The UVEA
The uveal tract is the densely pigmented, vascular, middle layer of the eye which lies between the sclera
externally and the retina internally . It is formed of three parts, the iris , the ciliary body and the
choroid.
THE IRIS
Anatomy of the iris
The iris is the anterior part of the uveal tract. It is a circular diaphragm that has a central perforation
called the pupil. It separates the space between the lens and the cornea into anterior and posterior
chambers.
Color:
At birth the iris is light gray in color (gray to light brown).The melanocytes show their full activity
during the first year of life giving the iris its definitive color.
Functions of the iris and pupil :
1. The iris and the pupil control the amount of light rays entering the eye by the effect of miosis
and mydriasis.
2. The iris prevents light rays from passing through the periphery of the lens that acts as a prism
causing aberrations.
3. Miosis increase depth of focus.
THE CILIARY BODY
The ciliary body is a triangular body with its base towards the root of the iris and the anterior
chamber angle . Its apex merges with the choroid. The ciliary body is composed of two section, the
anterior pars plicata and the posterior pars plana.
The pars plicata carries 70 ciliary processes. Each process has a central vascular core and is
covered by 2 layers of epithelium . The ciliary processes secrete aqueous humor, which circulates
through the posterior and anterior chambers, playing an important role in maintaining the IOP.
The ciliary Muscle
Consists of 3 parts:
i.
The longitudinal fibers: run between the supra- choroid and a small lip of the sclera called the
sclera spur. Contraction leads to opening of the trabecular meshwork and the canal of schlemm.
ii.
Circular fibers: arranged as a sphincter: contraction causes relaxation of the suspensory
ligament of the lens. This relaxes the tension on the lens capsule, causing increased convexity of
the lens surfaces, and hence increases its power. The action is called
accommodation.
iii. Radial fibers : are present between the longitudinal and circular fibers.
Functions of the ciliary body:
Secretion of aqueous humor from the ciliary processes.
Suspension of the crystalline lens.
Accommodation by the contraction of the ciliary muscle.
Helps aqueous humor drainage by contraction of the ciliary muscle.
THE CHOROID
The choroid forms the major part of the uveal tract. It lies between the sclera and the retina,
from the ora serrata to the optic nerve . This vascular layer supplies nutrition to the external half
of retina and is composed primarily of an inner layer of capillaries know as the choriocapillaris,
and externally by large collecting veins. Bruch's membrane is the part of the choroid which lies
between the choriocapillaris and the rods and cones.
DISEAES OF THE IRIS AND CILIARY BODY
Diseases that affect the iris and ciliary body include:
Congenital anomalies
Heterochromia: difference in color between the
two eyes.
Anomalies of the pupil:
i.
Polycoria : congenital multiple pupils.
ii.
Corectopia : abnormal displacement of the pupil.
Aniridia:
Is a bilateral absence of the iris which is never complete as there is a narrow rim of iris tissue
which usually blocks the angle of the anterior chamber with secondary glaucoma.
. albinism: is a deficient melanin in the iris leading to :
1. a. Reddish iris
2. b. Nystagmus (due to loss of central fixation)
Coloboma : A localized defect of the iris. It is present since birth and is typically located down
and nasally . The collarete surrounds the site of the coloboma. Which differentiates it from an
iridectomy
ACUTE IRIDOYCLITIS
Iridocyclitis is inflammation of the iris and the cliary body. Both commonly occur together since
they share a common blood supply. It is also called anterior uveitis. It may acute or chronic ,
endogenous or exogenous, granulomatous or non – granulomatous.
Etiology
May be endogenous or exogenous.
1.
Exogenous uveitis
Exogenous uveitis is caused by either external injury to the iris or by invasion of microorganisms
from outside e.g. during surgery or due to trauma. It results in suppurative inflammation know as
endophthalmitis.
2. Endogenous uveitis
a. Secondary to another disease in the eye :
i.
Keratitis
ii.
Rupture of the lens capsule releasing lens antigens (iritis phaco-anaphylactica)
Signs:
1. Mild lid edema.
2. The conjunctiva shows deep ciliary injection.
3. Corneal edema.
4. Keratic precipitates (KPs): these are inflammatory cells deposited on the corneal endothelium,
mostly in the middle and inferior zones of the cornea. They are detected by slit – lamp
examination.
5. Aqueous cells: these are inflammatory cells reaching the aqueous humor. When numerous, they
produce hypopyon.
6. Aqueous flare : This is the
earliest sign of iritis. It is due to leakage of proteins into the aqueous
through the damage blood vessels causing turbidity of the aqueous humor. It is detected by
slit – lamp examination.
7. Iris : is muddy in color with loss iris pattern due to accumulation of exudates on its surface.
8. Pupil : shows miosis due to spasm of the sphincter muscles.
9. Hyphema: Blood in anterior chamber as in herpetic and tuberculous iridocyclitis..
10. Vitreous : shows inflammatory cells, mainly in its anterior third.
11. Intraocular pressure is usually low in the acute phase, but secondary glaucoma may occur in
chronic and recurrent cases. In the acute phase, rise of pressure may occur due to plasmoid
aqueous.
.
Treatment of iridocyclitis
Local treatment :
1.
Atropine sulphate : it is most important line of treatment.
1-2% drops in adults and 1% ointment in children. Eye drops should be avoided in children to
avoid systemic toxicity . it is used 3 times daily.
Atropine relieves pain and headache from ciliary spasm, dilates the pupil and prevents posterior
synechia, and decreases exudation from the iris vessels.
2 . Corticosteroids
Prednisolone acetate 1% dexamethasone phosphate 0.1% in the form of drops or ointment.
Used frequently every 1-2 hours in the acute stage and tapered gradually.
Mechanism of action of corticosteroids:
i.
Decreases the release of inflamatory mediators by stabilization of lysosomal membranes.
ii.
Decrease vascular permeability.
iii.
Inhibit fibroblastic activity and diminish the formation of synechiae.
3. Hot fomentations : decrease pain and improve the circulation
4. Dark glasses : to decrease photophobia.
II. Systemic treatment
1.
Systemic steroids:
Indicated in severe cases and in large doses, usually 60-80 mg/day (1 mg/kg/day) tapering should
be gradual to avoid relapses.
Contraindications :
i.
Infective cases ( unless given under a good cover of antibiotics)
ii.
Diabetic patients (corticosteroids are diabetogenic)
iii.
Cardiac and renal disease
iv.
Tuberculosis.
Side effects:
i.
Salt and water retention
ii.
Hypokalaemia.
iii.
Hyperglycemia.
iv.
Acute gastric erosions.
v.
Psychosis.
2. Non – steroidal anti – inflammatory drugs (NSAIDs) :
NSAIDs inhibit prostaglandin synthesis.
They are given in combination with corticosteroids or as a substitute if steroids are
contraindicated.
3. Antibiotics
Used in infective cases, e.g. post – operative or post- traumatic endophthalmitis, and in bacterial
infections such as syphilis and tuberculosis.
3. Analgesics for pain.
5. Immunosuppressive drugs :
Examples of immunosuppressive drugs include cyclosporine and chlorambucil.
They are used in steroid – resistant cases, e.g. in some cases of Behcet's disease
CHRONIC IRIDOCYCLITIS
Etiology
A.
Non – granulomatous :
B.
Granulomatous :
1. Tuberculosis
2. Syphilis
3. Sarcoidosis
4. Brucellosis
5. Iritis phacoanaphylactica
Sympathetic ophthalmitis.
Characteristic features:
1. Long course with exacerbations and remissions.
2. Mutton – fat keratic precipitates ( large KPs formed by coalescence of small KPs) beige in color,
waxy in appearance.
3. Iris nodules:
a. Koeppe nodules: at the pupillary margin.
b. Busacca nodules : from the anterior surface of the iris.
4. Dust – like opacities in the vitreous , which are mainly wandering macrophages.
Iridocyclitis should be differentiated from other causes of red eye, mainly conjunctivitis, corneal
ulcers and, acute congestive glaucoma
INFLAMMATIONS OF THE CHOROID
Inflammation of the choroid is called choroditis or posterior uveitis. Posterior uveitis can affect
the retina, retinal vessels, RPE the choroid, and optic nerve . It may exudative, granulomatous or
suppurative.
1. Exudative : a non – specific response with marked exudation.
2. Granulomatous : due to allergy to bacterial toxins.
a.
To tuberculo- protein.
b.
To streptococcal toxins as in a septic focus.
3. Suppurative
a. Endophthalmitis
b. Panophthamitis
SUPPURATIVE CHOROIDITIS
The infection may be endogenous or exogenous and may lead to endophthalmitis or
panophthalmitis.
ENDOPHTHALMITIS
Endophthalmitis is a purulent inflammation of the intraocular tissues in response to infection
(exogenous or endogenous) trauma, immune reaction, physical or chemical changes, vacuities, or
neoplasm. The inflammation is confined to the intraocular structures, but the outer coat of the eye
( cornea, sclera ) and Tenon's capsule are free.
Classification :
1. Acute postoperative endophthalmitis : is the most common entity. It may be infectious,
secondary to bacteria or fungi. Acute sterile endophthalmitis can be caused by chemical insult
such as the use of irrigating agents, or retention of an inteaocular foreign body (IOFPB) such as
powder from gloves.
2. Traumatic, as in penetrating injuries if antibiotics were not started early.
3. Endogenous (metastatic) endophthalmitis as in immunocompromised patients (AIDS,
Cytomegalovirs).
Etiologic agent
1. Bacterial : staphylococcus epidermidis, staphylococcus aurous, gram- negative bacteria
( pseudomonas, Proteus, Escherichia coli).
2. Fungal : Candida, Aspergillus.
Classification :
1. Acute postoperative endophthalmitis : is the most common entity. It may be infectious,
secondary to bacteria or fungi. Acute sterile endophthalmitis can be caused by chemical insult
such as the use of irrigating agents, or retention of an inteaocular foreign body (IOFPB) such as
powder from gloves.
2. Traumatic, as in penetrating injuries if antibiotics were not started early.
3. Endogenous (metastatic) endophthalmitis as in immunocompromised patients (AIDS,
Cytomegalovirs).
Etiologic agent
1. Bacterial : staphylococcus epidermidis, staphylococcus aurous, gram- negative bacteria
( pseudomonas, Proteus, Escherichia coli).
Fungal : Candida, Aspergillus
Clinical picture :
1. Pain
2. Increased hyperemia
3. Lid edema
4. Diminution of vision , often with corneal edema.
5. Anterior chamber reaction ( hypopyon)
6. Vitreous reaction.
Management of bacterial endophthalmitis :
1. Hospitalization.
2. Vitreous aspiration for smears ( Gram and Giemsa) culture and sensitivity.
3. Anterior chamber paracentesis for smears, culure and sensitivity .
4. Antibiotics:
a. Intravitreal :
i.
1 mg of vancomycin (to cover gram – positive organism ) plus :
ii.
2.25 mg of ceftazidime or 0.4 mg of amikacin ( to cover gram- negative organisms)
b. Subconjunctival :
1. 25 mg of vancomycin
2. 100 mg of ceftazidime or 20 mg of amikacin.
c. Topical
1. Vancomycin drops 50 mg/ml
2. Ceftazidime drops 50 mg/ ml or fortified gentamycin drops 15 mg/ ml.
d. Systemic amikacin 14mg/kg i.v or i.m every 8 hours for 5 days , or ciprofloxacin 500mg every
12 hours for 5 days.
e. Topical and / or systemic steroids may be added
AT LEAST 24 HOURS AFTER STARTING
INTENSIVE ANTIBIOTIC THERAPY
f. Vitrectomy in addition to the above treatment is done in severe cases not responding to other
measures.
Mangement of fungal endopthalmits
1. Evaluation as in bacterial endophthalmitis
2. Amphotericin B systemically , intravitreally and topically.
PANOPHTHALMITIS
In panophthalmitis: the inflammation extends to involve all the ocular tissues including the outer
coat, Tenon's capsule and the orbit.
Symptoms:
1. Severe pain.
2. Loss of vision
3. General signs of infection ( fever, malaise , rapid pulse)
Signs :
4. Proptosis
5. Limitation of movement in all directions.
6. Severe edema of the and conjunctiva
7. Hypopyon in the anterior chamber
8. Yellow reflex due to pus in the vitreous
9. Pus bursts through the cornea.
10. Extension to the cavernous sinus is a risk.