CASE REPORT ANTERIOR UVEITIS

Created by : YULISA HANDAYANI I11109016

OPHTALMOLOGY DEPARTEMEN OF RSUD SOEDARSO FACULTY OF MEDICINE AND HEALTH SCIENCES TANJUNGPURA UNIVERSITY PONTIANAK 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, Created by :

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

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 Asburys, 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. (RiordanEva; 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 Bruchs 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 2050 years of age and accounts for 1020% 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, postoperative, 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. b.

Direct mechanical effects of trauma. Irritative effects of blood products after intraocular haemorrhage (haemophthalmitis).

c. d. e.

Microbial invasion. Chemical effects of retained intraocular foreign bodies 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 Anterior uveitis Primary site of inflammation Anterior chamber Include Iritis, Iridocyclitis,

Anterior cyclitis Intermediate uveitis Vitreous Pars Posterior Hyalitis Posterior uveitis Retina or choroid Focal, multifocal, or planitis, cyclitis,

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 and staphylococcus, The

streptococcus,

psuedomonas,

pneumococcus

gonococcus.

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 (Koeppes 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 56 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 eyeciliary 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 34 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 paleyellow 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 visionthreatening 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 nongranulomatous 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 antiinflammatory 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 624 months, after which gradual tapering and discontinuation of medication should be attempted over the next 312 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 Asburys, 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 flowershaped 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 Asburys, 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 nonmedicamentous:
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 antiinflammatory 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 Sex Age Address Ethnic Job Religion : Mr. A : Male : 70 years old : Dusun Tanjung Rengas Sambas : Melayu : Laborer : Moslem

Patient was examined on December 23rd, 2013

2. Anamnesis a. Main complaint b. History of disease : Blurry vision in left eye. : 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 didnt 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 Awareness Vital Signs: Heart Rate Respiration freq. : 56x/minute : 20x/minute : good : compos mentis

Blood Pressure Temperature

: 130/80 mmHg : 36 oC

4. Ophthalmological status Visual acuity: a. OD b. OS : 6/20 : 6/40 OD OS

Right eye ortho ptosis (-), lagoftalmos (-), edema (-) Redness (+), discharge (-) , fibrovascular growth (+) Conjunctiva Eye ball position Palpebra

Left eye Ortho ptosis (-), lagoftalmos (-), edema(+) Redness (+), injection (+) cililary injection discharge (-) , fibrovascular growth (-)

Clear, edema (-), defect (-), infiltrate (-) clear, deep Iris colour : brown Pupil: circular, 3mm,

Cornea

edema (+), defect (-), infiltrate (+)

COA Iris and pupil

opaque, deep Iris colour : brown, posterior synechiae

anisokor, reactive to light

Pupil: irregular, 6 mm, anisokor, not reactive to light

Clear Clear Normal papil with demarcated edge, C/D ratio 0,5

Lens Vitreous Fundus

opaque Clear Normal papil with demarcated edge, C/D ratio 0,5

Eye ball movement OD

+ + + +

OS
+ +

Tonometry Visual field test (confrontation) Ishihara test Fluorescein test Sensibility test

: not done : Normal : Not done : Not done : 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 didnt 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 its 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 Ad functionam : bonam : bonam

Ad sanactionam : bonam

OS Ad vitam Ad functionam : bonam : 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 didnt 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 its 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 patients 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 patients left eye decreasing suddenly can caused by defect in the cornea like keratitis or corneal ulcer, or from the uveal tract. Since the patient didnt 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. patient doesnt have any complaint to this. The

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

Cornea of the left eye has infiltrate, defect and edema. Its 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 pupils 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 its 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 didnt 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 cant 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 doesnt 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 cannt 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 inflammationinduced 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 hasnt pass the pupil and the patient doesnt complaint any symptom like discomfort in the eye or vision impairment. The treatment of uveitis has three main goals: to prevent visionthreatening 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 didnt 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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