Course 5-7 :

5. Cornea & sclera 6. Uveea 7. Lens & glaucoma

Course no.5. CORNEA AND SCLERA

Cornea
- The cornea is the anterior, transparent part of the sclera and together they form the outer tunic (membrane) of
the eyeball. It is approximately round at the front view and convex anteriorly at the profile view. The cornea
covers the iris, pupil, and anterior chamber. The cornea, with the anterior chamber and lens, refracts light, with
the cornea accounting for approximately two-thirds of the eye's total optical power. The refractive power of the
cornea is approximately 43 dioptres.

-The cornea has unmyelinated nerve endings sensitive to touch, temperature and chemicals; a touch of the cornea
causes an involuntary reflex to close the eyelid.

-Compared to other tissues, the density of nerve endings is highest in the cornea, reaching maximum in the center
and decreasing towards the periphery. These nerve endings provide pain sensitivity and contact sensitivity. There
is no thermal sensitivity in the cornea.

-Sensory innervation is provided by the ciliary nerves that originate in the nasal branch of the ophthalmic nerve.
The innervation also has a trophic role: damage to the ophthalmic branch of the trigeminal nerve causes total loss
of corneal sensitivity and the appearance of neuroparalytic keratitis.

- The healthy cornea does not have blood vessels within it, and for this reason it is transparent . Oxygen
dissolves in tears and then diffuses throughout the cornea. Nutrients are transported by diffusion from the tear
fluid through the outside surface and the aqueous humour through the inside surface. The cornea has a diameter
of about 11.5 mm and a thickness of 0.5–0.6 mm in the center and 0.6–0.8 mm at the periphery. Transparency,
avascularity, the presence of immature resident immune cells, and immunologic privilege makes the cornea a
special tissue.

-Certain sites of the human body have immune privilege, meaning they are able to tolerate the introduction of
antigens without eliciting an inflammatory immune response. Tissue grafts are normally recognised as foreign
antigen by the body and attacked by the immune system. In immune privileged sites, tissue grafts can survive for
extended periods of time without rejection occurring. One of the I mmunologically privileged sites is the eye.

-The passage area between the cornea and the sclera is at the level of the corneosceral limbus. In its thickness are
the anatomical elements of the camber angle, the drainage place of the aqueous humor.

Corneal injury
The cornea is particularly exposed to trauma due to its position in the anterior part
Injuries to the cornea can be categorized into traumatic and exposure-releated and can vary greatly, from minor
and insignificant to potentially vision-threatening.

1.Traumatic injuries most commonly include corneal abrasions and foreign bodies. Exposure-related
injuries to the cornea include burns from chemical, thermal, and radiation sources.
More severe corneal injuries include penetrating trauma with or without the involvement of the anterior and
posterior segment structures, ocular surface burns leading to limbal stem cell deficiency, and secondary
glaucoma.
  -corneal abrasion

Traumatic corneal erosions affect the corneal epithelium without crossing the Bowman's membrane.

1. I. Corneal abrasions may be caused by any number of objects including fingernails, contact lens wear, plant
branches, foreign bodies on the tarsal conjunctiva, deviated cilia or foreign objects blown or thrown into the
eyes.
subjective symptoms are very intense, disproportionate to the severity of the injury (the corneal epithelium is
richly innervated, and therefore, very painful when an injury occurs) : foreign body pain, tearing,
blepharospasm, photophobia. The pain disappears after the instillation of anesthetic eye drops. The epithelium
does regenerate quickly, with most abrasions healing within 24 to 48 hours.

Diagnosis is often by slit lamp examination after fluorescein dye has been applied (after the instillation of
anesthetic eye drops!!).
Epithelial abrasions have a variable shape: linear, punctiform, several vertical lines in the case of a foreign body
on the tarsal conjunctiva. Examination of the tarsal conjunctiva and the palpebral margin is necessary to exclude
conjunctival foreign bodies or deviated cilia.

Treatment is typically with antibiotic drops or ointment. In those who wear contact lenses moxifloxacin eye
drops is often recommended. Paracetamol or NSAIDs, and eye drops such as tropicamide that paralysis the pupil
can help with pain. No need eye patching for those with simple abrasions.

1.II. Impenetrable corneal wounds that extend beyond the Bowman's membrane are generally linear in shape
and are produced by hard, sharp bodies.
the symptoms are similar to those of corneal erosion but much more attenuated.
A particular shape is the corneal scalp which can be produced by fragments of broken windshield. The lesions
are usually multiple, with irregular edges and can retain in their depth remnants of windshield.
Perforated corneal wounds are a medical emergency, require suturing and radiological examination to detect any
intraocular foreign bodies.

1.III.Corneal foreign body

The corneal abrasions are the most common form of ocular trauma. and the corneal foreign body account for the
second one.
Corneal foreign body is foreign material on or in the cornea, usually metal, glass, or organic material.
Most commonly it is a combination of a lack of protective eye-wear and high-risk activities (grinding,
hammering, drilling, and welding)
The foreign bodies can lodge in any of the five layers and can continue forward, creating an open globe injury.
The history of present illness will typically be consistent with a sudden onset event.
Symptoms include a foreign body sensation, grittiness, irritation, pain, redness, photophobia, blurred vision and
excessive watering of the and difficulty with keeping the eye opened.
All ocular trauma patients should be administered adequate pain control to assist in obtaining an accurate exam.

1.III. *Metallic foreign bodies in the context of hammering or drilling metal-on-metal, particularly in the
absence of protective eyewear, may just embed in the corneal surface but can penetrate the eye if travelling at
sufficiently high velocity. In the case of globe penetration, urgent referral to the nearest emergency department
with ophthalmological care should occur. Foreign bodies involving organic material, such as those sustained
while gardening, carry a high risk of infection . Seeds , insect scales and caterpillar setae are infrequent, but have
vision threatening consequences
All patients suspected of having a corneal foreign body should also undergo a slit lamp examination.

Care should be taken to inspect the entire eye as well as flipping the upper lid, as foreign bodies can hide under
the tarsal plate and introduce micro-trauma with every blink of the eye. This should first be without fluorescein
dye

Upon adding the fluorescein, again a general inspection should be performed, looking for any corneal abrasions
or lacerations. The dye will also allows to perform the Seidel test, which when positive, indicates globe
perforation.
Foreign body removal should commence as soon as possible; within 24 hours is ideal, as, after this time, the
foreign body can become embedded within the stroma of the cornea, and this makes removal more difficult
Simple irrigation and a moist cotton swab is the first step. The majority of recent and superficial foreign bodies
can be successfully removed this way. If this is unsuccessful, the bevel of a needle is usable under slit lamp
guidance. The aim of the procedure is the safe and complete removal of the foreign body and any surrounding
rust ring

Upon successful removal off the corneal foreign body, treatment consists of pain control, follow up, and
consideration given to prophylactic antibiotics. When choosing an antibiotic, contact lens wearers should have
anti-pseudomonas coverage.
There has been considerable controversy over employing an eye patch. It is contraindicated in contact lens
wearers, as well as organic foreign bodies, as they can increase the rate of infection, although patches have not
shown to be of benefit in time to corneal healing, or reduction in symptomatic days
A.Metallic particle from drilling; B. Seed; C. Insect scale; D. Keratitis and endophthalmitis from a

contact lens.  

2. Keratitis is a painful inflammation of the eye. It can be caused by an infection or an injury. There are many
different types of keratitis, and each type needs different treatment.
The condition is often marked by moderate to intense pain and usually involves any of the following symptoms:
pain, impaired eyesight, photophobia (light sensitivity), red eye and a gritty sensation.

Based on the etiological agent, keratitis can be classified as:

2. I Infectious Keratitis
 A. Bacterial keratitis - including Pseudomonas, Staphylococcus, Streptococcus, Moraxella, Nocardia, and
Atypical Mycobacteria
B. Protozoal keratitis - including Acanthamoeba
C. Fungal keratitis - This includes infection by Aspergillus, Fusarium, Candida
D. Viral keratitis - This includes infection by Herpes simplex virus (HSV), Herpes zoster virus (HZV),
Adenovirus, and others.

2.II. Non-infectious Keratitis : Local causes - includes trichiasis, giant papillae, tarsal foreign body.
A.Peripheral ulcerative keratitis : Collagen vascular diseases, like rheumatoid arthritis, granulomatosis with
polyangiitis, polyarteritis nodosa, , systemic lupus erythematosus, and others
B. Neurotrophic corneal ulcer (post- herpes zoster ophthalmicus, trigeminal nerve damage due to surgery or
tumor)
C. Xerophthalmia

Classification (by stage of disease):Superficial punctate keratitis\ Ulcerative keratitis

Classification (by chronicity) Acute\Chronic

2.I.A Bacterial keratitis is a serious bacterial infection of the cornea which can, in severe cases, cause loss of
vision. Bacterial keratitis is also often referred to as a 'corneal ulcer'
-The most common risk factor for bacterial keratitis is contact lens wear. Overnight wear and inadequate lens
disinfection have been associated with increased risk of infection.
-Other predisposing risk factors include: trauma (including foreign bodies and chemical and thermal injuries),
contaminated ocular solutions, changes in the corneal surface (from dry eye, eyelid misdirection, and exposure),
altered ocular defense mechanisms, blepharitis and viral keratitis.
In younger patients, trauma and contact lens wear are the most common predisposing factors while in older
patients, chronic corneal disease such as dry eyes, surgical trauma are also important risk factors.

Stages of Corneal Ulcer (bacterial keratitis)

1.Stage of progressive infiltration
2.Stage of active ulceration
3. Stage of regression
4. Stage of cicatrization

History
Doctor should ask about the onset of symptoms, whether there was recent trauma to the eye, and whether the
patient engaged in activities such as swimming in contact lenses. Patients should be asked about contact lens. A
past ocular history should include whether there was a history of eye trauma, previous eye diseases, or eye
surgeries, medications.

Symptoms
Symptoms include rapid onset of ocular pain, redness, photophobia, discharge, and decreased vision. The rate of
progression of the symptoms is related to the virulence of the infecting organism.

Signs
Signs of bacterial keratitis might include conjunctival injection and focal white infiltrates (with epithelial
demarcation and underlying stromal inflammation). Flourescein can be used to highlight areas of epithelial cell
loss.
Other signs can include: corneal thinning, stromal edema, mucopurulent discharge, anterior chamber reaction
and hypopyon. Eyelid edema may be present in some cases. In severe cases, posterior synechiae, hyphema, and
rise the intraocular pressure may occur.

Diagnostic procedures
Corneal scrapings for smears and cultures are performed to determine the causative organism in all ulcers that are
either large, involve the middle to deep stroma, are sight threatening, are chronic in nature, are atypical, or are
unresponsive to treatment.

Differential diagnosis
The differential diagnosis of bacterial keratitis is large. Other infectious etiologies must be considered. Non-
infectious (or sterile) ulcers may be related to dry eye syndrome, exposure or neurotrophic keratopathy,
autoimmune diseases (such as rheumatoid arthritis), vernal keratoconjunctivitis, vitamin A deficiency. Round,
white scars from old foreign bodies may be confused with small infiltrates.

Treatment
-Contact lenses should be discontinued.
-Topical antibiotic drops should be prescribed. Oral antibiotics may be considered for patients with deep
ulcers or scleral involvement. Oral medication can be used for pain.
-Medical therapy
Topical broad spectrum antibiotic therapy should be used until culture results are available.
*Small non-staining peripheral ulcers may be started on antibiotics drops every 2 to 6 hours.
* For ulcers with epithelial defects and an anterior chamber reaction, a antibiotic drop every hour around
the clock is recommended.
* Large or vision threatening ulcers (with moderate to severe anterior chamber reaction and/or involving
thare usually treated with fortified antibiotics drops.
-Medical follow up
Daily follow up is needed until a response to antibiotic regimen is noted.
On follow up, assess the size of the epithelial defect, the size and depth of the infiltrate, the degree of pain and
the anterior chamber reaction.
Taper the antibiotics when ulcer improves
*In severe non-responding ulcers hospitalization for frequent monitoring and drop administration may be
required. Admission (to hospital) may be needed if there is scleral extension or corneal perforation and systemic
antibiotics and/or surgery are needed; the patient is unable to instill the medication as prescribed, he is unable to
return for follow up or is noncompliant.
* Surgery
A corneal transplant or patch graft is considered for impending or actual perforations.

Complications
Potential complications include scleral extension of the infection, residual corneal scarring, irregular
astigmatism, loss of vision, corneal perforation, and endophthalmitis .
Prognosis
The prognosis depends on the size, location, depth, and etiology of the corneal ulcer as well as any pre-existing
ocular conditions.

3. Fungal keratitis or keratomycosis refers to an infective process of the cornea caused by any of the multiple
pathologic fungi capable of invading the ocular surface. It is most typically a slow, relentless disease that must be
differentiated from other types of corneal conditions with similar presentation; especially its bacterial
counterpart, which accounts for the majority of the microbial corneal infections.
- Fungal keratitis is a serious ocular infection with potentially catastrophic visual results
- The list covers many fungi including but not limited to yeasts of Candida , Aspergillus , Fusarium.
Corneal ulcers unresponsive to broad-spectrum antibiotics, the presence of satellite lesions, and scanty secretions
in a large ulcer are some signs that should raise flags to the attending professional about the possibility of a

mycotic agent.  

Symptoms
Symptoms are similar to any corneal infection including blurred vision, redness, tearing, photophobia, pain,
foreign body sensation and secretions. In some cases the lesion are rather indolent which help to delay the
diagnosis and hence delay the treatment. Suspicion should be high in cases of trauma with vegetable matter.

Clinical diagnosis
Under the slit lamp, early on the lesion might look like an unhealed corneal abrasion with scanty infiltrates and
no secretions. With time however, the ulcer develops thicker infiltrates and fuzzy margins. The presence of
satellite lesions strongly suggests a fungal infection. Redness and periocular edema are also common.
For a definitive diagnosis, scrapings taken from deep within the lesion should be made and inoculated in
Sabouraud agar In general,

Treatement consists of medical therapy with the use of topical and/or systemic anti-fungal medications alone or
in combination with surgical treatment.

4. Viral keratitis
Viral diseases of the cornea result in four types of keratitis-punctate, dendritic,
disciform and other types of parenchymatous keratitis.

4.I Herpetic simplex keratitis is a form of keratitis caused by recurrent herpes simplex virus (HSV) infection in
the cornea
Evolution:
1.It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving
the cornea.
2. Primary infection typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis),
accompanied by small white itchy lesions on the corneal surface. The effect of the lesions varies, from minor
damage to the epithelium (superficial punctate keratitis), to more serious consequences such as the formation of
dendritic ulcers.

symptoms: Infection is unilateral, affecting one eye at a time. Additional symptoms include dull pain deep
inside the eye and mild to acute dryness. Most primary infections resolve spontaneously in a few weeks. Healing
can be aided by the use of oral and topical antivirals.
Recurrences may be more severe. The epithelial layer is destroyed as the dendritic ulcer grows, and mild
inflammation (iritis) may occur in the underlying stroma of iris. Sensation loss occurs in lesional areas,
producing generalised corneal anaesthesia with repeated recurrences.
Keratitis caused by HSV is the most common cause of cornea-derived blindness in developed nations. Therefore,
HSV infections are a large and worldwide public health problem.

Signs and symptoms

Corneal involvement is rarely seen in primary infection.
Recurrent herpes of the eye is caused by reactivation of the virus in a latently infected sensory ganglion, transport
of the virus down the nerve axon to sensory nerve endings, and subsequent infection of ocular surface.

4.II. Dendritic ulcer (Epithelial keratitis)

This classic herpetic lesion consists of a linear branching corneal ulcer (dendritic ulcer).
During eye exam the defect is examined after staining with fluorescein dye. The underlying cornea has minimal
inflammation.
Symptoms: Patients with epithelial keratitis complain of foreign-body sensation, light sensitivity, redness and
blurred vision. Focal or diffuse reduction in corneal sensation develops following recurrent epithelial keratitis.
* In immune deficient patients or with the use of corticosteroids the ulcer may become large and in these cases
it is called geographic ulcer.

Herpes keratitis:    

Treatment
Epithelial keratitis is treated with topical antivirals, which are very effective with low incidence of resistance.
Treatment of the disease with topical antivirals generally should be continued for 10–14 days. Cortisone-
containing eye drops are contraindicated.

4.III. Interstitial Keratitis is any non-ulcerating inflammation of the corneal stroma without the involvement of
either the epithelium or endothelium. The term refers to a common end for a number of diseases which primarily
manifest as inflammation and vascularization of the corneal stroma with minimal loss of tissue.The inflammation
and blood vessel invasion characteristic of interstitial keratitis can result in scarring of this layer resulting in
decreased vision.

Ocular zoster can affect any part of the eye from the conjunctiva to the optic nerve.

4.IV Acute Zoster Keratitis

Acute keratitis can occur up to 1 month following the onset of rashes . Some of the common symptoms:
manifestations include the following:
Punctate keratitis and pseudodendrites consist of swollen, poorly adherent epithelial cells and are usually seen in
the corneal periphery .
Nummular keratitis is characterized by coin-shaped (nummular) lesions that appear in the superficial stroma. The
lesions usually underlie areas of previous epithelial keratitis.

4.V. Chronic Zoster Keratitis

This form occurs up to several months following the initial HZO infection.
Mucous plaques can occur suddenly in an eye that has been nearly quiescent. They appear as stuck-on, grayish,
branching lesions and have minimal underlying inflammation Mucous plaques can be highly resistant to
treatment, and multiple recurrences can lead to scarring.
Interstitial keratopathy: HZO keratitis can lead to vascularization, with a leash of vessels leading up to the area
of scarring.

Long-Term Complications
As in HSV keratitis, neurotrophic ulcers can occur repeatedly and cause problems long after the acute episode
has resolved. In contrast to HSV keratitis, however, profound loss of corneal sensation can result from a single
episode of HZO, and these ulcers are more likely to perforate.
 * Neuralgia is almost always associated with acute HZO, but pain that lasts longer than 1 month constitutes
postherpetic neuralgia (PHN), perhaps the most debilitating sequela of HZO. PHN occurs in 10% to 30% of
patients with HZO, and its risk factors include increasing age, prodromal pain, more severe rash, greater acute
pain, and ophthalmic involvement.
symptoms: The pain is of variable quality and has been described by patients as burning, shooting, sharp,
throbbing, or tender. One classic feature of this pain is allodynia (pain following a stimulus that is normally non-
noxious, such as wind). The pain can be severe and unrelenting and can take over the patient's life, resulting in
decreased functioning and increased risk of depression.

Treatment
Topical antivirals have no role in the treatment of HZO. However, oral antivirals begun within 72 hours of onset
of symptoms can reduce the severity of the disease and of any long-term complications, including PHN. Recent
studies have indicated that in certain populations, such as immunocompromised patients, this 72-hour window
can be extended. For every patient with HZO, oral acyclovir can be used, 800 mg 5 times a day, for 7 to 14 days,.
Valacyclovir and famciclovir can also be used . For the treatment of HZO, a good rule of thumb is to double the
doses of the medications used for HSV keratitis.

      ZZ disciform keratitis 

   ZZ KERATIS: Late dendriform keratitis, which is

polymerase chain reaction-positive for herpes zoster virus.

The use of corticosteroids for the treatment of HZO is controversial.

As most long-term complications of HZO are related to the neurotrophic status and relative dryness of the
affected eye. Punctal occlusion, artificial tears, bandage contact lenses, tarsorrhaphy, eyelid reconstructive
surgery, and conjunctival flaps all have a role to play in the treatment of the various HZO complications.
Tarsorrhaphy is especially useful in recalcitrant cases of neurotrophic keratitis.

5. Corneal manifestations in general diseases: Neurotrophic keratitis

Neurotrophic keratitis is a degenerative corneal disease caused by damage of trigeminal nerve.
*Corneal nerves play an essential role in preservation of the normal metabolism and function of the ocular
surface. Loss of sensitivity impairs corneal wound healing, leading to epithelial changes including punctate
epithelial keratopathy, persistent epithelial defects, corneal ulcer, melting and perforation.
*Various ocular and systemic diseases can cause damage to the fifth cranial nerve at different levels, from
the trigeminal nucleus to the corneal nerve endings. Common causes are herpetic keratitis, diabetes, multiple
sclerosis chemical or surgical damage, abuse of anaesthetics or chronic topical treatments, chemical burns or, use
of contact lenses. and neurosurgical procedures.

The diagnosis, and particularly the treatment of neurotrophic keratitis are the most complex and challenging
aspects of this disease, as a satisfactory therapeutic approach is not yet available.
*Eye examinations:
 -Complete eye examination: examination of the eyelids, blink rate, presence of inflammatory reactions and
secretions, corneal epithelial alterations.
-Corneal sensitivity test: performed by placing a cotton wad or cotton thread in contact with the corneal
surface: this only allows to determine whether corneal sensitivity is normal, reduced or absent; or using an
esthesiometer that allows to assess corneal sensitivity.
-Tear film function test, such as Schirmer's test, and tear film break-up time.
Fluorescein eye stain test, which shows any damage to the corneal and conjunctival epithelium

Medical treatment consists mainly of supportive measures that do not address the underlying cause of the
disease. In addition, another viable therapeutic option is amniotic membrane graft, which has been shown to
play a role in stimulating corneal epithelium healing and in reducing vascularisation and inflammation of the
ocular surface.Other approaches used in severe forms include the administration of autologous serum eye drops.
Recently, novel promising treatments have been proposed and are currently under evaluation. These include
mainly topical treatment with nerve growth factor and surgical corneal neurotization.

Diseases of the sclera

1.Episcleritis is a benign, self-limiting inflammatory disease affecting the episclera. The episclera is a thin layer
of tissue that lies between the conjunctiva and the connective tissue layer that forms sclera. Episcleritis is a
common condition, and is characterized by the abrupt onset of painless eye redness.
There are two types of episcleritis, nodular and simple.
A. Nodular episcleritis lesions have raised surface.
Simple episcleritis lesions are flat.
There are two subtypes: A.1 In diffuse simple episcleritis, inflammation is generalized.
A.2. In sectoral simple episcleritis, the inflammation is restricted to one region.
Most cases of episcleritis have no identifiable cause, although about a third of cases are associated with various
systemic diseases. Often people with episcleritis experience it recurrently.
Episcleritis is caused by inflammation due to the activation of immune cells, including lymphocytes and
macrophages.
*Most of the time, the cause of episcleritis is never determined (idiopathic). Several diseases are associated
with episcleritis, including systemic vasculitis , connective tissue diseases (rheumatoid arthritis, relapsing
polychondritis, systemic lupus erythematosus), psoriatic arthritis, ankylosing spondylitis, rosacea, gout, atopy,
Crohn's disease, and ulcerative colitis.
*About 50 % of patients with relapsing polychondritis have either episcleritis or scleritis. Very rarely,
episcleritis is associated with infections, including Lyme disease, tuberculosis, syphilis, and herpes zoster.
*The redness in the eye associated with episcleritis is due to engorgement of the large episcleral blood vessels,
which run in a radial direction from the limbus.

Signs and symptoms

Symptoms of episcleritis typically include usually painless redness and watery eyes. When occurs,
the pain of episcleritis is typically mild, less severe than in scleritis, and may be tender to palpation.
There are two types of episcleritis:
A.1 the diffuse type, where the redness involves the entire episclera, The diffuse type of
episcleritis may be less painful than the nodular type.
 A.2 and the nodular type, where the redness appears more nodular, involving only a small, well-circumscribed
area. Sometimes, small nodules are present within the episclera, which move slightly over the sclera with gentle
pressure.
Discharge is absent with episcleritis, and vision is unaffected.
Episcleritis is a benign, self-limited condition that usually resolves completely over the course of a few weeks.  

Treatment
Often, treatment is not necessary, because episcleritis is a self-limiting condition. Artificial tears may be used to
help with irritation and discomfort. More severe cases can be treated with either topical corticosteroids or oral
non-steroidal anti-inflammatory drugs.
Episcleritis is defined as inflammation confined the more superficial episcleral tissue. Episcleritis is usually
idiopathic and non-vision threatening without involvement of adjacent tissues. Vessels have a reddish hue
compared to the deeper-bluish hue in scleritis. These superficial vessels blanch with 2.5-10% phenylephrine
while deeper vessels are unaffected.
.

Course no.6 UVEEA

The uvea consists of the middle layer of pigmented vascular structures of the eye and includes the iris, ciliary
body, and choroid.
Uveitis= Uveitis is the inflammation of the uvea.
Uveitis is an ophthalmic emergency and requires a thorough examination and urgent treatment to control the
inflammation.

Classification
A. Anatomical classification
I. Anterior uveitis - The anterior chamber is the primary site of inflammation. The most common form of
uveitis, it affects the iris the ciliary body. Anterior uveitis is sometimes referred to as iritis because the iris is the
part of the uvea that is usually inflamed. bacterial, viral,fungal, parasitis:
II. Intermediate uveitis it affects the area just behind the ciliary body (pars plana) and also the most forward
edge of the retina. This is the least common type of uveitis. The vitreous is the primary site of inflammation.
Lyme disease .
III. Posterior uveitis - A rare form of the disorder that affects the back part of the eye, the choroid, and can
affect also the retina and /optic nerve. Posterior uveitis refers to inflammation involving the
choroid(choroditis),retina (retinitis),both ( chororetinitis),or retinal vessels(retinal vasculitis).
This form is more difficult to treat, and is often associated with progressive loss of vision. toxoplasmosis,
tuberculosis, fungi(candida),Herpes simplex, zoster(ARN),cytomegalovirus

-Pan-uveitis - When inflammation affects all three areas of the uvea it is referred to as pan-uveitis.
Intermediate, posterior and pan-uveitis are very serious conditions and may cause
blindness if left untreated. .Uveitis may extend to involve the cornea(keratouveitis) or sclera (sclerouveitis).
syphilis ,tuberculosis and leptospirosis.

Classification based on etiology

1.Infectious: bacterial, viral,fungal, parasitis:
2. Noninfectious: with or without known systemic association
3. Masquerade: neoplastic or non-neoplastic.
4. Uveitis is also classified by onset (sudden or insidious), duration (limited or persistent), and course (acute,
recurrent, or chronic).
*Idiopathic disease heads the diagnosis list for adult cases of anterior uveitis followed in descending frequency
by HLA B27-related disease, herpetic disease (herpes simplex virus and varicella zoster virus [HSV and VZV]),
and trauma. All other diagnoses comprise only a small percentage of cases of anterior uveitis in adults.

Clinical course:
1.Acute (of sudden onset and limited duration)
 2.Recurrent (repeated episodes separated by untreated inactive periods)
3.Cronic (persistent duration with relapse less than 3 month after discontinuation of treatment)
Remission is defined an inactivity (no visible cells) for 3 month or longer.
*Uveitis is often idiopathic but may be triggered by genetic, traumatic, immune, or infectious mechanisms.

Immunology
The defense or immune system protects our body against various, i.e., pathogenic microorganisms and their toxic
constituents, degraded and degenerated cells, both foreign and self. Generally speaking it is subdivided into a A.
nonspecifi c and a B. specifi c immune system. These two entities are, however, closely connected functionally.

A. The nonspecific (natural or innate) immune system is fully functional from birth and is responsible for
immediate defense against pathogenic germs available at any time. It is not able to “learn” during life, although
its effectiveness is enormously increased by the influence of the specific immune system. Cell agents of the
nonspecific defenses are in particular neutrophils, macrophages, and NK ( natural killer) cells. Humoral factors
also play an important role.

B. The specific (acquired or adaptive) immune system gets underway rather slowly after birth and then
advances its effectiveness during life enormously. Its main agents are lymphocytes and distinct accessory cells
(e.g., dendritic cells); macrophages are also involved. The specific defense system possesses two compartments
which use different strategies but cooperate closely:
humoral immune defense (B cells) and cell-mediated immune defense (T cells).

Humoral Immune Defense (B Cells) This function is carried out by B - lymphocytes (B cells).
-Their weapons are soluble antibodies (immunoglobulins , Ig ) which bind specifically to an antigen and thus
dispose it.
- The effector cells – the cells which conduct the real action – are plasma cells . They develop from antigen-
stimulated B cells
1.Ig.Isotype
2. IgM is most effective for agglutination of bacteria and particles
3. IgG Predominant Ig-fraction in blood plasma; among other functions complement binding and
activation, opsonization of pathogenic germs, and neutralization of toxins; transport via transcytosis through the
placental barrier; and also serves in passive immunization of the newborn
4. IgA Secreted by subepithelial plasma cells ; protection of mucosa and exocrine glands; also contained in
breast milk; protection of intestinal mucosa of the infant
5. IgE Opsonization of worm larvae (recognition through eosinophils); bound to the cell surface of mast
cells and basophils, upon antigen-binding activation of primary allergic response.

Cell-Mediated Immune Defense (T Cells) This function is carried out by T lymphocytes (T cells). These
are subdivided into two large fractions:
(1) T - helper cells ( T H cells ) secrete cytokines that are responsible for many activities of the adaptive
and innate defense.
(2) Cytotoxic ( cytolytic ) T cells ( CTC ) kill other cells by specifi c mechanisms after recognition of
antigenic cell surface structures that display these cells as virus-infected or abnormal cells.

Course of Immune Response

1. Upon first contact with an antigen consisting of protein, 1–2 weeks may pass until the immune response with
effective antibody secretion becomes noticeable (primary response).
2 .A second contact with the same anti-gen only needs a few days (secondary response).
3. Memory cells of all three compartments can sur-vive for a long time (possibly years) and can induce a rapid
and strong immune response following renewed contact with the same antigen.

Definition of Autoimmunity
Autoimmune processes are characterized by the presence of autoantibodies or autoreactive lymphocytes, i.e.,
antibodies or cells which react with self-antigens.

Definition of Autoinflammation
Autoinflammatory diseases (AIDs) have emerged as a distinct group of diseases and can be defi ned as “clinical
disorders marked by abnormally increased inflammation, mediated predominantly by the cells and
molecules of the innate immune system” ; i.e., in contrast to autoimmune disorders, autoantibodies or
autoreactive T cells are usually absent.

Ocular Immune Privilege

Antigens introduced into the AC (?) elicit a unique form of immune deviation in which classical Th1 immune
responses, such as DTH(?) and complement- fixing antibody production, are suppressed, while the generation of
non-complement- fi- xing antibodies is preserved.
Antigens introduced into the posterior regions of the eye induce a similar immune devi-ation, although this form
of immune regulation is less well understood.

Implications for Therapy

Inhibition of the inflammatory cascade is the most important therapeutic strategy. Glucocorticoids and
nonsteroidal antiinflammatory (NSAIDS) drugs have been applied as soon as the inflammatory origin of
autoinflammatory disorders was identified. Colchicine and chloroquine have also been used, and also
immunosuppressant agents have been shown to be effective.

Immunology of Clinical Uveitis

Uveitis can be induced by various mechanisms and multiple antigens.
* Microbial antigens, the only ones known, may lead directly to uveitis in case of severe pathogenicity of the
antigen but may also induce an immune reaction after being recognized by antigen- presenting cells with
activation of T cells. In an autoinfl ammatory way microbial antigens seem to induce interleukin 1 (IL-1) with
activation of T cells. The role of autoantigens in clinical uveitis is still unclear.
The role of any other antigens inducing uveitis still is unclear.

I. Anterior uveitis
Anterior uveitis includes iridocyclitis and iritis. Iritis is the inflammation of the anterior chamber and iris. -
Iridocyclitis is inflammation of iris and the ciliary body with inflammation predominantly confined to ciliary
body. Up to 90% of uveitis cases are anterior in location (iritis). This condition can occur as a single episode and
subside with proper treatment or may take on a recurrent or chronic nature.

Causes of anterior uveitis: In most cases we don’t know what causes it. For some patients, Anterior uveitis
can occur regularly. The following conditions contribute to the cause of Anterior uveitis including rheumatoid
arthritis, juvenile rheumatoid arthritis, anklylosing spondlyitis, lupus, syphilis, gout, herpes virus infection,
Chron’s disease, ulcerative colitis, psoriasis, and eye injury.
Blood tests or x-rays can be done to find a potential cause.

Anterior uveitis tends to be the most symptomatic, especially when acute.

Symptoms include: pain, redness, photophobia, decreased vision (to a variable degree), watery discharge,
sometimes preceded by mild ocular discomfort for a few days.
Chronic anterior uveitis may have less dramatic symptoms and present with irritation or decreased vision.
Visual acuity is variably impaired depending on the severity of inflammation and the presence of
complications. It is frequently only mildly reduced in acute anterior uveitis

Diagnosis: Slit-lamp findings include keratic precipitates (white blood cell clumps on the inner corneal
surface), cells and flare (a haze) in the anterior chamber (aqueous humor), miosis and posterior synechiae.
With severe anterior uveitis, white blood cells may layer in the anterior chamber (hypopyon).

Signs include hyperemia of the conjunctiva adjacent to the cornea (ciliary flush or limbal injection).

1.Ciliary injection is due to involvement of deeper blood vessels and is typically seen in anterior uveitis on
acute onset. This sign is characteristically absent in cronic anterior uveitis.
2.Miosis, due to pupillary sphincter spasm predisposes to the formation of posterior synechiae.
-Anterior chamber cells are dependable indicator of inflammatory activity.
 3.Tyndall phenomenon means scattering of a beam of light by a medium containing small suspended
particles—e.g., smoke or dust in a room, which makes visible a light beam entering a window. In the anterior
chamber, this effect is made by cells witch are present in the aqueous humor. We will note Tyndall +, or ++ .
4.Hypopion refers to a whitish purulent exudate composed of inflammatory cells in the inferior part of the
anterior chamber forming an horizontal level under the influence of gravity.
5.Keratic precipitates are deposits on the corneal endothelium composed of inflammatory cells. They are
usually concentrate inferiorly, often in a triangular pattern with apex pointing up, under the influence of
gravity and aqueous convection currents.
Their characteristic indicate the probable type of uveitis: tipically smaller in the non-granulomatous
inflammation typic in acute anterior uveitis and medium to large (classically chronic) granulomatous

inflammations. HYPEREMIA:    

  -HYPOPION ANTERIOR UVIETIS

Posterior synechiae
6. Large greasy- appearing granulomatous keratic precipitates are said to have a ”mutton fat ”
appearance. Long standing k. precipitates may become pigmented.
7. Aqueous flare is haziness of the normally clear fluid in the anterior chamber, reflecting the presence of
protein due to breakdown of the blood aqueous barrier.
The presence of flare indicates active inflammation with a resultant higher risk of complications.
8. Fibrinous exudate in the anterior chamber is common in severe acute anterior uveitis. he exudates are
also deposited in the pupillary field, and at first it is resorbed under treatment in a few days. If the exudate
from the pupillary field is not resorbed, it is organized in the form of a membrane, an aspect called pupillary
occlusion.
9. Iris nodules on the pupillary margin or involving the stroma
10.Posterior synechiae are inflammatory adhesion between pupil margin and the anterior lens capsule.
PICTURE: LEFT Chronic Cytomegalovirus anterior uveitis showing fine to
large keratic precipitates with a small area of mild stromal edema
PICTURE RIGHT (SMALLER PUPIL):  Granulomatous KP (keratic precipitates) plastered on
the back surface of the cornea

   
11. Adhesions are loose at first and break easily when mydriatic instillation. If the synechiae are for
several days, the posterior face of the irisukui remains adherent to the anterior crystalloid and the pupil dilates
irregularly. When these synechiae break, remnants of pigment epithelium remain on the anterior crystalloid.
If they do not break, the pupil acquires a clover shape.( )
-in severe cases, when the adhesions are strong, the pupil does not dilate at all under the action of mydriasis.
These are annular iridescent synechiae or pupillary seclusion.
-The seclusion and the pupillary occlusion cause the circulation of the aqueous humor to stop, from the
posterior chamber to the anterior one; aqueous humor accumulates in the posterior chamber and causes
secondary glaucoma.

12. Odher signs include: iris atrophy, hetechromia iridis, iris neovascularization
- Intraocular pressure may be reduced or elevated.
Posterior segment examination should alwais performed to detect a masquerading cause of anterior uveitis or
complications such macular cystoid edema.

Fibrinous anterior uveitis:

green eye picture: Slit-lamp photograph showing

acute anterior uveitis with fibrin in the anterior chamber and a hypopyon in a
patient human leukocyte antigen (HLA)-B27-positive with ankylosing spondylitis. 
 

II. Intermediate uveitis is typically painless and manifests with floaters

decreased vision
The primary sign is cells in the vitreous humor. Aggregates and condensations of inflammatory cells often
occur, appearing as "snowballs." Vision may be decreased because of floaters or cystoid macular edema,
which results from fluid leakage from blood vessels in the macula. Confluent and condensed vitreous cells and
snowballs over the pars plana (part of the ciliary body that extends posteriorly beyond the junction of the iris
and sclera) may cause a classic "snowbank" appearance, which can be associated with neovascularization of
the retinal periphery.
  - iris atrophy (viral uveitis)

III. Posterior uveitis may give rise to various symptoms but most commonly causes floaters and
decreased vision as occurs in intermediate uveitis.
Signs include
1.Cells in the vitreous humor
2. White or yellow-white lesions in the retina (retinitis), underlying choroid (choroiditis), or both
3. Retinal vasculitis
4. Optic disc edema
Panuveitis may cause any combination of the previously mentioned symptoms and signs. Panuveitis, also
known as Diffuse uveitis, is the inflammation of all uveal components of the eye with no particular site of
predominant inflammation.

Complications
Serious complications of uveitis include profound and irreversible vision loss, especially when uveitis is
unrecognized, inadequately treated, or both.
The most frequent complications include:
- Cataract (secondary to the disease process and / or to corticosteroid treatment)
- Glaucoma (secondary to the disease process and / or to corticosteroid treatment)
- Retinal detachment
- Neovascularization of the retina, optic nerve, or iris
-Cystoid macular edema (the most common cause of decreased vision in patients with uveitis)
- Hypotony (an intraocular pressure that is too low to support the health of the eye)

Diagnosis
-Slit-lamp examination
- Ophthalmoscopy after pupil dilation
- Uveitis should de suspected in any patient who has ocular pain , redness , photophobic, floaters ,
decreased vision .
- Patients with unilateral anterior uveitis have ocular ache in the affected eye if light is shined in the
unaffected eye (true photophobia), which is uncommon in conjunctivitis.

Diagnosis of anterior uveitis is by recognizing cells and flare in the anterior chamber. Cells and flare are
seen with a slit lamp and are most evident when using a narrow, intensely bright light focused on the anterior
chamber in a dark room.
Findings of intermediate and posterior uveitis are most easily seen after dilating the pupil. If uveitis is
suspected, patients should be referred immediately for complete ophthalmologic evaluation.

Masqueraders
Many conditions that cause intraocular inflammation can mimic uveitis and should be considered in the
appropriate clinical settings.
Such conditions include: * severe conjunctivitis (eg, epidemic keratoconjunctivitis),
* severe keratitis (eg, herpetic keratoconjunctivitis, peripheral ulcerative keratitis)
* and severe scleritis .
- Acute angle-closure glaucoma can cause redness and severe pain similar to that of uveitis, which is why it
is important to check intraocular pressure at every visit.

-Uveitis is often (but not always) associated with a low intraocular pressure, whereas pressure is typically
high in acute angle-closure glaucoma. Uveitis can also be distinguished from angle-closure glaucoma by the
absence of corneal haze and the presence of a deeper anterior chamber.
 -Other masqueraders include * intraocular cancers in the very young (typically retinoblastoma and leukemia)
and in older people (intraocular lymphoma).
-Much less commonly, retinitis pigmentosa can manifest with mild inflammation, which may be confused
with uveitis.

Treatment
*Corticosteroids (usually topical) and sometimes other immunosuppressive drugs: corticosteroids given
topically (eg, prednisolone acetate 1% one drop every hour while awake) or by periocular or intraocular
injection along with a cycloplegic-mydriatic drug.
Particularly severe or chronic
*Cycloplegic-mydriatic drugs
*Sometimes antimicrobial drugs: treat infectious uveitis
*Sometimes surgical therapy
Particularly severe or chronic cases may require systemic corticosteroids (eg, prednisone 1 mg / kg orally once
/ day), systemic noncorticosteroid immunosuppressive drugs , laser phototherapy, cryotherapy applied
transsclerally to the retinal periphery, or surgical removal of the vitreous (vitrectomy).

III. CHOROIDITIS (POSTERIOR UVEITIS)

III.1. Endophthalmitis means bacterial or fungal infection inside the eye involving the vitreous and or
aqueous humors. Is a form of choroiditis.
- Most cases are exogenous and occur after eye surgery, after penetrating ocular trauma, or as an extension of
corneal infection. An increasing number of cases are occurring after intravitreal injections of anti-vascular
endothelial growth factor (VEGF) medications.
-Endophthalmitis may also be endogenous, arising from bacteraemic or fungaemic seeding of the eye.

-The most common pathogens in endophthalmitis vary by category.

*Coagulase-negative staphylococci are the most common causes of post-cataract endophthalmitis, and these
bacteria and viridans streptococci cause most cases of post-intravitreal anti-VEGF injection endophthalmitis,
*Bacillus cereus is a major cause of post-traumatic endophthalmitis, and Staphylococcus aureus and
streptococci are important causes of endogenous endophthalmitis associated with endocarditis.
* Endogenous fungal endophthalmitis in hospitalized patients is usually caused by Candida species,
particularly Candida albicans.

-Most cases of endophthalmitis present acutely, with hours to a few days of symptoms. These cases are
medical emergencies, as delay in treatment may result in permanent vision loss.

Symptoms include decreased vision (95%), red eye (80%), and eye pain (75%) Patients feel otherwise well and
are afebrile.
diagnosis: On physical examination, vision is decreased, eyelids are normal to slightly swollen, the conjunctiva
is injected, and a hypopyon is present in >80% of cases 15.
Treatment
The most important component of therapy is the direct injection of antibiotics into the eye. The second
component of treatment is vitrectomy. Vitrectomy surgically debrides the vitreous humor, similarly to draining
an abscess, and is the fastest way of clearing infection in eyes with fulminant endophthalmitis.

III. 2.Panophthalmitis
Definition: Acute suppurative inflammation of the inner eye with necrosis of the sclera (and sometimes the
cornea) and extension of the inflammation into the orbit. Pain may be severe and the globe may rupture. In
endophthalmitis the globe does not rupture.

III.3.Toxoplasma chorioretinitis, more simply known as ocular toxoplasmosis, is possibly the most common
cause of infections in the back of the eye (posterior segment) worldwide. The causitive agent is Toxoplasma
gondii.
 -The diagnosis is made by examination of the eye, using ophthalmoscopy. Sometimes serologic testing is used
to rule out the disease, but due to high rates of false positives, serologies are not diagnostic of toxoplasmic
retinitis.

-Sign and symptoms: A unilateral decrease in visual acuity is the most common symptom of toxoplasmic
retinitis
Under ophthalmic examination, toxoplasmic chorioretinitis classically appears as a focal, white retinitis with
overlying moderate inflammation of the vitreous humour.
-A unifocal area of acute-onset inflammation adjacent to an old chorioretinal scar is virtually pathognomonic
for toxoplasmic chorioretinitis.
-Focal condensation of vitreous and inflammatory cells may be seen overlying the pale yellow or gray-white
raised lesion in the posterior pole.

-Pathophysiology
1.Toxoplasma gondii is an intracellular parasite that causes a necrotizing chorioretinitis
2. Congenital disease: occurs due to the acquisition of the organism by a pregnant woman exposed to tissue
cysts or oocytes in uncooked meat or substances contaminated with cat feces. Spontaneous abortion may result if
the disease is acquired during the first trimester.
3. Retinochoroiditis is the most common manifestation, occurring in 3/4 of cases.

In congenital toxoplasmosis, the disease is bilateral in 65–85% of cases and involves the macula in 58%.
Chronic or recurrent maternal infection during pregnancy is not thought to confer a risk of congenital
toxoplasmosis because maternal immunity protects against fetal transmission. In contrast, pregnant women
without serologic evidence of prior exposure to Toxoplasma should take sanitary precautions such as having
someone else clean and maintain litter boxes and avoiding undercooked meats.

In acquired toxoplasmosis, the ocular form of the disease occurs much less frequently. Previously, only 1-3% of
patients with acquired infection were believed to develop ocular toxoplasmosis. However, serologic studies
suggest that ocular toxoplasmosis is more commonly associated with acquired infection than was previously
believed.

Diagnosis
In most instances, the diagnosis of toxoplasmic retinochoroiditis is made clinically on the basis of the appearance
of the characteristic lesion on eye examination.
1. Seropositivity (positive blood test result) for Toxoplasma is very common and therefore not useful in
diagnosis; however,
2. a negative result i.e. absence of antibodies is often used to rule out disease.
3. Serology is useful to confirm active toxoplasmic retinochoroiditis, not only by showing positivity but by
also showing a significant elevation of titers:
*The mean IgG values were 147.7 ± 25.9 IU/ml for patients with active disease versus 18.3 ± 20.8 IU/ml for
normal individuals.
* Antibodies against Toxoplasma:
-IgG : appear within the first 2 weeks after infection, typically remain detectable for life, at low levels
and may cross the placenta.
-IgM : rise early during the acute phase of the infection, typically remain detectable for less than 1 year,
and do not cross the placenta.
-IgA : Measurement of IgA antibody titers may also be useful in a diagnosis of congenital
toxoplasmosis in a fetus or newborn because IgM production is often weak during this period and the presence of
IgG antibodies may indicate passive transfer of maternal antibodies in utero. IgA antibodies however usually
disappear by 7 months.

*In atypical cases, ocular fluid testing to detect parasite DNA by polymerase chain reaction or to determine
intraocular production of specific antibody may be helpful for establishing etiology.
Neuroimaging is warranted in AIDS patients presenting with these findings because intracranial toxoplasmic
lesions have been reported in up to 29% of these patients who have toxoplasmic chorioretinitis.

Prevention
Toxoplasma infection can be prevented in large part by:
-cooking meat to a safe temperature (i.e., one sufficient to kill Toxoplasma)
-peeling or thoroughly washing fruits and vegetables before eating
-cleaning cooking surfaces and utensils after they have contacted raw meat, poultry, seafood, or unwashed fruits
or vegetables
-pregnant women avoiding changing cat litter or, if no one else is available to change the cat litter, using gloves,
then washing hands thoroughly
-not feeding raw or undercooked meat to cats to prevent acquisition of Toxoplasma
Prolonged and intense rainfall periods are significantly associated with the reactivation of toxoplasmic
retinochoroiditis. Changes promoted by this climatic condition concern both the parasite survival in the soil.

Treatment
Small extramacular lesions (lesions not threatening vision) may be observed without treatment.
- Sight-threatening lesions are treated for 4–6 weeks with triple therapy consisting of
1. Pyrimethamine: During treatment with pyrimethamine, leukocyte and platelet counts should be monitored
weekly.
2. sulfadiazine, and
3. folinic acid.: protects against the decrease in platelets and white blood cells induced by pyrimethamine.
--AFTER: Prednisone may be used for 3–6 weeks to reduce macular or optic nerve inflammation and can be
started on day 3 of antibiotic therapy.
- Corticosteroids should not be used without concurrent antibiotic treatment or in immunocompromised
patients due to the risk of exacerbation of the disease.
- Currently, there is no published evidence from randomized controlled trials demonstrating that
corticosteroids would be an effective adjunct for treating ocular toxoplasmosis
- Trimethoprim-Sulfamethoxazole has been shown to be equivalent to triple therapy in the treatment of
ocular toxoplasmosis and may be better tolerated.
- Clindamycin and azithromycin can also be considered as alternative therapies.
- Spiramycin may be used safely without undue risk of teratogenicity and may reduce the rate of
transmission to the fetus.
AIDS patients require chronic maintenance treatment.

III.3. Uveal Melanoma

Uveal melanoma is a cancer of the eye involving the iris, ciliary body, or choroid (collectively referred to as the
uvea). Any part of the uveal tract may be affected; however, choroidal melanoma is the predominant type.
evolution: Tumors arise from the pigment cells (melanocytes) that reside within the uvea and give color to the
eye. These melanocytes are distinct from the retinal pigment epithelium cells underlying the retina that do not
form melanomas.  When eye melanoma is spread to distant parts of the body, the five-year survival rate is
about 15%
Risk factors: -fair skin, blond hair, light eye color, and inability to tan.
-more commonly seen in older age groups, with a progressively rising age-specific incidence rate
that peaks at age 70 years. The age-adjusted incidence of uveal melanoma is higher in males compared with
females.

Signs and Symptoms

Ocular Melanoma may present without symptoms depending upon the location and size of the tumor. When
symptoms do occur, they can include :
* blurred vision,Diplopia, irritation, pain, a perception of flashes of light in the eye (photopsia)
a reduction in the total field of vision, loss of vision, a sensation of a foreign body in the field of vision (floaters),
redness, proptosis, a change in the shape of the pupil, pressure within the eye, metamorphopsia (a distortion of
vision where, when a person looks at a grid of straight lines, the lines appear wavy and parts of the grid appears
blank.
* Examination of patients with suspected ocular melanoma includes slit-lamp biomicroscopy and diagnostic
testing, such as B-scan ultrasonography, which is useful for characterizing and measuring the tumor
Choroidal melanoma usually presents as a dome- or mushroom-shaped subretinal mass.  
(choroidal melanoma)
Ciliary body melanoma may be associated with a wide dilated pupil, presents as a dome-shaped or sessile
lesion, and may cause lens displacement with consequent refractive and accommodation disturbances, localized

cataract or increased intraocular pressure.   (seen behind pupil)

*examination: Ultrasound biomicroscopy allows for excellent visualization of tumors of the iris and ciliary
body, and fluorescein angiography may also aid in the diagnosis.
Melanoma of the iris is usually asymptomatic and manifests as growth of a previously noted iris lesion or as a

pigmented spot on the iris.   (iris melanoma)

Multifocal and bilateral lesions are more consistent with choroidal metastasis. Hemorrhage, inflammation and
pain are rare, but may be seen in large tumors.
An atypical presentation is diffuse melanoma, which is <5 mm in thickness and encompasses more than a
quarter of the uvea. Small lesions are difficult to diagnose.

Metastasis
Because there are no lymphatic channels to the uveal tract, metastasis occurs through local extension and/or
blood-borne dissemination.
-The most common site of metastasis for uveal melanoma is the liver. Other common sites of metastasis
include the lung, bones, and just beneath the skin (subcutaneous). Approximately 50 percent of patients will
develop metastases within 15 years after treatment of the primary tumor.
Uveal metastasis originates from cancer in the breast, lung, kidney, GI tract, cutaneous melanoma, or others. to
the deeper-bluish hue in scleritis