uveal tract.pptx..........................

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FACULTY OF MEDICINE
DEPARTMENT OF OPTHALMOLOGY
FIFTH-YEAR
TOPIC: Diseases Of the Uveal
PRESENTERS:
EMMANUEL SWAKA
LUCY WILSON SEBIT
SUPERVISOR: DR.KENNETH LADO LINO SUBE
DR. EMMANUEL ORYEM
SOUTH UNIVERSITY OF MEDICINE, SCIENCE, AND TECHNOLOGY
(SUMST)

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CONTENT
Introduction
Classification
Clinical Pictures
Diagnosis
Management(Medical and Prevention and Control)

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APPLIED ANATOMY
• The uveal tract consists of
iris, ciliary body and
choroid.
• Anatomically, they are
continuous and so disease
of one part may spread to
the other. The uveal tract is
the vascular layer of the
eye.

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Components of the Uveal Tract
Iris:
• The iris is the anterior part of the uveal tract and is responsible for
controlling the amount of light that enters the eye through the pupil.
• It is a thin, circular structure that contains muscles (sphincter and
dilator muscles) that adjust the size of the pupil in response to light
conditions.
• The iris also contributes to eye color due to its pigmentation.

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Ciliary Body:
• Located behind the iris, the ciliary body plays a vital role in
accommodation, allowing the eye to focus on objects at varying distances.
• It contains ciliary muscles that change the shape of the lens and is also
responsible for producing aqueous humor, which maintains intraocular
pressure and nourishes the eye.

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Choroid:
• The choroid is the posterior part of the uveal tract, situated between
the retina and the sclera. It is a highly vascular layer that provides
oxygen and nutrients to the outer layers of the retina. The choroid
also helps absorb excess light, preventing reflections that could
interfere with vision.

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Macroscopic appearance of anterior surface
of iris

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Microscopic structure of iris and ciliary body

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Blood supply
• The uveal tract is supplied by three
sets of arteries
1. Short posterior ciliary arteries.
2. Long posterior ciliary arteries.
3. . Anterior ciliary arteries.

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pathophysiology
• The term uveitis strictly means inflammation of the uveal tissue only.
However, clinically there is always some associated inflammation of
the adjacent structures such as retina, vitreous, sclera and cornea.
Due to close relationship of the anatomically distinct parts of the
uveal tract, the inflammatory process usually tends to involve the
uvea as a whole.

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Classification of uveitis
• Uveitis is classified into 4 types mainly
1. Anatomical uveitis.
2. Clinical uveitis.
3. Pathological uveitis.
4. Etiological classification(Duke Elder’s).

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Anatomical uveitis
• 1. Anterior uveitis
• It is inflammation of the uveal tissue from
iris up to pars plicata of ciliary body.
• It may be subdivided into:
• Iritis, in which inflammation predominantly
affects the iris.
• Iridocyclitis in which iris and pars plicata
part of ciliary body are equally involved.
• Anterior cyclitis, in which pars plicata part
of ciliary body is predominantly affected.

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Signs and symptoms
• Eye pain or aching
• Redness
• Photophobia
• Blurred vision
• Irregular pupil shape

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Intermediate uveitis
• Intermediate uveitis refers to inflammation involving pars plana
ciliaris, peripheral retina, choroid and vitreous base.
Epidemiology
• Accounts for 10% of all cases of uveitis and 20% of cases of uveitis in
children,
• Bilateral in 80% of cases,
• Males and females are equally affected,
• Age: onset typically in 2nd and 4th decade (bimodal).

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Etiology
• Idiopathic in about 85% cases.
• Immunogenic predisposition is reported with a positive correlation
with HLA-DR2.
• Known causes (15% cases) include tuberculosis, syphilis, sarcoidosis,
and Lyme disease.

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Signs and symptoms
• Floaters
• Blurred vision
• Minimal eye pain or redness
• Vitreous cells
• Snowbanking
• Cystic macular edema

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3. Posterior uveitis. It refers to inflammation of the choroid
(choroiditis). Almost always there is associated inflammation of retina
and hence the term ‘chorioretinitis’ is used.
4. Panuveitis. It is inflammation of the whole uvea.

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Clinical classification
1. Acute uveitis. It has got a sudden symptomatic onset and the
disease lasts for 3 months or less.
2. Chronic uveitis. It frequently has an insidious and asymptomatic
onset. It persists longer than 3 months and is usually diagnosed when it
causes defective vision.
3. Recurrent uveitis. This is characterised by repeated episodes
separated by inactive periods of >3 months without treatment.

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Pathological classification
• Suppurative or purulent uveitis.
• Nonsuppurative uveitis. It has been further subdivided into two
groups (Wood’s classification).
• i. Nongranulomatous uveitis, and
• ii. Granulomatous uveitis.

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Etiological (Duke Elder’s) classification.
1. Infective uveitis
2. Immune-related uveitis
3. Toxic uveitis
4. Traumatic uveitis
5. Uveitis associated with non infective systemic diseases
6. Idiopathic uveitis.

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Infective uveitis
• In this, inflammation of the uveal tissue is induced by invasion of the
organisms.
• Uveal infections may be exogenous, secondary or endogenous.
• i. Exogenous infection wherein the infecting organisms directly gain
entrance into the eye from outside.
• ii. Secondary infection of the uvea occurs by spread of infection from
neighbouring structures, e.g., acute purulent conjunctivitis
(pneumococcal and gonococcal), keratitis, scleritis, retinitis, orbital
cellulitis and orbital thrombophlebitis.

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.
• iii. Endogenous infections are caused by the entrance of organisms
from some source of infection situated elsewhere in the body, by way
of the bloodstream. Endogenous infections play important role in the
inflammations of uvea.

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• Types of infectious uveitis
• Depending upon the causative organisms, the infectious uveitis may be classified as
follows:
• i. Bacterial infections. These may be granulomatous, e.g., tubercular, leprotic, syphilitic,
brucellosis or pyogenic such as streptococci,staphylococci, pneumococci and
gonococcus.
• ii. Viral infections associated with uveitis are herpes simplex, herpes zoster and
cytomegalovirus (CMV).
• iii. Fungal uveitisis rare and may accompany systemic aspergillosis, candidiasis and
blastomycosis. It also includes presumed ocular histoplasmosis syndrome.
• iv. Parasitic uveitis is known in toxoplasmosis, toxocariasis, onchocerciasis and
amoebiasis.
• v. Rickettsial uveitis may occur in scrub typhus and epidemic typhus.

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Immune related uveitis
• Immune related uveitis is one of the commonest occurrence in clinical
practice. It may cause uveitis in the following mechanism.
I. .Microbial allergy.
II. . Anaphylactic uveitis.
III. Atopic uveitis.
IV. Autoimmune uveitis.

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Toxic uveitis
• Toxins responsible for uveitis can be,
I. Endotoxins produced inside the body play a major role.
II. Endocular toxins are produced from the ocular tissues.
III. Exogenous toxins causing uveitis are irritant chemical substances of
inorganic, animal or vegetative origin.

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Traumatic uveitis
• It is often seen in accidental or operative injuries to the uveal tissue.
Different mechanisms which may produce uveitis following trauma
include:
• Direct mechanical effects of trauma,
• Irritative effects of blood products after intraocular haemorrhage
(haemophthalmitis),
• Microbial invasion,
• Chemical effects of retained intraocular foreign bodies, and
• Sympathetic ophthalmia in the other eye.

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Uveitis associated with non-infective systemic
diseases
• Certain systemic diseases frequently complicated by uveitis include:
• Sarcoidosis,
• Collagen related diseases (polyarteritis nodosa (PAN), disseminated
lupus erythematosus (DLE), rheumatic and rheumatoid arthritis),
• Metabolic diseases (diabetes mellitus and gout),
• Disease of the central nervous system (e.g., disseminated sclerosis),
and
• Diseases of skin (psoriasis, lichen planus, erythema nodosum,
pemphigus and so on)

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Idiopathic uveitis
It may be specific or nonspecific.
i. Idiopathic specific uveitis entities include the conditions which have
certain special characteristics of their own, e.g., pars planitis,
sympathetic ophthalmitis and Fuchs’ heterochromic iridocyclitis.
ii. Nonspecific idiopathic uveitis entities include the condition which do
not belong to any of the known etiological groups. About more than
25% cases of uveitis fall in this group.

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Diagnosis
Ocular examination and investigation
• Visual acuity Test.
• Measuring of intraocular pressure.
• Slit lamp examination to assess the anterior Chamber and Vitreous.
• Fundoscopy.

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• Laboratory tests include
1. Haematological investigations
• TLC and DLC to have a general information about inflammatory response of
body.
• ESR to ascertain existence of any chronic inflammatory condition in the body.
• Blood sugar levels to rule out diabetes mellitus.
• Blood uric acid in patients suspected of having gout.
• Serological tests for syphilis, toxoplasmosis and histoplasmosis.
• Tests for antinuclear antibodies, Rh factor, LE cells, C-reactive proteins
antistreptolysin-0, ACE (for sarcoidosis).

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2. Urine examination for WBCs, pus cells, RBCs and culture to rule out
urinary tract infections.
3. Stool examination for cyst and ova to rule out parasitic infestations.

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Radiological investigations include:
• X-rays of chest, paranasal sinuses, sacroiliac joints and lumbar spine.
• CT scan high resolution. CT scan of thorax should be considered for
suspected sarcoidosis cases.
• MRI scan of head for suspected sarcoidosis, demyelination and
lymphomas.

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Skin tests.
• These include tuberculin test, Kveim’s test for sarcoidosis,
toxoplasmin test, lepromin test and pathergy test for Behcet’s
disease.

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Principles management
1. Cycloplegic drugs.
• Commonly used drug is 1% atropine sulfate eye ointment or drops
instilled 2-3 times a day.
2. Corticosteroids.
• Commonly used steroidal preparations contain dexamethasone,
betamethasone, hydrocortisone or prednisolone. steroids are used as
(i) eye drops 4–6 times a day, (ii) eye ointment at bed time, and (iii)
Anterior sub-Tenon injection is given in severe cases (a single dose of
triamcinolone 20 – 40mg).

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3. Broad spectrum antibiotic drops
• Fluoroquinolones (moxifloxacin eg vigamox 0.5%) gatifloxacin or
besifloxacin often 3-4 times daily.
• Aminoglycosides (tobramycin 0.3% 4-6 times daily or o.5% of
gentamicin ).

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3. Immunosuppressive drugs
• Methotrexate ( oral 7.5-25 mg/week).
• Mycophenolate mofetil (500-1500 mg twice daily).
• Azathioprine(1-3mg/kg/day).
• Cyclosporine (2.5-5mg/kg/day).
• Adalimumab (40mg every 2 weeks) subcutaneous.

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Prevention and control

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ACUTE IRIDOCYCLITIS
• It is an acute inflammation of the iris (iritis) and the ciallary
body (cyclitis).
SYMPTOMS
• Redness- Redness—It is due to circumciliary congestion.
• Pain—It is worse at night. There is severe neuralgic pain
referred to forehead, scalp, cheek, malar bone, nose and teeth
(as the iris is richly supplied by sensory nerves from the
ophthalmic division of 5th nerve).
• Lacrimation and photophobia may be present (without any
mucopurulent discharge) due to associated keratitis.
• Impaired vision—It is mainly due to hazy plasmoid aqueous
and opacity in the media.
• Photophobia- is due to pain induced by pupillary constriction
and ciliary spasm because of inflammation.

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SIGNS
1. Circumciliary congestion—There is
hyperaemia around the limbus which is dull
purple-red in colour.
2. Anterior chamber :There is plasmoid
aqueous containing leucocytes, minute flakes
of coagulated proteins and fibrinous network.
The slit-lamp examination shows the presence
of :
a. Milky ‘flare’ or ‘aqueous flare’—Dust-like
particles are seen moving in the beam of
slit lamp similar to Tyndall effect.
b. Keratic precipitates (kp)—The exudate
tends to stick to the damaged
endothelium in the lower part of cornea in
a triangular .

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Cont…..
1. . Fresh kp—These are multiple, circular and grey-
white coloured. They consist of lymphocytes
predominantly.
2. Old kp—These are pigmented, small with
crenated edges.
3. Mutton fat kp—These are few, large, yellow,
greasy waxy kps.
2. Hypopyon—In severe cases of iritis
polymorphonuclear leucocytes are poured out which
sink to the bottom of the anterior chamber forming
hypopyon.
3. Hyphaema—Blood in the anterior chamber
rarely occurs due to spontaneous haemorrhage.

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CONTINUATION OF SIGNS
3. Pupil—It is constricted due to water logging and
vasodilatation. It reacts sluggishly to light due to
irritation of the third nerve endings in iris.
4. Iris
1. There is loss of normal pattern of the iris.
2. Iris appears muddy due to the collection of
exudates.
5. Synechiae—It is an adhesion or attachment of iris
to the adjacent structures
6. Lens
1. Complicated cataract—There is typical posterior
cortical cataract with bread crumb appearance
and polychromatic lustre
2. Pseudoglioma—It is seen in young children.

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CONT…
• 7. Vitreous—Vitreous opacities due to leuco cytes, coagulated fibrin and
exudates may be present in severe cases.
• 8. Intraocular tension
1. In active stage
i. Hypertensive iridocyclitis may be present due to increase pressure in
dilated capillaries and outpouring of leucocytes.
ii. The sticky albuminous aqueous drains with difficulty thus raising the
tension.

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2. In later stage :
i. Secondary glaucoma may be present due to
pupillary blocii.
ii. Phthisis bulbi (hypotony) may be present due to
atrophy of the ciliary body.

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COMPLICATION AND SEQUELAE
1. Complicated cataract: it is common complication of iridocyclitis.
2. Secondary glaucoma: it may occur as an early or late complication of
iridocylitis.
I. Early glaucoma: In active phase of the disease, presence of exudates and
inflammatory cells in the anterior chamber may block the trabedular
meshwork.
II. Late glaucoma: is the result of pupil block.
• 3. Cyclitic member: it result due to fibrosis of exudates present behind the
lens.
• 4. Choroiditis: It may develop in prolonged cases of iridocyclitis owing to
their anatomical continuity.

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Cont…
5. Retinal complication: These include cystoid
macular oedema , macular degeneration,
exudative retinal detachment and secondary
periphlebitis retinae.
6. Band-shaped keratopathy: It occurs as a
complication of long-standing chronic uveitis,
especially in children having Still’s disease.
7. Phthisis bulbi: it is the final stage end result
of any form of chronic uveitis. In this
condition, ciliary body is disorganised and
atrophied.

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INVESTIGATION OF ACUTE
IRIDOCYCLITIS
• Clinical Examination:
I. Visual Acuity Test: Assesses the impact on vision.
II. Tonometry: Measures intraocular pressure , which may be low (ciliary
body shutdown) or high (trabeculitis).
III. Slit-Lamp Biomicroscopy: The goldern standard for identifying
inflammatory cells and protein flare in the anterior chamber.
IV. Fundus Examination: Dilated exam to rule out immediate or posterior
involvement.
• Laboratory investigations(Tailored Approach):
I. Complete Blood Count and inflammatory Markers: ESR and CRP for systemic
inflammation.
II. Serology for infections: Syphilis (VDRL/RPR,FTA-ABS), Lyme disease,
Toxoplamosis.
III. Genetic Testing: HLA-B27, commonly associated with acute anterior uveitis and
ankylosing spondylitis.

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Cont…
iv. Autoimmune Markers: ANA (especially for
pediatric cases),RF.
V. Specific Markers: Angiotensin-converting enzyme
(ACE) and lysozyme foe sarcoidosis.
• Imaging and special procedures:
I. Chest X-ray/CT: To rule out sarcoidosis or
tuberculosis.
II. Optical Coherence Tomography: To detect
macular edema.
III. Ultrasound Biomicroscopy: Used if the view is
obscured or to check for ciliary body issues.
IV. Anterior Chamber paracentesis: Rarely, for PCR
analysis of infectious agents (e.g ,Herpes, CMV).

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Medical Prevention
• Manage Underlying Conditions: A significant number
of cases are associated with autoimmune disorders
(e.g ankylosing spondylitis, rheumatoid arthritis).
• Regular Eye Exam: Routine, comprehensive eye exams
(at least every 1-2years, or more frequently if you have
a known systemic condition).
• Prevent Eye Injury:
• Smoking Cessation:
• Nutritional Support:
• Prompt Infection Treatment:

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MANAGEMENT
I. Nonspecific treatment
a. Local therapy
1. Cycloplegic drugs. These are very useful
and most effective during acute phase of
iridocyclitis. Commonly used drug is 1%
atropine sulfate eye ointment or drops
instilled 2-3 times a day.
2. 2. Corticosteroids, administered locally, are
very effective in cases of iridocyclitis.
(i) eye drops 4–6 times a day, (ii) eye ointment
at bed time, and
(iii) Anterior sub-Tenon injection is given in
severe cases.

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CONT….
• 3. Broad spectrum antibiotic drops.
b. Systemic therapy
1. Corticosteroids.
2. Non-steroidal anti-inflammatory drugs (NSAIDs)
3. Immunosuppressive drugs: cyclophosphamide, chlorambucil,
azathioprine.
4. Azithromycin or tetracycline or erythromycin.

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CHRONIC IRIDOCYCLITIS

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CHRONIC IRIDOCYLITIS
Primary Etiologies of Chronic Iridocyclitis
• Autoimmune and Systemic Disease ( Most
Common):
• Juvenile Idiopathic Arthritis: A leading cause,
particularly in children.
• Sarcoidosis: A systemic granulomatous disease.
• Seronegative Spondyloarthropathies: Includes
Ankylosing Spondylitis, psoriatic Arthritis, and
Reactive Arthritis(often HLA-B27 associated).
• Behcet’s Disease: known to cause chronic ,
recurrent inflammation.
• Inflammatory Bowel Disease: Such as Crohn’s
disease or ulcerative colitis.
• Tubulointerstitial Nephritis and Uveitis syndrome:
A cause often identified in specific cases.

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• Chronic Infections:
• Tuberculosis(TB): Can present as chronic
granulomatous iridocyclitis.
• Syphilis: A known cause of chronic uveitis.
• Herpes Simplex or Varicella –Zoster Virus: While
often acute, these can cause chronic or recurrent
iridocyclitis.
• Toxoplasmosis: Often causes retinochoroiditid but
can present as chronic iridocyclitis.
• Lyme Disease:
• Ocular Syndromes(Specific Entities):
• Fuch’s Heterochromic iridocyclitis: A common ,
usually unilateral , chronic, and often asymptomic
form of iridocyclitis.
• Lens-induced Uveitis:

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• Idiopathic:
• Asignificant proportion of chronic iridocylitis cases
(often 50% or more) remain idiopathic, meaning no
specific cause is identified despite evaluation.
Key Association and Risk Factors
• HLA-B27Genotype: Strongly linked to chronic forms
of anterior Uveitis.
• Genetic Factors: Family history of autoimmune
diseases.
• Immune Status: Compromised immune systems can
lead to increased risk.

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Clinical Features and
Symptoms
• Subtle, Insidious Onset: Unlike acute iridocylitis, the
chronic form may not present with a “red eye” or
significant pain initially.
• Reduced Vision / Blurry Vision: Often the primary, or
only, symptom, resulting from complications like
cataracts, macular edema, or vitreous haze.
• Mild to No pain : While acute cases are severely
painful, chronic cases often present with minimal
discomfort, causing them to go unnoticed.
• Floasters: Patients may complain of dark spots in their
field of vision.
• Mild injection: Mild redness may be present around
the iris.
• Irregular Pupil/Miosis: The pupil may be contracted or
irregularly shaped due to scar tissue formation
(synechiae).

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Signs Found On Examination(Slit-
Lamp)
• Cells and Flare: Presence of inflammatory cells and
protein in the aqueous humor.
• Keratic Precipitates(KPs): White, inflammatory
deposites on the back of the cornea.
• Posterior Synechiae: Adesions of the iris to the lens,
causing an irregular pupil shape.
• Iris Nodules: Koeppe nodules( at pupil margin) or
Busacca nodules (in the iris stroma).
• Iris Atropy: Thinning and loss of color in the iris stroma
(common in Fuch’s heterochromic iridocyclitis).
• Band Keratopathy: Calcium deposits on the cornea,
frequently seen in chronic cases, especially JIA.

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Common Complications
If left untreated , chronic iridocyclitis can cause signifant,
permanent vision loss due to:
• Cataracts: Increased eye pressure(intraocular
pressure).
• Cystoid Macular Edema: Swelling in the central
part of the retina.
• Phthisis Bulbi: Ashrunken,non-functional eye in
advanced, untreated cases.
• Vitreal Debris: Coarse opacities in the vitreous.

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Investigation Of Chronic
Iridocyclitis
 Comprehensive Eye Examination: Slit-lamp exam to
evaluate anterior chamber cells, flare, keratic precipitates.
 Imaging & Tonometry: Optical Coherence Tomograpy for
macular edema, tonometry to monitor high intraocular
pressure, and ultrasound.

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SYSTEMIC SCREENING
Inflammatory Markers: Antinuclear Antibody for Juvenile idiopathic Arthritis,
HLA-B27 for ankylosing spondylitis.
Infection Screen: VDRL/TPHA for syphilis , Mantoux or QuantiFERON-TB Gold
for tuberculosis.
Sarcoidosis Screening: Serum Angiotensin- Converting Enzyme and Chest X-
ray or HRCT-Scan.
Aqueous Humor Analysis (paracentesis): Used to detect infectious causes (e.g
Herpes Simplex, Varicella zoster , CMV) Using PCR,or for Goldmann- Witmer
coefficient calculation in, for e.g Fuch’s heterochromic iridocyclitis.

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PREVENTION AND CONTROL
1. Therapeutic Management Of Underlying Conditions
Autoimmune Disease Control: e.g juvenile idiopathic arthritis. Management
of underlying condition is the primary preventive measure.
Immunodulatory Therapy: e.g methotrexate are used for long term control
of inflammation and to prevent recurrence.
Biologic Agent: For refractory or severe, non-infectious chronic uveitis, TNF-a
inhibitors . Used to reduce flares.
Infectious Disease Control: e.g herpes simplex virus, long term prophylactic
antiviral therapy (such as oral acyclovir) can be used to prevent recurrent
episodes.

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2.Sustained Pharmacological Control
Topical Corticosteroids(firs –line): Potent steroid drops such as
prednisolone acetate 1% or difluprednate 0.05% are the mainstay of
treatment to reduce inflammation.
Cycloplegic/ Mydriatic Agent: Eye drops like atropine 1% or
homatropine are used to paralyze the ciliary muscle, relieving pain
and preventing the iris from sticking to the lens.
Periocular and intraocular Steriods: (e.g triamcinolone acetonide)

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ETIOLOGY
1. Exogenous—It is usually due to infected wound
which may be accidental, operative or after
corneal ulcer perforation.
The common pathogens are Pneumococcus,
Staphylococcus, Streptococcus, E. coli, Pseudomonas
pyocyanea, Bacillus subtilis, C. welchii, etc.
2. Endogenous—It is due to metastasis of the
infected embolus in the retinal artery and choroidal
vessels.

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Clinical Features
1.There is severe pain and limitation of the
movements of eye.
2. There is rise in temperature, headache, vomiting
and rapid failure of vision.
3. The lids are red and swollen with marked
conjunctival chemosis.
4. Purulent conjunctival discharge, marked
conjunctival and ciliary congestion.
5. Corneal wound appears to be necrotic and
hypopyon may be present.
6. Yellow reflex is seen through the pupil (vitreous
abscess).
7. Fundus examination—Media is hazy so the yellow
oedematous retina is faintly visible or often invisible.

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Complications
1. Cyclitic membrane is present due to
organized exudates.
2. Papillitis—Inflammation of optic disc and
surrounding retina may occur.
3. Pus may burst through the globe just behind
the limbus.
4. Phthisis bulbi occurs eventually.

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LABORATORY INVESTIGATIONS
Ocular Fluid Sampling: Anterior Chamber and Vitreous tapes are the
Gold standard.
Microbiology
Gram stain
Culture
Fungal Staining: Use Calcogluor white, and sabouraud agar for
suspected cases.
Molecular Methods: PCR on vitreous fluid provides high sensitivity.
IMAGING: B-Scan checking Vitritis, foreign bodies.

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Preoperative Care
Povidone-iodine: The golden standard is applying 5% povidone-iodine
to conjunctival sac 3-5 minutes before surgery .
Lid Hygiene: Treating blepharitis and cleaning the eyelid margins,
preferably with 10% povidone-iodine, reduced flora.
Antibiotics: e.g moxifloxacin
Intraoperative Measures
Intracameral Antibiotics: such as (1mg cefuroxime) to reduce infection.
Sterile Technique: To exclude eyelashes
Antibiotic Irrigation:

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 Postoperative Care
Prompt Monitoring: Early identification of symptoms- several pain,
rapid vision loss, eyelid swelling is crucial.
Antibiotic Drops: Continuing with postoperative topical antibiotics to
prevent late- onset infection.

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Treatment
1. Corticosteroids—Topical, subconjunctival injection and systemic
administration of corticosteroids is essential. They are anti-
inflammatory in action and preserve the ocular structure.
2. Atropine—Topical administration by drops or ointment and
subconjunctival injection are given. It provides rest to the eye by
paralysing the ciliary muscle.

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Surgical
1. Vitrectomy may be done early to save useful vision.
2. Evisceration is done when eye cannot be saved and the patient is
completely blind with no perception of light.
• It saves the patient from severe agonising pain.

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ETIOLOGY
 It occurs most commonly as an acute process 1-7 days
following intraocular surgery such as cataract extraction
and filtering operation.
 In India the incidence rate varies from 1 to 3%. Chances of
infection are much greater if there is associated vitreous
loss as vitreous is a very good culture medium for
organisms.
It is commonly caused by :
i. Bacteria—Staphylococcus, Pseudomonas, Pneumococcus,
etc.
ii. Fungus—Aspergillus fumigatus, Candida albicans, etc. It
occurs after injury with vegetable matter such as thorn or
wooden stick.

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SOURCE
• Bacterial flora of the eyelids, conjunctiva and lacrimal
passage.
1. Contaminated instruments, solutions, environmental
flora including that of surgeon and operating room
personnel.
2. penetrating injury with an infected object, e.g. wooden
splinter, iron particle.
3. Perforation of suppurative corneal ulcer of
Pseudomonas pyocyanea or fungal origin.
4. Systemic infection may cause metastatic infection
(septic emboli), e.g. AIDS, viral fever, septicemia. It may
occur in immunodeficient host and uncontrolled diabetic
patients.

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CLINICAL FEATURES
Bacterial Endophthalmitis
1.There is sudden onset with severe pain and redness in the
eye in acute cases.
2. Marked visual loss with defective projection of rays is an
important feature.
3. Lid oedema, chemosis and corneal haze are present.
4. There is low intraocular tension (hypotony) due to
cyclitis.
5. Fibrinous exudate or hypopyon is seen in the anterior
chamber.
6. There is associated vitritis and haze in the vitreous.
7. There is yellowish reflex seen behind the lens. There is
absence of red fundus reflex and inability to visualize the
fundus even with indirect ophthalmoscope.

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Fungal Endophthalmitis
1. It has an incubation period of several weeks.
2. There is mild pain and redness with transient hypopyon.
3. It affects the anterior vitreous and anterior uvea causing
thick, organized hypopyon.
4. The whole vitreous turns into a granulomatous mass.

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Differential Diagnosis
1. Retained cortical lens material following lens
extraction may be associated with severe
anterior uveitis.
2. Toxic reaction to the irrigating fluid,
chemicals or foreign material.
3. Panophthalmitis—There is associated
inflammation of extraocular tissues resulting
in lid oedema, chemosis and painful
limitation of movements of eyeball.

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Complications
1. Panophthalmitis
2. Papillitis
3. Phthisis bulbi.

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Investigation
 Identification and culture and sensitivity of the
causative organism from the aqueous and vitreous
taps confirms the diagnosis.
LABORATORY DIAGNOSIS
Ocular Fluid Sampling: Anterior Chamber and Vitreous
tapes are the Gold standard.
Microbiology
Gram stain
Culture
Fungal Staining: Use Calcogluor white, and sabouraud
agar for suspected cases.
Molecular Methods: PCR on vitreous fluid provides
high sensitivity.
IMAGING: B-Scan checking Vitritis, foreign bodies.

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TREATMENT
• 1. Broad-spectrum antibiotics which cover gram-positive and gram-
negative organisms are given.
i. Intravitreal—An aminoglycoside (gentamicin or amikacin) and
vancomycin should be injected slowly into the midvitreous cavity using a
25-gauge needle.
ii. Periocular injections or subconjunctival injections of:
• Vancomycin 25 mg and ceftazidine 100 mg daily for 5-7 days.
• Gentamicin 20 mg and cefuroxime 125 mg daily for 5-7 days.
iii. Topical therapy every 30-60 minutes
. iv. Systemic—Intravenous ceftazidine (2 gm every 72 hours), cefotaxime
(1 gm twice daily) • Oral ciprofloxacin (750 mg every 8 hours).

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2. Corticosteroids are given topically, systemically and by periocular
subconjunctival injections.
3. Atropine and analgesics are useful in giving rest to the eye and
relieving pain.
4. Vitrectomy if done early may be useful in severe and resistant cases
only.
It is indicated particularly in fungal endophthalmitis along with
intravitreal and systemic amphotericin B.

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• 1. Treatment of pre-existing infections before surgery, e.g.
staphylococcal blepharitis, conjunctivitis and dacryocystitis should be
done.
• 2. Preoperative prophylactic topical broad-spectrum antibiotics are
instilled to decrease patients conjunctival bacterial flora.
• 3. Postoperative subconjunctival injection of antibiotics and steroids is
a must.
• 4. Meticulous attention to aseptic surgical technique is given

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POSTERIOR UVEITIS (CHOROIDITIS)

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CHOROIDITIS
 There is inflammation of the posterior uveal
tract (choroid). It may be focal, multifocal and
diffuse in location.
 As the outer layers of retina depend upon the
choroid for nutrition, there is always associated
inflammation of retina (chorio-retinitis).
Clinical Forms
It occurs in two forms which is similar to anterior
uveitis.
1. Granulomatous choroiditis is due to direct
pathogenic infection.
2. Non granulomatous choroiditis or exudative
choroiditis is due to allergic reaction.

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SYMPTOMS
1. There is diminution of vision due to retinal lesions and
opacities in the vitreous (floaters).
2. Photopsia—Flashes of light are seen due to irritation of
the retina.
3. Metamorphopsia—Straight line appears wavy due to
oedema of the retina.
4. Micropsia—The objects appear smaller than they
actually are due to separation of rods and cones.
5. Macropsia—The objects appear larger than they
actually are due to overcrowding of rods and cones.
6. Positive scotoma—Patient complains of seeing a black
spot in front of the eye corresponding to the retinal lesion.
7. Negative scotoma—A black spot is present in the field
of vision similar to the blind spot, corresponding to the
retinal lesion

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SIGNS
Fundus Examination
1. In early stage one or more yellowish areas with ill-defined
edges are seen deep to retinal vessels.
This appearance is due to infiltration of the choroid and
presence of exudates which hide the choroidal vessels. There
may be sheathing of retinal vessels.
2. Black spots are seen floating in the vitreous (vitritis).
3. ‘Spill over’ uveitis—Anterior segment inflammation such as
posterior synechia, kp, aqueous flare may be present.
4. In the healing stage—Yellow lesions become white due to
fibrosis and the lesions are surrounded by black pigments

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Differential Diagnosis
It includes
 toxoplasmosis,
 peripheral toxocariasis
 syphilis,
 multiple sclerosis
 sarcoidosis.

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Clinical Types
 Choroiditis is usually classified according to number
and site of lesions.
1. Disseminated (diffuse) choroiditis—The lesions are
seen scattered all over the fundus, e.g. as in syphilis
and tuberculosis.
2. Anterior choroiditis—The lesions are seen in the
peripheral parts (near equator) of the fundus, e.g. as
in syphilis.
3. Central choroiditis—It involves the macular area or
posterior pole, e.g. as in toxoplasmosis,
histoplasmosis.
4. Juxtapapillary choroiditis (of Jensen)—The lesions
are present around the optic disc. It occurs in young
persons.

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Complications
In late stages following complications are
seen:
 Complicated cataract.
 Secondary glaucoma.
 Choroidal neovascularization.
 Retinal detachment.

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Investigations
IMAGING
• Fundus Fluorescein Angiography: Used to detect inflammatory activity, vascular
leakage, or nonperfusion.
• Optical Coherence Tomography: Evaluate structural changes like subretinal fluid,
retinal thickening.
• Fundus Autofluorescence: Identifies active vs old lesion
LABORATORY BLOOD TEST
Infectious screening
Autoimmune:CBC, ESR
Genetic Markers: HLA-A29

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Treatment
 It is usually unsatisfactory as great damage is usually
done to the retina before the condition can be
controlled,
1. Atropine provides rest to the eye by paralysing the
ciliary muscles.
2. Heat application by diathermy or an electric pad may
be useful.
3. Corticosteroids—Systemic administration of
corticosteroids or ACTH cuts short an attack and hastens
healing.
4. Specific treatment is required for causative organism
such as toxoplamosis, toxocariasis, tuberculosis, syphilis,
etc.

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• Hygiene and Infection Prevention.
• Toxoplasmosis Prevention.
• Preventative Eye Care.
• Sun Protection.

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References
• AK khurana –Comprehensive Ophthalmology
• R-jogi –basic-ophthalmology
• Clinical ophthalmology-Rotation

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