CASE REPORT

ANTERIOR UVEITIS

Created by :YULISA HANDAYANI

I11109016

OPHTALMOLOGY DEPARTEMEN OF RSUD SOEDARSOFACULTY OF MEDICINE AND HEALTH SCIENCES

TANJUNGPURA UNIVERSITYPONTIANAK

2013

LEGALIZATION SHEET

Case presentation is legal with title :

ANTERIOR UVEITIS

This working paper was arranged to fullfil the requirement of Ophthalmology

Module Clinical Assistant

Opthalmology Stage

Approved by,

Pontianak, November 2013

Consulent,

dr.M. Iqbal, Sp.M, M.kes

Created by :

Yulisa Handayani

NIM. I11109016

CHAPTER I

INTRODUCTION

Uveitis is one of the major causes of blindness in the world. Uveitis is

composed of a diverse group of disease entities, which in total has been estimated

to cause approximately 10% of blindness. Uveitis is broadly classified into

anterior, intermediate, posterior and panuveitis based on the anatomical

involvement of the eye. (Agrawal et al, 2010)

Uveitis has many subtypes and many potential associations with systemic

conditions and has always been one of the most challenging diagnoses in

ophthalmology (Babu; Rathinam, 2010).

Anterior uveitis is the commonest form of intraocular inflammation with a

varying incidence in the general population of various countries around the world.

The potential severe consequences of recurrent or untreated anterior uveitis are

probably underestimated. Anatomically, anterior uveitis involves inflammation of

the iris alone (iritis), anterior part of ciliary body (anterior cyclitis) or both

structures (iridocyclitis). (Agrawal et al, 2010)

Anterior uveitis can caused by trauma, chronic diarrhea, Reiter disease,

herpes simplex, Behcet syndrome, Posner Schlosman syndrome, post-operative,

adenovirus, parotitis, influenza, chlamydial infection, rheumathoid arthritis and

etc. (Ilyas S, 2007)

Traumatic cataract can occur by penetrating eye injury or blunt trauma that

can be seen in days or years (Ilyas S, 2007). The lens becomes white soon after

the entry of a foreign body, since interruption of the lens capsule allows aqueous

and sometimes vitreous to penetrate into the lens structure. (Vaughan and

Asbury’s, 2007).

Pterygium is Wing-shaped fold of fibrovascular tissue arising from the

interpalpebral conjunctiva and extending onto the cornea. Usually nasal in

location. It is Elastotic degeneration of deep conjunctival layers, related to

sunlight exposure and chronic irritation. More common in individuals from

equatorial regions (Elhers, 2008). Both blue and ultraviolet light have been

implicated in its causation, as demonstrated in watermen. Outdoor work in

situations with high light reflectivity, including from sand and water, enhances

pterygium development, and the use of hats and sunglasses is protective. (Yanoff,

2009).

.

CHAPTER II

LITTERATURE REVIEW

2.1 Anatomy of Uvea

The uveal tract (also known as the vascular pigmented layer, vascular tunic,

and uvea) takes its name from the Latin uva (grape) because the dark

pigmentation and shape of the structure are reminiscent of a grape. The uveal tract

lies between the sclera and retina. (Lang, 2000)

The uveal tract is the vascular coat of the eye, lying between the sclera and the

neuroepithelium. It consists of the iris, ciliary body, and choroid. The former

represents the anterior part, the latter the posterior part, and the ciliary body forms

the middle part. The uvea contains nerves, supporting connective tissue, and a

variable number of melanocytes that are responsible for its distinctive color. The

uvea is supplied anteriorly by long posterior ciliary arteries and the anterior ciliary

arteries. Posteriorly the uvea is supplied by several posterior ciliary arteries that

enter the choroid around the optic nerve. (Yanoof, 2008)

Anatomy of Uvea

2.1.1 Iris

The iris is the anterior extension of the ciliary body. It presents as a

flat surface with a centrally situated round aperture, the pupil. (Riordan-

Eva; Whitcher, 2007)

The iris consists of two layers: the anterior mesodermal stromal

layer and the posterior ectodermal pigmented epithelial layer.The posterior

layer is opaque and protects the eye against excessive incidentlight. The

anterior surface of the lens and the pigmented layer are so closetogether

near the pupil that they can easily form adhesions in inflammation. (Lang,

2000).

The iris forms a diaphragm in front of the crystalline lens. The iris

controls the amount of light transmitted into the eye by changes in the

pupillary size. The vascular supply to the iris originates in the anterior and

long posterior ciliary arteries. The iris color is determined by the number

and degree of melanin granules in the superficial stromal melanocytes.

(Yanoof, 2008)

2.1.2 Ciliary Body

The ciliary body, roughly triangular in cross-section, extends

forward from the anterior end of the choroid to the root of the iris (about 6

mm). It consists of a corrugated anterior zone, the pars plicata (2 mm), and

a flattened posterior zone, the pars plana (4 mm).The ciliary processes

arise from the pars plicata. (Riordan-Eva; Whitcher, 2007)

The ciliary muscle is responsible for accommodation. The double

layered epithelium covering the ciliary body produces the aqueous humor.

(Lang, 2000)

2.1.3 Choroid

The ciliary body extends from the base of the iris and becomes

continuous with the choroid at the ora serrata. It is approximately 6-6.5

mm in anteroposterior dimension. It consists of an anterior portion called

the pars plicata and a posterior portion called the pars plana. (Yanoff,

2009)

The choroid is the middle tunic of the eyeball. It is bounded on the

interior by Bruch’s membrane. The choroid is highly

vascularized,containing a vessel layer with large blood vessels and a

capillary layer.The blood flow through the choroid is the highest in the

entire body.The choroid regulates temperature and supplies nourishment to

the outer layers of the retina. (Lang, 2000)

2.2 Uveitis

2.2.1 Definition

The term "uveitis" denotes inflammation of the iris (iritis,

iridocyclitis), ciliary body (intermediate uveitis, cyclitis, peripheral uveitis,

or pars planitis), or choroid (choroiditis). Common usage, however, includes

inflammation of the retina (retinitis), retinal vasculature (retinal vasculitis),

and intraocular optic nerve (papillitis). Uveitis may also occur secondary to

inflammation of the cornea (keratitis), sclera (scleritis), or both

(sclerokeratitis). (Riordan-Eva; Whitcher, 2007)

2.2.2 Epidemiology

Uveitis usually affects people 20–50 years of age and accounts for

10–20% of cases of legal blindness in developed countries. Uveitis is more

common in the developing world than in the developed countries, due in

large part to the greater prevalence of infections that can affect the eye, such

as toxoplasmosis and tuberculosis. (Riordan-Eva; Whitcher, 2007)

Large series of uveitis patients show variation in terms of the relative

prevalence of different forms of uveitis. In surveys of patients referred to

tertiary centers, anterior uveitis has been shown to account for 28-66% of

cases, intermediate uveitis for 5-15%, posterior uveitis for 19-51%, and

panuveitis for 7-18%. (Yanoff, 2009)

2.2.3 Ethiology

Uveitis can caused by trauma, chronic diarrhea, Reiter disease,

herpes simplex, Behcet syndrome, Posner Schlosman syndrome, post-

operative, adenovirus, parotitis, influenza, chlamydial infection,

rheumathoid arthritis and etc. (Ilyas S, 2007)

Traumatic uveitis is often seen in accidental or operative injuries to

the uveal tissue. Different mechanisms which may produce uveitis

following trauma include (Khurana, 2007):

a. Direct mechanical effects of trauma.

b. Irritative effects of blood products after intraocular haemorrhage

(haemophthalmitis).

c. Microbial invasion.

d. Chemical effects of retained intraocular foreign bodies

e. Sympathetic ophthalmia in the other eye.

2.2.4 Classification

Depend on the anatomical location, uveitis can be classified as:

Anatomical Classification of Uveitis

Type Primary site of inflammation Include

Anterior uveitis Anterior chamber Iritis, Iridocyclitis,

Anterior cyclitis

Intermediate uveitis Vitreous Pars planitis,

Posterior cyclitis,

Hyalitis

Posterior uveitis Retina or choroid Focal, multifocal, or

diffuse choroiditis,

Chorioretinitis,

Retinochoroiditis,

Retinitis,

Neuroretinitis

Panuveitis Anterior chamber, vitreous,

and retina or choroid

Anatomical Classification of Uveitis

Acute uveitis describes the course of a specific uveitis syndrome

characterized by sudden onset and limited duration.Chronic uveitis

describes persistent inflammation characterized by prompt relapse (in less

than 3 months) after discontinuation of therapy. Recurrent uveitis is

characterized by repeated episodes of uveitis separated by periods of

inactivity without treatment lasting at least 3 months. (Kanski, 2011)

2.2.5 Occular Manifestation

The clinical manifestations of uveitis vary depending on several

factors - the primary site of involvement in the eye, the course of the

inflammatory process (e.g., acute or chronic), and the presence of secondary

complications arising from the uveitis itself. (Yanoff, 2009)

The symptoms of acute anterior uveitis (e.g., human leukocyte

antigen HLA-B27-related entities, such as ankylosing spondylitis) generally

include pain, redness, photophobia, and blurred vision, which typically

develop over a period of hours or days. On the other hand, patients who

have chronic anterior uveitis, such as that seen with JIA or Fuchs’

heterochromic iridocyclitis, may present merely with blurring of vision or

mild redness, with little pain or photophobia. Patients who have

intermediate or posterior uveitis typically present with floaters or impaired

vision secondary to cystoid macular edema or chorioretinal involvement.

Patients who have panuveitis may present with any or all of these

symptoms. (Yanoff, 2009)

2.2.6 Examination Method

The slit lamp is used to examine the surface of the iris under a

focused beam of light. Normally no vessels will be visible. Iris vessels are

only visible in atrophy of the iris, inflammation, or as neovascularization in

rubeosis iridis.Where vessels are present, they can be visualized by iris

angiography afterintravenous injection of fluorescein sodium dye. Defects

in the pigmented layer of the iris appear red under retroillumination with a

slit lamp. Slit lamp biomicroscopy visualizes individualcells such as

melanin cells at 40-power magnification. The anterior chamber is normally

transparent. Inflammation can increase the permeability of the vessels of the

iris and compromise the barrier between blood and aqueous humor. The

pigmented epithelium of the retina permits only limited evaluation ofthe

choroid by ophthalmoscopy and fluorescein angiography or

indocyaninegreen angiography. Changes in the choroid such as tumors or

hemangiomascan be visualized by ultrasound examination. (Lang, 2000)

2.2.7 Pathology of Uveitis

Inflammation of the uvea fundamentally has the same characteristics

as any other tissue of the body, i.e, a vascular and a cellular response.

However, due to extreme vascularity and looseness of the uveal tissue, the

inflammatory responses are exaggerated and thus produce special results.

(Khurana, 2007)

Pathologically, inflammations of the uveal tract may be divided into

suppurative (purulent) and nonsuppurative (non-purulent) varieties. Wood

has further classified non-suppurative uveitis into a nongranulomatous and

granulomatous types. (Khurana, 2007)

Purulent inflammation of the uvea is usually a part of

endophthalmitis or panophthalmitis occurring as a result, of exogenous

infection by pyogenic organisms which include staphylococcus,

streptococcus, psuedomonas, pneumococcus and gonococcus. The

pathological reaction is characterised by an outpouring of purulent exudate

and infiltration by polymorphonuclear cells of uveal tissue, anterior

chamber, posterior chamber and vitreous cavity. As a result, the whole uveal

tissue is thickened and necrotic and the cavities of eye become filled with

pus. (Khurana, 2007)

The pathological alterations of the nongranulomatous reaction

consists of marked dilatation and increased permeability of vessels,

breakdown of blood aqueous barrier with an outpouring of fibrinous exudate

and infiltration by lymphocytes, plasma cells and large macrophages of the

uveal tissue, anterior chamber, posterior chamber and vitreous cavity. The

inflammation is usually diffuse. As a result of these pathological reactions

iris becomes waterlogged, oedematous, muddy with blurring of crypts and

furrows. As a consequence its mobility is reduced, pupil becomes small in

size due to sphincter irritation and engorgement of radial vessels of iris.

Exudates and lymphocytes poured into the anterior chamber result in

aqueous flare and deposition of fine KPs at the back of cornea. Due to

exudates in the posterior chamber, the posterior surface of iris adheres to the

anterior capsule of lens leading to posterior synechiae formation. In severe

inflammation, due to pouring of exudate from ciliary processes, behind the

lens, an exudative membrane called cyclitic membrane may be formed.

(Khurana, 2007)

The pathological reaction in granulomatous uveitis is characterised

by infiltration with lymphocytes, plasma cells, with mobilization and

proliferation of large mononuclear cells which eventually become

epithelioid and giant cells and aggregate into nodules. Iris nodules are

usually formed near pupillary border (Koeppe’s nodules). Similar nodular

collection of the cells is deposited at the back of cornea in the form of

mutton fat keratic precipitates and aqueous flare is minimal. Necrosis in the

adjacent structures leads to a repairative process resulting in fibrosis and

gliosis of the involved area. (Khurana, 2007)

2.2.8 Anterior Uveitis

Though anterior uveitis, almost always presents as a combined

inflammation of iris and ciliary body (iridocyclitis), the reaction may be

more marked in iris (iritis) or ciliary body (cyclitis). Clinically it may

present as acute or chronic anterior uveitis. Main symptoms of acute

anterior uveitis are pain, photophobia, redness, lacrimation and decreased

vision. In chronic uveitis, however the eye may be white with minimal

symptoms even in the presence of signs of severe inflammation. (Khurana,

2007)

External examination shows ciliary (circumcorneal) injection which

has a violaceous hue. (Kanski, 2011)

Ciliary Injection

Miosis due to sphincter spasm may predispose to the formation of

posterior synechiae unless the pupil is pharmacologically dilated.

Endothelial dusting by a myriad of cells is present early and gives rise to a

‘dirty’ appearance True keratic precipitates (KP) usually appear only after a

few days and are usually non-granulomatous. (Kanski, 2011)

Endothelial dusting by cells

Aqueous cells indicate disease activity and their number reflects

disease severity. Grading of cells is performed with a 2 mm long and 1 mm

wide slit beam with maximal light intensity and magnification. This must be

performed before mydriasis because in normal eyes cells and pigment

clumps may develop after pupillary dilatation. Worsening is defined as

either a two-step increase in the level of activity or an increase to the

maximum grade. Anterior vitreous cells indicate iridocyclitis. (Kanski,

2011)

Hypopyon is a feature of intense inflammation in which cells settle in

the inferior part of the anterior chamber (AC) and form a horizontal level.

(Kanski, 2011)

Hypopion

Posterior synechiae may develop quickly and must be broken down

before they become permanent . Low intraocular pressure (IOP) may occur

as a result of reduced secretion of aqueous by the ciliary epithelium.

(Kanski, 2011)

Extensive posterior synechiae

Fundus examination is usually normal, but should always be

performed to exclude ‘spillover’ anterior uveitis associated with a posterior

focus, notably toxoplasmosis and acute retinal necrosis (Kanski, 2011).

With appropriate therapy the inflammation tends to completely

resolve within 5–6 weeks.The prognosis is usually very good.

Complications and poor visual prognosis are related to delayed or

inadequate management. Steroid-induced hypertension may occur but

glaucomatous damage is uncommon (Kanski, 2011).

Chronic anterior uveitis (CAU) is less common than the acute type

and is characterized by persistent inflammation that promptly relapses, in

less than 3 months, after discontinuation of treatment. The inflammation

may be granulomatous or non-granulomatous. Bilateral involvement is more

common than in AAU. Presentation is often insidious and many patients are

asymptomatic until the development of complications such as cataract or

band keratopathy. Because of the lack of symptoms patients at risk of

developing CAU should be routinely screened; this applies particularly in

patients with juvenile idiopathic arthritis. (Kanski, 2011).

External examination usually shows a white eye. Occasionally the

eye may be pink during periods of severe exacerbation of inflammatory

activity.Aqueous cells vary in number according to disease activity but even

patients with numerous cells may have no symptoms. Aqueous flare may be

more marked than cells in eyes with prolonged activity and its severity may

act as an indicator of disease activity. (Kanski, 2011). It is due to leakage of

protein particles into the aqueous humour from damaged blood vessels. It is

demonstrated on the slit lamp examination by a point beam of light passed

obliquely to the plane of iris. In the beam of light, protein particles are seen

as suspended and moving dust particles. This is based on the ‘Brownian

movements’ or ‘Tyndal phenomenon’. (Khurana, 2007).

Aqueous Flare and Cells

Keratic precipitate are clusters of cellular deposits on the corneal

endothelium composed of epithelioid cells, lymphocytes and polymorphs.

(Kanski, 2011).

Keratic Precipitate

The duration is prolonged and in some cases the inflammation may

last for many months or even years. Remissions and exacerbations of

inflammatory activity are common and it is difficult to determine when the

natural course of the disease has come to an end.The prognosis is guarded

because of complications such as cataract, glaucoma and hypotony. (Kanski,

2011).

2.2.9 Intermediate Uveitis

Intermediate uveitis affects mainly the intermediate zone of the eye

—ciliary body, principally the pars plana, peripheral retina, and vitreous.

The cause is unknown in most cases, although syphilis, tuberculosis, Lyme

disease, and sarcoidosis should be ruled out with appropriate laboratory and

ancillary testing. Multiple sclerosis should also be considered. Intermediate

uveitis is seen mainly among young adults, affects men and women equally,

and is bilateral in up to 80% of cases. (Riordan-Eva; Whitcher, 2007)

Common complaints include painless floaters and decreased vision.

Minimal photophobia or external inflammation. Usually age 15 to 40 years

and bilateral.Vitreous cells, white exudative material over the inferior ora

serrata and pars plana (snowbank), cellular aggregates floating in the

inferior vitreous (snowballs). Younger patients may present with vitreous

hemorrhage. (Elhers, 2008)

Pars planitis/intermediate uveitis with snowballs

Posterior subcapsular cataract and cystoid macular edema are the most

common causes of decreased vision. In severe cases, cyclitic membranes

and retinal detachments may occur. Secondary glaucoma is rare.

Corticosteroids are used mainly to treat cystoid macular edema or retinal

neovascularization. Topical corticosteroids should be tried for 3–4 weeks to

identify patients predisposed to development of corticosteroid-induced

ocular hypertension. If no improvement is noted and ocular hypertension

does not develop, a posterior sub-Tenon or intraocular injection of

triamcinolone acetonide, 40 mg/mL, may be effective. Patients with

intermediate uveitis usually do well with cataract surgery. (Riordan-Eva;

Whitcher, 2007)

2.2.10 Posterior Uveitis

Posterior uveitis refers to inflammation of the choroid (choroiditis).

Since the outer layers of retina are in close contact with the choroid and also

depend on it for the nourishment, the choroidal inflammation almost always

involves the adjoining retina, and the resultant lesion is called

chorioretinitis. (Khurana, 2007)

Presentation varies according to the location of the inflammatory

focus and the presence of vitritis. For example a patient with a peripheral

lesion may complain of floaters whereas a patient with a lesion involving

the macula will predominantly complain of impaired central vision. (Kanski,

2011)

Blurred vision, floaters, pain, redness, and photophobia typically

absent unless anterior chamber inflammation is present. (Elsher, 2008)

Various visual symptoms experienced by a patient of choroiditis are

summarised below (Khurana, 2007):

a. Defective vision. It is usually mild due to vitreous haze, but may

be severe as in central choroiditis.

b. Photopsia. It is a subjective sensation of flashes of light resulting

due to irritation of rods and cones.

c. Black spots floating in front of the eyes. It is a very common

complaint of such patients. They occur due to large exudative

clumps in the vitreous.

d. Metamorphopsia. Herein, patients perceive distorted images of

the object. This results due to alteration in the retinal contour

caused by a raised patch of choroiditis.

e. Micropsia which results due to separation of visual cells is a

common complaint. In this the objects appear smaller than they

are.

f. Macropsia, i.e., perception of the objects larger than they are, may

occur due to crowding together of rods and cones.

g. Positive scotoma, i.e., perception of a fixed large spot in the field

of vision, corresponding to the lesion may be noted by many

patients.

Lesions of the posterior segment of the eye can be focal, multifocal,

geographic, or diffuse. Those that tend to cause clouding of the overlying

vitreous should be differentiated from those that give rise to little or no

vitreous cells. The type and distribution of vitreous opacities should be

described. Inflammatory lesions of the posterior segment are generally

insidious in onset, but some may be accompanied by abrupt and profound

visual loss. (Riordan-Eva; Whitcher, 2007)

Retinitis

Vitreous opacities due to choroiditis are usually present in its middle

or posterior part. These may be fine, coarse, stringy or snowball opacities

(Khurana, 2007).

Features of a patch of choroiditis in active stage it looks as a pale-

yellow or dirty white raised area with ill-defined edges. This results due to

exudation and cellular infiltration of the choroid which hide the choroidal

vessels. The lesion is typically deeper to the retinal vessels. The overlying

retina is often cloudy and oedematous. In atrophic stage or healed stage,

when active inflammation subsides, the affected area becomes more sharply

defined and delineated from the rest of the normal area. The involved area

shows white sclera below the atrophic choroid and black pigmented clumps

at the periphery of the lesion (Khurana, 2007).

2.2.11 Treatment

The treatment of uveitis has three main goals: to prevent vision-

threatening complications, to relieve the patient's complaints and, when

feasible, to treat the underlying disease. (Babu; Rathinam, 2010)

a. Mydriatic and Cycloplegic Agents

These topical medications are used to treat the ciliary spasm that

frequently occurs with acute anterior uveitis and to break recently

formed posterior synechiae and/or prevent the development of new

synechiae. Longer acting agents, such as homatropine, scopolamine,

or atropine, are utilized to relieve ciliary spasm, whereas the shorter

acting agents (tropicamide or cyclopentolate) may play a role in

preventing new posterior synechiae formation in patients who have

chronic iridocyclitis (e.g., secondary to JIA) and minimal

photophobia in whom the pupil should be kept relatively mobile.

(Yanoff, 2009)

b. Corticosteroids

Corticosteroids are the drugs of choice in most types of uveitis.

They inhibit the inflammatory process by suppressing the

arachidonic acid metabolism and activation of complement. (Babu;

Rathinam, 2010)

When administered systemically they have a definite role in non-

granulomatous iridocyclitis, where inflammation, most of the times,

is due to antigen antibody reaction. Even in other types of uveitis,

the systemic steroids are helpful due to their potent non-specific anti-

inflammatory and antifibrotic effects. Systemic corticosteroids are

usually indicated in intractable anterior uveitis resistant to topical

therapy. (Khurana, 2007)

In panuveitis, both topical and systemic corticosteroids are

needed. Depending upon the severity of the disease, oral

prednisolone is started in a loading dose of 1 mg/kg/day. As the

inflammation subsides, tapering of corticosteroids by 5-10 mg per

week is begun within two to four weeks of initiating therapy. Once

the eye is completely quiescent, the patient is followed on a

maintenance dose ranging from 2.5-10 mg daily of prednisolone. A

reasonably long period of low-dose corticosteroids is required as

maintenance therapy in VKH(Vogt Koyanagi-Harada) syndrome and

SO.(Babu; Rathinam, 2010)

The normal response to the corticosteroid therapy may be

interrupted by recurrence of uveitis in which case the frequency of

instillation of topical drops is increased besides raising the oral

corticosteroid to the initial high-dose levels. Unilateral cases may be

given a trial with periocular injection of depot corticosteroids into

the posterior subtenon space. The side-effects and complications of

topical or systemic corticosteroids must be looked for at every

follow-up visit of the patient. These include secondary glaucoma,

posterior subcapsular cataract, increased susceptibility to infection

(ocular or systemic), hypertension, gastric ulcer, diabetes, obesity,

growth retardation, osteoporosis and psychosis. (Babu; Rathinam,

2010)

c. Antimetabolites

Indicate for sight-threatening uveitis, which is usually bilateral,

non-infectious, reversible and has failed to respond to adequate

steroid therapy. Steroid-sparing therapy in patients with intolerable

side-effects from systemic steroids or those with chronic relapsing

disease requiring a daily dose of prednisolone of more than 10 mg.

Once a patient has been started on an immunosuppressive drug and

the appropriate dose ascertained, treatment should continue for 6–24

months, after which gradual tapering and discontinuation of

medication should be attempted over the next 3–12 months.

However, some patients may require long-term therapy for control of

disease activity. (Kanski, 2011)

d. Vitrectomy in panuveitis

Vitrectomy for uveitis began in the late 1970s for diagnostic

purposes and for treating infections. Diagnostic vitrectomy

combined with PCR can significantly improve diagnostic yield in

otherwise idiopathic uveitis, and can frequently make a diagnosis in

cases complicated by media opacity or other features that make

traditional exam-based diagnosis difficult or impossible. Vitrectomy

may be considered as a therapeutic option when uveitis persists

despite maximum tolerable medical treatment with corticosteroids

and/or other immunosuppressants. It may also be indicated when

visual loss occurs due to complications of longstanding

inflammations, such as a densely opacified vitreous, scar tissue

pulling on the ciliary body causing hypotony, cystoid macular

edema, an epiretinal membrane, a dense posterior lens capsule

opacification or a tractional retinal detachment.Vitrectomy removes

the lodged lymphocytes in the vitreous, inflammatory debris,

immune complexes and autoantigens. It also increases the uveal

penetration of anti-inflammatory cells. Besides providing a better

access for complete removal of the cataractous lens material along

with posterior capsule, the combined approach of pars plana

lensectomy and vitrectomy allows easy performance of intraocular

maneuvers and prevents formation of cyclitic membrane. (Babu;

Rathinam, 2010)

2.3 Traumatic Cataract

The incidence of these lens opacities is higher in men than in women due to

occupational and sports injuries. (Lang, 2000)

Traumatic cataract can occur by penetrating eye injury or blunt trauma that

can be seen in days or years (Ilyas S, 2007). The lens becomes white soon after

the entry of a foreign body, since interruption of the lens capsule allows aqueous

and sometimes vitreous to penetrate into the lens structure. (Vaughan and

Asbury’s, 2007).

Blunt trauma does not result in rupture of the capsule, may cause an

anterior and/or posterior subcapsular cataract or both. Initially, fluid influx causes

swelling and thickening of the lens fibers. Later the fibers become less swollen;

the anterior subcapsular region whitens and may develop a characteristic flower-

shaped pattern, or an amorphous or punctate opacity. (Yanoff, 2009)

Small perforation caused by penetrating injury will close immediately

because of ephitelial proliferation so the opacity only in the small area (Ilyas,

2007). A small capsular penetrating injury may result in a localized lens opacity.

A larger rupture results in rapid hydration and complete opacification. Penetrating

injuries can be caused by accidental or surgical trauma such as a peripheral

iridectomy or during a vitrectomy. (Yanoff, 2009)

Traumatic Cataract

Traumatic cataract and iridodialysis

Concussion cataract occurs mainly due to imbibition of aqueous and partly

due to direct mechanical effects of the injury on lens fibres. It may assume any of

the following shapes (Khurana, 2007):

a. Discrete subepithelial opacities are of most common occurrence.

b. Early rosette cataract (punctate). It is the most typical form of

concussion cataract. It appears as feathery lines of opacities along the

star-shaped suture lines; usually in the posterior cortex.

c. Late rosette cataract. It develops in the posterior cortex 1 to 2 years after

the injury. Its sutural extensions are shorter and more compact than the

early rosette cataract.

d. Traumatic zonular cataract. It may also occur in some cases, though

rarely.

e. Diffuse (total) concussion cataract. It is of frequent occurrence.

f. Early maturation of senile cataract may follow blunt truma.

2.4 Pterygium

Pterygium is a growth onto the cornea, usually nasally, of fibrovascular

tissue that is continuous with the conjunctiva. It occurs in the palpebral fissure

area, much more often nasally than temporally, although either or both (“double”

pterygium) occur. Elevated whitish opacities (“islets of Vogt”) and an iron

deposition line (“Stocker”) may delineate the head of the pterygium on the cornea.

(Yanoff, 2009)

It is thought to be an irritative phenomenon due to ultraviolet light, drying,

and windy environments, since it is common in persons who spend much of their

lives out of doors in sunny, dusty, or sandy, windblown surroundings. The

pathologic findings in the conjunctiva are degenerative and hyperplastic condition

of conjunctiva. The subconjunctival tissue undergoes elastotic degeneration and

proliferates as vascularised granulation tissue under the epithelium, which

ultimately encroaches the cornea (Khurana, 2007). In the cornea, there is

replacement of Bowman's layer by hyaline and elastic tissue. (Vaughan and

Asbury’s, 2007)

Figure Pterygium

A fully developed pterygium consists of three parts: head (apical part

present on the cornea), Neck (limbal part), and Body (scleral part) extending

between limbus and the canthus. Depending upon the progression it may be

progressive or regressive pterygium. Progressive pterygium is thick, fleshy and

vascular with a few infiltrates in the cornea, in front of the head of the pterygium

(called cap of pterygium). Regressive pterygium is thin, atrophic, attenuated with

very little vascularity. There is no cap. Ultimately it becomes membranous but

never disappears. (Khurana, 2007)

The symptom of pterygium is irritation, redness of eye, decreased vision

or may be asymptomatic (Elhers, 2008). Visual disturbances occur when it

encroaches the papillary area or due to corneal astigmatism induced due to fibrois

in the regressive stage (Khurana, 2007).

The stage of pterygium is:

a. Grade I : not pass the limbus

b. Grade II : passed the limbus but not reach the pupil

c. Grade III : covered the pupil

d. Grade IV : pass the pupil

Complications like cystic degeneration and infection are infrequent.

Rarely, neoplastic change to epithelioma, fibrosarcoma or malignant melanoma,

may occur. (Khurana, 2007)

Pterygium must be differentiated from pseudopterygium.

Pseudopterygium is a fold of bulbar conjunctiva attached to the cornea. It is

formed due to adhesions of chemosed bulbar conjunctiva to the marginal corneal

ulcer. It usually occurs following chemical burns of the eye. (Khurana, 2007)

The treatment for pterygium is including medicamentous and non-

medicamentous:

a. Protect eyes from sun, dust, and wind (e.g., sunglasses or goggles if

appropriate).

b. Lubrication with artificial tears four to eight times per day to reduce ocular

irritation.

c. For an inflamed pterygium:

Mild: Artificial tears q.i.d.

Moderate to severe: A mild topical steroid . A non-steroidal anti-

inflammatory drop may be used 2 to 4 times per day to decrease

symptoms.

d. If a delle is present, then apply artificial tear ointment q2h.

Surgical excision is the only satisfactory treatment, which may be

indicated for: (1) cosmetic reasons, (2) continued progression threatening to

encroach onto the pupillary area (once the pterygium has encroached pupillary

area, wait till it crosses on the other side), (3) diplopia due to interference in

ocular movements. (Khurana, 2007)

Recurrence of the pterygium after surgical excision is the main problem

(30-50%). However, it can be reduced by any of the following measures

(Khurana, 2007) :

a. Transplantation of pterygium in the lower fornix (McReynold's

operation) is not performed now.

b. Postoperative beta irradiations (not used now).

c. Postoperative use of antimitotic drugs such as mitomycin-C or

thiotepa.

d. Surgical excision with bare sclera.

e. Surgical excision with free conjunctival graft taken from the same eye

or other eye is presently the preferred technique.

f. In recurrent recalcitrant pterygium, surgical excision should be

coupled with lamellar keratectomy and lamellar keratoplasty.

CHAPTER III

CASE

1. Patient identity

Name : Mr. A

Sex : Male

Age : 70 years old

Address : Dusun Tanjung Rengas Sambas

Ethnic : Melayu

Job : Laborer

Religion : Moslem

Patient was examined on December 23rd, 2013

2. Anamnesis

a. Main complaint : Blurry vision in left eye.

b. History of disease : Patient complains blurry vision in left eye since 2

weeks ago after the patient stabbed by wire in the eyelid. The patient felt

pain in the eyelid, the eye is red, headache, dazzled (photophobia), the

patient didn’t get fever or has watery or purulent discharge in his eye.

c. Past clinical history: Patient claims that there is no history of the same

symptoms before. History of using contact lens (-), history of using

another drugs (-) {such as steroid, or topical traditional drug, etc}.

Hypertension history (-), DM history (-), another disease (-).

d. Family history : There are no one of his family have the same complaint.

3. General Physical Assessment

General condition : good

Awareness : compos mentis

Vital Signs:

Heart Rate : 56x/minute

Respiration freq. : 20x/minute

Blood Pressure : 130/80 mmHg

Temperature : 36 oC

4. Ophthalmological status

Visual acuity:

a. OD : 6/20

b. OS : 6/40

OD OS

Right eye Left eye

ortho Eye ball position Ortho

ptosis (-), lagoftalmos

(-), edema (-)

Palpebra ptosis (-), lagoftalmos (-),

edema(+)

Redness (+), discharge

(-) , fibrovascular

growth (+)

Conjunctiva Redness (+), injection (+)

cililary injection discharge

(-) , fibrovascular growth

(-)

Clear, edema (-), defect

(-), infiltrate (-)

Cornea edema (+), defect (-),

infiltrate (+)

clear, deep COA opaque, deep

Iris colour : brown

Pupil: circular, 3mm,

anisokor, reactive to

Iris and pupil Iris colour : brown,

posterior synechiae

Pupil: irregular, 6 mm,

++

+

+

+

+

+

+

++

+

+

+

+

+

+

OD OS

light anisokor, not reactive to

light

Clear Lens opaque

Clear Vitreous Clear

Normal papil with

demarcated edge, C/D

ratio 0,5

Fundus Normal papil with

demarcated edge, C/D

ratio 0,5

Eye ball movement

• Tonometry : not done

• Visual field test (confrontation) : Normal

• Ishihara test : Not done

• Fluorescein test : Not done

• Sensibility test : Positive

5. Resume

Patient complains blurry vision in left eye since 2 weeks ago after the

patient stabbed by wire in the eyelid. The patient felt pain in the eyelid, the

eye is red, headache, dazzled (photophobia), the patient didn’t get fever or has

watery or purulent discharge in his eye. He works as a laborer, that always

have contact with dust, dust from wood, wire, and etc.

Vital signs of this patient are in normal range only the blood pressure in

the prehypertension stage. Visual acuity of OD is 6/20, and OS is 6/40.

Eyelids are normal in right eye, but edema in left eye. Conjunctiva of the right

eye has fibrovascular growt called pterygium. Cornea of the left eye has

infiltrate, defect and edema. The anterior chamber is deep and clear in the

right eye and opaque and deep in the left eye. Iris is brown there is posterior

synechiae, pupil are anisokor, the right pupil is 3 mm in diameters and 6 mm

in left pupil and it’s not reactive to light. The lens is opaque in the left eye and

clear in the right eye. The vitreous is clear. The fundus is normal in the right

eye and left eye.

6. Diagnose

Working Diagnose:

OD : pterygium grade II

OS : anterior uveitis and traumatic cataract

Differential diagnose:

OD: pinguecula

OS: keratitis, panuveitis for anterior uveitis and senile cataract and

lens dislocation for traumatic cataract.

7. Plan for examination

Tonometry

USG

Full blood count

8. Treatment:

- Non medicamentous :

o Using of protective glasses, wear hat when the patient work

- Medicamentous :

OD

Artificial tears 3 x 1 topical

OS

o Prednisone oral 1-2 mg/kg/day 14 days, tapering off

o Prednisolone acetate 1% 2 drops 4 times /day

o Ranitidine 150 mg x 2 for 14 days

o Atropine 1% 2 drops x 4

o Combination of neomycin/polymixin B/gramicidin 2 drops x 6

(every 4 hours)

9. Prognosis

OD

Ad vitam : bonam

Ad functionam : bonam

Ad sanactionam : bonam

OS

Ad vitam : bonam

Ad functionam : dubia ad bonam

Ad sanactionam : bonam

CHAPTER IV

DISCUSSION

A man, 70 years old, work as a laborer. Patient complains blurry vision

in left eye since 2 weeks ago after the patient stabbed by wire in the eyelid.

The patient felt pain in the eyelid, the eye is red, headache, dazzled

(photophobia), the patient didn’t get fever or has watery or purulent discharge

in his eye. From the ophthalmic examination the visual acuity of OD is 6/20,

and OS is 6/40. Eyelids are normal in right eye, but edema in left eye.

Conjunctiva of the right eye has fibrovascular growt called pterygium. Cornea

of the left eye has infiltrate, defect and edema. The anterior chamber is deep

and clear in the right eye and opaque and deep in the left eye. Iris is brown

there is posterior synechiae, pupil are anisokor, the right pupil is 3 mm in

diameters and 6 mm in left pupil and it’s not reactive to light. The lens is

opaque in the left eye and clear in the right eye. The vitreous is clear. The

fundus is normal in the right eye and left eye.

Blurry vision is can caused from the refractive media such as cornea or

the lens, from uvea tract like iris, cilliar corpus, choroid, or the retina. The

patient felt pain in the eyelid because of there is inflammation in the eyelid

and in the eye after the patient stabbed by wire and corneal epithelial damage

typically produces a superficial sharp pain or foreign body sensation

exacerbated by blinking. The patien also complaint about photophobia.

Photophobia is intimately, likely inextricably, linked to pain sensation. The

trigeminal nerve and its nuclei are the primary mediators of pain sensation to

the head. The conjunctiva, cornea, sclera, and uvea (iris, ciliary body, and

choroid) are densely innervated with trigeminal fibers, and exquisitely

sensitive to pain. Any painful stimulus to these areas (e.g. iritis, uveitis)

invariably causes photophobia. The patient feel headache is caused by referred

pain from the eye.

The patient’s left eye is red because of cilliar injection. Ciliar injection

is dilatation of pericorneal blood vessel ( a. cilliar anterior) that can caused by

inflammation in the cornea, corneal ulcer, corpus alienum, inflammation in the

uveal tract, glaucoma, endophtalmitis or panophtalmitis. It is not clearly

discernible, brightly (purple) colored nonmobile vessels in the episclera near

the limbus and can accompanied with pain sensation, lacrimation,

photophobia, and pupil irregular in size.

From the ophthalmologic examination, the visual acuity is 6/20 for OD

and 6/40 for OS. Decreasing of visual acuity can caused by aging process

because the patient is 70 years old and in aging process there is weakness in

cilliary muscle and sclerosing of the lens that can cause weakness of the

accommodation process. Visual acuity also can decrease because of defect in

the cornea, opacity in the lens, inflammation in the uveal tract, retinal

impairment, etc. The visual acuity in the patient’s left eye decreasing suddenly

can caused by defect in the cornea like keratitis or corneal ulcer, or from the

uveal tract. Since the patient didn’t complaint about any discharge from his

eye, it can caused by inflammation in uveal tract such as anterior uveitis.

Uveitis is inflammation of the iris (iritis, iridocyclitis), ciliary body

(intermediate uveitis, cyclitis, peripheral uveitis, or pars planitis), or choroid

(choroiditis). Anterior uveitis is iritis and iridocyclitis. Uveitis can cause by

corneal infection, systemic infection like syphilis, tuberculosis, systemic

immunological disease like sarcoidosis, Vogt-Koyanagi-Harada, arthritis

rheumatoid, and trauma, etc.

The eyelid of patient left eye is edema, it can caused by inflammation

after the patient stabbed by the wire. Conjunctiva on the right eye has

fibrofascular growth called pterygium. Pterygium is Triangular fold of

conjunctiva that usually grows from the medial portion of the palpebral fissure

toward the cornea. Pterygium can caused by chronic irritation, dryness,

ultraviolet light exposure and previous history of trauma, the patient work as a

laborer who always contact with dust, sand, and dust from wood. The

pterygium is in grade 2: passed the limbus but not yet pass the pupil. The

patient doesn’t have any complaint to this.

Cornea of the left eye has infiltrate, defect and edema. It’s can caused

ecause there is inflammation in the cornea. In anterior uveitis, the infiltrate can

caused by chronic inflammation resulting debris in the anterior chamber that

stick to the inner surface of the corneal endothelium and make keratic

precipitate. The defect in the cornea is possibly the port of entry of the wire

that can caused inflammation to the iris (anterior uveitis) . The anterior

chamber is opaque and deep in the left eye can caused by accumulation of

inflammatory cell, debris or fibrin. Iris is brown and there is posterior

synechiae that is The iris is adherent to the lens in several places as a result of

previous inflammation, causing an irregular, fixed pupil. The adhesion may

alter the sphincter pupil’s muscle movement. So the pupil will be anisokor, as

seen in the pupil examination the right pupil is 3 mm in diameters, regular and

6 mm in left pupil, irregular and it’s not reactive to light.

Posterior Synechiae

The lens is opaque in the left eye and clear in the right eye. Opacity of

the lens can caused by cataract. Cataract is any opacity of the lens. Aging is

the most common cause of cataract, but many other factors can be involved,

including trauma, toxins, systemic disease (such as diabetes), smoking, and

heredity. Cataract can caused blurred vision but the patient didn’t complaint

about blurred vision in the left eye or “white eye” before so the most possible

cause for the opacity of the lens in the patient is trauma. The lens becomes

white soon after the entry of a foreign body or blunt trauma, since interruption

of the lens capsule allows aqueous and sometimes vitreous to penetrate into

the lens structure. Blunt trauma does not result in rupture of the capsule, may

cause an anterior and/or posterior subcapsular cataract or both. Initially, fluid

influx causes swelling and thickening of the lens fibers. Later the fibers

become less swollen; the anterior subcapsular region whitens and may develop

a characteristic flower-shaped pattern, or an amorphous or punctate opacity.

The vitreous is clear. The fundus is normal in the right eye and left eye. If the

vitreous body is unclear and the fundus can’t be seen, we can suspect it as

panuveitis that is involvement of vitreous body and retina/choroid.

The differential diagnose for pterygium grade II in OD is pinguecula

and pseudopterygium. Pinguecula appear as yellow nodules on both sides of

the cornea (more commonly on the nasal side) in the area of the palpebral

aperture. The nodules, consisting of hyaline and yellow elastic tissue, rarely

increase in size, but inflammation is common. Pseudopterygium is a fold of

bulbar conjunctiva attached to the cornea. It is formed due to adhesions of

chemosed bulbar conjunctiva to the marginal corneal ulcer. Psudopterygium is

not always in the palpebral aperture and the patient should has defect or ulcer

in the cornea before.

The differential diagnose for OS is keratitis and panuveitis . Keratitis

can caused by viral, bacterial, or fungal infection with or without trauma

before. The symptom is the patient feel usually blurred, there is watery or

purulent discharge, change in corneal surface related to cause, there is cilliar

injection and conjunctival injection, the pupil is normal or myosis but the

pupil still reactive to the light. In the patient, there is no discharge, and the

pupil is irregular and doesn’t reactive to the light so keratitis can be disregard.

Panuveitis is involvement of vitreous body and retina/choroid we should do

USG to see that. And for the traumatic cataract the differential diagnose is

senile cataract and traumatic lens dislocation. Since the opacity of the lens

happened after the patient stabbed by wire, the senile cataract can be

disregard. Small perforation caused by penetrating injury will close

immediately because of ephitelial proliferation so the opacity only in the small

area like found in the patient. Lens dislocation can occur after a trauma and

can be no symptom if the dislocation is partial but if the lens floating in the

vitreous the patient will have blurred vision and red eye. Iridodonesis, a

quivering of the iris when the patient moves the eye, is a common sign of lens

dislocation and is due to the lack of lens support. This is present both in

partially and in completely dislocated lenses. But in the patient, iridodonesis

cann’t be find.

The intraocular pressure should be measured in uveitis patient because

sometimes increasing of intraocular pressure is occur due to secondary

glaucoma. Or decreasing intraoccular pressure due to the inflammation-

induced decrease in aqueous production. Long-standing uveitis or cyclitic

membrane-induced ciliary body detachment may result in hypotony and

eventual phthisis bulbi. Full blood count is needed to know does the patient

has systemic infection.

The non medicamentous treatment in this patient is use eyeglasses when

the patient work to avoid exposure to dust, wood, foreign body, and ultraviolet

light. For the pterygium grade II in the OD, we can use artificial tears 3x1

daily topical to avoid dry eye. Surgical treatment is not indicated because the

pterygium hasn’t pass the pupil and the patient doesn’t complaint any

symptom like discomfort in the eye or vision impairment.

The treatment of uveitis has three main goals: to prevent vision-

threatening complications, to relieve the patient's complaints and, when

feasible, to treat the underlying disease. For the anterior uveitis in OS, we can

give systemic corticosteroid like prednisone 1-2 mg/kg/day 14 days, than we

do tapering off. Corticosteroid has the function to reduce the inflammation of

the eye by inhibit cyclo-oxygenase and lipoxygenase pathways, decrease

complement level, migration of lymphocytes, production of vasoactive amines

and interleukin, circulating monocytes and macrophage activity. As the

inflammation subsides, tapering of corticosteroids by 5-10 mg per week is

begun within two to four weeks of initiating therapy. For the topical therapy

we can use prednisolone acetate 1%. Topical therapy is only helpful in the

treatment of the anterior segment therapy. The side-effects and complications

of topical or systemic corticosteroids must be looked for at every follow-up

visit of the patient. The H2 blocker is given for prevent gastric ulcer.

Mydriatic agent is given to promote comfort by relieving spasm of the

ciliary muscle and pupillary sphincter and to break down recently formed

posterior synechiae. For this patient we could use intensive atropine 1%, 2

drops up to four times daily.

For the treatment of the ocular infection, and prevention for further

inflammation, we can give the combination of neomycin/polymixin

B/gramicidin combo, 2 drops every 4 hours (6 times a day) for 7-10 days.

CHAPTER V

CONCLUSION

A man 70 years old complaint blurred vision in the left eye after stabed by

wire. Examination show cilliar injection, irregular pupil and not reactive to light,

posterior synechiae, opacity in lens and the anterior chamber. In the right eye

there is fibrovascular growth until the limbus but the patient didn’t has any

complaint. The working diagnose is pterygium grade II for OD and anterior

uveitis and traumatic cataract for OS. The therapy include non-medicamentous

(wearing eyeglasses or hat when patient works) and medicamentous (artificial

tears for the right eye and systemic and topical corticosteroid, topical antibiotic

and mydriatic agent for the left eye).

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