 ANATOMY

Regions

The uvea lies between the corneosclera (outermost layer of the eye) and the
retina (innermost layer/in the back of the eye). It is traditionally divided into 3
or 4 regions, the iris, ciliary body, pars plana and choroid. These
distinctions are based on their different structures as seen under light
microscopy, and continued use of these terms is appropriate in anatomical
studies. For clinical use, the terms anterior uvea (ie, iris and ciliary body) and
posterior uvea (ie, choroid) are now in common use, since diseases often
spread beyond a single anatomical region of the uvea.

Histology

In general the uvea consists of a pigmented, highly vascular loose fibrous

tissue. The pigment is produced and held in numerous dendritic melanocytes,
similar to normal dermal melanocytes. The blood vessels show patterns which
are specific to the region of the uvea, ( iris, ciliary body, pars plana and
choroid). The stroma also contains large nerves, which are branches of the
posterior ciliary nerves. They enter the eye around the optic nerve, and
run forwards in the uvea to reach their termination in the cilary body or iris.
These parts of the uvea also contain smooth muscle.

 What is uveitis

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Uveitis is a general term denoting intraocular inflammation that either primarily
or secondarily involves one (or more) components of the uveal tract. Although
components of the uveal tract are comprised of the iris, ciliary body, and
choroid, all layers of the eye may be involved by inflammation. Because the
uveal tract is supplied by the systemic circulation, systemic diseases and local
diseases that affect blood vessels can involve the uvea as well as contiguous
ocular tissues and structures.

 CLASSIFICATION

 Importance Of Classification

Classification and standardization of uveitis is important, as it enhances the

precision and comparability of clinical research from different centers and
assists in the development of a complete picture of the course of the disorders
and their response to treatment. Attempts have been made to standardize
some aspects of uveitis, and various classification criteria, inflammation
grading schema, and outcomes criteria have been described.

Uveitis may be classified in a number of ways, according to several systems

and multiple descriptors. Mastering one, solid, replicable process to best
evaluate, diagnose, and treat patients with intraocular inflammation is
essential for the astute clinician dealing with ocular inflammation.

 The most commonly used classification

The most widely used classification of uveitis was devised by the International
Uveitis Study Group (IUSG) in 1987 based on the anatomical location of the
inflammation.

In 2005, the Standardization of Uveitis Nomenclature (SUN) Working Group

devised additional classification criteria for uveitis. The consensus by the group
members was that an anatomical classification of uveitis should be used and
that this classification should serve as a framework for subsequent work on
diagnostic criteria for specific uveitic diagnoses. A standardized grading
schema for anterior chamber cells, anterior chamber flare, and vitreous haze
was developed. Outcomes and results reporting were also standardized.

 Classification parameters

Uveitis may be classified according to numerous parameters, to include the

following:

1. Patient demographics
2. Location of the inflammatory process (anatomical)
3. Duration, onset, and course of inflammation
4. Clinicopathological classification
5. Etiology of the inflammation

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 The intellectual exercise of naming each parameter allows the clinician to focus
upon those diagnoses most likely attributed to each patient's disease. Thus, a
specifically tailored, cost-effective uveitis evaluation may be obtained to
further process the differential for a given constellation of parameters.

1. Patient demographic

Demographic information provides essential data in formulating a differential

diagnosis. Age, sex, sexual orientation, race, geographic location, travel
history, social habits, and occupation all contribute to the diagnostic synthesis.
Therefore, a thorough and comprehensive history is the most important
component of the uveitis workup.

Age

The age of the patient often is helpful in focusing the differential diagnosis.

 Common types in Children → Juvenile idiopathic arthritis (JIA),

retinoblastoma, and toxocariasis
 Common types in Young adults → Fuchs heterochromic iridocyclitis,
multiple sclerosis, Behcet syndrome, acute posterior multifocal placoid
pigment epitheliopathy (APMPPE), and pars planitis
 Common types in Middle aged patients → Reiter syndrome, ankylosing
spondylitis, birdshot retinochoroidopathy, and VKH syndrome
 Types occur at any age → Tuberculous and luetic uveitis
 Elderly patients rarely present with primary uveitis.

Sex

The sex of the patient may provide useful information.

 Uveitis associated with ankylosing spondylitis, Behcet syndrome, and

Reiter syndrome is more common in males.
 while uveitis associated with JIA more frequently occurs in females.
 Fungal endophthalmitis and sympathetic ophthalmia are more common
in males due to either injury or intravenous drug use.
 However, most uveitic syndromes have no particular sexual or racial
predilection.

Race

The race of the patient may focus the differential even further.

 Human leukocyte antigen B27 (HLA-B27)–associated arthritides are more

common in whites and include ankylosing spondylitis, psoriatic arthritis,
and Reiter syndrome.
 Sarcoidosis most commonly presents in blacks.
 VKH is seen mostly in patients of Asian and American Indian descent.
 Behcet syndrome is a disease of the ancient Eurasian silk route, from
China to Turkey.
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  However, most uveitic syndromes have no particular sexual or racial
predilection.

Sexual habits

Sexual orientation may play a role in diagnosis because young, sexually active
males are more likely to contract HIV and other AIDS-related infections, such as
cytomegalovirus (CMV) retinitis, Kaposi sarcoma, or herpes zoster
ophthalmicus. Sexually active individuals are also at increased risk of
contracting a sexually transmitted disease, such as syphilis or gonorrhea,
which may cause a primary uveitis, or chlamydia, which itself may trigger a
HLA-B27-related uveitis.

Geographic history

When suspecting infectious etiologies of uveitis, it is wise to adequately

address the geographic location and recent travel of the patient. The endemic
nature of histoplasmosis within the Mississippi-Ohio-Missouri River valleys
should make the ophthalmologist suspicious of this illness in patients from that
area. Histoplasmosis also is relatively localized to the 45° north and 45° south
latitudes worldwide. Histoplasmosis is not endemic to Australia, New Zealand,
Europe, England, or Japan. Coccidioidomycosis is found predominantly in the
southwest United States.

Family history

Family history is important, as some diseases have a genetic predisposition or

there may be a greater likelihood that a particular disease will develop by
direct transmission from a family member. For example:

 Inflammatory diseases, such as ankylosing spondylitis, Reiter syndrome,

and inflammatory bowel disease, develop in families with HLA-B27.
 Ocular toxoplasmosis is usually a late result of congenital transmission.
 A history of infectious diseases (eg, tuberculosis) in a family is helpful
when such an entity is suspected.

Social habits

A history of ingestion of raw or undercooked meat is important in arousing

suspicion for ocular toxoplasmosis. Contact with feline feces containing oocytes
of Toxoplasma gondii may occur in the handling of cat litter or by playing in
sand boxes. If ocular toxocariasis is suspected, a history of contact with
unwormed cats or dogs is important

Contagious disease exposure

Leptospirosis infection has an increased incidence in sewer workers and those

with exposure to rodent urine. Other cases include a history of exposure to
contaminated water. A history of exposure to a patient with active tuberculosis
may assist in the diagnosis when tuberculosis is being considered as a possible
cause of uveitis.
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 When sexually transmitted diseases, such as syphilis, AIDS, and Reiter
syndrome, are being considered, a directed sexual history, including inquiring
about previous sexually transmitted diseases, genitourinary symptoms, and
sexual practices, may obviate an expensive diagnostic workup. Additionally, a
history of intravenous drug abuse may be useful in arriving at a smaller
differential diagnosis.

Travel history

Travel and immigration are important components of the uveitis history. Past
exposure to tuberculosis or dysentery may be directly related to a recent or
recurrent ocular inflammatory episode. Exposure to malaria, yellow fever,
typhoid fever, hepatitis A, B, and C, as well as trachoma, leprosy, or
onchocerciasis must be considered in rare cases. The local immigration and
health departments may provide critical information regarding endemic
diseases in specific travel and immigration destinations.

Occupational exposure

Occupational and hobby exposure may provide useful clues to the determined
diagnostician, particularly in the farming or animal husbandry environment.
Brucellosis may occur in livestock workers and slaughterhouse workers, while
some cases of brucellosis are caused by consumption of unpasteurized milk
products. Leptospirosis previously was seen in miners or sewer workers;
however, most cases today follow exposure to water contaminated by domestic
animals carrying the bacteria. Chlamydia psittaci infection results from parrot
exposure. Cat scratch disease caused by Bartonella henselae infection and
toxoplasmosis can follow feline exposure.

2. Location of the inflammatory process

The anatomical location of the inflammatory process is one of the most

important clues to pathogenesis and treatment.

Anterior uveitis

 Anterior uveitis comprises inflammation, primarily affecting the anterior

segment, and includes iritis, iridocyclitis, and anterior cyclitis.
 It is the most common form of intraocular inflammation.
 In a general or comprehensive ophthalmology practice, most patients
presenting do not have an underlying systemic disease. Instead, usually
at least 50% of the patients presenting with inflammation have
predominantly anterior disease caused by either trauma or, most
commonly, an idiopathic postviral syndrome. Most physicians and
authors do not perform a thorough systemic diagnostic evaluation in
patients with first episode mild-to-moderate anterior segment
inflammation in the absence of systemic disease or complaints. The
directed uveitis history is key in this situation.

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  Uveitic syndromes associated with primarily anterior segment
involvement include HLA-B27 syndromes, herpes simplex and herpes
zoster disease, Fuchs heterochromic iridocyclitis, and many arthritic
syndromes. Secondary iatrogenic disease often is seen postoperatively,
particularly following complications of surgery, trauma, scleral or seton
implants, corneal transplants, capsular disruption, or fixed haptic and iris
fixated intraocular lens implantation.

Intermediate uveitis

Middle uveitis, cyclitis, intermediate uveitis, pars planitis, peripheral uveitis, or

chronic cyclitis often indicates a more severe form of ocular inflammation than
isolated anterior disease.

According to the SUN classification system,

 the term intermediate uveitis is used when the primary site of

inflammation is in the middle portion of the globe and includes posterior
cyclitis, hyalitis, choroiditis, and chorioretinitis.
 Pars planitis should be used only for that subset of intermediate uveitis
where there is snowbank or snowball formation occurring in the absence
of an associated infection or systemic disease (ie, idiopathic).
 If there is an associated infection (eg, Lyme disease) or systemic disease
(eg, sarcoidosis), then the term intermediate uveitis should be used.
 Sometimes, spillover uveitis (middle inflammation or anterior vitreous
cells) may occur, indicating that the primary source of disease is anterior.
 Intermediate uveitis or cyclitis is commonly associated with major
granulomatous diseases (eg, tuberculosis, sarcoidosis, Lyme disease,
lues).

Posterior uveitis

Posterior uveitis is inflammation of the choroid and the retina and

includes retinochoroiditis, retinitis, and neuroretinitis.
 Spillover into the adjacent choroid, creating a retinochoroiditis or a
chorioretinitis, may occur.
 Retinitis typically manifests by toxoplasmic or herpetic infection.
 Choroiditis may occur with any of the granulomatous uveitides (eg,
tuberculosis, sarcoidosis, Lyme disease, lues), histoplasmosis, or more
unusual syndromes, such as birdshot or serpiginous chorioretinitis.
 Papillitis may occur with toxoplasmosis, viral retinitis, lymphoma, or
sarcoidosis.

Panuveitis (diffuse)

 The term panuveitis is reserved for those situations in which there is no

predominant site of inflammation, but inflammation is observed in the
anterior chamber, vitreous, and retina and/or choroid (ie, retinitis,
choroiditis, retinal vasculitis).

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 Diffuse uveitis, panuveitis, or endophthalmitis generally occur with
overwhelming infections, such as infantile toxocariasis, postoperative
bacterial endophthalmitis, or severe toxoplasmosis.

 Many of the granulomatous uveitides may produce a highly disseminated

pattern, especially when delayed diagnosis occurs

3. Clinicopathologic classification

I) Suppurative

o It is an inflammation characterized by polymorphonuclear cellular

infiltration
o The purulent infection may be due to staphylococci, streptococci,
pneumococcal, meningococci, gonococci, b.pyocyanea, b.proteus, or
b.coli.
o According to the source of infection, suppurative uveitis may be:
a) Exogenous : postoperative or perforating injury
b) Secondry to an eye lesion as acomplication of corneal ulcer
c) Endogenous ( metastatic ) infection is rare
Suppuritive uveitis may be present as one of the following clinical types
a) Localized suppuritive uveitis :
Anterior uveitis : suppuritive iritis
suppuritive iridocyclitis
Posterior uveitis : suppuritive choroiditis
b) Diffuse suppuritive uveitis : endophthalmitis
panophthalmitis

II) Exudative

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 o It is inflammation characterized by lymphocytes and plasma cell
infilteration
o It may be sub acute or chronic and is rarely recurrent.
o According to the source of inflammation, it may be:
a) Exogenous
Infection :virus or bacteria oflow virulance
Trauma : injury, or operative
Chemicals : corrosives, acids or alkalis.
b) Secondry to other lesions : intraocular haemorrhage
Subretinal fluid in retinal detachment
Degeneration in intraocular tumours
c) Endogenous : allergic, collagen disease, skin disease, focal infectionor
metabolic diseases
Clinically exudative uveitis may be
a) Localized exudative (serous or plastc) uveitis:
Anterior: exudative iritis, exudative cycitis, exudative iridocyclitis.
Posterior : exudative choroiditis
b) Diffuse exudative uveitis (rare) : diffuse choroiditis
Exudative pan uveitis

III) Granulomatous

o Definition It is chronic inflammation characterized by infilteration eith

histiocytes, epithiliod cells, giant cells, lymphocytes and plasma cells
arranged in nodules or granuloma.
o The center of granuloma is formed of histiocytes and macrophages
and it is periphery is formed of lymphocytes and plasma cells.
o Pathophysiology :--The exact pathophysiology of granulomatous iritis
is unknown. It may result from an autoimmune reaction or from the
host's immune response to a systemic infectious process, such as
syphilis, Lyme disease, tuberculosis (TB), or local reactivation of
herpetic viral infection.
o According to the source of inflammation, it may be :

1. Exogenous : retained intraocular organic foreign body

2. Secondry to eye lesions : lens matter
Keratitis or scleritis ( syphilitic, tuberculous or
leprotic )
3. Endogenous : specific infection, vogt-koyanagi-harada disease,
sarcoidosis, juvenile xanthogranuloma, sympathetic ophthalmia.
Clinically gralomatous uveitis may be
a) Localized :
Anterior : nodular iritis, granulomatous cyclitis, granuloamtus
iridocyclitis
Posterior: granulomatous choroiditis
b) Diffuse : granulomatous pan uveitis
Complicated by
1. Visual impairment .
2. Complicated Cataract.
3. Secondary glaucoma.
4. Corneal decompensation.
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 5. Chronic cystoid macular edema.

4. Etiology of the inflammatory process

When diagnostic testing has been performed, the specific etiology of the
underlying process may be identified. Sometimes, only the category, but not
the actual cause of inflammation may be known. This knowledge alone may be
sufficient to initiate appropriate therapy. For instance, when history rules out
trauma, age rules out ischemia, and comprehensive serologies rule out
infection in the presence of arthritis, systemic anti-inflammatory therapy may
begin despite the absence of a specific diagnostic syndrome.

Etiology provides the ultimate classification system. A useful technique to

classify an inflammatory process, or any process within the eye for that matter,
uses the 7 "I" system. This system places every source of ocular inflammation
into 1 of 7 categories, with an eighth case for the process of elimination and
frustration when all diagnostic means fail to reveal a specific etiology, as
follows:

1. Inflammatory - Primary autoimmune disease

2. Infectious - Due to known ocular and systemic pathogens
3. Infiltrative - Referring to invasive neoplastic processes
4. Injurious - Trauma commonly seen in general offices
5. Iatrogenic - Surgery, inadvertent trauma, or medication
6. Inherited - Metabolic or dystrophic disease
7. Ischemic - Impaired circulation can cause inflammation
8. Idiopathic

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 A diagnosis of idiopathic uveitis implies not only that a thorough, specific,
tailored, cost-effective diagnostic workup was performed, but it also implies
that treatable infectious diseases have been acceptably ruled out.

 Clinical Picture and complication Different Types Of

Uveitis:

 The most commonly used parameter of classification is the anatomical

classification.

 Thus each part of the uveal tract ( iris, ciliary bdy, choroid ) may be
inflamed.
 So there is iritis, cyclitis, and choroiditis.
 Each may be ( exogenous, secondary to eye lesion, or endogenous
according to the source of inflammation)
 And may be ( suppuritive, exudative or granulomatous ) according to the
pathology of disease.
 And may be ( localized or diffuse ) according to the clinical state of the
disease

Anterior uveitis ( iritis, cycltis and iridocyclitis

 Iritis
Iritis is usually of exudative endogenous type. and it may be suppuritive , but rarely to
be granulomatous

 Symptoms

1. Diminished Vision : due to turbidity of the aquous, exudates covering

the lensor occluding the pupil, reflex spasm of the ciliary muscle
(irritative myopia) or secondry glaucoma

2. Red Eye due to ciliary injection

3. Pain { dull aching of the involved eye and surrounding orbit }.

4. Photophobia excessive tearing

5. Refered Headache along the distribution of the ophthalmic nerve

6. History of similar attacks

 Signs

1. Eye Lids :mild to moderate congestion of the lids, resulting in

pseudoptosis
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2. ciliary injection

3. K. ps (keratic precipitates) { Small to medium in nongranulomatous iritis

while large with a greasy or "mutton-fat" granular appearance in granulomatous
iritis.

4. Aquous flare : early sign to appear

5. Iris :muddy iris

Lost iris pattern ( as iris furrows and crypts are ffilled with fibrinous or purulent
exudates

Iris also show Inflammatory nodules (Koeppe and Busacca) In granulomatous

Uveitis

6. Koeppe nodules are found at the pupillary border. Busacca nodules are located
on the surface of the iris

7. Hypopyon { in severe cases}

8. Peripheral anterior synechiae and posterior synechiae form between the

pupil margin and the lens iris bombé

9. Cystoid Macular Edema { in severe cases }

10.Pupillary Miosis

11. Intraocular Pressure :

• may be diminished because of ciliary body dysfunction {in

acute cases }

• may be increased because of acute trabeculitis and iris bombé

12. Inflammatory by-products may accumulate in the trabeculum { in

chronic cases. }+

 Prognosis

o Suppuritive Iritis may resolve completely or usually ends with

endophthalmitis or panophthalmitis

o Exudative Iritis may resolve spontaneously but usually recure again

and again

o Granulomatous Iritis is achronic destructive lesion which may end with

keratitis, cyclitis, pan uveitis or sclera necrosis

 Complication

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 1. Cornea : ring abcess, interstial keratitis or PAS

2. Secondry Glaucoma (due to iris bombi)

3. Iris Atrophy

4. Distortion Of The Pupil

5. Complicated Cataract : complicated anterior cortical catarct in relation

to synechia or complicated posterior cortical catarct

6. Spread Of Inflammation to ciliary body

D.D acute iritis from acute glaucoma

 Cyclitis
o It is rarely acute but usually chronic insidious

o It is usually of endogenous cause from the exudative type but may be

granulomatous

o Suppuritive cyclitis is not a separate entity but it is usually a part of

suppurative iridocyclitis

 Symptoms

1. Mainly deterioration of vision

2. Also symptoms of irritation are present as photophobia, lacrimation

and blepharospasm

3. Condition may be recurrent and of long course

 Signs
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 1. Ciliary injection : not marked

2. Tenderness over the region of the ciliary body

3. Aquous flare and few K.PS

4. A.C : appear deep when retinal detachment occur as acomplication

5. PUPIL : irregular – sluggish reactive – posterior synechia

6. Cyclitic membrane : due to exudation in the retrolental space when it

contracts it will cause R.D

7. Tension : in the uncomplicated cases it is usually soft due to the

serous detachment of the ciliary epithelium

 Complication

1. Retinal detachment : exudative or secondry to cyclitic membrane

2. Retinal vasculitis, macular edema and degeneration or optic neuritis

3. Complication of synechia and cyclitic membrane

4. Atrophy of ciliary body → atrophia bulbi

5. Complicated posterior cortical cataract

 Iridocyclitis

o It is the common presenting clinical picture of inflammation of the iris

and ciliary body because pure iritis or cyclitis is rare.

o It may be granulomatous or non granulomatous ( suppuritive or

exudative )

o It may be exogenous but commonly endogenous

o It may be acute or chronic and is usually recurrent

A. Acute Nongranulomatous Anterior Uveitis

Acute nongranulomatous anterior uveitis often is associated with the
histocompatibility antigen HLA-B27 and linked with a predisposition
for developing ankylosing spondylitis.
Ninety percent of the patients who have the two diseases
concomitantly are also positive for the HLA-B27 marker.
Other diseases associated with this form of acute ocular
inflammation include ulcerative colitis, Crohn's disease, Reiter's
syndrome, psoriatic arthritis, and gastroenteropathies secondary to
Yersinia and Klebsiella pneumoniae infections.

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 These disease associations should be looked for in any individual
presenting with acute nongranulomatous anterior uveitis.
The HLA-B27 genotype is often the link that binds them together.
B. Chronic Iridocyclitis of Juvenile Rheumatoid Arthritis
Chronic iridocyclitis associated with juvenile rheumatoid arthritis is
an indolent, smoldering disease that usually begins between ages 3
and 15, occurring more often in girls than boys.
Signs and symptoms and complications of iridocyclitis are the
combination of those of the iritis and cycclitis. Vision is markedly
diminished, pain is more severe and the signs involove the anterior
and posterior segments. Complications are expected and of serous
prognosis. Condition is usually bilateral

Intermediate uveitis

 Pars planitis
o Bilateral ocular inflammatory disease

o Usually affect adolescents

o It is also called peripheral uveitis and chronic cyclitis

 Symptoms

1. floaters → it is the main complaint of patient in pars planiti, it is due

to the inflammatory celluler reaction in the vitrous

2. minimal pain, redness, and photophobia

3. diminished vision { if macular edema occurs }

 Signs

1. Minimal aqueous cell and flare { anterior cellular activity may be

more pronounced in children and in patients with multiple sclerosis }

2. Snow banking : whitish yellow exudative material on the peripheral

retina and the pars plana or (snowballs : clumps of inflammatory
cells )

3. Retinal periphlebitis and edema of the disc and macula { in patients

with active pars planitis }

4. Cataracts, especially posterior subcapsular

 Complications

1. Posterior Vitreous Detachment

2. Cystoid Macular Edema

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 3. Retinal Neovascularization { as a result of ischemia } causing
vitreous hemorrhages and vitreous fibrosis can cause traction on the
peripheral retina and lead to retinal detachment

4. Optic nerve edema

5. A vascular cyclitic membrane can exercise traction on the ciliary body

and lead to hypotony and phthisis bulbi.

 Fuchs' Heterochromic Cyclitis

o It is usually unilateral inflammatory disease that affect the anterior or the
intermediate part of the uvea
o It usually affect the adult age in female more than males.
o It is chronic in its course
 Symptoms are minimal and include floaters
 Signs include low-grade aqueous cell and flare reaction, stellate, white,
granulomatous KPs, heterochromia

 Complication include posterior synechiae are rare, glaucoma and

cataract formation

Posterior uveitis (choroiditis)

Pathologically it may be:

 Purulent
 Exudative

 granulomatous

Etiologically : it may be a part of systemic disease or syndrome as the

following:
 Toxoplasmosis
 Sarcoidosis

 Syphilis

 Behçet disease

 Histoplasmosis

 Toxocara

 Symptoms. Patients are free of pain, although they report blurred vision
and
floaters.

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 Signs: Ophthalmoscopy reveals isolated or multiple choroiditis foci. In
acute disease they appear as ill-defined white dots. Once scarring has
occurred the foci are sharply demarcated with a yellowish-brown color.
Occasionally the major choroidal vessels will be visible through the
atrophic scars. No cells will be found in the vitreous body in a primary
choroidal process.
However, inflammation proceeding from the retina (retinochoroiditis) will
exhibit cellular infiltration of the vitreous body.
 Complication.

1. Destruction of the retina, retinitis or chorioretinitis, follows destruction of

choriocapillaries and Bruch's membrane.

2. Spread of inflammation to the anterior uvea.

3. Neuritis and optic atrophy

4. Complicated posterior cortical cataract

5. Scleritis specialy in granulomatous lesions.

 Prognosis.The inflammatory foci will heal within 2–6 weeks and form
chorioretinal scars. The scars will result in localized scotomas that will
reduce visual acuity if the macula is affected.
Now we are going to discuss choroiditis according to its pathological picture
( suppuritive, exudative and granulomatous)

 Suppuritive choroiditis

Clinicopathologically it may be:

 Diffuse due to exogenous or endogenous cause
In exogenous cases, aretained foreign body in the posterior segment
carries the infection and a suppuritive retinitis ocurr first then followed
by suppuritive choroiditis. In endogenous metastasis, the infection start
in choroid

 Localized purulent choroiditis (rare) secondry ot metastatic emboli with

purulent organism .the lesion may be single or disseminated. Rarely, it
resolves but usually become diffuse

 Exudative choroiditis

o The commonest type

o The lesion may be

1. Diffuse involving a large area of choroid. It is usually due to syphilis or

tuberculosis. The lesion is greyor yellow, and the overlying retina is
16
 edematous. The lesion heal with a white scar. Pigment hypertrophy
within the lesion may be extensive and give apicture similar to retinitis
pigmentosa but pigmentations is irregular and in clumps. Ring scotoma
and night blindness are characteristic in both lesions.

2. Dissiminated : lesions are scattered and inbetween the healthy

choroid. An active lesion is a yellowish elevation under aretinal vessel. A
healed lesion is a scar with a pigmented margin due to chorioretinal
atrophyand fibrosis with hypertrophy of pigment epithelium of the
retina. The optic disk show secondary optic atrophy and vessels are
attenuated. dissiminated choroiditis may be anterior (peripheral) or
posterior (central).

3. Localized (circumscribed) : a large patch ( about one disk diameter)

may be seen. It may be single or multiple. There are K.Ps and vitrous
turbidity

a) Juxtapapillary choroiditis (of JENSEN) is alocalized choroidal lesion

near the optic disk. when it is nasal, there is a sector shaped
scotoma. When it affects the arcuate fibres, a bjerrum scotoma
results and if the papilla-macular bundle is destroyed, a cacco-
central scotoma results.

b) Central (macular) choroiditis : there is an obsolete central scotoma,

lesion is seen in congenital toxoplasmosis .

 Granulomatous choroiditis

o This due to tuberculosis, syphilis, sarcoidosis or brucellosis.

o It may be diffuse, disseminated or localized.

o Caseaton may ocurr ending with destruction of the eye and phthisis
bulbi

Diffuse uveitis

 Endophthalmitis
Definition: This refers to acute or chronic intraocular inflammation of Microbial
or immunologic causes .In the strict sense, any intraocular inflammation is
endophthalmitis. However, in clinical usage endophthalmitis refer to diffuse
suppuritive choroiditis with a secondary abcess in the vitrous, and suppuritive
retinitis.

Etiologically endophthalmitis may be due to :

a. Exogenous infection : following retained intraocular foreign body or
postoperative, exogenous endophthalmitis is more violent while
endogenous endophthalmitis may be chronic or insidious
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 b. Secondary (as a complication of) to iridocyclitis or astage of
panophthalmitis

c. Endogenous metastasis :the second most common cause after

exogenous.

 Symptoms.

a) Acute vitreous inflammation or endophthalmitis. Characteristic

Symptoms include
1. acute loss of visual acuity accompanied by
2. deep dull ocular pain that responds
3. Severe reddening of the conjunctiva is present.
4. Amaurotic cat's eye reflex where the whitish or yellowish appearance
of the pupil of the child attracts the attention of the mother
In contrast to bacterial or viral endophthalmitis, mycotic endophthalmitis
begins as a subacute disorder characterized by slowly worsening chronic
visual impairment. Days or weeks later, this will also be accompanied by
severe pain.
b) Chronic vitreous inflammation or endophthalmitis: The clinical course is
far less severe, and the loss of visual acuity is often moderate.

 Signs
1. Amauritic cat's eye reflex

2. K.PS, aquous flare, hypopyon and ciliary injection

3. There is no proptosis or limitation of eye movement (D.D from

panophthalmitis).

4. Red reflex is absent and examination of the posterior segment reveals

a yellow or white reflex with cyclitic membrane and total detachment
later on

5. The eye gradually atrophies and exacerpation of inflamtion may ocurr.

6. Vision is lost due to destruction of the retina or choriocapillaries.

 Complications
1. Panophthalmitis

2. Pseudo glioma

3. Atrophia bulbi

4. Act as aseptic focus to the other eye.

 Clinical course and prognosis. The prognosis for acute microbial

endophthalmitis depends on the virulence of the pathogen and how

18
 quickly effective antimicrobial therapy can be initiated. Extremely virulent
pathogens such as Pseudomonas and delayed initiation of treatment (not
within a few hours) Worsen the prognos is for visual acuity. With
postoperative inflammation and poor initial visual acuity, an immediate
vitrectomy can improve the clinical course of the disorder. The prognosis is
usually far better for chronic forms and secondary vitreitis in
uveitis/vitreitis.

Endogenous endophthalmitis Exogenous endophthalmitis

Endogenous endophthalmitis is usually
associated with systemic infection. In
immunocompromised individuals, such as
those receiving long-term intravenous
therapy or hyperalimentation or those
debilitated from other causes, an infectious
nidus of bacteria or fungi reaches the eye
through the choroidal or retinal circulation.
The initial symptoms may be minimal, such
as spots and floaters. Severe visual loss may
result from opacification of the vitreous; full-
thickness inflammation of the retina, choroid,
and sclera; and opacification in the anterior
segment. Initially, the findings may mimic
acute nongranulomatous anterior uveitis, but
the rapid progression and the nature of the
clinical picture are usually characteristic of
endogenous endophthalmitis
D.D from : panophthalmitis & tenonitis
Exogenous endophthalmitis refers to
intraocular infection, usually bacterial,
which occurs after intraocular surgery or
penetrating ocular trauma. The offending
agents can occur from many sources,
although the usual source in postsurgical
endophthalmitis is patient flora or
contamination of instruments or fluids,
yielding an infectious culture in the eye.
Depending on the series reported
The clinical features include
postoperative pain out of proportion to
normal postoperative healing within 24
hours to 1 week after surgery, a steamy
inflammation of the cornea with a
fibrinoid anterior chamber reaction, and
hypopyon (Fig. 8.64). The size of the
hypopyon often reflects the bacterial
load or aggressiveness of the offending
organism. Gram-positive bacteria, such
as Staphylococcus epidermidis, are some
of the more common causes of
postoperative endophthalmitis and
generally produce milder disease.
Staphylococcus aureus, Streptococcus
pneumoniae, and Gram-negative
organisms usually produce much more
severe clinical findings. The onset of
pain, redness, and hypopyon and,
sometimes, complete opacification of the
cornea with intraocular pus formation
can occur within 8 hours (Fig. 8.65).
Endophthalmitis after penetrating ocular
trauma can be caused by multiple
organisms, including Bacillus cereus, a
particularly virulent organism, which can
lead to rapid destruction of the eye

 Panophthalmitis
Definition it is diffuse suppuritive inflammation of all coats of the eye with
Tenon's capsule.it is dramatic acute inflammation that usually ends with
destruction of the eye.

19
Etiology :
a) Exogenous : after operation penetrating injuries, corneal ulcers, or an
infected trephining operation. Rarely an iris inclusion
b) Endogenous ( metastatic ) : some cases of panophthalmitis are
metastatic infections specialy in diabetes or during fevers such as
pneumonia, puerperal fever, or meningitis
c) Secondary ( as acomplication of ) to cavernous sinus thrombosis or
orbital cellulitis.

 Symptoms
There are severe pain in the eye, fever, general malaise, headache, swelling
of both lids bulging of eye, congestion of the conjunctiva and loss of vision.
 Signs
1. Proptosis and limitation of eye movement (D.D from endophthalmitis).
2. The lids are edematous and tender
3. Conj and ciliary injection with chemosis of conjunctiva which may bulge
as chemotic folds through the palpebral fissure.
4. The cornea, in exogenous cases shows a suppurating wound or a
perforated ulcer and in the endogenous group shows a ring abcess.
Finally, in both groups the cornea slouphs out with complete necrosis.
5. Total hypopyon masks a purulent iritis
6. Vision is lost

 Complication

1. Necrosis of the cornea and discharge of the purulent intraocular

contents which leads to phithisis bulbi

2. Sloughing of the sclera at the weak foramina and discharge of the

intraocular contents into tenon's capsule and the orbital tissues to
develop orbital cellulitis

3. Spread of infection through a spreading thrombophlebitis into the orbit

or the cavernous sinus.

4. Spread of infection through the meninges of the optic nerve leading to

meningitis or cavernous sinus thrombosis

5. Metastatic pyamic complication

6. Resolution of inflammation, spontaneously or after treatment with the

following complication

a. Atrophia bulbi or shrunken globe

b. Cyclitic membrane and retinal detachment (pseudo glioma).

c. All types of synechia with atrophy of the iris.

20
 d. Complicated cataract.

7. The shrunken eye remain irritated and acts as a septic focus.

8. Degenerative changes such as fatty degeneration and bone formation.

D.D from : endophthalmitis, tendonitis, orbital ceeulitis and cavernous sinus

thrombosis.

table Orbita Caverno tenoni endophthal panophthal

l us sinus tis mitis mitis
celluli thrombo
tis sis
Symptoms
• Pain ++++ ----------- ++++ ----------- ++++
• Loss of -------- ----------- --------- ++++ ++++
vision
• Diplopi ++++ ++++ ++++ -------- --------
a ++++ ++++ ++++ --------- ++++
• Proptos ++++ ++++ ++++ ------- ++++
------- ++++ -------- -------- --------
is
• Fever
• coma
Signs
• Prptosi ++++ ++++ ++++ --------- ++++
s +all Lat.rectus +all ---------- +all
• Limit
movme clear clear clear opaque opaque
nt seen seen seen yellow yellow
• Media good good good lost lost
• Fundus ++++ --------- ++++ ++++ ++++
+R.R
• Vision
• tendern
ess

Surgical draina tarsorrhap draina enucleation eviceration

ttt ge hy ge

 Sympathetic ophthalmia
Definition: Specific bilateral inflammation of the uveal tract due to chronic
irritation of one eye, caused by a perforating wound to the eye or intraocular
surgery, produces transferred uveitis in the fellow eye.
Epidemiology. Sympathetic ophthalmia is very rare.
Etiology. Sympathetic ophthalmia is currently thought to be an autoimmune
inflammatory response toward ocular antigens, specifically a delayed

21
hypersensitivityto melanin-containing structures from the outer segments of the
photoreceptor layer of the retina. The immune system, which normally is not
exposed to ocular antigens, is introduced to the contents of the eye following
traumatic injury. Once exposed, it senses these antigens as foreign, and begins
attacking them. The onset of this process can be from days to years after the
inciting traumatic event.

Clinical picture. Floating spots and loss of accommodation are among the
earliest symptoms. The disease may progress to severe iridocyclitis with pain
and photophobia. Commonly the eye remains relatively painless while the
inflammatory disease spreads through the uvea. The retina, however, usually
remains uninvolved, although perivascular cuffing of the retinal vessels with
inflammatory cells may occur. Papilledema, secondary glaucoma, vitiligo, and
poliosis of the eyelashes may accompany.
 Complications :-

1. iridocyclitis
2. Papilledema.
3. secondary glaucoma.
4. vitiligo, and poliosis
5. Optic nerve injury
 Differential diagnosis. The disorder should be distinguished from
iridocyclitis and choroiditis from other causes.

 Vogt-Koynanagi Harada Syndrome

Definition Vogt-Koyanagi-Harada (VKH) syndrome is a rare and unusual form of diffuse
granulomatous uveitis. This condition is usually more severe in more highly pigmented individuals.
In the United States, the VKH syndrome is seen most commonly in individuals of Native American
or Asian ancestry.
 Clinical Features

1. Acute serous detachment of the retina is the hallmark of the VKH syndrome (Fig. 8.41)
and may be accompanied by multiple areas of yellowish or yellowish-white edema of the
retinal pigment epithelium.
2. retinal vasculitis
3. swelling of the optic disc.
4. Associated anterior iritis may be severe and may be either granulomatous or
nongranulomatous in appearance.
5. Some patients will experience associated headache and stiffness of the neck or other
neurologic symptoms such as tinnitus.

6. With time, many patients will manifest associated dermatologic changes including poliosis
(whitening of the lashes) and vitiligo (patchy depigmentation of the skin). Neither the
vitiligo nor poliosis is generally present at the outset of the disease.

 Pathophysiology :-
-The etiologic and pathogenic factors in VKH syndrome remain unclear. The clinical course of
VKH syndrome with an influenza like episode suggests a viral or post-infectious origin. Some
studies invoke a possible role of Epstein-Barr virus reactivation in this disease. Although a viral
cause has been proposed, no virus has been isolated or cultured from patients with VKH syndrome.
22
Morris and Schlaegel found virus like inclusion bodies in the sub-retinal fluid of a patient with
VKH syndrome.
-Clinical and experimental data continue to support an immunologic etiology. An autoimmune
reaction seems to be directed against an antigenic component shared by uveal, dermal, and
meningeal melanocytes.

 BEHECET'S DISEASE
Definition Behecet's disease is a form of diffuse bilateral uveitis of unknown cause that is
associated with significant dermatologic and vascular features. It is found in young adults, and
although
rare in the United States, it is the most common form of uveitis in Japan. The ophthalmologist may
be the first to recognize the condition because of the unusual presentation and clinical findings.

Clinical Features
o Major features
 Recurrent aphthous ulceration of the oral mucous membrane
 Skin lesions - Erythema nodosum–like lesions, subcutaneous
thrombophlebitis, folliculitis (acnelike lesions), cutaneous hypersensitivity
 Eye lesions - Iridocyclitis, chorioretinitis, retinouveitis, definite history of
chorioretinitis or retinouveitis
 Genital ulcers
o Minor features
 Arthritis without deformity and ankylosis
 Gastrointestinal lesions characterized by ileocecal ulcers
 Epididymitis
 Vascular lesions
 Central nervous system symptoms
o Diagnosis
 Complete - Four major features
 Incomplete - (1) 3 major features, (2) 2 major and 2 minor features, or (3)
typical ocular symptom and 1 major or 2 minor features
 Possible - (1) 2 major features or (2) 1 major and 2 minor features

Uveitis and systemic diseases

Systemic diseases has a broad wide effect on the eye and the uvea because the uvea is supplied by
the systemic diseases. Systemic diseases mostly cause diffuse uveitis, with the consideration that
organisms show variation in the preferable site.

Systemic diseases affecting the eye can be classified into:

23
A. Bacterial Systemic
I) Tuberculosis
Tuberculosis is a chronic disease caused by Mycobacterium tuberculosis. Any organ system,
including the eye, can be affected. Ocular tuberculosis is rare, although it is becoming more
common with the advent of AIDS and the use of immunosuppressive agents in the treatment of
other diseases.

Clinical Features
o A posterior granulomatous choroiditis is the most common finding in ocular tuberculosis
(Fig. 8.47).
o Retinal vasculitis in the form of sheathing of the veins and arteritis is common.
o Blurred vision is usually the presenting symptom and is generally related to vitritis.
o Chronic iridocyclitis may also occur, although it may be solely immunologic in nature,
without active organisms.
o In overwhelming systemic infections, tuberculous endophthalmitis has been reported.
As with many of these rare conditions, a high index of suspicion is necessary for the initial
diagnosis. Skin testing and a chest radiograph are indicated as part of the ophthalmologist's workup,
but an internal medical consultation also is indicated before determining the diagnosis and
treatment.

II) Syphilis
Ocular syphilis may occur as both an acquired and a congenital form of disease, and can confuse the
uveitis diagnosis. In acquired syphilis, eye involvement can occur in the secondary, latent, and
tertiary phases of the disease. Untreated acquired syphilis and congenital syphilis are associated
with multisystem abnormalities.

Clinical Features
a) Acquired syphilis
o may be acute or chronic in nature, and are often
o granulomatous in character.
o Any portion of the ocular system may be involved.
o Some characteristic findings of acute ocular infection are
1. anterior uveitis,
24
 2. diffuse and focal chorioretinitis,
3. retinal vasculitis
4. optic neuritis (Fig. 8.45).
5. Late findings include interstitial keratitis, chorioretinal scars, (salt-and-pepper)‌
retinal pigment epithelial scarring, and optic atrophy.
6. The Argyll-Robertson pupil, which fails to react to light but preserves
accommodation, classically has been associated with syphilis. .
b) Congenital syphlis
o Ocular findings associated with congenital syphilis may include
1. anterior uveitis
2. chorioretinitis : is usually seen in the healed stage and pigmentation may take one or
more of the following pictures ::
a) salt and pepper fundus where pigmented spots lie on ayellowish bachground
and usually the lesion is peripheral.
b) Peripheral isolated pigmented spots.
c) Coarsely pigmented peripheral areas
d) Atrophic white patchs
3. interstitial keratitis
4. optic atrophy.
III)Gonorrreal uveitis
IV)Brucellosis
V) leprosy

B. Parasitic systemic
diseases

I) Toxoplasmosis
Causative organism : Toxoplasma gondii

Stages of the parasite : 1- sporocyst :excreted in cat's faeces

2- bradyzoites : present in tissues

3- tachyzoites : proliferate and causes tissue

destruction

 Signs :

1. foci of chorioretinal atrophy and scarring with pigmented borders (old

lesion)

2. focal retinitis with overlying vitrous haze ( active lesion ) severe vitritis
causes " headlight in the fog " appearance , where the inflammatory
focus is difficultly seen through the hazy vitrous

3. 3-Papillitis

25
 4. Atypical lesion : – occurs in immuno-compromised patients

– consists of discrete foci of retinitis with no scars

 Prognosis : Healing within 1-4 months with clearing of vitrous haze .

 Complications :Loss of vision ( from involvement of fovea ,optic disc

papillo-macular bundle or from retinal detachment )

 Diagnosis : by detection of toxoplasma antibodies by haemeagglutination

or ELISA

II) Onchcerchiasis
Onchocerca volvulus (blinding worm) is a wide spread infection in central Africa.

Man is the definitive host and simulium fly is the intermediate host.

 Ocular lesions

1. Onchocercomata (nodules) in the skin of the eye lid and forehead

2. Proptosis with high eosinophila

3. Movement of the larve under the conjunctiva

4. Interstitial keratitis

5. Moving larva within aquous

6. A grey brown mass of dead larva in te angle of the anterior chamber with iris atrophy

7. Spongy iris (pumice-stone iris)

8. Inverted pear shaped pupil

9. Posterior synechia

10. Pigmented K.ps

11. Central (posterior) degenerative chorioretinitis with star like or bone-corpuscle

pigmentation

12. Finally consecutive optic atrophy

III)Loasiasis
Loa loa (African eye worm), rarely affects the eye. The adult worm can move under the skin or the
conjunctiva, in the anterior chamber, in the vitrous or protruding through a macular hole

IV)Toxocariasis
Causative organism : Toxocara canis .

26
 Stages of the parasite :

1- Ova :excreted in dog's faeces .

2- Larvae : penetrate human intestine { after ingestion of ova } then

migrates to the eye , when they die they cause inflammation followed by
granuloma .

Forms :

1. Chronic endophthalmitis

2. Posterior pole granuloma

3. Peripheral granuloma

Chronic Posterior pole Peripheral granuloma

endophthalmitis granuloma
Age Between 2 and Between 6 and During adolescence
incdenc 9 years 14 years and adultlife
e
Sympto Leucocoria Unilateral visual Symptomless or
ms ,Unilateral loss Unilateral visual loss (
visual loss and from macular
Squint heterotopia or retinal
detachment )
Signs Anterior uveitis Absent uveitis Absent uveitis
Dense grayish- Rounded Peripheral white
white exudate yellowish white hemispherical
on pars plana granuloma at the granuloma
similar to "snow macula or the Vitrous bands
banking" disc
Complica
tions Tractional Tractional retinal
retinal Vascular detachment
detachment distortion macular heterotopia
Hypotony Hard exudates leading to peudo-
Cataract Retinal strabismus
detachment

V)cysticercosis
Tainea solium rarely causes intraocular cysts. These cysts are commonly subretinal with detachment

VI)Echinococcosis (Hydatid Cyst)

Taenia echincoccus, rarly causes orbital cysts. Occasionally, a subretinal cyst with painful absolute
granuloma ocurrs.

C. Non infective systemic

27
 I) Sarcoidosis
Characters of the disease
o Sarcoidosis is a multisystem systemic disease of unknown cause in which lymphoid tissue
develops noncaseating, granulomatous inflammation.
o Usually, sarcoidosis is a disease that affects 20- to 40-year-old individuals, with persons of
African descent and women more predisposed than other patient subgroups.
o The lungs are the most frequently involved organs, but the skin, liver, spleen, joints, and
heart may also be involved.
o Ocular involvement occurs in 17% of cases of systemic involvement. Ocular sarcoidosis can
take many forms, but it is often the presenting sign of the systemic disease.

Clinical Features
1. Acute iridocyclitis may be the earliest form of sarcoid uveitis.
2. Patients complain of ocular pain, photophobia, and redness,
3. flare and cells are seen in the anterior chamber.
4. The uveitis may be granulomatous or nongranulomatous.
5. Fine, gray KPs initially may be seen on the posterior surface of the cornea.
6. The condition often becomes chronic, and mutton-fat KPs develop as the disease process
continues.
7. The granulomatous nature of sarcoidosis is responsible for some of the ocular features,
including conjunctival granulomas, mutton-fat KPs, Busacca nodules within the iris
stroma, and Koeppe nodules along the pupil margin (Fig. 8.33).
8. Posterior segment findings in ocular sarcoidosis may include vitritis, pars plana
snowbanking, cyclitis, choroiditis, optic neuritis, cystoid macular edema, retinal arteritis,
retinal phlebitis, and optic nerve granulomas (Figs. 8.34; 8.35A, B). All or none of these
may be found. White, fluffy opacities may be seen in the inferior vitreous, and yellow-white
exudates, called candle-wax drippings, and sheathing of the peripheral retinal veins may be
seen (Fig. 8.36).
The characteristic granulomatous anterior, posterior, or diffuse uveitis should alert the clinician to
search for systemic involvement. The workup should include a chest x-ray, serum angiotensin-
converting enzyme assay, and if necessary, a gallium scan limited to the head, neck, and
mediastinum. Biopsy of ocular tissues such as conjunctival granulomas (Fig. 8.37) or lacrimal gland
granulomas may be helpful in confirming the diagnosis

II) Metabolic diseases

1. Gout

Gouty (uratic) iritis is usually preceded by episcleritis or scleritis. The attack is usually
asscociated with acute rise of tension. The un complicated attack of iridocyclitis usually
resolves in a week's time with only pigment dispersion on the anterior lens capsule. Urates
are not deposited in the uveal tract and inflammation is recurrent.

2. Diabetes mellitus

Non inflammatory changes in uveal tract are more common in diabetes mellitus. The
pigment epithelium of the iris shows edema, glycogen infliteration and finally
ruputure. The muscles of the iris are infiltrated with glycogen and the papillary
reaction are affected. Rubeosis iridis, with recurrent hyphema and haemorrhagic
glaucoma are seen in advanced cases.
28
 True diabetic iritis is rare. There are albuminous exudates that fill the pupil,
neovascularization around the pupil that disappear with subsidence of the attak, and
pigmented posterior synechiae. The papillary response to mydriatic is poor.

 MANAGEMENT

Lines of treatment:-
A-Accurate diagnosis
B-Non specific treatment
C-specific treatment
D-treatment of complication
A-Accurate diagnosis: by both etiological and clinical methods this needs
the following:

a- Proper examination of the eye to exclude other causes for red eye

b- General medical examination to detect a systemic cause

c- Special investigations for :

- Eye: - we do paracentesis of anterior chamber to take a specimen of

aqueous to be examined by histological, biochemical, biological,
bacteriological and immunological methods.

- Systemic investigations by :-

i- Skin test :

Tuberculin for T.B

Bruceilin for brucellosis

Kvein reaction for sarcoidosis

Behecetine for Behecet's disease

ii- Serological tests:

C-reactive proteins for collagen diseases

Anti-streptococcal tests

Compliment fixation test

B- Non specific treatment:

29
 I- Local treatment

II- General treatment

I-Local treatment

1-Mydriasis and cycloplegia using: atropine (1-2%), scopolamine (0.2-0.5%),

homatropine (2-5%).

Advantage:

- Mydriasis results in mechanical decongestion of iris, cutting newly

forming synechia, relieving pain from spastic miosis.

- Cycloplegia relives pain from spasm of accommodation, improves

passive congestion, minimizes protein exudation into aqueous and
vitreous and puts the uveal tissue at a physiological rest.

2-Dark glasses

3-Hot fomentations

4-Corticosteroids: as eye drops, ointment or subconjunctival injections

5-Anti-bacterial drugs as eye drops, ointment or subconjunctival injections

6-Paracentisis of anterior chamber when there is extensive hypopyon, with or

without secondary glaucoma or to drain aqueous and allow fresh plasmoid
aqueous to reform with its high content of anti bodies or to have a specimen of
aqueous for investigations.

II-General treatment

1-Corticosteriods: prednisilone tabelets beginng with 40-80 mg then maintain

treatment with 10-20 mg

2-Corticotrophin to avoid complications of prolonged steroid therapy

3-Anti-inflammatory drugs: salicylates, butazolidine or indocid.

4-Anti-bacterial drugs

5-Non specific protein therapy

6-Anti-histaminics

7-tonics and vitamins

8-Diamox to guard against secondary glaucoma

30
C-Specific treatment: according to the results of investigations IF
a case of :
1-Acute iritis:

a- Infective group: give specific chemotherapy or antibiotic

b- Allergic group: specific desensitization

c- Septic foci are treated either medically or surgically

2-Cyclitis: follows the same lines previously discussed under iritis

3- Iridocyclitis:

Acute nongranulomatous Chronic Iridocyclitis of Juvenile

Rheumatoid Arthritis
The management of acute nongranulomatous The management of this form of chronic
anterior uveitis involves the intensive use of iridocyclitis involves the use of cycloplegics to
cycloplegic and steroidal agents, and the prevent synechiae formation. Because this is a
secret to successful therapy is prompt long-term disease process, the extended use of a
aggressive treatment. Cycloplegics such as cycloplegic, such as Atropine, may be indicated
1% Cyclogyl administered four times daily or, to keep the pupil from binding and producing
in severe cases, 1% Atropine administered secondary complications such as iris bomb ‫©أ‬.
four times daily help to dilate the pupil, Typically, one to four drops daily of low-dose
relieve ciliary spasm, and reduce pain. topical steroids are needed to reduce the
However, a side effect of this therapy is potential for side effects of the inflammation.
blurred near-range vision, which may Long-term steroid use, however, is associated
incapacitate younger individuals. Fortunately, with the risks of cataract formation and
these effects are dose dependent. Topical glaucoma. Over many years of treatment, these
steroids are the primary antiinflammatory are the two most feared complications. The
agents, with an initial treatment rate of one former may be successfully treated with
drop every hour while awake. If no intraocular surgery. If topical antiglaucoma
improvement occurs within 24 to 48 hours, medications are ineffective, surgery may also
high-dose topical steroid therapy can be correct the latter condition. In end-stage disease,
supplemented with subconjunctival injections often occurring in the patient's later years, ciliary
of intermediate-acting steroids or occasionally dysfunction and hypotony are the more sinister
supplemented with a short course of high- problems. This expected course has prompted
dose oral steroid therapy (60 to 100 mg/day in some ophthalmologists to treat the initial and
divided doses). If an infectious process is long-term disease aggressively with oral
identified, appropriate antibiotic or antiviral nonsteroidal antiinflammatory agents or even
therapy should be started. with cytotoxic or alkylating medications to
attempt to resolve all traces of inflammation.
The rationale of aggressive treatment is that
intraocular integrity may be better maintained
over the many years the disease is present, but
the added risks of aggressive treatment make
this approach controversial.
Intermediate Uveitis

31
4-pars planitis (Intermediate uveitis): Treatment usually consists of cautious
observation in patients who do not have significant cystoid macular edema,
severe or disabling floaters, or significant anterior segment inflammation. In
those patients who do require treatment, use of intensive high-dose topical
steroid therapy is often effective in gradually achieving control of the
inflammation, and may be very useful in unmasking steroid responders for
whom treatment with periocular injection with depot corticosteroid agents is
contraindicated. Subtenons steroid injections and/or oral steroid therapy are
often helpful in resolving or controlling inflammation that has not responded
satisfactorily to high-dose topical steroid therapy. Treatment with stronger
agents such as cyclosporine or alkylating agents is rarely indicated.

5- fuch's Heterochromic cyclitis: Atropine and cortisone are of no value.

Glaucoma is treated medically if this fails, an externally fistulizing operation is
done.

6- Choriditis: it follows the same principles as in iritis. But usually treatment is

of limited value in stopping the progress of the lesion but may prevent
recurrence.

7-Endophthalmitis:
- Conservative treatment is tried first.
- We give general anti-bacterial drugs.
- Locally we give atropine and anti bacterial drugs by every possible route such
as sub-conjunctival or intra-vitreal injections of penicillin or vancomycin
-If medical treatment failed and the eye is irritade we do enucleation of the
eyeball

8-Panophthalmitis:
- Medical: as endophthalmitis but usually without effect
- Surgical: we do evisceration to evacuate the intra-ocular purulent
content. Under general anaesthesia we remove the cornea. Then curette
all the intra-ocular contents with a scoop. The inside of sclera is washed

9-sympathetic ophthalmitis: treatment is essentially prophylactic because once

sympathetic ophthalmitis starts it continues inspite of the prolonged medical
treatment. Immediate or early enucleation of an eye with a penetrating injury,
beyond a useful surgical repair, must not be delayed. Proper surgical repair of
the injured eye is essential, avoiding incarceration of uveal tissue. If the eye,
after repair remains irritated with low tension enucleation is done.

Active treatment in the established cases includes:

1- Cortisone: locally and generally for at least 6 months to 2 years
2- ACTH: generally to avoid systemic complications of corticosteroids

32
 3- Atropine, neosyniphrine , etc.

4- Anti-inflammatory drugs: salicylates, iodides, tnderil etc.

5- Diamox and osmotherapy when secondary glaucoma

Operative treatment of secondary glaucoma is of bad prognosis and

recurrent hyphaema after the operation is a dangerous complication.

10- Vogt-Koyanagi-Harada Syndrome: Successful management of VKH requires

a high index of suspicion for the disease based on the characteristic physical
findings. A spinal tap may reveal leukocytosis, and other laboratory tests can
exclude other granulomatous conditions. Affected individuals are often positive
for the Dw-54 marker.
Treatment of this immunologic condition includes the use of systemic
corticosteroids and sometimes includes immunosuppressive agents such as
chlorambucil or methotrexate. Cyclosporine may also be used in the treatment
of this condition. The final outcome depends on the control of inflammation and
prevention of scar formation. Visual function may remain quite good, although
the course may be long term and indolent (Fig. 8.42).

11- Behecet's Disease: Successful treatment requires prompt recognition and

suppression of inflammation. Laboratory studies may be helpful, and patients
commonly have the HLA-B5 marker. Therapeutic agents include systemic
corticosteroids, cyclosporine, and immunosuppressive agents such as
chlorambucil. The final outcome depends on the amount of damage caused by
the initial vasculitis, which often results in arterial occlusion and retinal
necrosis. The end result, however, may be satisfactory if the process is
diagnosed and treated promptly. Localized treatment, such as laser therapy for
the ischemic complications of vasculitis, is sometimes helpful, and the proper
management of Behecet's disease should include consultation with a skilled
internal medicine specialist.

12-Tuberclosis : Treatment is accomplished with antitubercular medications,

which include isoniazid and rifampin. Because resistant strains commonly
develop, single drug therapy should not be used. Topical corticosteroids and
cycloplegics may be used to treat anterior uveitis. Posterior uveitis may be
treated with the judicious use of systemic corticosteroids after consultation
with the internist.

13-Syphilis : Ocular syphilis is treated with oral, intramuscular, or intravenous

antibiotics. A full systemic course is indicated for ocular and extraocular
involvement. If macular scarring is minimized, good vision may be obtained.
The VDRL test result falls slowly after treatment and is useful in following
patients over time. Because the spirochetes are slow-growing organisms,
recurrences are possible, and follow-up VDRL testing is indicated.

14-Toxoplasmosis: Treatment is aimed at prompt resolution of the infectious process in vision-

threatening areas. Classically, sulfadiazine and the folic acid antagonist pyrimethamine have been
used. Folinic acid is administered to reduce the bone marrow toxicity of pyrimethamine. Antibiotics
such as clindamycin, trimethoprim-sulfamethoxazole, and tetracycline, which affect the organism's
33
pathways of protein transcription, have been used. Corticosteroids have also been advocated for
severe inflammation, although caution is indicated because high doses of these drugs, especially in
the form of periocular injections, may be contraindicated because of their immunosuppressive
action, which may potentiate the infectious process (Fig. 8.18).
The drugs used in the treatment of ocular toxoplasmosis may have significant side effects, and
patients undergoing treatment must be closely monitored. Because the folic acid antagonists may
cause bone marrow suppression, a platelet and complete blood count should be obtained at least
weekly. With sulfadiazine, the rare but devastating complication of Stevens-Johnson syndrome must
be watched for. Clindamycin may cause necrotizing enterocolitis, and tetracycline should not be
prescribed for pregnant patients. Corticosteroids given topically or systemically are not without
hazards. These treatment regimens, however, are often effective in reducing intraocular scarring and
preserving visual function. For small, peripheral lesions or those that do not threaten vision,
observation only may be a viable option.
15-Toxocariasis : Thiabendazole, the treatment of choice for visceral larval
migrans, is not indicated for treatment of ocular toxocariasis because the
organism has generally perished by the time that the eye changes are noted;
secondary inflammation is responsible for the ocular symptoms and findings.
Ocular inflammation may be self-limited in many cases, although active iritis
and/or vitritis may require treatment with topical and/or periocular steroid
injection. Vitrectomy may become a consideration in patients with chronic
smoldering active inflammation, and removal of the antigen-laden vitreous in
these patients often results in permanent quiescence of intraocular
inflammation.

16-sarcoidosis : The management of sarcoidosis is related to the level of eye

inflammation and its structural damage. Topical, periocular, or systemic
corticosteroids are the basic elements of treatment. Cycloplegic agents may
also be helpful in reducing synechiae formation. The ophthalmologist should
work with the internist to determine whether systemic therapy would benefit
extraocular areas.
Oral steroid therapy may be needed initially in patients with severe
inflammation, and chronic low-dose oral steroid therapy, such as 20 mg of
prednisone daily, may be needed to control chronic inflammation or reduce
exacerbations. If inflammation is not controlled, secondary scarring can occur.
This can result in corneal scars, iris bomb ‫ ©أ‬from synechiae between the
pupillary margin and the lens surface, cataract formation, chronic cystoid
macular edema, optic nerve dysfunction, and vascular ischemic events caused
by inflammatory obstructive phenomena

D- Treatment of complication:
1- Secondary glaucoma: continue atropine. Give diamox and osmotherapy.
Do paracentesis if necessary.

2- Occlusio and seclusio pupillae: after the eye becomes quite and
iridectomy is necessary both for secondary glaucoma and for vision.

3- Peripheral anterior synaechiae with secondary glaucoma: do external

fistulizing operation

34
 4- Complications include cataracts and a slightly higher incidence of retinal
detachment, which can be treated surgically. The long-term prognosis is
good, especially if the inflammation is mild. The disease may resolve,
sometimes after many years' duration.

 References

 Classification

• e.medicine classification
• DR. ABDEL-BASSET ELNAGGAR. Diseases of uveal tract in his book (THE
EYE AND ITS DISEASES). Second edition 1976. TANTA UNIVERSITY.
• Bloch-Michel E, Nussenblatt RB: International Uveitis Study Group
recommendations for the evaluation of intraocular inflammatory disease.
Am J Ophthalmol 1987 Feb 15; 103(2): 234-5[Medline].
• Gritz DC, Wong IG: Incidence and prevalence of uveitis in Northern
California; the Northern California Epidemiology of Uveitis Study.
Ophthalmology 2004 Mar; 111(3): 491-500; discussion 500[Medline].
• Jabs DA, Nussenblatt RB, Rosenbaum JT: Standardization of uveitis
nomenclature for reporting clinical data. Results of the First International
Workshop. Am J Ophthalmol 2005 Sep; 140(3): 509-16[Medline].
• Karcioglu ZA, Brear R: Conjunctival biopsy in sarcoidosis. Am J
Ophthalmol 1985 Jan 15; 99(1): 68-73[Medline].
• Sheppard JD: Posterior uveitis. Ophthalmol Clin North Am 1993; 6: 1.
• Sheppard JD, Garovoy MR: The major histocompatibility complex in
ophthalmology. In: Friedlander MH, ed. Duane's Basic Ophthalmologic
Science. Vol. 1. 1991.
• Sheppard JD, Nozik RA: Practical diagnostic approach to uveitis. In: Duane
JA, Jaeger EW, ed. Duane's Clinical Ophthalmology. Vol. 4. 1989.
• Smith RE, Nozik RA: Uveitis: A Clinical Approach to Diagnosis and
Management. 2nd ed. Baltimore: Williams & Wilkins; 1988.

 Clinical Picture And Complication

• DR. ABDEL-BASSET ELNAGGAR. Diseases of uveal tract in his book (THE

EYE AND ITS DISEASES). Second edition 1976. TANTA UNIVERSITY.
• WILLIAM TASMAN & EDWARD A.JAEGER. Chapter Of Intraocular
Inflammation In The Their Book ( THE WILLS EYE HOSPITAL ATLAS OF
CLINICAL OPHTHALOMOLGY) second edition.
• Prof Gerhard K. Lang,MD Professor and Chairman University Eye Hospital
Ulm, Germany.chapter of the uveal tract. Ophthalmology A Pocket
Textbook Atlas. Second edition

 Management

• DR. ABDEL-BASSET ELNAGGAR. Diseases of uveal tract in his book (THE

EYE AND ITS DISEASES). Second edition 1976. TANTA UNIVERSITY.
35
 • WILLIAM TASMAN & EDWARD A.JAEGER. Chapter Of Intraocular
Inflammation In The Their Book ( THE WILLS EYE HOSPITAL ATLAS OF
CLINICAL OPHTHALOMOLGY) second edition.

36