2. Presentation layout
Anatomy of uvea
Uveitis introduction
Classification of uveitis
Anterior uveitis introduction
Etiology of AU
Clinical features,complications and D/D
Investigations
Treatment of AU
3. Anatomy of uvea
UVEA constitutes- middle vascular coat
3 parts-
a)iris
b)ciliary body
c)choroid
Developmentally, structurally and functionally- indivisible
color varies from light blue to dark brown
4. Developmental milestones
9TH WEEK GESTATION-
12TH WEEK GESTATION-
5TH MONTH- all layers of choroid seen & iris fully developed
6TH MONTH- dilator muscle begins to form, sphincter muscle is fully formed
POSTNATAL PERIOD- dilator muscle fully formed by 5 years,
iris stromal pigment develops after birth
5. MACROSCOPIC APPEARANCE OF IRIS
TWO SURFACES
A)ANTERIOR SURFACE
Collarette- zigzag line, 2mm from pupil, thickest, represents attachment of pupillary
membrane
Divides surface into-
a) CILIARY ZONE- c/b
b) PUPILLARY ZONE-
Between collarette and pigmented frill
B)POSTERIOR SURFACE-
dark brown/black Contains-
A) Schwalbe’s contraction folds
B) Schwalbe’s structural furrows
C) Circular furrows
6.
7. FOUR LAYERS-
a)Anterior limiting layer-
b) Iris stroma-
•Forms main bulk
•Consists of collagenous tissue with mucopolysaccharide
C) Anterior epithelial layer
D)Posterior pigmented epithelial layer
Anterior continuation of non pigmented epithelium of ciliary body
8.
9. Ciliary body
Forward continuation of choroid at ora serrata
Triangular in cut section, ant side of its form part of angle, in
middle attached to iris and outer part lies against sclera
Triangle – two parts
a) Anterior part- ciliary processes (pars plicata) 2-2.5mm
b)Posterior part- smooth (pars plana) 5mm wide temporally
& 3mm nasally
10. Structure of ciliary body
MICROSCOPIC STRUCTURE
1.SUPRACILIARY LAMINA- outermost part
2. 2.STROMA-
Consists Ciliary muscle- non striated, triangular in cut section, 3 parts
a.Longitudnal/meridional fibres- origin from scleral spur, inserts into suprachoroidal lamina
b.Circular fibres- in inner portion, nearest to lens
c.Radial fibres- obliquely placed
3)Layer of pigmented epithelium- forward continuation of RPE
4)Layer of non pigmented epithelium- forward continuation of sensory retina
5)Internal limiting membrane-lines NPE Forward continuation of internal limiting
membrane of retina
11. Choroid
Posterior most part
Extension- optic disc to ora serrata
Inner surface- smooth, brown and in contact with RPE
Outer surface-rough and in contact with sclera
Thickness- posteriorly 0.22mm
anteriorly 0.10mm
12. Microscopic structure of choroid
1) Suprachoroidal lamina- lamina fusca
Thin layer, continues anteriorly with supraciliary lamina of ciliary
body
2) Stroma – plenty of pigmented cells, macrophages,mast and
plasma cells
3) choriocapillaris- rich capillary network
4)Basal lamina- Bruch’s membrane/lamina vitrae-Innermost
layer
13. Uveitis
Term uveitis- inflammation of uvea
However, clinically there is some association from the nearby
structures
14. Classification of uveitis
A. Anatomical classification
Acc to SUN, uveitis is classified anatomically :
a. Anterior uveitis
b. Intermediate uveitis
c. Posterior uveitis
d. Pan uveitis
16. Anterior uveitis
Inflammation of the uveal tract from the iris upto the plars plicata of ciliary body i.e …..
It may be sub divided into
A. Iritis
B. Iridocyclitis
C. Anterior cyclitis
Aetiology
Uveitis (anterior)
Anterior uveitis (the most common form of uveitis: 75% of all cases of uveitis). Annual
incidence 12 per 100,000 population
it may affect all ages, although it is most common in individuals in the third and fourth
decades.
(https://www.college-optometrists.org/guidance/clinical-management-guidelines/uveitis-anterior-acute-and-recurrent-
.html)
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6095364/)
17. Etiology of uveitis/AU
Depending upon the offending agent of uveitis,
A. infectious
i. exogenous
ii.secondary
iii.endogenous
B.non infectious
i.auto-immune
a.HLA-associated
b.others
ii.Atopic
iii.Toxic
iv.Idiopathic
specific
nonspecific
19. Clinical features
Clinically it may be present as acute or chronic uveitis:
Acute: Symptoms more severe like photophobia, redness,
lacrimation and decreased vision
Chronic: Signs more severe than symptoms, however eye may
be presented white as that of very minimal symptoms
20. Symptoms
Pain:
complain of skull aching which typically Worsen at night
Acute Severe Radiates along V1 nerve distribution
dominant symptom of AAU
Redness:
feature of AAU, and occur due to circum corneal congestion, as a result of
hyperemia of anterior ciliary vessels due to the effect of toxins, histamines
and histamine like substances and axon reflexes.
Photophobia and Blepharospasm:
in AAU, due to reflex between sensory fibers of fifth CN {WHICH ARE
IRRITATED} and motor fibres of seventh CN supplying the orbicularis oculi
21. Lacrimation
occurs as a reflex of Vth CN (afferent) and secretomotor
of seventh CN(efferent)
Diminution of vision
a. Ciliary spasm –induces ?
b. Vitreous exudates
c. Exudates in pupillary area {pupillary block}
d. CME
e. Sec. glaucoma
f. Turbid aqueous
g. Complicated Cataract
22. Signs
A . Lid Edema
Mild, may accompany a severe attack of AAU
B . Ciliary congestion
ccc is marked in AU, it may be differentiated from superficial
congestion occurring in acute conjunctivitis
23.
24. C. Corneal signs
1.KPs:
KPs are pathogenic sign of AU.
Are proteinaceous cellular deposits occurring at the back of the cornea
mostly arranged in triangular fashion occupying the centre and inferior part of the
cornea due to convetion currents in the aqueous humour.
Different morphology of KPs are
Mutton fat KPs
in granulomatous iridocyclitis and composed of epitheloid cells and macrophages
Large,thick ,fluffy and lardaceous KPs ,having greasy or waxy appearance
usually a few -10-15 in no
Small and medium KPs
small,discrete,dirty white KPs arranged irregularly at the back of cornea
they may be numerous
these are pathognomic of nongranulomatous uveitis and are composed of
lymphocytes
25. Fine KPs :
also also called as ‘satellite’ KPs,typically cover entire corneal endothelium and form the so
called endothelial dusting.
Are seen in Fuchs heterochromic iridocyclitis,herpetic iritis and CMV retinitis.
Old KPs
are sign of healed uveitis
either of the abive described KPs with healing process shrink,fade,become pigmented and
irregular in shape(crenated margin)
old mutton fat KPs usually have a ground glass appearance due to hyalinization
2.cornea edema
toxic endothelitis and raised IOP when present
3.Posterior corneal opacity
may be formed in long standing cases of iridocyclitis
28. D.ANTERIOR CHAMBER SIGNS:
Aqueous cells
Early sign
On oblique illum.:1 mm long 1mm wide slit with max light and
magnifications
Grading:
29. Aqueous flares
D/t leakage of protein into the aqueous humor from the leaky vessels
On oblique illumination: a point of beam projected on the iris plane
Protein particles seen floating the beam of light: Tyndall phenomenon
Grading:
Hypopyon:
sterile pus in AC
Changes in depth and shape of AC
Changes in the angle of anterior chamber
32. E.Iris signs
1. Loss of normal pattern
2. Muddy in color in active stage & hyper/ hypopigmented
3. Iris nodules: Aggregations of lymphyocytes and epitheloid
cells.
Koeppe’s nodules ….
Busacca’s nodules….
4. Posterior synechiae
Adhesion of posterior surface of iris to anterior surface of
cornea
a. Segmental
b. Annular
c. Total
38. G.Lens signs
1. Pigment dispersion on lens surface
2. Fibrin exudates on lens surface
3. Complicated cataract: Polychromatic lusture
4. Bread crumb appearance
5. Cyclitic membrane:
retrolental, fibrovascular membrane which stretches across the back of the lens
42. I.Changes in IOP
1. Normal
2. Increased (sec glaucoma)
3. Decreased (in acute iridocyclitis - acute ciliary shock
chronic,longlasting iridocyclitis -atrophy of ciliary process
leading to phthisis bulbi)
55. INVESTIGATIONS
A.Hematological Examination
It includes following tests:
• TLC/DLC: Gross idea of inflammatory response of body
• ESR: r/o Chronic infection
• Blood sugar: r/o DM
• Blood Uric Acid: r/o Gout
• Seological Test: Syphilis, toxoplasmosis & histoplasmosis
• Test for: Anti Antinuclear Antibodies CRP Rh factor Anti-
streptolysin O LE cells
56. B.Urine Examination:
For WBC, Pus cells, RBS
Culture : r/o Urinary tract infection
C.Stool Examination ;
For Cysts & ova to r/o parasitic infestations.
D . Radiological Investigation :
CXR , Paranasal sinus, Sacroiliac joints , Lumbar spine.
E. Skin Tests:
Tuberculin test, Kveims test & Toxoplasmin test
57.
58. Treatment of iridocyclitis
I. Non specific treatment
a.Local therapy
b.systemic therapy
c.Physical measures
II. Specific treatment for the cause
III. Treatment complications
1) Cycloplegics
2) Corticosteroids
3) Broad spectrum antibiotics.
1. Corticosteroids
2. Non-Steroidal Anti inflammatory Drugs(NSAIDS)
3. Immunosupressives
70. C. Physical Measures
1. Hot fomentation
more antibodies are brought and toxins are drained
2. Dark goggles
helps in photophobia,lacrimation and blepharospasm
74. Just as different fads that seize the imagination of the general public are often carried to
excess, so diagnostic or therapeutic fads may take over in the practice of medicine.
Analysis of 33 surveys of the causes of uveitis reported by ophthalmologists over the
course of 120 years shows how some diagnoses such as syphilis and tuberculosis fell from
favor because tests ruled out these diseases, whereas others such as toxoplasmosis
became popular because of the finding of the organism in a few cases by a famous
ophthalmic pathologist. Yet others (pars planitis, sarcoidosis) were not even causes of
disease, but rather merely descriptive, or the ocular component of a systemic disease
whose etiology and pathogenesis remain unknown. We will examine the waxing and
waning of these diagnostic categories and the impressive confidence of some clinicians in
their own diagnostic acumen as they made diagnoses often unsupported by objective
evidence.
(https://pubmed.ncbi.nlm.nih.gov/9657289/)
75.
76. 1. Comprehensive ophthalmology by AK Khurana
2. Kanski’s clinical ophthalmology 8th edition
3. Parson’s eye disease
4. Americal Academy of ophthalmology(AAO)
5. American Optometric Association(AOA)
6. https://www.college-optometrists.org/guidance/clinical-management-
guidelines/uveitis-anterior-acute-and-recurrent-.html