Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

One of the suspected causes of Fuch’s heterochromic cyclitis is congenital in origin, it can be seen at any age in both the sexes, 10% cases are bilateral. However, some consider it be inflammatory or degenerative and do not put in category of congenital anomalies.

Gyrate atrophy of choroid

This is an inborn error of aminoacid metabolism. It is associated with raised level of ornithine in plasma, aqueous, CSF and urine. The condition is heriditory bilateral presenting in the first decade as progressive night blindness. There is progressive atrophy of choroid as well as retina. The lesions start in mid periphery as oval patches with scalooped border.

The size and shape of the lesion vary, they merge with each other to form a larger patch and girdle the mid periphery. Choroid and retina are absent over the patch but the retinal blood vessels remain normal for long time and then attenuate. Macular involvement is late either as macular edema or a patch may cover the macula. Secondary cataract is common EOG and ERG are sub normal.

There is no specific treatment. Constant supplementation of diet with pyridoxine (B6) is supposed to delay the progress. Low protein diet is also recommended.

Choroideremia

This is a bilateral progressive disease, seen only in males, women are carriers who show mild form of the disease. The condition is first noticed between five to ten years of age as progressive night blindness which is misdiagnosed as vitamin A deficiency by general physician or as retinitis pigmentosa unless fundus is examined. The fundus has no resemblance to retinitis pigmentosa. The two features common among the two conditions are night blindness and ring scotoma in the peripheral field. The disease progresses to legal blindness in ten to twenty years. Central vision is retained till late. The disease is caused due to atrophy of choroid and retinal pigment epithelial. There is no known treatment. Low vision aids and mobility support may help. Ultimately the patient has to be rehabilitated as visually challenged.

Choroidal sclerosis

Choroidal sclerosis has two forms: 1. Adult and 2. Juvenile. The adult form is probably is degenerative process. The juvenile form is most probably congenital in nature and manifest round about fifteen years of age. The lesion begins on the macula that looks similar to patch of choroiditis. The central vision is poor. There is no specific treatment. Low vision aid and rehabilitation are the only paliatives available.

Uveitis in children

General consideration

The term uveitis means inflammation of any part of the uvea. It is the commonest disorder of the uvea. No age sex or ethnic group is spared. It can be unilateral or bilateral. Due to proximity of lens, retina, vitreous and optic nerve to the uvea, these parts are invariably drawn into the clinical manifestation of uveitis as well as complication.

Commonest age group inflicted by uveitis is between second to sixth decade after which incidence of uveitis diminishes rapidly. About five percentage of all uveitis is seen in pediatric age group. Uveitis in children may range between mild self limiting anterior uveitis to sever

vision threatening endophthalmitis involving all parts of uvea as well vitreous. In one third of all uveitis cases no definite cause can be pinpointed as causative factor. This rises to fifty percent in uveitis in children. Undetected uveitis in children may result in permanent sub normal vision leading to strabismus and amblyopia. Some of the uveitis in children are due to systemic infection and are bilateral i.e. tuberculosis, syphilis, toxoplasmosis.

There is no satisfactory way to classify uveitis. Various classifications have been put forward depending upon 1. Parts of the uvea involved. 2. Mode of onset and duration. 3. Etiology. 4. Pathology. 5. Associated with various systemic manifestation. 6. Masquerade syndromes.

1. Anatomical classification

(i) Anterior uveitis. This is inflammation localized to iris and or ciliary body. Due to lack of anatomical barrier between iris and ciliary body the inflammation may involve both resulting in to iridocyclitis. Inflammation limited to iris is called iritis while that involving ciliary body (pars plicata) is known as cyclitis.

(ii) Intermediate uveitis. Here the process involves posterior part of the ciliary body (parsplana) peripheral choroid and retina and called as parsplanitis.

(iii) Posterior uveitis. The part involved is mostly choroid, that may involve the whole of choroid, may be localized to macula, may be near the disc or involve the periphery. Choroiditis invariably involves retina and the condition is called chorioretinitis as seen in tuberculosis syphilis or retinochoroiditis when the primary lesion begins in the retina i.e. toxoplasmosis.

(iv) Pan uveitis. All the parts of uvea are involved as in sympathetic ophthalmia.

(v) Endophthalmitis. In this sight threatening condition there is pan uveitis with involvement of vitreous, not extending beyond sclera.

(vi) Panophthalmitis. Panophthalmitis is the severest form of uveitis involving all coats of eye and periocular tissue. It is a blinding condition.

(vii) Keratouveitis. This is a very common form where primary lesion starts in cornea and involvement of anterior uvea is due to spread of toxins to the endothelium. In case of interstitial keratitis the inflammation starts in the uvea and spreads to the cornea.

(viii) Juxta papillary22. The lesion is a choroidal inflammatory patch near the disc producing sector shaped lesion and corresponding field defect.

(ix) Disseminated choroiditis. Small areas of inflammation are scattered all over the fundus behind the equator.

(x) Central choroiditis. It is located in the posterior pole involving the macula. (xi) Sclero uveitis is involvement of uvea along with sclera.

2. Onset (Chronological)

On the basis of mode of onset, uveitis can be

I.Acute II. Chronic

III. Recurrent

IV. Acute exacerbation on chronic.

3. Etiological

Etiological classification of uveitis is most logical from point of management but it is not possible to pinpoint the exact cause in about one third cases.

Eiologically uveitis can be divided into : (i) Microbial

(a) Endogenous.

(b) Exogenous.

(a) Endogenous microbial uveitis is either caused due to direct invasion of uvea by micro organism or due to immune reaction of the micro organism to the uvea.

(b) Exogenous microbial uveitis is due to direct entry of pathogenic organism, following perforation of globe, accidental and surgical or spread from outer coat of the eye mostly as a result perforating corneal ulcer.

The organism can be bacteria, viruses, fungi, protozoa and nematodes.

All bacteria are capable of producing some type of uveitis or other if they get access to the uvea. They can produce acute or chronic lesions. Acute lesions are generally produced by cocci i.e. gonococcus and pneumococcus. The bacilli generally produce chronic uveitis i.e. tuberculosis, syphilis, leprosy23.

Viruses that cause uveitis are herpes simplex, herpes zostor Epistein Barr virus, rubella, influenza, measles and mumps.24

Fungi that produce uveitis are candida, fusarium.

Out of many protozoan infection that produces uveitis is Toxoplasma gondi.25 It generally produces bilateral congenital or acquired posterior uveitis.

Toxocara canis and catis are two round worms of dogs and cats that produce unilateral posterior uveitis in children that is always vision threatening, but not fatal and must be differentiated for more serious retinoblastoma which is both sight threatening as well as life threatening. Both present with white reflex in pupillary area. Other nematodes that cause uveitis are cysticerosis and onchocercisasis.

(ii) Auto immune disease. Auto immune disorders that generally have systemic manifestation form the largest group of diseases that produce both acute and chronic uveitis. They are generally associated with certain specific HLA type. These are juvenile rheumatoid arthritis, ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome, Vogt Koyanagi Harada disease, Behcet disease. HLA typing is now considered an important diagnostic test in uveitis.24 Sympathetic ophthalmia is presumed to be due to hypersensitivity to uveal pigment. Lens protein sensatization cause phacogenic uveitis.

(iii) Other non specific uveitis are—Pars planitis, Fuch’s heterochromatic iritis, sarcoidosis, malignant tumor of eye, long standing retinal detachment, iritis glaucomatosa, retained intra ocular foreign bodies specially pure copper, anterior segment ischaemia following squint surgery, pulse less disease also produces uveitis but all are not seen in children.

4. Pathological classification

The pathological classification most widely used was suggested by Woods in 194727,28, that divides uveitis into two groups i.e. granulomatous and non-granulomatous, on the basis of histopathology presentation without sharp line of demarcation in clinical presentation.

The granulomatous uveitis generally involves all the part of uvea with predilection for choroids. It is more commonly a bilateral involvement. There is general actual invasion of the uvea by organism. There is a proliferation of tissue. The proliferation of tissue due to microbial invasion depends upon the virulence of the organism and the state of immunity of the tissue. The onset is generally insidious without much pain, the keratic precipitates are large mutton fat in nature, aqueous flare is relatively low with scanty cells. Hypopyon is unusual, the vitreous shows marked flare and cells. The posterior synechia are thick, broad and difficult to break. In late cases peripheral anterior synechia are seen. The iris develops nodules. The condition has long slow course.

The non-granulomatous uveitis has an acute painful onset, generally uniocular to begin-with, other eye gets involved later, mostly self limiting. An episode lasts for four to six weeks without treatment. There is marked circumciliary congestion. There may be ciliary tenderness. This may involve all parts but anterior uveitis is more common. KPs are generally small and numerous. There may be fibrinous exudation and formation of hypopyon. Anterior chamber reaction is marked with flare and cells. Vitreous does not show cells, pupil is miotic. Posterior synechia are small and narrow, break with ease. In late stages there may be peripheral anterior synchia. Iris module are generally not formed.

Division of uveitis into two classes of granulomatous and non granulomatous is not always clinically possible. A case of acute anterior uveitis of non infectious origin may show large mutton flat KPs or a case of chronic anterior uveitis may show indolent character of granulomatous uveitis. Some of the examples are—uveitis due to leptospirosis should cause a granulomatous uveitis but in fact it presents as a non granulomatous uveitis. Similarly lens induced uveitis is expected to be an allergic reaction to lens protein and should behave like non granulomatous which on slit lamp, looks like granulomatous. Similarly sympathetic uveitis also presents as granulomatous lesion with epithelial cells and giant cells when it is supposed to be an allergic reaction. Sarcoidosis is a non infective multi systemic disorder. Logically it should produce non granulomatous uveitis but in most of the eye, it present as granulomatous uvietis with nodule formation.

Clinical features of uveitis in general

Symptoms and signs in uveitis greatly differ in different types. There may just be blurring of vision without pain or redness as seen in pars planitis, white iritis in girls and Fuch’s heterochromic iritis to severe loss of vision with pain as in endophthalmitis. Symptoms of posterior uveitis may differ from those of anterior uveitis in such an extent that they may look like two separate entities. Many conditions may masquerade as uveitis when in fact they are either life threatening serious conditions of intra ocular malignancy or benign condition like persistant primary hyper plastic vitreous. Complications and sequaelae may change this clinical picture entirely.

It is better to divide clinical features related to following types of uveitis, i.e. those belonging to 1. anterior uveitis, 2. posterior uveitis, 3. intermediate uveitis, 4. pan uveitis in separate groups. Moreover the signs and symptoms differ greatly between acute and chronic uveitis. Complications like glaucoma or cataract may overshadow the primary features of uveitis.

Symptoms of acute anterior uveitis

1.Onset. Generally sudden and unilateral but may occasionally be bilateral. Simultaneous onset is extremely rare.

2.Pain. Pain may be the first symptoms of acute anterior uveitis. The pain ranges from dull ache to throbbing pain, radiating along the distribution of ophthalmic branch of fifth nerve on the same side. This pain is worst at night. Tenderness of the globe is indicative of ciliary involvement.

3.Lacrimation and photophobia are common symptoms due to irritation of sensory supply to anterior uvea. They are more marked in children.

4.Redness. The eye may present as red eye due to circum ciliary congestion caused by dilated anterior ciliary vessels.

5.Diminished vision. Initially patient may not have diminished vision. Diminished vision if at all present, develops after three four days, or from the beginning in a case of recurrent attack.

Causes of diminished vision are—Edema of corneal epithelium, deposition of precipitates on the posterior surface of cornea, turbid aqueous, small constricted pupil, exudates in the papillary area, anterior vitreous cells and flares, spasm of ciliary body resulting in the myopia, secondary glaucoma. Recurrent anterior uveitis is commonly associated with macular edema, sometime there may be papillitis result in diminished vision.

Signs of anterior uveitis

1.Mild edema of the lids : Exact cause of such edema is not well understood.

2.Circum corneal congestion.

Redness around the cornea starts as a pink hue that becomes gradually darker red. The congestion fades towards periphery. The circum ciliary congestion does not blanch with weak solution of vasoconstrictor.

3.Keratic precipitates:

Keratic precipitates are deposition of cells, macrophases, uveal pigments or RBC on the endothelium of cornea. It may be a passive process where cells circulating in the aqueous come in contact with the swollen endothelium and settle on the endothelium or as an active process where the endothelial cells become phagocytic and engulf the circulating cells in the aqueous.27

The large keratic precipitates may be visible on bright oblique illumination with corneal loupe. However, to visualise them in details they should be examined with good illumination of slit lamp. The number, shape, size and distribution depend up on severity and duration of inflammation. Large to medium sized keratic precipitates are generally deposited in a triangular fashion with apex up towards the pupil. Fine KPs are generally dusted all over the endothelium, few KPs may be deposited in an irregular fashion.

Various types of keratic precipitates according to their size, colour and characteristic are: large mutton fat KP., medium KP, endothelial dusting, pigmented KP and red KP.

Mutton fat KP. These are largest KPs arranged in a broad based triangular distribution. The apex of the triangle is upwards, larger KPs occupy lower position. Larger KPs may reach upto 1 mm. in size. They are called mutton fat KPs due to their greasy lardaceous appearance. Mutton fat KPs primarily consists of macrophages and clusters of epithelial cells, they have a sandy white colour, they may at times be pigmented, their number varies between ten to twenty. They are generally seen in so called granulomatous uveitis but may be seen in recurrent non granulomatous uveitis also. Common causes being—Tuberculosis, toxoplasmosis, endophthalmitis anaphylectica, sympathetic ophthalmia, sarcoidosis. As inflammation subsidies they become hylanised and fade in colour.

Small and medium sized KPs are due to lymphocytes and plasma cells, their borders are clear cut. There may be as many as forty to fifty in one eye. They are seen in nongranulomatous anterior uveitis both acute and chronic.

Endothelial dusting is caused by very small KPs that may run into hundreds. They are scattered all over with predilection for lower part, commonly seen in acute nongranulomatous anterior uveitis and recurrence of such conditions.

Pigmented KPs. These are seen in chronic inflammation of long duration. They are due to entanglement of iris pigment in white KPs or the iris pigment has been engulfed by the cells.

Red KPs are seen in uveitis that cause hyphaema i.e. herpes simplex and herpes zoster.

Old KPs. As time passes, KPs shrink in size, fade in colour, these borders become crenated, they have ground glass appearance and may be pigmented.

4. Anterior chamber reaction. Normal aqueous is colourless, clear fluid. In inflammation there is outpouring of protein from the anterior uvea resulting into plasmoid aqueous giving it a turbid appearance. Increased turbidity of aqueous is due to suspended particles : cells fibrin, protein, RBC etc.

The cells. In aqueous cells originate in the iris and ciliary body due to active migration from uvea to aqueous humor. The cells may circulate in the aqueous by convection current or settle on the endothelium. They may be seen on the iris, ciliary body, trabeculum lens, suspensory ligament and anterior vitreous face.27 Initially the cells are poly-morphonuclear, as days pass, they are replaced by lymphocytes, plasma cells and macrophages. More are the cells, more is the involvement of ciliary body. The cells are examined by the slit lamp with maximum illumination and magnification by a 3 mm. × 1 mm. slit. The cells should be counted and graded between 0 to 4+ where 0 stands for absence of cells and 4+ means over 50 cells per field.

Aqueous flare. Presence of protein in the aqueous makes it turbid as beam of light passes through the turbid aqueous the suspended particles stand out as shining bodies against the iris background, this phenomena is called aqueous flare. To see a flare an intense beam of light 2 mm. wide is directed on the iris at an oblique angle and obscuration of details of the iris is noted. Clearer details denote less flare and total obscuration is maximum flare. Flare is again graded between 0 to 4+. Flare in not always a sign of active uveitis, it can be seen due to

leak of damaged vessels without iridocyclitis. To diagnose uveitis a combination of cells and flare must be present.

Fibrenous exudates in the AC. In severe anterior uveitis the cells may get enmeshed in fibrinous aqueous and form a sheet over the iris surface and lens capsule. Presence of fibrinous aqueous is called plastic iritis which is a form of severe iritis.

Pus in AC. In severe cases of uveitis there is down powering of WBC, that due to their weight gravitate at the bottom of AC. Accumulation of pus in AC is called hypopyon that is sterile.

5.Iris. The iris gets fluid laden due to dilation of radial vessel and cellular infiltration of the stroma. The iris looses its roughness, the contours of the pits and collarettes are lost. As the iris gets fluid filled and increases in thickness it spreads towards the centre causing shrinkage in pupillary diameter. Nodules on iris are late phenomenon mostly seen in recurrent and chronic uveitis. A swollen peripheral iris may come in contact with posterior surfaces of cornea resulting in peripheral anterior synechia.

6.Pupil. It is miotic which on careful examination looks irregular that reacts poorly to light. Causes of miosis are engorged radial vessels, infiltration of stroma by cells, relatively stronger sphincter muscles and irritative action of toxins on the nerve ending. The pupil becomes irregular due to presence of posterior synechia between the posterior surface of iris and anterior surface of lens in phakic eye. Irregularity of pupil becomes more marked when pupil is dilated by mydriatic. Initially the pupil does not dilate at the site of synechia, but dilates inbetween the synechia. This gives the pupil a scalooped or festooned appearance. With repeated use of mydriatic, the synechia are broken resulting into a round dilated pupil and leaving iris pigment on the anterior lens capsule which lasts for days but disappear ultimately.

If the synechia persists for few weeks, but do not break, they require stronger mydriatic cum cycloplegia. Long standing posterior synechia are the site where future anterior capsular opacities may develop. In untreated cases posterior synechia may spread all along the circumference and bind down the pupillary margin all around, resulting in to a ring or annular posterior synechia that prevents aqueous from passing through the pupil resulting in rise of pressure in the posterior chamber that pushes the iris forward in a bow like fashion called the iris bombe. Deposition of exudates that obscures pupillary area is called occlusio pupil with loss of third Purkinje image.

7.Lens. In early stages that lens is clear, later the iris gets adhered to it which on dilatation leave fragments of iris pigment on the lens, varying in number and size. In long standing and recurrent cases anterior capsular cataract develops at the site of posterior synechia. In case of recurrence complicated cataract develops starting from posterior capsule which on slit lamp give a polychromatic lusture. In fibrinous iridocyclitis a membrane similar to occlusio pupil develops behind the posterior capsule and is called posterior cyclitic membrane.

8.Vitreous. Changes in vitreous are common specially when ciliary body in inflamed, the changes are in content and structure. Vitreous involvement is directly proportionate to severity of inflammation. The anterior vitreous can be seen by a bright beam of slit lamp. The changes can be in the form of opacities that are due to cells, coagulated exudates and fibrin. Presence of cells in the anterior vitreous is seen in anterior uveites while that in the posterior

vitreous is due to inflammation of choroid. A comparison between the cell count in anterior chamber and posterior chamber gives a rough idea differentiating involvement of iris and ciliary body. In case of cyclitis cell density in anterior vitreous is more than in anterior chamber, in case of iritis the finding is reversed.

9. Fundus changes

A.The media may look hazy due to presence of KPs, fibrin in pupillary area, posterior capsular opacification and vitreous debris. In case of a small rigid pupil fundus may not be visible.

B.The retinal changes can be diffuse, peripheral or macular. Diffuse retinal edema may be present in anterior uveitis. Macular changes are seen mostly as cystoid macular edema (CME), best seen by Goldman three mirror lens or Volks + 68 to + 90D and fluorescein angiography. The macular edema is a self limiting feature but may leave permanent pigmentation. Peripheral changes are seen in pars planitis.

C.The disc may be blurred due to optic neuritis, this is more common in cyclitis.

10. Intraocular pressure. Intraocular pressure changes are variable, while in most of the eyes it remains normal, in some cases it may become abnormal in initial few days, especially in children. Lowering of intraocular pressure is more pronounced in cyclitis due to lowered secretion in ciliary process. Intraocular pressure rise in acute anterior uveitis is due to plasmoid aqueous and cells obstructing the trabecular meshwork, trabeculitis, peripheral anterior synechia.

Symptoms of Intermediate Uveities24, 27, 30, 31

Intermediate uveitis is also known as pars planitis and chronic cyclitis. The symptoms are floaters, diminished or foggy vision that may worsen over years without any attributable cause. Children complaining of floaters in eye should not be dismissed as simple floaters unless proved other wise. Pars planitis is a disease of children and young adults. In 70% cases it is bilateral.

Signs of intermediate uveitis

There is hardly any sign visible on oblique illumination the eye is white in most of the cases. There are very few cells in anterior chamber. There may be fine KPs in the lower part, the iris is normal, so is the pupil. The anterior vitreous shows more cells than in aqueous, the posterior vitreous is clear.

The real diagnosis lies in the peripheral fundus examined by indirect opthalmoscope and scleral dentation that shows peripheral retinitis, perivasculitis and vitritis. The inferior periphery shows maximum changes in the form of white fluffy exudates as spherical deposits or plane sheat referred to as snowball and snow banking.

The macula gets involved in late stages in the cystoid macular edema. Rarely there may be papillitis. Posterior sub capsular cataract is a common late feature. Shrinkage of perivascular membrane may lead to traction detachment.

Symptoms of posterior uveitis

Posterior uveitis can be acute or chronic. It may be localized either in posterior pole or periphery, may be diffuse, scattered all over the choroids. Retina and optic nerve are frequently involved. The symptoms and signs depend upon the above factors.

Pain : In contrast to anterior uveitis pain is almost always absent unless associated with anterior segment involvement specially in the form of secondary glaucoma. Lacrimation, photophobia, redness and ciliart tenderness are also absent.

Diminished vision : Diminished vision is a prominent feature of posterior uveitis specially if the lesion involves the macula, maculopapillar bundle and optic nerve. Peripheral lesions do not produce much of visual symptoms. They are mostly associated with floaters in the field of vision. Acute posterior uveitis with muscular involvement have deterioration of vision that may be preceded by metamorphopsia.

Causes of diminished vision in posterior uveitis consists of simple macular edema, cystoid macular edema, pigmentation of the macula, scar or the macula, vitreous haze, papillitis, lenticular opacity and secondary glaucoma. An unilateral lesion of central choroiditis may present as strabismus and amblyopia in a child. In case of congenital toxoplasmosis loss of vision may be detected only when the child is brought as a case of squint.

Signs of posterior uveitis are better divided into 1. Acute and 2. Chronic.

Signs of posterior uveitis are mostly localized in the posterior pole, however, whole of the fundus should be scanned with a direct ophthalmoscope as far as possible, followed by indirect opthalmoscopy with scleral indentation.

Acute lesion of choroids is a patch of choroiditis seen as an area over which retina is invariably involved, the edema may not obscure the retinal vessel, border of the lesion is well defined. Colour of the area involved is yellowish or grayish. A large area in the posterior pole may give grayish reflex and retinoscopy that disappears from retinoscopy field on movement of the eyeball. The posterior polar lesions are best seen with slit lamp. Vitreous changes are very prominent in acute lesions of the choroids. They are in the form of vitreous floaters, vitreous flare and posterior vitreous detachment. In case of endophthalmitis there may be severe vitreitis with accumulation of exudates. In a case of acute choroiditis, sudden loss of red reflex denotes onset of endophthalmitis.

The vitreous opacities may vary in shape and size. They may be fine coarse, large or stringy. Fine opacities are due to inflammatory cells. Large opacities on the periphery and snow ball opacities are seen commonly in pars planitis, candidiasis and sarcoidosis32. The vitreous opacities are graded by number of cells counted in a field by direct opthalmoscope and graded between 0 to 4 +.29 This grading has a disadvantage that it fails to measure the actual inflammatory activity in the vitreous which is best seen by indirect opthalmoscope with intermediate magnification, medium field, with diminished illumination, examined by + 20 D lens.33 Visibility of three fundus landmarks i.e. optic nerve head, retinal blood vessels and retinal nerve layer are noted and graded between 0 to 4+. Zero being clear is view of nerve fibre striation and four plus stands for obscuration of optic nerve head.32

Other changes noted on fundus examination are retinitis, vasculitis, papillitis and exudative retinal detachment.

Symptoms of chronic posterior uveitis

The symptoms are same as in acute posterior uveitis i.e. there is no pain, redness, photophobia or lacrimation. However, seeing of floaters, scotomas and diminished vision persists.

Causes of diminished vision in chronic posterior uveitis are

Complicated cataract mostly posterior capsular opacification with polychromatic lusture, vitreous haze, vitreous bands, scar over the macula and maculopapillar bundle. Cystoid macular edema, macular pigmentation, macular hole, sub retinal neovascularisation, periphlebitis, secondary glaucoma and traction detachment.

Signs of chronic posterior uveitis are same as seen in acute choroiditis with changes due to passage of time. Some of the lesions get healed, other may develop satellite lesion adjacent to healed or healing lesion or there may be development of new lesions independent of original lesion.

Vitreous floaters which are hallmark of acute posterior uveitis subsides to a great extent, however, some haze may persist. Posterior vitreous detachment is more common with development of traction bands.

A healed patch of choroiditis has an irregular margin with clumps of uveal pigment on the periphery. The retina generally disappears over the healed patch but the vessels persist, there may be clumps of choroidal pigment away from the patch. The floor of the patch is white due visible sclera over which the choroid has been destroyed. Large areas of the choroiditis may result into a scotoma that becomes negative with passage of time. Other fundus changes consists of sheathing of blood vessels, traction detachment, post neuritic optic atrophy, macular scar, membrane formation over macula and neovascularisation. Intraocular tension may be normal or raised. Hypotony is general far less frequent than seen in acute anterior uveitis.

Complication in acute anterior uveitis:

Common complications are secondary glaucoma, hypotony, massive deposit of KPs on the endothelium, changes in refraction, cystoid macular edema, papillitis, hypopyon and hyphaema.

Secondary glaucoma in acute anterior uveitis is generally open angle glaucoma but can be narrow angle as well due to extremely narrow angle that gets blocked by swollen iris at the periphery or due to dilatation of pupil by strong cycloplegic like atropine.

Causes of secondary open angle glaucoma in acute anterior uveitis are many that may act separately or in combination, they are—Obliteration of the trabecular mesh work by swelling of the meshwork in the form of trabeculitis. These already narrowed channel may further be clogged by fibrinous aqueous. Obstruction of aqueous flow from posterior to anterior chambers is caused due to ring synechia, aqueous flow can be hampered due to small pupil, extensive contact of iris over the lens without the formation of actual synechia.

Hypotony

In initial phase of acute iridocyclitis aqueous secretion by ciliary body is diminished more is the inflammation lower is the tension. This is popularly known as ciliary shutdown, complete stoppage of aqueous production never takes place. The hypotony presents as flattering of cornea, shallowing of AC resulting in increased iridocorneal contact that ends in formation of peripheral anterior synechia. In most of the eyes production of aqueous returns to normal and the tension building up to normal level or may overshoot the normal limit to result in glaucoma. In some cases hypotony persists. The tension may be as low as 6 mm to 7 mm.