than fungal endophthalmitis. Parasitic endophthalmitis is far more common than expected, about 16% of all white reflexes in pupillary area are caused by toxocara.71

Many fungi have been isolated as causative factor but common are Candida and Aspergillus. Candida is more frequent than aspergillus. Candidal infection starts in the choroids as multifocal round lesions that spread to cause perivasculitis, retinal haemorrhage, may lead retinal necrosis. The symtoms are more indolent as compared to Aspergillus which is more severe, painful and associated with hypopyon.

Endogenous endophthalmitis is more effectively treated by parental antibiotic. As the lesion starts and remains under the internal limiting membrane. For the same reason vitrectomy is less effective in endogenous endophthalmitis. Systemic steroids help in controlling inflammation in bacterial endophthalmitis but are contra indicated in fungal endophthalmitis. Local antibiotic drops are prescribed to combat secondary corneal and conjunctival infection while combination of local cycloplegic and steroids are given for anterior uveitis.

Exogenous endophthalmitis

Exogenous endophthalmitis is three times more common than endogenous endophthalmitis. In adult common type of exogenous endophthalmitis is post surgical, which is less common in children whose accidental wounds with or without retained foreign bodies cause more inflammatory reaction. Retained organic foreign bodies more inflammatory than inorganic. Some of the organic foreign bodies are inert and do not cause any inflammatory reaction but foreign bodies containing copper and iron cause various degrees of chemical changes. Pure copper produces more severe endophthalmitis than copper alloys. Pure copper causes severest form of endophthalmitis. However, sometimes inert foreign bodies can also cause sterile endophthalmitis. Thus exogenous endophthalmitis can be 1. Bacterial 2. Fungal 3. Sterile. All of them can follow surgery or be accidental.

Bacterial exogenous endophthalmitis is commonest form of endophthalmitis.72 Post surgical endophthalmitis is more common than accidental. Exact percentage of post operative endophthalmitis is just a guess. It has been reported to be in the range of 0.05% to 0.2%. It is more common following secondary I0L than primary I0L. In penetrating keratoplasty it is perhaps the micro organism in donor cornea that is responsible for the infection. Break down of asepsis and antisepsis protocol is the commonest cause of post surgical endophthalmitis.

Organism get access into intraocular structure via—1. Contaminated instrument, irritating fluid, visco-elastic, 2. Saprophytes from the lid and conjunctiva that become opportunistic, 3. Undiagnosed nasolacrimal duct obstruction.

There are three forms of endophthalmitis according to the onset of the disease

1.Acute within first forty eight hours following surgery, always bacterial, caused by gram negative bacteria and gram positive cocci i.e. streptococci and staphylococcus aureus.

2.Delayed between seven to tens days mostly caused by staphylococcus epidermis and coagulase negative cocci.

3.Late—after four to six weeks, commonest organisms being various fungi, P. acne and staphylococcus epidermis.

4.Remote infected bleb, prolapsed uvea.

All types of bacteria both gram positive or negative are capable of causing post operative exogenous endophthalmitis. However, gram positive strains are responsible for 90 to 95% of endophthalmitis.71 Gram negative organism are more virulent, spreads fast and produce endotoxin. In children streptococci are more common causative organism than staphylococci which is a major cause of endophthalmitis in adults. Propioni bacterium acne, which is an anaerobic gram positive commensal is becoming more frequent cause of chronic post surgical endophthalmitis.

Symptoms and signs of acute post surgical endophthalmitis are—Pain more than usually expected pains of surgery, lacrimation, photophobia, drop of vision below anticipated level. On examination, the lids are swollen, the conjunctival congestion is prominent, their may be chemosis of conjunctiva, hazy cornea. Intense flare and cells may have fibrinous aqueous or frank hypopyon, edema of iris. Non reacting, small pupil if cycloplegics have not been used. Exudative membrane over the I0L or vitreous face, retrolenticular flare and cells in phakic eye. The fundal glow is either very faint or absent on retinoscopy and direct ophthalmoscopy. An indirect ophthamoscope may circumviate the exudates in the vitreous and allow visualization of the fundus behind. It also gives extent and depth of the vitreous abscess that can be used to assess progress of the disease. The movements of the eyeball are normal and there is not proptosis. Loss of ocular movement and onset of proptosis denotes panophthalmitis. At this stage ultra sonography may clinch the diagnosis.

Delayed post operative endophthalmitis undergoes same pathological process as acute but in a milder form. The symptoms consist of chronic reduced vision. On examination all signs of persistent uveitis are present that are initially responsive to steroids. Thus masking the exact pathology resulting into delay in treatment. On slit lamp examination there are large KPs with 2+ to 3+ flare and cells, aqueous may have fibrous strands. Lower angle of AC should be carefully scrutinized for small hypopyon that changes its level and position with the eyeball. There is generally exudates in the pupillary area. There may be exudates behind the posterior capsule. Generally there is formation of vitreous abscess. Marked reduction of vision and loss of fundal glow are two ominous signs. Fundus when visible may show retinal hemorrhages and exudates.

Late onset post surgical endophthalmitis

This is generally due to otherwise non virulent commonsels. The eye remains congested with mild to moderate pain and vision that was good is lost in days. On examination, there are signs of recurring pan uveitis with loss of fundal glow or a white reflex in pupillary

area. Intraocular tesion is variable. Rise of tension results in unexplained pain that makes the child restless. Ultrasonography at this stage helps to clinch the diagnosis and differentiate from other condition that may mimic endophthalmitis.

Post operative fungal infection is more often missed than diagnosed, as it has relatively less symptoms than bacterial endophthalmitis, most of these eyes have generally received usual high doses of steroids. The exact features may be masked, even the eye may be relatively white. The child invariably does not complain of lowering of vision. It takes several weeks to months for fungal endophthalmitis to develop. Generally there is a fixed thick hypopyon and rise of intraocular pressure. Vitreous may show snowball and fluffy opacities that may mistaken as cortical matter.

Sterile post operative endophthalmitis24,71 is mostly iatrogenic in nature, less frequent than infective endophthalmitis. The condition has to be kept in mind to be correctly diagnosed. The inflammation is caused due to chemical insult of irrigating agents, residue from chemicals sterilizers, lens matter, monomers on the I0L. Too much manipulation of anterior uvea, vitreous disturbance. Inadvertent intraocular injection of xylocain during peribulbar injection and antibodies / steroid during periocular injection talc from the surgical gloves, cotton swabs, suture material are some of the frequent causes of sterile post operative endophthalmitis. Sterile endophthalmitis have an acute or delayed onset and respond fairly well to medical treatment, non responding cases may require vitrectomy.

Post traumatic endophthalmitis

About 5% of eyes sustaining accidental penetrating injury develop endophthalmitis. Onset may be as short as 1-2 days or as long as 2 to 3 months depending upon the virulence of the organism, size of the inoculum, immune status of the eye and treatment received. Accidental trauma has been found to be responsible for about one third of all cases of exogenous endophthalmitis. Increased frequency of endophthalmitis following accidental injury is high because they are caused by infected objects that are mostly vegetable in nature and carry virulent organism with them along with dirt, dust contaminated fluid etc. Common causes of perforating injuries in children are - Bow and arrow, tip cat (gilli), sling shot (gulel), twigs and leaves, protruding nails from walls, latches of the door. In fact any relatively sharp object cause penetrating injury. They are more common in rural set up and in boys. Most of the time they are uniocular. The overall profile of the organism isolated from post traumatic endophthalmitis are similar to post surgical endophthalmitis.71

Fulminating endophthalmitis develops in short period when infected by B Cereus the organism that has never been isolated in post surgical endophthalmitis. Late onset of endophthalmitis is generally seen in fungal infection.

Diagnosis of post traumatic traumatic endophthalmitis is not difficult. The presentation is similar to post surgical endophthalmitis. The difference being disorganization of the globe due to involvement of multiple ocular structures. The eyes are generally soft, they may have retained intraocular foreign body. X-ray orbit is required to exclude presence of radio opaque foreign body. Ophthalmic ultrasonography gives information like position of lens, vitreous haemorrhage, retinal detachment, presence of foreign body.

Management consists of prompt repair of wounds as per standard method. Construction of anterior segment. Prophylactic use of broad spectrum antibodies is debatable. Once the endophthalmitis develops, it should be treated as any endophthalmitis.

Differential diagnosis of post surgical and post traumatic endophthalmitis consists of endophthalmitis phaco anaphylactica, dislocated lens nucleus, large fragments of cortical material, unresolved haemorrhage, ciliochoroidal detachment, retinal detachment.

Management of endophthalmitis

I. Endogenous -

1.Supportive treatment by cycloplegic and steroid locally.

2.Systemic antibiotic

3.Systemic steroid under umbrella of systemic antibiotic

4.Systemic antifungal

5.Vitrectomy

II. Exogenous endophthalmitis (post surgical) is an ocular emergency that requires urgent and intense treatment by way of sub conjunctival and intra vitreal injection of antibiotic alone or with steroid as per standard dose. Role of vitrectomy is not yet clear.

Panophthalmitis

This is acute purulent infection of all the structures of the eye including Tenon’s capsule, extraocular muscles and orbital tissues. Panopthalmitis is generally bacterial in nature, all pus forming bacteria can cause pan opthalmitis. The organism reach the exterior of the globe following exogenous endophthalmititis which generally follow intraocular surgery or accidental penetrating wound. It may take few days for panophthalmitis to develop following penetrating injury surgical or otherwise. It may also result following perforation of a sloughing corneal ulcer. Xerophthalmic children and eyes with lagophthalmos are more likely to develop panophthalmitis. Sometimes the period may be few hours only and starts with malaise, headache, fever, pain in and around the eye.

On examination the lids are swollen red and hot. The interpalpebral fissure is obliterated. Pus trickles through the lids, the conjunctiva is chemosed and hyperemic. Initially the cornea is steamy but later on develops purulent keratitis and sloughs, the anterior chamber is full of pus. Details of this structure beyond the hypopyon is not visible. The whole of the uvea is smothered with pus and the vitreous is almost a bag of pus, the lens may dislocate. The globe is immobile and proptosed. Absence of perception of light is the rule.

In post operative eyes pus may exude through the section. It is sometimes difficult to differentiate between severe endophthalmitis and early panophthalmitis. The condition is to be differentiated from orbital cellulitis which generally does not involve the globe and vision is retained. Absence of perception of light and immobile globe is more in favour of panopthalmitis than endophthalmitis.

Treatment of panophthalmitis is one of the most frustrating things. Broad spectrum antibiotic may suppress the infection. Visual recovery is almost impossible. The eye when untreated goes into phthisis after a prolonged course. The main role of antibiotics in panophthalmitis is to prevent septicemia, meningitis and cavernous sinus thrombosis.

Definitive treatment is evisceration of the eye

Masquerade syndrome51

This consists of a group of intraocular disease that are not uveitis per se but mimic uveitis in many ways hence diagnosed and managed as uveitis with disastrous result. They are seen mostly under 15 years of age in both the sexes, but may be seen as early as first year of life. Some of them are malignant and potentially life threatening, others may be non malignant growth or non inflammatory conditions.

Two common malignant disorders are retinoblastoma and myelogenous leukemia. Medulo epithilioma is a locally invasive tumor, may be malignant. While juvenile xantho granuloma is a benign dermatological condition that causes spontaneous hyphaema in children.

Intra ocular foreign bodies and peripheral retinal degeneration are two common non neoplatic condition that may present as uveitis. Other less common conditions are retinitis pigmemtosa, multiple sclerosis and post vaccination status.

All the above conditions may cause aqueous flare, cells in AC, posterior synechia, cells in vitreous.

Retinoblastoma is generally seen is children under five years of age with strabismus, redness, photophobia which on examination shows a posteriorly placed growth or may come with white reflex in pupillary area, congestion pain. KP flare cells in AC and accumulation of pus like fluid in AC (pseudo hypopyon) which is infact accumulation of tumor cells, posterior synechia, nodules on iris, tension is invariably raised. Pseudo hypopyon may disappear and uveitis subside with local steroid and cycloplegic only to reappear. X-rays shows intera ocular calcification ophthalmic ultrasonography may outline the tumor and intraocular calcification. Serum and aqueous LDH may be raised. Aqueous tap may reveal tumor cells.

Leukemia : Acute myeloid leukemia may present as anterior uveitis in children. Spontaneous hypheama, heterochromia and glaucoma. Fundus examination may show Roth’s spot. Examination of blood gives clue to presence of leukemia. The child is generally ill and pale.

Differential diagnosis consists of all causes of white reflex in pupillary area.

Investigation includes : Routine Hb%, TLC, DLC, ESR, X-ray chest and orbit, ultrasonography, CT of orbit and MRI.

Management depends upon causative factor. All cases of uveitis in children that improves with cycloplegic and steroid and recur should be suspected to be masquerade syndrome.

New growth of uvea in children24, 42, 51, 74

New growths of uvea are rare in children, when present they are generally benign or locally invasive. However, malignant melanoma which is malignant growth of sixth decade can sometimes be seen in second decade. Such occurrences are extremely rare. However, malignant melanoma of iris is more common in children than adults. Benign tumor of the iris are hemangioma, may be associated with angioma of the lid and cause secondary angle closure glaucoma.

Neuro fibroma of iris is seen as nodule on the iris in association with generalized neurofibromatosis. They do not require any treatment.

Nevi are common tumors of the iris that make their presence felt just before puberty. They do not require any treatment, unless they start growing in size or there is change in pigmentation, which may be sign of malignant change.

Juvenile xanthogranuloma73 is a benign dermatological tumor seen at the age of one year. The skin lesions are yellow multiple nodules. There may be visceral involvement. Ocular lesions are generally associated with cutaneous lesions.

Ocular involvement are—Iris nodules, spontaneous hyphema, secondary glaucoma and uveitis. They lesions may involve all parts of the eye. The condition of self limiting. Hyphema and uveitis are treated with local steroids.

Diktyoma75: This is a rare tumor, mostly arising from ciliary body but may arise from iris, retina or optic nerve. It is a congenital growth, commonest age of presentation is between two to four years. It is unilateral slowly progressive may remain confined to globe or may become locally invasive. Metastasis is rare, only occurring when the growth becomes extra ocular. It is also known as medullo epithelioma because it was thought to arise from medullary epithelium of fore brain. The term diktyoma is derived from its lace like appearance when it invades the iris.76

There are two types of medullo epithelioma - The teratoid and the non teratoid. The former besides ciliary epithelium contains hyaline, cartilage, rhabdomyocytes, brain tissue etc. Both types can be benign or malignant. One third of the medulla epitheliomas are malignant. On histology it shows rosettes similar to retinoblastoma. The tumor is very often mistaken as retinoblastoma because retinoblastoma is commonest ocular growth in the same age group. Medullo epithelioma may present as white reflex in pupillary area, secondary glaucoma and proptosis, which are common features of retinoblastoma as well. However, incidence of bilateral retinoblastoma is common presenting feature which is extremely rare in medullo epithelioma.

There is no known genetic predisposition or known family history. Presenting features depend upon site, duration and location of the growth. It may only be detected accidentally when the child presents with diminished vision and squint. Otherwise common presenting features include diminished vision, pain and redness of the eye, whitish reflex in the pupillary area, buphthalmos and late proptosis.

Diagnosis is difficult, however, unilateral growth without extra ocular involvement, absence of intra ocular calcification should arouse suspicion of medullo epithelioma. All cases should be examined with indirect ophthalmoscope. X-ray, CT, MRI, USG may help to differentiate medullo epithelioma from other disorders.

Treatment

There is no definite treatment77 for small growth of iris and cilliary body be cured by wide iridectomy or irido cyclectomy. Eyes with large tumors are best enucleated. Role of chemotherapy and radiation are not well established.

REFERENCES

1.Miller S.J.H. : Parson’s disease of the eye, 17th edition, p. 151, Churchill Livingstone, London, 1984.

2.Nema H.V. : Anatomy of the eye and its adnexa, 2nd edition p. 19 to 30, Jay Pee Brothers, New Delhi, 1991.

3.Jogi Renu : Basic ophthalmology, 1st edition, p. 148, Ajeet Publication New Delhi, 1994.

4.Miller S.J.H. : Parson’s disease of the eye, 17th edition, p. 6, Churchill Livingstone, London, 1984.

5.Duke Elders S. : System of ophthalmology, Vol. III, p. 167-184, Henry Kimpton, London, 1963

6.Khurana A.K. : Ophthalmology, 2nd edition, p. 152-156, New Age International (P) Limited, 2000, New Delhi.

7.Nancy Anderson Hamming, Apple D. : Anatomy and embryology of eye in Principle and practice of ophthalmology, Vol. 1, First Indian edition, pp 33-44, Jay Pee, Brothers, New Delhi, 1987.

8.Banumathy S. P. : Anatomy of the eye, 1st edition p. 52, Arvind Eye Hospital, Maduri.

9.Ahmed E : A text book of ophthalmology, First edition, p. 24, Oxford University Press, Calcutta, 1993.

10.Duke Elder’s : System of ophthalmology, Vol. III, Part I, pp. 158 to 162, 1st edition Henry Kimpton London 1963.

11.Vaughan D., Asbury T. : General Opthalmology tenth edition, p. 10-11, Lange Medical Publication, California, 1983.

12.Duke Elder’s : System of ophthalmology Vol. III part I, p. 36-40 1st edition. Henry Kimpton London 1963.

13.Duke Elder’s : System of ophthalmology Vol. III Part II, p. 573, First edition. Henry Kimpton London, 1963.

14.Walton D.S. : Aniridia in Current ocular therapy, 5th edition, p. 508-509, Edited by Fraunfelder F.T. and Roy F.H., WB Saunders Company, Philadelphia, 2000.

15.Deborah Pavan Langston : Pediatric ophthalmology in Manual of ocular diagnosis and therapy. Third edition, p. 290.

16.Duke Elder’s : System of ophthalmology, Vol. III, p. 775, Ist edition, Henry Kimpton, London, 1963.

17.Nema H.V. : Anatomy of the eye and its adnexa, Second edition, p-150, Jay Pee Brothers, New Delhi 1991.

18.Biswas J. : Disease of uveal tract in Modern ophthalmology, Vol. 2, Second edition, p. 559, Jay Pee Brothers, New Delhi, 2000.

19.Sorsby A. : Albinism in Modern ophthalmology, Vol. 2, p. 37-39, Butterworth London, 1963.

20.Kanski J.J. : Heriditory disorders of the retina and choroids in Clinical ophthalmology, 2nd edition, p. 385-386, Butterworth, London, 1989.

21.Sharma P. : Essentials of ophthalmology, first edition, p. 155, Modern Publication, New Delhi, 2000.

22.Ahmed E. : Disease of the uveal tract in A text book of ophthalmology. First edition,

p.227, Oxford University Press, Calcutta, 1993.

23.Miller S.J.H. : Disease of the uveal tract in Parson’s disease of the eyes. Seventeenth edition, p. 157, Churchil Livingstone London, 1984

24.Carolene R Baumal : Granulomatous uveitis in ophthalmology secretes. edited by Vander JF and Gault JA. First Indian edition, p. 258, Jay Pee Brothers New Delhi, 1998.

25.Debora Pawan Langston : Uveal tract iris ciliary body and choroids in Manual of ocular diagnosis and therapy, 3rd edition, p. 174-213.

26.Gittinger J.W. : Asdorian G K—Toxoplamosis in Manual of clinical problems in ophthalmology. First edition, p. 147, Little Brown and Co., Boston, 1998.

27.Sharma P. : Uvea and its diseases in Essentials of ophthalmology. First edition, p. 156-175, Modern Publishers, New Delhi, 2000.

28.Coles R.S. : Uveitis in Modern Opthalmology, Vol 4, edited by Sorsby A. First edition

p.636-686. Butterworth, London 1964

29.Wood A.C. : Endogenous inflammation of the uveal tract, Williams and Willkino, Baltimore 1961

30.Hogan M.H., Kimura S. J. and Thygeson P. : Signs and Symptoms of uveities I. Anterior uveitis AJO 47-155, 1959.

31.Tesseler M. : Uveitis in Principle and practice of ophthalmology Vol. 2, First Indian edition, Edited by Peyman G A, Sanders D and Goldberg FM, p. 1554-1566, Jay Pee Brothers, New Delhi 1987.

32.Biswas J. : Intermediate uveitis (Pars Planitis) in, Vol. 2, Second edition, Edited by Dutta L C, p. 571-580, Jay Pee Brothers, New Delhi 2000.

33.Kanski J.J. : Uveitis in Clinical ophthalmology, second edition p. 136-177, Butterworth, London, 1989.

34.Nussenblat R.B. : et al. Standardisation of vitreal inflammatory activity in intermediate and posterior uveitis. Opthalmology, 92-467-471, 1985.

35.Duke Elders in Systems of ophthalmology, Vol. III part II p. 893-902, Henry Kimpton, London, 1963.

36.Doughman D.J. : Olson G.A. and Nolan S. : Experimental band Keratopathy, Arch Oph 81: 264; 1969.

37.Barua C.K. and Dutta L.C. : Corneal degeneration and dystrophies in Modern Opthalmology Vol. 1, Second edition, edited by Dutta L C, p. 183-184, Jay Pee Brothers New Delhi, 2000.

38.Tran D.B. and Schanzlin D.J. : Corneal and conjunctival calcification in Current of ocular therapy. 5th edition page 329-330 edited by Fraunfelder F.T., Roy F.H., Randall J., W. B. Saunders Company, Philadelphia, 2000.

39.O’Brat DPS, Gantry D S et al. : Treatment of band keratopathy by excimer photo keratectomy BJO 77: 702-708 1993.

40.Igerscheimer J. : Spirochaetal infection-Aquired syphilis in Modern Opthalmology Vol. II, edition second, p. 217-219 Butterworth London 1963.

41.Dutta L.C. : Ophthalmology : Principles and practice, 1st edition, p. 121-122, Current Book International, Calcutta.

42.Rosenbaum J.T. and George R.K. : Uveitis in Current ocular therapy, 5th edition p. 519-521. edited by Franfelder F.T. and Roy F.H. and Randall J., W.B. Saunders Company Philadelphia, 2000.

43.Knox D.L. : Disorders of the uveal tract in Paediatric Ophthalmology, Vol. I, second edition, edited by Harley R.D., W.B. Saunders Company, Philadelphia 1983.

44.Biswas J. and Wagle A. : Anterior uveitis and arthritis in Modern Ophthalmology. Vol. 2, Edited by Dutta L.C., p. 566-571, Jay Pee Brothers, New Delhi, 2000.

45.Vaishali Gupta and Gupta A : Ocular toxoplasmosis in Modern Ophthalmology, Vol. 2, edition 2, edited by Dutta L.C. p. 580-585, Jay Pee Brothers New Delhi 2000.

46.Shaffer D B : Paediatric ophthalmology in Text books of ophthalmology. 9th Edition, edited by Scheic H.G. and Albert, D M, WB Saunders company Philadelphia, 1977.

47.Shalaby I.A. and Dunn J.P. : Acquired and congenital syphilis in Current therapy. Ed 5, Edited by Fraunfelder F.T., Roy F.H., Randell J., p. 2-5, W.B. Saunders Company Philadelphia, 2000.

48.Wood A.C. : Chronic bacterial infection: Ocular tuberculosis in Modern ophthalmology. Vol II, first edition, edited by Sorsby A., p. 116-153, Butterworth, London, 1963.

49.Pamela S. Chavis : Tuberculosis in Current ocular therapy, fifth edition, edited by Fraunfelder F.T., Roy F.H. and Randel J., p. 78-81, W.B. Saunders Company Philadelphia 2000.

50.Helm C.J. : Holland G.N. and Ocular tuberculosis, Survey ophthalmology 38 : 229256 1993

51.Gittinger J.W. : Herpes simplex keratitis in Manual of clinical problems in ophthalmology, first edition, edited by Gittinger J.W. and Asdaurion G.K., p. 46-47, Little Brown and Co. Boston, 1998.

52.Gillespie S.H. : Ocular toxocariasis in Current ocular therapy, edition 5, p. 97-98, edited by Fraunfelder F.T., Roy F.H. and Randall J., W.B. Saunders Company Philadelphia 2000.

53.Gupta V. and Gupta A. : Pediatric posterior uveitis in Modern Ophthalmology. Vol. II, edition two, edited by Dutta L.C., p. 561-565, Jay Pee Brothers, New Delhi 2000.

54.Asdourian G.K. : Toxocariasis in Manual of Clinical Problems in Ophthalmology, first edition, edited by Gittinger J.W. and Asdourian G.K., p. 149-151, Little Brown, Boston 1998.