Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

The drug should always be prescribed under supervision of oncologist. Their benefit should always be weighed against their potential dangers. All of them produce cytopenaea and liver toxicity. The dose used in ophthalmology is comparatively low. Hence side effects encountered in ophthalmic use are fewer in comparison to malignancy.

They are mostly used in sympathetic ophthalmia, Vogt-Koyanagi- Harada disease, Baheet’s disease and serpiginous choroditis. They may be used in parsplanitis, chronic cyclitis, retinal vasculitis. Their role in childhood paraplanitis is questionable. Cytotoxic drugs are not available as drops or ointment commonly used drugs are cyclophosphamide, cyclosporin, chlorambucil, azathioprine, methotrexate. Cyclosporine does not come under true antimetabolite, it is basically an antibiotic. Combination of steroid with cyclosporin reduces total dose of cyclosporin which is available as drops.

Specific type of uveitis in children:

While pediatric population comprises of 15% of general population, incidence of pedriatric uveitis ranges between 2 to 10 percent27, 42, average being 5%. These figures are definitely less when compared to adult uveitis, however, it is important not to miss uveitis in children because it can be bilaterally sight threatening. Some of the peculiarities of pediatric uveitis are :

1.Incidence of bilateral uveitis in children is more than adult uveitis.

2.Unilateral chronic uveitis (white uveitis syndrome) may go undetected.

3.Girls are effected more than boys in a ratio of 6:4 except sympathetic uveitis where boys outnumber girls.

4.Endogenous uveitis is commonest form of childhood uveitis.

5.Acute anterior uveitis is less frequent than chronic recurrent uveitis.

6.One third of childhood uveitis have undetermined etiology.

7.Prognois is poor due to chronicity, uncertain etiology, late diagnosis, poor response and poor compliance.

8.It can be congenital or acquired.

Though all adult form of uveitis can inflict patients under fifteen, some are seen less commonly in children.

Pediatric uveitis can be:

Congenital—Toxoplasmosis, rubella, herpes simplex syphilis.

Acquired—

1.Infective : Generally chronic but may be acute. They may be due to tuberculosis, syphilis, streptococcal, gonococcal. Other organism causing uveitis are pneumococcus, staphylococcus, bacillus cereus, leprosy (rare in children), leptospirosis, propioni bacterium, lyme disease, various fungi, toxoplasmosis, toxocara, herpessimplex herpeszoster, aids.

2.Connective tissue diseases effecting joints43 : Juvenile rheumatoid arthritis, juvenile Reiters syndrome, juvenile spondylitis, inflammatory bowel disease.

3.Trauma : Sympathetic ophthalmia, sensitization to lens protein following rupture of lens capsule, retained in intraocular foreign body.

4.Others : Vogt Koyanagi - Harada syndrome, Behcet’s syndrome, sarcoidosis, Fuch’s heterochronic uveitis. All these are very infrequently seen in children. All except Fuch’s heterochronic iritis generally produce bilateral chronic pan uveitis. Pars planitis is common in children that produce intermediate uveitis. Other causes are ischeamic ocular inflammation following squint and retinal surgery.

5.Masquerade syndromes : These disorders are mostly non inflammatory in nature diagnosed as chronic idiopathetic uveitis. They can be life threatening malignant lesions or non malignant lesions in children. Common examples are—Retinoblastoma leukemia, medulo epithelioma, intraocular foreign body, Coats disease, peripheral retinal detachment.

Toxoplamosis uveitis

Toxoplasmosis has emerged as commonest cause of posterior uveitis. It is caused by protozoa, toxoplasma gondi that is an obligatory, intra cellular parasite. Cat is the first definite host and humans are the intermediate hosts. In cat it is an intestinal parasite that reproduces sexually in the gut and is shed in stool as oocytes which infect the human being by ingestion of food contaminated by oocytes. The food may be directly infected by the dirt containing the parasite or may be transmitted to exposed food by vectors like house fly and cockroach.Toxoplasma can be transmitted via unpasteurised milk, half cooked meat. It is also transmitted by way of inhalation, through blood transfusion, skin wounds and transplants. Once it reaches human intestine it multiplies there and pass to the regional lymph nodes. From the lymph nodes they get circulated in regional circulation44, 45 In intermediate host toxoplasma multiplies within, asexually and form a protective cyst within the cells where the cyst remains protected from the immune system hence dormant occasionally. So long as the organism is intracellular it does not give a positive serological test. Titer of serological test is not related to ocular involvement, however, a rising titer is indicative of recurrence that is very common. Toxoplasmosis occurs in two forms i.e. acquired that is very mild and self limiting does not require any treatment and gives immunity to reinfection, but recurrence due to rupture of toxoplasma cyst is possible. However a pregnant mother who is infected during pregnancy can transmit the infection to the growing foetus. The foetus is infected via plancental blood or by direct extension from a dormant lesion on the uterine wall. A mother who is sero positive for toxoplasma before first pregnancy will not infect the foetus nor the subsequent foetuses. Thus only one of the pregnancies is at risk. There is no prophylaxis against toxoplasma.

Congenital toxoplasmosis

Once it was thought that all ocular and brain lesions of toxoplasmosis were congenital and consequently lesion as recurrences. However now it is known that these lesions can be acquired also. The congenital lesions have predilection for brain and retina. In the brain it produces encephalitis, the patches of which get calcified in long term. In eye the lesion are patches of retinochoroiditis in the posterior pole on the macula, close enough to the macula to cause loss of vision or juxta papillary. Scattered smaller patches away from the posterior pole without visual symptoms, these lesions are detected only on routine fundus examination by indirect ophthalmoscope.

All lesions are generally bilateral : The lesions starting at early pregnancy may heal and the child born with a patch of healed choroiditis. The healed patch is not noticed unless looked for particularly. A healed patch is oval in shape may be larger than disc, has patches of pigment on the periphery. The center of the patch is white. The blood vessels pass over the patch. There are no cells in the vitreous or aqueous. A child infected late in pregnancy has active lesion in the posterior pole with fluffy appearance, the retina is edematous. There are no pigments on the periphery, vitreous may have cells.

A child with congenital toxoplasmosis has three Cs representing Chorioretinitis, Calcification and Convulsion. All neonates with convulsions should undergo fundus examination and X-ray skull. However, the child may have only ocular lesions. In severely infected child, there is microcephally and mental retardation.

Children with ocular lesion are generally diagnosed when they are examined forinfentile strabismus which is invariably estropia or diminished vision. Some times there may be nystagmus unilateral cases are generally amblyopic.

Recurrence is seen between ten years and forty years. They are more common in teen age girls 24,42 Recurrences generally occur either on the periphery of the healed lesions or as satellite lesion adjacent. The recurrence has all the characteristics of acute lesion with involvement of vitreous that is studded with cells and floaters sufficient to reduce the visibility of the lesion in a head light in the fog manner24. Posterior vitreous detachment is common, the detached vitreous is dusted with vitreous precipitates similar to Kps. Other involvement’s are - papillitis and vasculitis. Some times the lesions may be punctate, scattered on wide area of retina without much vitreous reaction.

Complications include cataract, glaucoma, subretinalneovascularisaton, exudative retinal detachment45 Vitreous haemorrhage, nystagmus, opportunistic systemic infection in immuno compromised individual.

Differential diagnosis consist of congenital coloboma of macula, tubercular choroiditis, cytomegalo virus infection, retinoblastoma, herpes simplex chorio retinitis.

Diagnosis : Diagnosis of congenital toxoplasmosis is straight forward when the child is brought with systemic symptoms of convulsion, mental retardation, microcephaly and squint. On examination a typical patches of central choroiditis is visible. On X-ray there is invariably intracranial calcification. CT and MRI may show small lesions in the cortico medulary region. Other investigation are (1) serological test for serum antitoxoplasma antibody. Any titer of serum antibody is significant.45 2. Elisa test, 3. IgG and 3 IgM titer - A positive IgG may be present without ocular involvement, positive IgM is indicative of recent infection.

Management

There is no prophylaxis for toxoplasmosis. There is no treatment for infected cats as cats may be asymptomatic. Best way is to look after personal hygiene, avoid raw vegetables. Meat should be well cooked.

Once diagnosis has been confirmed the treatment is by anti-toxoplasmosis chemotherapy, cortico steroid, photo coagulation of peripheral lesions and management of uveitis.

Chemotherapy

Drugs available for treatment are—Pyrimethamine, Sulphadiazine alone, triple sulpha, sulpha methoxazole with trimethoprim, clindamycin, spiromycin, minocylin and atovaquone, vancomycin, tetracycline. The dose should be administered in consultation with pediatrician who should also monitor for side effects.

Once the lesion has healed no treatment is required, but chemotherapy may prevent recurrence. Pregnant mothers who test positive should be given full course of treatment in consultation with gynecologist and neonatologist. For active lesion a combination of pyrimethamine triple sulpha with systemic steroid is the best combination available. Steroid alone may suppress an acute attack for some times only to flare up later. The chemotherapy should be continued for weeks, the steroid is generally tapered after seven to ten days. Pyrimethamine can cause marrow suppression, nausea and leucopenia. Hence it is necessary to get weekly WBC count to overcome the side effects. 5 mg. of leucovorin (folinic) acid is given twice a week. Eye with multiple recurrence and vitreous haemorrhage may require vetrectomy.

Rubella uveitis

Rubella uveitis in children is part of congenital rubella and over shadowed by congenital cataract and glaucoma. In seventy percent of cases it produces non progressive chorioretinitis giving a pepper and salt fundus appearance with good central vision and normal ERG. Other causes of pepper salt fundus should be excluded. In some percentage of cases, there may be iritis or iridocyclitis. The iris stroma is severely damaged leading to partial hole formation that trans-illuminates reflected ray, pupil is generally small and dilates poorly with atropine. Both dilator and sphincter muscle may be involved. There is no specific treatment, congenital rubella can be prevented only if the mother has been immunized in childhood.

Herpes simplex uveitis24, 42, 49

In children herpes simplex uveitis is generally secondary to herpetic keratitis but can be due to systemic involvement as well. It is mostly produced by type II herpes simplex virus, however, type I can also cause cutaneous lesions that are self limiting. Virus may migrate to trigeminal ganglion only to be reactivated with reduced resistance. It can cause non granulomatous anterior uveitis with or without evidence of cutaneous or corneal involvement. It can also cause chorioretinitis and retinitis in older children. The condition is painful with intense lacrimation and photophobia with evidence of active keratitis or stromal keratitis, cells, flares, posterior synechia and occasional hypopyon. The neonate gets the infection during passage through birth canal and lesion develops between two weeks to 18 months after. It may occasionally be life threatening. Other common age groups to be affected is between 6 months to five years.

Management is by way of cycloplegic for lacrimation, and photophobia, three times a day and weakest possible steroids under supervision if cornea is not involved. Systemic anti viral drugs should be administered in consultation with pediatrician.

Syphilitic uveitis in pediatric age group

Syphilis has been called greatest imitator in clinical medicine. It can inflict any age of both sexes, all ethnic groups and involve any part of body in various combinations. It used to

be a major cause of uveitis both acute and chronic before present era of antisyphilitic treatment came into vogue. In children commonest form of uveal involvement is associated with congenital syphilis, however, acquired syphilis can also be seen in pediatric age group due to frequent child abuse and precocity. Uveal involvement in children may be (1) congenital and quiet at birth, (2) active at birth, (3) may become active at teens, (4) may be acquired in teens.24 There is no primary stage in congenital syphilis. The congenital syphilis in initial years are comparable with secondary syphilis becoming tertiary, if not treated.45,47 Hence uveal involvement in children may show features of secondary or tertiary syphilis. It can be acute

(1)Associated with interstitial keratitis

(2)Without involvement of cornea

(a) Acute iritis

(b) Diffuse chorioretinitis.

Uveitis in interstitial keratitis preceeds corneal involvement, however, corneal reaction may be severe enough to obstruct examination of the iris and anterior chamber. Finding of the uveitis may only be visible after the cornea has cleared.

Corneal endothelium may be damaged by KPs and secondary guttatae may develop, hyaline strands may project in anterior chamber, angle may get hyalinised resulting in glaucoma. The iris may be atrophic.30 Other syphilitic lesions include chronic iridocylitis, chorioretinitis, retinal phlebitis, vitreous opacity.45 Pupillary changes can be due to involvement of iris stroma or part of neurosyphilis.

Acute iritis can start as network of fine capillaries, vascular papules and nodules.24 There are multiple synechia resulting into miosis which does not respond to atropine, flare and cells in anterior chamber are common.39

Posterior segment involvement results in salt and pepper spots of chorioretinitis. It is generally bilateral and peripheral may involve posterior pole or a quadrant. There is no visual loss. In later stages, salt and pepper spots may be confused as retinitis pigmentosa.

Diagnosis of syphilitic uveitis is often missed as it is generally thought that syphilitic uveitis is only seen in adults. Interstitial keratitis related anterior uveitis is easy to diagnose and responds well to treatment. The diagnosis is confirmed by variety of serological tests.

The laboratory investigations in syphilis are same for all ages. They can be

(1)Nontreponemal—VDRL and rapid plasma regain

(2)Specific treponemal—FTA - ABS - Flourescent treponemal antibody absorption MH4TP - Micro hemo agglutination test.

Non treponemal test V.D.R.L. becomes negative in late stages even with or without treatment but FTA-ABS never become negative.

Treatment

Treatment of syphilitic uveitis with interstitial keratitis does not pose much difficulty. Difficulty arises when uveitis in children is suspected to be due to secondary or tertiary stage. In all such cases it should be confirmed by FTA-ABS and treated as acquired syphilis in consultation with pedriatician.

Local treatment consist of atropine ointment under five, drops may be used in older children with caution. Once desired mydriasis has been achieved, atropine may be replaced by 1% cyclopentolate. Topical steroids are administered as per severity, to begin with its can be as often as hourly to be reduced to three times a day. Steroids drops may have to be used for months and the child monitored constantly for possibility of side effects. In older children peribulbar steroid can be given in recalcitrant cases. Oral steroids are not required.

Uveal involvement is generally hematogenous. As anterior and posterior uvea have different blood supply, the involvement is independent of each other but can be concurrent.

Surprisingly involvement of uvea is rare along with active pulmonary lesion. Miliary tubercle of choroids is common in military tuberculosis and meningitis. Tubercular lesion of uvea is thought to be due to sensitization of uvea to tuberculosis protein. The sensitization depends on systemic resistance and host immunity. Inflammatory and destructive process is due to hyper sensitivity while healing is due to host immunity and host resistance.

In children, following primary infection a fast developing hypersensitivity takes place due to low or absent immunity. It is possible to get either anterior or posterior uveitis separately or together to results in a pan uveitis. Uveal involvement is generally granulomatous with mutton fat KP, aqueous flare and cells in anterior chamber, edema of iris and ciliary body. Formation of Koeppe nodules at the pupillary margin, broad posterior synechia, exdates over the anterior lens capsule. Formation of tubercular nodule all over the uvea, either as solitary or miliary tuberculosis. Tuberculoma is now a days extremely rare. Vitritis is common, there may be papillitis. Macular involvement leads to early and permanent loss of central vision. A self limiting acute iritis develops following cutaneous injection of tuberculin. This is non granulomatous and without synechia.

Posterior uveitis is less common in children than in adults. Common presentations are :

(1)Miliary tubercle in the choroid secondary to tuberculous meningitis

(2)Circumscribed lesion in the posterior pole

(3)Involving the macula. A healed macular involvement may be confused as congenital coloboma of macula or toxoplasmic chorioretinitis. Occasionally there may be perivasculitis with sheathing and new vessel formation that may cause vitreous haemorrhage ranging from small pre retinal haemorrhage to full blown vitreous haemorrhage.

Diagnosis

Diagnosis of uveal tuberculosis is one of baffling problems. It is done by exclusion, presumption and confirmation. Tuberculosis should be differentiated from other forms of granulmatous uveitis like toxoplasmosis, syphilis, and sarcodosis.

Presumptions

In case of presumed uveal tuberculosis—the child has raised ESR and lymphocytosis. The uveitis does not respond favourably to local cycloplegic and steroids or becomes worse. A therapeutic trial with isonniazide 10 to 20 mg/Kg per day not exceeding 300 mg is administered to the child as a single dose daily for 2 to 3 weeks with local treatment. If there is significant

improvement other systemic anti tubercular antibiotic agents are added in consultation with pediatrician.57E

Confirmatory investigations : (1) Routine TLC, DLC and ESR. (2) X-ray chest to exclude pulmonary involvement is undertaken. (This generally comes out to be negative.) (3) A thorough examination of abdomen and lymph nodes are done to exclude extra pulmonary tuberculosis and if found to be positive a full course of three drugs anti-tuberculosis chemotherapy is started.

Skin test (Mantoux test). Purified protein derivative is used. First 5(TU) of PPDT is used as interdermal injection and reaction is red after 48 hours. If this test is negative 25(TU) is used for confirmation. Any reaction even erythema is suggestive of tubercular origin. However, a positive test is seen in children who have received BCG as a part of immunization or suffered from tuberculosis in the past.

Other test : Anti tubercular immunoglobin IgA. IgG and IgM.

Polymerase chain reaction is very sensitive in pulmonary tuberculosis and less sensitive in extra pulmonary tuberculosis.

Management of tubercular uveitis

Management of tubercular uveitis consists of local treatment by cycloplegic and steroids. Posterior synechia of tubercular iridocyclitis are difficult to break hence they require prolonged use of strong cycloplegic like atropine used with usual caution. Once the pupil has been dilated atropine may be replaced by cyclopentolate or a combination of cyclopentolate with phenylephenine. Local steroids have to be used for long time than other non infectious uveitis and gradually tapered off over months. The child should get minimum three drugs for systemic anti tubercular chemotherapy for 6 to 9 months.

Toxocara infection of uvea (See page 489 also)

Toxocarasis is a nematod infection. It is a c ommon cause of chronic posterior uveitis. It is caused due to ingestion of embryonated ova of an intestinal parasite—Toxocara canis round worm of the dogs.50 The puppies that are most infectious, the puppies get infected via two sources—1. a more common way is ingestion of infected food and 2. Less common by trans placental infection.42 In both instances this ova hatches in the small intestine to form larvae. The larva penetrates the intestinal wall and is taken up by systemic circulation to reach distant organs. Some larvae reach the trachea and are coughed up. The coughed larvae is reswallowed to reach the intestine and get converted into an adult worm.51 A female adult worm produces 200,000 eggs per day, that are excreted in feces of the dog. The eggs can survive in the soil for years without hatching. They only hatch in the intestine of either dogs or human being. The second stage of infection develops in the intestine of a toddler who may ingest either the soil or food contaminated with by ova. The ova form larvae in the intestine that penetrate the intestinal wall, from where they are carried to distant organs including eye. The larvae do not mature to become mature worm in human beings, nor they return to the gut, hence they are not excreted in the feces of human being. The systemic infection of by toxocara has two distinct stages. (1) Stage of viscereal larva migrans. (2) Distant spread to liver, lungs, brain, muscle and eye. Involvement of eye is commonly referred to as ocular toxocariasis.

Visceral larva migrance is characterized by malaise, fever, cough, hepato spleenomegaly, leucocytosis, eosionphilia and cutaneous lesion without ocular manifestation.

Ocular toxocariasis is a late feature of systemic involvement. It is rarely seen with systemic involvement. Average age of a child with visceral larval migrans is two years while ocular toxocariasis is seen between 18 months to 18 years, average being 7.5 years.51 There is a latent period of few years between visceral larval migrans and ocular toxocariasis. Ocular toxocariasis is always unilateral condition, seen mostly in male, exact cause of this preference is not known. All races are equally affected. Its incidence in under developed countries must be more than reported. Once this larvae reache the eye, it can produce various types of posterior uveitis.51, 52 A typical lesion is posteriorly placed. Anterior segment signs and symptoms are minimal but not altogether absent. Children are mostly brought with strabismus, diminished vision or rarely white reflexes in pupillary area. On examination the eye is generally white with minimum cells and flare in aqueous. Ocular toxocariasis generally produce one of the following types of lesions.

1.Solitary posterior polar granuloma in the macular region or between the macula and nerve head.

2.Peripheral granuloma

3.Chronic endophthalmitis.

Solitary posterior polar granuloma is most common type of lesion that causes diminished vision due to involvement of macula. It is mostly seen in age group 6 to 14 years. The lesion is one or two disc diameter, raised yellowish white area, may be surrounded by hard exudates. Retinal vessels disappears in the lesion. There may be peri retinal gliosis with traction lines, there may subretinal haemorrhage with serous retinal detachment. The lesion is discovered either during routine eye examination or by chance or when the child closes the normal eye and discovers diminished vision in uncovered eye or the child may be brought for squint, more rarely with a white reflex in pupillary area.

Peripheral retinal granuloma. This is generally associated with parsplanitis, seen above 6 years of age, may be discovered in adults by chance. The peripheral lesion is a solitary mass associated with extensive peripheral gliosis. There may be vitreous bands extending from the lesion to the macula, disc or both causing traction displacement of macula that may present as pseudo squint. As the lesion is peripheral vision remains unaffected unless macula is involved. The vitreous band may cause retinal breaks that lead to localized, or extensive tractional retinal detachment.

Chronic endophthalmitis. This type of lesion is generally seen in younger children who are brought with either diminished vision squint or white reflex in pupillary area. There may be involvement of anterior segment with cells, flare, posterior synechia, even hypopyon. The vitreous is infiltrated with cells. In late cases a cyclitic membrane may develop. Vision is grossly diminished and it becomes difficult to visualize the fundus, macular edema and cataract further worsens the vision. Tractional or rhegmatisgenous retinal detachments are common.

Less common presentations are—Exudative retinal detachment, diffuse chorioretinitis, diffuse unilateral sub acute neuro retinitis (DUSN)50, 51, optic neuritis unilateral pars planatis.

Differential diagnosis

Most commonly mistaken diagnosis is retinoblastoma which cannot always be differentiated clinically, however, toxocariasis does not show intraocular calcification on X-ray and ultrasonography, it is extremely rare to get bilateral toxocariasis. Anterior chamber aspiration does not show tumour cells but gives polymerase chain reaction to toxocara antigens. Other disorders that form differential diagnosis are : Coats disease, other forms of endophthalmitis, persistent hyper plastic primary vitreous, retinopathy of prematurity.

Diagnosis

Diagnosis of ocular toxocariasis is alwayspresumptive. All cases of unilateral granuloma in a white eye should be suspected to have ocular toxocariasis unless proved otherwise. Contact with infected puppies is so common in general population that history of contact with puppies is of hardly any use, so are the skin changes of viscerallarval migrans. Differential count may show eosinophilia, X-ray orbit, ocular USG, CT and MRI are negative for intraocular calcification. Most reliable test is ELISA test to detect toxocara antibodies in serum, aqueous or vitreous. A titer of 1:8 in serum is diagnostic. However, sometimes serum may give negative results while aqueous/vitreous give positive results that is reliable.

Management

1.Prophylaxis. There are no sure way to prevention except personal hygiene and non consumption of uncontaminated food, however, pica cannot be stopped in toddlers who are most susceptible. Role of routine deworming of child may not be sufficient to expel the larvae. However, regular deworming of puppies from second week has been recommended. It is virtually impossible to deworm stray puppies that are the main source of contamination of soil.

2.Therapeutic.

(A)Medical

I.Anti helminths : Though broad spectrum anti helminths are routinely prescribed in children suspected to be suffering from toxocariasis. There role has been questioned. Anti helminths may cause increased inflammatory reaction due to deaths of the organism. Anti helminths whenever administered should be given under umbrella of full dose of cortico steroids in uveal toxocariasis.

II.Corticosteroids : Corticosteroids can be used in conjunction with anti helminths or alone. They can be used orally or by way of periocular injection.

Anterior segment reaction is managed by local cycloplegies and steroids.

(B)Surgical method. Vitreous surgery not only removes all inflammatory process and antigen but also vitreous bands and helps in placing of scleral buckle. The material removed by vitrectomy may be used for confirm diagnosis. Vitrectomy may be used to remove posterior cyclitic membrane as well.

Laser photo coagulation51 of live nematod when detected, should be tried only when the nematode is away from posterior pole.

Cryo freezing24: When laser is not available trans scleral cryo coagulation of peripheral lesion may be attempted under direct vision.

Acquired immuno deficiency syndrome and uveitis

Acquired immuno deficiency syndrome is an infectious disease with world wide distribution, both sexes are affected. No age is immune. AIDS can be congenital due to transplacental transmission of human immunodeficiency virus type I (HIV-I) or infection may be acquired during the passage of the child through birth canal of infected mother. Number of children affected by AIDS is increasing. Children who receive blood transfusion regularly due to various blood disorders are also at high risk. In older children HIV can be acquired due to use of contaminated needle especially in drug users. The HIV virus targets the CD4 lymphocytes and destroy it.

The HIV virus is a retrovirus known as human immuno deficiency virus type I. It has only RNA in its structure, it uses patient’s cellular reproductive system to manufacture DNA for multiplication.53 Fifty percent of HIV positive persons are transient non infectious. However, about 90 percent will develop AIDS which is uniformally fatal over the years. There is a gap of few years when an HIV infected person is converted to AIDS. 50% to 75% of AIDS patients will ultimately develop ocular lesion, which may result into blindness.

The HIV virus has affinity for T helper lymphocytes (CD4) which are destroyed by HIV virus leading to sever immune deficiency as a result of some organism which may otherwise lie dormant and become active. There may be many fold increase in virulence of infective organism in the body. Some of the microorganisms have greater predilection for AIDS patients. These opportunistic organism can be bacteria—mycobacteria, fungi, herpes simplex, herpes zoster, cytomelagic virus, Epstein Barr virus, adeno virus, toxoplasma and pneumocystis.

Ocular manifestation may be either due to 1. AIDS itself or 2. AIDS related complex.24 3. AIDS by itself can clog this micro vasculature by deposition of immune complexes or 4. AIDS related opportunistic organism and malignancies.

The uveal lesion may be a nongranulomatous pan uveitis due to HIV or due to herpes simplex or herpes zoster. Commonest type of ocular infection is CMV retinitis that cause multiple cottonwool spots, acute retinal necrosis or retinal detachment.53 CMV retinitis is cell CD4 dependent.53 It is seen in patients who have CD4 count less than 50 cells/mm3. The disease is bilateral due to haemotogenous spread. Other ocular manifestations may involve any or many parts of the eye from simple follicular conjunctivitis to severe retinal necrosis leading to bilateral blindness. They include keratitis, retinal vasculitis, retinal haemorrhage, Roth’s spot, microaneurysm, papillitis and ischemic maculopathy.

Kaposi sarcoma is commonest form of malignancy met in patients with AIDS. Though this is malignancy of adults it occurs in teens in patients with AIDS as well. The tumor is of endothelial origin 54, it is seen in 35% of with HIV infection. It involves lids more often than conjunctiva, orbit is involved rarely. It is mostly seen in males. It is considered to be an indicator that the patient has reached the last stage of primary disease55. Once Kaposi sarcoma develops life, expectancy is less than two years. Extremities are involved earlier than periocular structures. The lesions are multicentric.

Diagnosis

A person is said to have AIDS if following criteria are present.53