ANTERIOR UVEITIS (IRIDOCYCLITIS)

CLINICAL FEATURES
Though anterior uveitis, almost always presents as a
combined inflammation of iris and ciliary body
(iridocyclitis), the reaction may be more marked in iris
(iritis) or ciliary body (cyclitis). Clinically it may
present as acute or chronic anterior uveitis. Main
symptoms of acute anterior uveitis are pain,
photophobia, redness, lacrimation and decreased
vision. In chronic uveitis, however the eye may be
white with minimal symptoms even in the presence of
signs of severe inflammation.
Symptoms
1. Pain. It is dominating symptom of acute anterior
uveitis. Patients usually complain of a dull aching
throbbing sensation which is typically worse at night.
The ocular pain is usually referred along the
distribution of branches of fifth nerve, especially
towards forehead and scalp.
2. Redness. It is due to circumcorneal congestion,
which occurs as a result of active hyperaemia of
anterior ciliary vessels due to the effect of toxins,
histamine and histamine-like substances and axon
reflex.
3. Photophobia and blepharospasm observed in
patients with acute anterior uveitis are due to a reflex
between sensory fibres of fifth nerve (which are
irritated) and motor fibres of the seventh nerve,
supplying the orbicularis oculi muscle.
4. Lacrimation occurs as a result of lacrimatory reflex
mediated by fifth nerve (afferent) and secretomotor
fibres of the seventh nerve (efferent).
5. Defective vision in a patient with iridocyclitis may
vary from a slight blur in early phase to marked
deterioration in late phase. Factors responsible for
visual disturbance include induced myopia due to
ciliary spasm, corneal haze (due to oedema and KPs),
aqueous turbidity, pupillary block due to exudates,
complicated cataract, vitreous haze, cyclitic
membrane, associated macular oedema, papillitis or
secondary glaucoma. One or more factors may
contribute in different cases depending upon the
severity and duration of the disease.
Signs
Slit lamp biomicroscopic examination is essential to
elicit most of the signs of uveitis (Fig. 7.8).
I. Lid oedema usually mild, may accompany a severe
attack of acute anterior uveitis.
II. Circumcorneal congestion is marked in acute
iridocyclitis and minimal in chronic iridocyclitis. It
must be differentiated from superficial congestion
occurring in acute conjunctivitis.
III. Corneal signs include; corneal oedema, KPs
and posterior corneal opacities.

1. Corneal oedema is due to toxic endothelitis and
raised intraocular pressure when present.
2. Keratic precipitates (KPs) are proteinaceouscellular
deposits occurring at the back of cornea.
Mostly, these are arranged in a triangular fashion
occupying the centre and inferior part of cornea due
to convection currents in the aqueous humour (Fig.
7.9). The composition and morphology of KPs varies
with the severity, duration and type of uveitis.
Following types of KPs may be seen:
i. Mutton fat KPs. These typically occur in
granulomatous iridocyclitis and are composed of
epithelioid cells and macrophages. They are large,
thick, fluffy, lardaceous KPs, having a greasy or
waxy appearance. Mutton fat KPs are usually a
few (10 to 15) in number (Fig. 7.9B).
ii. Small and medium KPs (granular KPs). These are
pathognomic of non-granulomatous uveitis and
are composed of lymphocytes. These small,
discrete, dirty white KPs are arranged irregularly
at the back of cornea. Small KPs may be hundreds
in number and form the so called endothelial
dusting.

iii. Red KPs. These are formed when in addition to
inflammatory cells, RBCs also take part in
composition. They may be seen in haemorrhagic
uveitis.
iv. Old KPs. These are sign of healed uveitis. Either
of the above described KPs with healing process
shrink, fade, become pigmented and irregular in
shape (crenated margins). Old mutton fat KPs
usually have a ground glass appearance due to
hyalinization.
3. Posterior corneal opacity may be formed in longstanding
cases of iridocyclitis.
IV. Anterior chamber signs
1. Aqueous cells. It is an early feature of iridocyclitis.
The cells should be counted in an oblique slit-lamp
beam, 3-mm long and 1-mm wide, with maximal light
intensity and magnification, and graded as :
– = 0 cells,
± = 1–5 cells,
+1 = 6–10 cells,
+2 = 11-20 cells,
+3 = 21–50 cells, and
+4 = over 50 cells
2. Aqueous flare. It is due to leakage of protein
particles into the aqueous humour from damaged
blood vessels. It is demonstrated on the slit lamp
examination by a point beam of light passed obliquely
to the plane of iris (Fig. 7.10). In the beam of light,
protein particles are seen as suspended and moving
dust particles. This is based on the ‘Brownian
movements’ or ‘Tyndal phenomenon’. Aqueous flare
is usually marked in nongranulomatous and minimal
in granulomatous uveitis. The flare is graded from ‘0’
to +4. Grade :
0 = no aqueous flare,
+1 = just detectable;
+2 = moderate flare with clear iris details;
+3 = marked flare (iris details not clear);
+4 = intense flare (fixed coagulated aqueous
with considerable fibrin).
3. Hypopyon. When exudates are heavy and thick,
they settle down in lower part of the anterior chamber
as hypopyon (sterile pus in the anterior chamber)
(Fig. 7.11).
4. Hyphaema (blood in the anterior chamber): It may
be seen in haemorrhagic type of uveitis.

5. Changes in depth and shape of anterior chamber
may occur due to synechiae formation.
6. Changes in the angle of anterior chamber are
observed with gonioscopic examination. In active
stage, cellular deposits and in chronic stage peripheral
anterior synechiae may be seen.
V. Iris signs
1. Loss of normal pattern. It occurs due to oedema
and waterlogging of iris in active phase and due to
atrophic changes in chronic phase. Iris atrophy is
typically observed in Fuchs’ heterochromic
iridocyclitis.
2. Changes in iris colour. Iris usually becomes muddy
in colour during active phase and may show
hyperpigmented and depigmented areas in healed
stage.
3. Iris nodules (Fig. 7.12). These occur typically in
granulomatous uveitis.

Koeppe’s nodules are situated at the pupillary
border and may initiate posterior synechia.
Busacca’s nodules situated near the collarette
are large but less common than the Koeppe’s
nodules.
4. Posterior synechiae. These are adhesions between
the posterior surface of iris and anterior capsule of
crystalline lens (or any other structure which may be
artificial lens, after cataract, posterior capsule (left
after extracapsular cataract extraction) or anterior
hyaloid face. These are formed due to organisation
of the fibrin-rich exudates. Morphologically, posterior
synechiae may be segmental, annular or total.
i. Segmental posterior synechiae refers to adhesions
of iris to the lens at some points (Fig. 7.8).
ii. Annular posterior synechiae (ring synechiae are
360o adhesions of pupillary margin to anterior
capsule of lens. These prevent the circulation of
aqueous humour from posterior chamber to
anterior chamber (seclusio pupillae). Thus, the
aqueous collects behind the iris and pushes it
anteriorly (leading to ‘iris-bombe’ formation) (Fig.
7.13). This is usually followed by a rise in
intraocular pressure.
iii. Total posterior synechiae due to plastering of
total posterior surface of iris with the anterior
capsule of lens are rarely formed in acute plastic
type of uveitis. These result in deepening of
anterior chamber (Fig. 7.14).
5. Neovascularsation of iris (rubeosis iridis)
develops in some eyes with chronic iridocyclitis.

VI. Pupillary signs
1. Narrow pupil. It occurs in acute attack of
iridocyclitis (Fig. 7.8B) due to irritation of sphincter
pupillae by toxins. Iris oedema and engorged radial
vessels of iris also contribute in making the pupil
narrow.
2. Irregular pupil shape. It results from segmental
posterior synechiae formation. Dilatation of pupil with
atropine at this stage results in festooned pupil
(Fig. 7.8A and Fig. 7.15).
3. Ectropion pupillae (evertion of pupillary margin).
It may develop due to contraction of fibrinous exudate
on the anterior surface of the iris.

4. Pupillary reaction becomes sluggish or may even
be absent due to oedema and hyperaemia of iris which
hamper its movements.
5. Occlusio pupillae results when the pupil is
completely occluded due to organisation of the
exudates across the entire pupillary area.
VII. Changes in the lens
1. Pigment dispersal on the anterior capsule of lens
is almost of universal occurrence in a case of anterior
uveitis.
2. Exudates may be deposited on the lens in cases
with acute plastic iridocyclitis.
3. Complicated cataract may develop as a
complication of persistent iridocyclitis. Typical
features of a complicated cataract in early stage are
‘polychromatic luster’ and ‘bread-crumb’ appearance
of the early posterior subcapsular opacities. In the
presence of posterior synechiae, the complicated
cataract progresses rapidly to maturity (Fig. 7.15).
VIII. Change in the vitreous
Anterior vitreous may show exudates and
inflammatory cells after an attack of acute iridocyclitis.
COMPLICATIONS AND SEQUELAE
1. Complicated cataract. It is a common
complication of iridocyclitis as described above.
2. Secondary glaucoma. It may occur as an early or
late complication of iridocyclitis.
i. Early glaucoma. In active phase of the disease,
presence of exudates and inflammatory cells in
the anterior chamber may cause clogging of
trabecular meshwork resulting in the decreased
aqueous drainage and thus a rise in intraocular
pressure (hypertensive uveitis).
ii. Late glaucoma in iridocyclitis (postinflammatory
glaucoma) is the result of pupil
block (seclusio pupillae due to ring synechiae
formation, or occlusio pupillae due to organised
exudates) not allowing the aqueous to flow
from posterior to anterior chamber. There may
or may not be associated peripheral anterior
synechiae formation.
3. Cyclitic membrane. It results due to fibrosis of
exudates present behind the lens. It is a late
complication of acute plastic type of iridocyclitis.
4. Choroiditis. It may develop in prolonged cases
of iridocyclitis owing to their continuity.

5. Retinal complications. These include cystoid
macular oedema, macular degeneration, exudative
retinal detachment and secondary periphlebitis
retinae.
6. Papillitis (inflammation of the optic disc). It may
be associated in severe cases of iridocyclitis.
7. Band-shaped keratopathy. It occurs as a
complication of long-standing chronic uveitis (Fig.
5.17), especially in children having Still’s disease.
8. Phthisis bulbi. It is the final stage end result of
any form of chronic uveitis. In this condition,
ciliary body is disorganised and so aqueous
production is hampered. As a result of it the eye
becomes soft, shrinks and eventually becomes a
small atrophic globe (phthisis bulbi).
DIFFERENTIAL DIAGNOSIS
1. Acute red eye. Acute iridocyclitis must be
differentiated from other causes of acute red eye,
especially acute congestive glaucoma and acute
conjunctivitis. The differentiating features are
summarised in Table 7.1.
2. Granulomatous versus non-granulomatous
uveitis. Once diagnosis of iridocyclitis is established,
an attempt should be made to know whether the
condition is of granulomatous or non-granulomatous
type. The main clinical differences between the two
are summarised in Table 7.2.
3. Etiological differential diagnosis. Efforts should
also be made to distinguish between the different
etiological varieties of iridocyclitis. This may be
possible in some cases after thorough investigations
and with a knowledge of special features of different
clinical entities, which are described under the subject
of ‘special types of iridocyclitis’ (see page 154).
INVESTIGATIONS
These include a battery of tests because of its varied
etiology. However, an experienced ophthalmologist
soon learns to order a few investigations of
considerable value, which will differ in individual case
depending upon the information gained from
thorough clinical work up. A few common
investigations required are listed here:
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 and antistreptolysin-
0.
2. Urine examination for WBCs, pus cells, RBC
and culture to rule out urinary tract infections.
3. Stool examination for cyst and ova to rule out
parasitic infestations.
4. Radiological investigations include X-rays of
chest, paranasal sinuses, sacroiliac joints and
lumbar spine.
5. Skin tests. These include tuberculin test, Kveim’s
test and toxoplasmin test.
TREATMENT OF IRIDOCYCLITIS
I. Non-specific treatment
(a) Local therapy
1. Mydriatic-cycloplegic drugs. These are very
useful and most effective during acute phase of
iridocyclitis. Commonly used drug is 1 percent
atropine sulfate eye ointment or drops instilled 2-3
times a day. In case of atropine allergy, other
cycloplegics like 2 percent homatropine or 1 percent
cyclopentolate eyedrops may be instilled 3-4 times a
day. Alternatively for more powerful cycloplegic effect
a subconjunctival injection of 0.25 ml mydricain (a
mixture of atropine, adrenaline and procaine) should
be given. The cycloplegics should be continued for
at least 2-3 weeks after the eye becomes quiet,
otherwise relapse may occur.
Mode of action. In iridocyclitis, atropine (i) gives
comfort and rest to the eye by relieving spasm of iris
sphincter and ciliary muscle, (ii) prevents the
formation of synechiae and may break the already
formed synechiae, (iii) reduces exudation by
decreasing hyperaemia and vascular permeability and
(iv) increases the blood supply to anterior uvea by
relieving pressure on the anterior ciliary arteries. As
a result more antibodies reach the target tissues and
more toxins are absorbed.
2. Corticosteroids, administered locally, are very
effective in cases of iridocyclitis. They reduce
inflammation by their anti-inflammatory effect; being

anti-allergic, are of special use in allergic type of
uveitis; and due to their antifibrotic activity, they
reduce fibrosis and thus prevent disorganisation and
destruction of the tissues. Commonly used steroidal
preparations contain dexamethasone, betamethasone,
hydrocortisone or prednisolone (see page 428).
Route of administration: Locally, 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.
3. Broad spectrum antibiotic drops, though of no use
in iridocyclitis, are usually prescribed with topical
steroid preparations to provide an umbrella cover for
them.
(b) Systemic therapy
1. Corticosteroids. When administered systemically
they have a definite role in non-granulomatous
iridocyclitis, where inflammation, most of the times,
is due to antigen antibody reaction. Even in other
types of uveitis, the systemic steroids are helpful due
to their potent non-specific anti-inflammatory and
antifibrotic effects. Systemic corticosteroids are
usually indicated in intractable anterior uveitis
resistant to topical therapy.
Dosage schedules. A wide variety of steroids are
available.Usually, treatment is started with high doses
of prednisolone (60-100 mg) or equivalent quantities

of other steroids (dexamethasone or betamethasone).
Daily therapy regime is preferred for marked
inflammatory activity for at least 2 weeks. In the
absence of acute disease, alternate day therapy
regime should be chosen. The dose of steroids is
decreased by a week’s interval and tapered completely
in about 6-8 weeks in both the regimes.
Note: Steroids (both topical and systemic) may cause
many ocular (e.g., steroid-induced glaucoma and
cataract) and systemic side-effects. Hence, an eagle’s
eye watchfulness is required for it.
2. Non-steroidal anti-inflammatory drugs (NSAIDS)
such as aspirin can be used where steroids are
contraindicated. Phenylbutazone and oxyphenbutazone
are potent anti-inflammatory drugs of particular
value in uveitis associated with rheumatoid disease.
3. Immunosuppressive drugs. These should be used
only in desperate and extremely serious cases of
uveitis, in which vigorous use of steroids have failed
to resolve the inflammation and there is an imminent
danger of blindness. These drugs are dangerous and
should be used with great caution in the supervision
of a haematologist and an oncologist. These drugs
are specially useful in severe cases of Behcet’s
syndrome, sympathetic ophthalmia, pars planitis and
VKH syndrome. A few available cytotoxic
immunosuppressive drugs include cyclophosphamide,
chlorambucil, azathioprine and
methotrexate. Cyclosporin is a powerful anti-T-cell
immunosuppressive drug which is effective in cases
resistant to cytotoxic immunosuppressive agents, but
it is a highly renal toxic drug.
(c) Physical measures
1. Hot fomentation. It is very soothing, diminishes
pain and increases circulation, and thus reduces the
venous stasis. As a result more antibodies are brought
and toxins are drained. Hot fomentation can be done
by dry heat or wet heat.
2. Dark goggles. These give a feeling of comfort,
especially when used in sunlight, by reducing
photophobia, lacrimation and blepharospasm.
II. Specific treatment of the cuase
The non-specific treatment described above is very
effective and usually eats away the uveal
inflammation, in most of the cases, but it does not
cure the disease, resulting in relapses. Therefore, all
possible efforts should be made to find out and treat
the underlying cause. Unfortunately, in spite of the
advanced diagnostic tests, still it is not possible to
ascertain the cause in a large number of cases.
So, a full course of antitubercular drugs for
underlying Koch’s disease, adequate treatment for
syphilis, toxoplasmosis etc., when detected should
be carried out. When no cause is ascertained, a full
course of broad spectrum antibiotics may be helpful
by eradicating some masked focus of infection in
patients with non-granulomatous uveitis.
III. Treatment of complications
1. Inflammatory glaucoma (hypertensive uveitis).
In such cases, drugs to lower intraocular pressure
such as 0.5 percent timolol maleate eyedrops twice a
day and tablet acetazolamide (250 mg thrice a day)
should be added, over and above the usual treatment
of iridocyclitis. Pilocarpine and latanoprost eye drops
are contraindicated in inflammatory glaucoma.
2. Post-inflammatory glaucoma due to ring
synechiae is treated by laser iridotomy. Surgical
iridectomy may be done when laser is not available.
However, surgery should be performed in a quiet eye
under high doses of corticosteroids.
3. Complicated cataract requires lens extraction with
guarded prognosis in spite of all precautions. The
presence of fresh KPs is considered a contraindication
for intraocular surgery.
4. Retinal detachment of exudative type usually
settles itself if uveitis is treated aggressively. A
tractional detachment requires vitrectomy and
management of complicated retinal detachment, with
poor visual prognosis.
5. Phthisis bulbi especially when painful, requires
removal by enucleation operation.