Uveitis- a photoessay
Uveitis can be defined as inflammation of the uvea, the middle, vascular
coat of the eye (Greek uva- grape)
The uvea consists of the iris, ciliary body and the choroid. The International
Uveitis Study Group classification separates uveitis anatomically by location
of observed disease according to visible signs- anterior posterior or intermediate.
Iritis is a synonym for anterior uveitis. (1,2,3,4,5,6,7)
Additionally, uveitis is described in relation to specific disease syndromes,
for example Fuchs Heterochromic Cyclitis or occurring in relation to systemic
disease such as sarcoidosis or toxoplasmosis. (1,2,3,4,5,6,7)
Uveitis may affect not only the uvea but also the optic nerve retina and
vitreous. Uveitis is a major cause of visual impairment and may account for
10-15% of blindness in the USA. Of people aged under 65 who are registered
legally blind, 10% are visually compromised because of uveitis and
its complications, very nearly the same number affected by diabetic
retinopathy. This paper will embrace
uveitis and also other inflammatory ocular manifestations of systemic diseases
commonly encountered by physicians. (1,2,3,4,5,6,7)
International
Classification of Uveitis
________________________________________________________________
Table- International Classification of Uveitis
Temporal-
Acute versus Chronic ( >3 months)
In
acute uveitis symptoms and signs occur suddenly and typically lasts up to 6
weeks. In chronic uveitis the onset is usually
gradual and the inflammation lasts longer than three months.
Anatomical
____________________________________________________(1,2,3)______________
The above classification attempts to characterize uveitis appropriately
based upon anatomical description of the major clinical signs. Once the type of
uveitis has been identified, the process of meshing can be used to determine the
appropriate etiology or syndrome. Even if an etiology cannot be established, a
prognosis and suitable treatment regimen can often be formulated.
(5,6,7)
Overview of the Investigation
and Management of Uveitis
The management of the patient with uveitis may involve
the following,
Following history-taking and examination a short differential diagnostic
list is compiled, taking into consideration the clinical features and the causes
of uveitis seen in the patients age group. The most practical approach with
regard to the type of investigations to be arranged is one which is tailored
to the individual patient. (1,2,3)
Epidemiology of uveitis in the United Kingdom
A uveitis register at the Leicester Royal Infirmary consisted of data
collected on all uveitis patients except minor easily resolved, anterior uveitis
cases. The diagnoses of these patients were classified by the aetiological method.
A total of 712 patients was entered into the register over a period of 10 years
starting from January 1985. In the study, 73.0% of the cases fit into named
clinical syndromes while 27.0% of the cases were diagnosed as idiopathic or
uncategorised. The commonest definable cause of anterior uveitis was HLA-B27-related
acute anterior uveitis, comprising 15.2% of all uveitis cases ( in some series
up to 50% of uveitis is related to HLA B27 antigen ). Intermediate uveitis accounted
for 7.9% of all cases while the commonest definable cause of posterior uveitis
was toxoplasmosis, forming 4.6% of all uveitis cases.
(8)
The annual incidence in Western countries is approximately 17/100,000
while the prevalence of uveitis is estimated as about 38/100,000.
(1,3)
Ethnicity
Ethnicity affects uveitis, for example- HLAB27 antigen is the commonest
factor responsible for uveitis in Caucasians, in the Afro-Caribbean community
sarcoid is common whist Bechets disease affects those of Asian and
Middle Eastern origins (HLA B5 ). (1,2,3,4,5,6,7)
________________________________________________________________________
Table-
Aetiology of Anterior uveitis
Intermediate
uveitis
Aetiology
of Posterior uveitis
Clinical features of Anterior Uveitis
In acute uveitis symptoms and signs occur suddenly and last up to 6
weeks. Typically the patient has pain, ocular redness, blurred vision,
photophobia and epiphora. The redness tends to be perilimbal with a violaceous
hue.

Keratic precipitates
Occasionally the eye may be white with minimal pain. Examination of
the anterior chamber with the slit lamp microscope reveals the presence
of white cells and flare. There may be small collections of white cells on the
corneal endothelium (keratic precipitates). Mononuclear cells may collect to
form iris nodules. The pupil may be irregular due to the presence of adhesions
between the pupil margin and the anterior lens surface (posterior synechiae).
Cells in the vitreous and occasionally oedema of the central retina (i.e.
macular oedema) may be noted. (1,2,3)

Keratic precipitates (retroilumination )
Hypopyon
Clinical features of Intermediate and
Posterior Uveitis
Disturbance of the central retina (macula) may cause blurred or
distorted vision.
Cellular debris in the vitreous may cause floaters. The retina may
appear cloudy and white from
oedema. Choroidal or retinal lesions may appear yellow or white, sometimes with
black pigmented borders. Neovascularisation of the retina or optic nerve may be
seen. Occasionally there may be swelling or pallor of the optic nerve head
Debris in vitreous
The retinal vessels may be cuffed with inflammatory exudate. (1,2,3)

Retinal scarring from past toxoplasma.
Histopathology of Uveitis
The time course and the anatomical site of the inflammation can be
determined in almost every case. Thus, at least these two aspects can be
considered for every patient with uveitis (e.g.,
chronic iridocyclitis, acute retinitis). Acute disease usually starts
abruptly and lasts 2 to 6 weeks, while chronic disease begins insidiously and
has no defined endpoint, often lasting longer than 6 weeks.
Ocular inflammation involves vessel dilatation and increased vessel
permeability with fluid extravasation and leucocyte migration. The ocular
inflammation has acute and chronic phases. During the acute phase chemical
mediators are elaborated, including prostaglandins, histamine, serotonin,
kinins, complement and leukotriene.
The chronic inflammatory phase can be granulomatous or non-granulomatous.
Granulomatous inflammation is
characterized by infiltration with epithelioid cells, giant cells, plasma cells
and lymphocytes. In non-granulomatous inflammation there is infiltration mainly
with plasma cells and lymphocytes. Protein may leak from inflamed blood vessels
and leucocytes may migrate from inflamed vessels, giving rise to so-called
aqueous flare and cells. (1,2,3)
Investigations
The most practical approach is one which is tailored to the individual
patient. and determine an appropriate management scheme can be aided by this
system. It is not possible to review the many investigations routinely ordered
for ocular inflammation individually but the following are worth stressing.
(1,2,3)
HLA-B27 Antigen
The test can be useful in cases of recurrent anterior uveitis. HLA-B27
denotes a genotype located on chromosome 6. It is present in 4% of the general
population and up to 50% of patients with acute iritis. Many
patients with acute iritis therefore have a genetic predisposition.
Factors which may trigger the occurrence of acute iritis are often unknown. In
general, the importance of tissue tying for HLA B27 is under appreciated, the
investigation has a high yield, is inexpensive, and gives patients an
explanation of an often recurrent problem. (9)
Ankylosing spondylitis, Reiters syndrome, psoriatic arthritis and
inflammatory bowel disease are all associated with iritis, spondylitis and the
presence of HLA-B27 positivity.
(1,2,9)
________________________________________________________________________
Differential
Diagnosis Of Uveitis- It is of paramount importance to note that uveitis can be
caused or mimicked by the following-
Masquerade
Syndromes- neoplasms mimicking uveitis
Ocular
malignant melanoma
Retinoblastoma
Reticulum
Cell Sarcoma ( Primary Intraocular Lymphoma )
Leukaemia
Lymphoma
Ocular
Metastasis
Other-
Endophthalmitis
Retinal
detachment
Intraocular
foreign body
(1,2,3,4,5,6,7)
_____________________________________________________________________
Table Uveitis - Investigations
General
Investigations
ESR /
Plasma Viscosity/ C Reactive Protein
CXR
FBC
Syphilis
Serology- TPHA, VDRL
Urine
analysis ( Diabetes Mellitus )
Specific
Investigations
HLA B27
Ag; HLA B29 ( birdshot
retinochoroidopathy )
Angiotensin
Converting Enzyme
Rheumatoid
Factor , Lupus Group Autoantibodies including anti-neutrophil cytopasmic
antibody ( Wegeners Granulomatosis ) Anticardiolipin Antibody- ( the yield of
these investigations is actually low except in children with Juvenile Chronic
Arthritis )
Toxoplasma
Serology / IgG antibodies ( if negative on undiluted serum to exclude congenital
toxoplasmosis )
Toxocara
ELISA
HIV
Pathergy
Test
Mantoux
Test, Sputum Acid Fast Bacilli
X Ray
Hands and SI Joints
B Scan
for Masquerade Leisions or Posterior Scleritis
Kveim
Test
Immune
Complexes -Polyethylene Glycol Method
DNA
Polymerase Chain Reaction ( Herpes virus, Propionebacter )
CT scan
of chest ( sarcoidosis)
MRI( non
Hodgkins lymphoma, neurosarcoid, demyelination )
Choroidal
biopsy ( Non Hodgkins Lymphoma )
Physician
Referral
Rheumatological
Referral
Broncho-alveolar
lavage ( Sarcoid)
CSF
studies ( non Hodgkins lymphoma, neurosarcoid, VKH )
Venereological
Referral HIV, Reiter's,
Syphilis
A recent
retrospective review showed the following abnormal results, plasma viscosity/
esr 34.2%, VDRL/TPHA (4.3%) Angiotensin converting enzyme (10.8%) Chest X ray (
14.6%)
(1,2,3,4,5,6,7)
_______________________________________________________________________
Some
Systemic Diseases Commonly Associated with Uveitis
Ankylosing Spondylitis
About 30% of patients with Ankylosing spondylitis develop iritis. The
iritis may precede the onset of back stiffness and pain. Rarely there may be
retinal vasculitis and vitritis. (9,10,11)
------------------------------------------------------------------------------------------------
Table
Ankylosing Spondylitis
30% of
AS patients develop iritis, especially if male; iritis may precede arthritis
rarely
retinal vasculitis / vitritis.
Acute
anterior uveitis lasting 2-6 weeks, good prognosis
Investigations
in suspected ankylosing spondylitis
X-ray
sacroiliac joints ( 2 yearly Sacroiliac joint X rays in males if initial X ray
normal.)
ESR
Rheumatoid
factor
HLA B27
(positive in more than 90% )
Need 2
yearly Sacroiliac joint X rays in males if initial X ray normal
(9,10,11)

Arthritis associated with uveitis
This syndrome is characterised by the triad of arthritis, urethritis and
conjunctivitis or less commonly, iritis. ( Conjunctivitis and iritis affect 60%
and 20% of patients respectively.)
There may be also be associated episcleritis and keratitis.
_________________________________________________________________________
Table-
Reiter's Syndrome
triad
of: arthritis (weight bearing
joints, sacroiliitis),
conjunctivitis
or iritis
urethritis
(cervicitis).
(9,10,11)
________________________________________________________________________
________________________________________________________________________
Table-
Associations of Reiter's Syndrome
Occurs
if genetically predisposed (HLA B27); 60
- 90% association
M>F
Exposure
to certain urethritis / dysentery organisms: e.g.
Chlamydia,
Yersinia, Shigella, Salmonella, Campylobacter.
The
order of manifestation is normally: urethritis conjunctivitis
arthritis.
Ocular
20%
anterior uveitis,
60%
conjunctivitis,
episcleritis,
keratitis, post-uveitis.
Reiters
disease can sometimes result in hypopyon formation
(9,10,11)
________________________________________________________________________
Juvenile Chronic Arthritis
In juvenile chronic arthritis, a seronegative inflammatory arthritis
affecting children, the patient often suffers from chronic anterior uveitis. The
uveitis is most commonly seen in girls who are ANF positive and have
pauciarticular disease. The uveitis is usually bilateral and may be complicated
by the development of cataract, band keratopathy and glaucoma.
(12,13)
________________________________________________________________________
Table-
Juvenile Chronic Arthritis
Chronic
AAU , usually bilateral Commoner in
female patients, the young, ANF positive. Pauciarticular disease <5 joints.
Complications
Glaucoma
(20%)
Cataract
(40%)
Band
Keratopathy (40%) (12,13)
________________________________________________________________________
The anterior uveitis is typically initially asymptomatic; the eyes are white
rather than red
The visual prognosis may be adversely affected by a delay in diagnosis.
Screening of affected children is therefore regarded as mandatory
________________________________________________________________________
Table-
Monitoring Children with Juvenile Chronic Arthritis
High
Risk
Early
Onset , < 6 years, Pauciarticular Disease , ANA Positive
3 months
for first year , then 6 months for five years , then annually
Medium
Risk
polyarticular
disease ANA positive , pauciarticular -disease ANA negative
6
monthly intervals for 5 years then annually
Low Risk
Systemic
JCA , B27 associated arthritis , disease starting after age 11
Duration
For ten
years after onset of JCA or until age 12, whichever is shorter.
Source RCOphth (UK),
British Paediatric Association (1994) (12)
_____________________________________________________________________
Treatment includes topical corticosteroids, mydriatics, NSAID's and oral
prednisolone Chlorambucil may
occasionally be required in severe cases. Reading glasses may be helpful if
mydriatics are being used for both eyes as accommodation is paralysed by
cycloplegics. Surgical treatment of cataract, glaucoma and band keratopathy may
also be required.
(12,13)
Toxoplasmosis
Toxoplasmosis gondii is an obligate intracellular protozoa causing up to
50% of cases of posterior uveitis .Ocular infection is characterised by focal
necrotising retinochoroiditis with vitritis.In congenital infection the eye may
also be affected by cataract, microphthalmos, and optic atrophy. (1,2,3)
_________________________________________________________________________
Table-
Congenital Toxoplasmosis
Highest
transmission occurs in the IIIrd trimester
90% of
congenital infections have no clinical signs
Earlier
infection occurs in pregnancy - worse potential outcome
Triad:-
convulsions,
cerebral
calcification
and
chorioretinitis
Eye -
chorioretinitis, cataracts, microphthalmos, panuveitis, optic atrophy
(1,2,3)

Toxoplasma focus
Complications include direct involvement of the fovea, papillomacular
bundle, or optic disc. Cystoid macular oedema, subretinal neovascular membrane
formation, tractional and rhegmatogenous detachment and retinal
neovascularisation may also occur. (1,2,3)
________________________________________________________________________
Table-
Investigation of Toxoplasmosis
ELISA
IgM in neonates, rising IgG in adults (although not that helpful in adults).
Fluorescein
angiography (hypofluorescence in the early stages and then progressive leakage).
Indocyanine
angiography - multiple small dark spots may be seen around the visible lesions
implying the affected retina is greater than apparent initially. This sign may
be useful in assessing the effect of treatment. (5,6,7)
_________________________________________________________________________
Some authorities argue that any
active chorio-retinal lesion should be treated in order to decrease the risk of
macular traction, secondary retinal detachment and cystoid macular
oedema. Medications used for treatment include pyramethamine, clindamycin,
sulfadiazine and prednisolone.
Rarely, vitrectomy may be indicated for the removal of vitreous opacities
and haemorrhage and for the release
of vitreoretinal traction.
________________________________________________________________________
Table-
Some indications for active treatment of toxoplasmosis
Lesions
that involve the macula,
papillomacular bundle or optic disc
and
large, active lesions should be treated.
Immunocompromised
patients should be treated.
___________________________________________________(1,2,3)_________________
Behcets Disease
This idiopathic systemic disease consists of an obliterative vasculitis
and usually effects young males of Japanese and eastern Mediterranean origin.
The eye may be involved with conjunctivitis, episcleritis, keratitis and uveitis.
The anterior uveitis is usually acute with recurrent episodes. Severe disease
may be indicated by the presence of a hypopyon. The eye may be white. Chronic
uveitis is less common. (1,14,15)
_________________________________________________________________________
Table -
Behcets Disease
Idiopathic,
systemic disease consisting of an obliterative vasculitis possibly due to
circulating immune complexes
Young
males, Japanese and eastern Mediterranean, HLA-B5 associated
Clinical
Oral
ulceration-100%, may pre-date eye disease, painful, recurrent
Genital
ulceration- 90%, may be asymptomatic in females
Skin-
erythema nodosum, pustules, ulceration, cutaneous hypersensitivity
Arthritis-
non-destructive, wrists and ankles
CNS-
palsies, brainstem syndrome, meningoencephalitis, affects 25% and major cause of
mortality
(1,14,15)
_________________________________________________________________________
Posterior uveitis is more
common than anterior uveitis. There may be vitritis; this is usually associated
with anterior uveitis. Diffuse vascular leakage may lead to retinal oedema,
cystoid macular oedema and optic disc oedema. Retinal vasculitis, predominantly
periphlebitis, can lead to branch retinal vein occlusion and retinal
neovascularization. Retinitis may be manifest as transient white necrotic
infiltrates and intraretinal haemorrhages.
(1,14,15)

Aphthous ulcers
Anterior uveitis is treated with topical corticosteroids and mydriatics.
Posterior uveitis is treated with oral prednisolone, usually with
immunosuppression suc as azothiaprine chlorambucil and cyclophosphamide. The
visual prognosis is often poor.
(16)
Sarcoidosis
This chronic non-caseating granulomatous systemic disease of unknown
aetiology affects women more commonly than men and is more common in individuals
of Afro-Caribbean ethnicity. (16,17,18)
Ocular Manifestations
About 30% of patients with sarcoidosis have ocular involvement.
Iritis may be acute or
chronic; it may be unilateral or bilateral. Patients with posterior uveitis
usually have anterior uveitis as well. Vitritis is also common and tends to
occur in older patients.
"Mutton fat" KPs
There may be retinal periphlebitis; the vessels may display an exudative
cuff
(so called candle wax drippings). Inflammation of the retina may
lead to macular oedema, retinal granuloma, preretinal nodules and retinal
haemorrhage. Inflammation of the optic nerve may cause optic disc oedema,
granuloma and neovascularization.
Branch retinal vein occlusion and retinal neovascularisation are
uncommon. (16,17,18)
__________________________________________________________________
Table-
Sarciodosis - Investigations
Chest
X-ray
Serum
ACE (angiotensin converting enzyme)- this is elevated in active disease
urine
and serum calcium levels- hypercalciuria is common; hypercalcaemia is less
common
Conjunctival
biopsy may show granulomata
Broncho-Alveolar
Lavage (7,8,19)
_________________________________________________________________________
Treatment
Anterior uveitis is treated with topical corticosteroids and mydriatics.
Orbital floor steroids, such as Depomedrone,
dexamethasone 40mg, can be given for unilateral posterior uveitis. Oral
prednisolone may be given for bilateral posterior uveitis. Some patients may
require immuno-suppression. (1,20,21,22,23)
Tuberculosis ( Ocular Manifestations )
The eyelids may be affected by lupus vulgaris with skin nodules
surrounded by erythema.The orbit may be affected by cellulitis, dacryoadenitis,
dacryocystitis, osteomyelitis and abscess formation.There may be
chronic conjunctivitis, episcleritis or scleritis.The cornea may be
affected by keratoconjunctivitis or interstitial keratitis.
TB Vasculitis
Uveitis is the most common ocular manifestation. There may be chronic
granulomatous anterior uveitis, multifocal choroiditis, exudative retinitis,
vasculitis and optic nerve oedema. Anti-tuberculous
medications -isoniazid, ethambutol and rifampicin are given for at least 6
months. The use of prednisolone in ocular disease
is controversial. (16,17,18)
Table-
Ocular Manifestations of Tuberculosis
Affects 2% of sufferers of active tuberculosis , uveitis is commonest manifestation. Systemic disease is often apparent.
Eyelids-
lupus vulgaris (nodules surrounded by erythema)
Orbit-
cellulitis, dacryoadenitis, dacryocystitis, osteomyelitis, abscess
Conjunctiva-
rarely affected, chronic conjunctivitis
Cornea-
phlyctenular keratoconjunctivitis, interstitial keratitis (unilateral, sectorial,
superficial vascularisation)
Sclera-
episcleritis, nodular scleritis
Uveitis-
chronic granulomatous anterior uveitis, multifocal choroiditis, exudative
retinitis, vasculitis, optic nerve oedema, papilloedema (16,17,18)
_________________________________________________________________________
Herpes Zoster Ophthalmicus
Herpes Zoster Ophthalmicus is commonly seen in the elderly. A vesicular
rash is seen affecting the ophthalmic trigeminal distribution. The presence of
vesicles on side of tip of nose (Hutchinsons sign) indicates involvement of
the external nasal branch of nasociliary nerve and is associated with a
high rate of ocular disease. Immunosuppression is
a risk factor for development of the disease.
There is often chronic anterior uveitis. Complications include sectoral
iris atrophy, glaucoma, cataract, hypotony and phthisis bulbi. Posterior segment
inflammation is seen including vitritis, retinal vasculitis and optic neuritis.
Therapy includes the following. Acyclovir ointment
(5 X day) is given. Topical corticosteroids
and mydriatrics are given for anterior uveitis. Anti-glaucoma medications
are required occasionally. Prednisolone may be given if neurological, orbital or
optic nerve involvement occurs. (1,2,3)
_________________________________________________________________________
Table-
Herpes Zoster Ophthalmicus
50% of
varicella infected patients will develop zoster by 80yrs
15%
trigeminal, 50% thoracic
Age is
the most common predisposing factor, immunosuppression occurs in 1-2 % only.
Pathology
is related to ischaemic vasculitis caused by viral invasion.
#10%
will have ophthalmic involvement and of these 50% will develop complications
3-5 days
of pain in trigeminal distribution maculopapular rash - vesicular (may not
develop rash - zoster sine herpete)
Hutchinsons
sign- involvement of external nasal branch of nasociliary nerve - vesicles on
side of tip of nose 93% will develop ocular disease
Lid
margin vesicles 100% ocular involvement)
________________________________________________________(2)_______________
Ocular Manifestations Of Acquired Syphilis
Uveitis may be acute or chronic, unilateral or bilateral. Interstitial
keratitis affects a small percentage of acquired cases and is often unilateral.
Chorioretinitis is bilateral in 50% of cases; multifocal or diffuse yellow
exudate is seen. (25,26)
The chorioretinitis may resolve, leaving extensive bone spicule
pigmentation. The appearance may resemble retinitis pigmentosa. There may be
retinal oedema, haemorrhages, exudates, cotton wool spots and vascular
sheathing. Optic disc oedema may also be seen.
Investigations for suspected syphilitic uveitis include VDRL and FTA-ABS
tests.
The VDRL test is useful for screening; false positive results may occur.
The FTA-ABS test remains positive for life, even after treatment. (7,8)
Treatment- Syphilitic may be cured with treatment, in other types of
uveitis, the condition is usually suppressed
by topical steroids. Medications
that may be considered include penicillin, erythromycin, doxycycline and
ceftriaxone. (25,26)
Guidelines for the Treatment of Uveitis
The exact nature of the clinical features, their severity and their time
course will vary between individual patients. Appropriate treatment requires
knowledge of the patients type of uveitis and awareness of the details of the
individuals clinical features. In addition, the risks and benefits of various
treatment options need to be considered.
The nature of the uveitis and any limitations of treatment should be
outlined to the patient. (1,3)
________________________________________________
Table Treatment of
Uveitis
Specific vs. Nonspecific
Local Ocular vs. Systemic
Medical vs. Surgical
Specialist referral, for
example to a rheumatologist, paediatrician or infectious disease specialist, may
be helpful in many cases. A useful specialist report is more likely to be
obtained if one indicates to the specialist the diagnostic possibilities that
are being considered (e.g. juvenile rheumatoid arthritis, sarcoidosis).
(27)
Specific treatment, such as antimicrobial medication for infectious
uveitis, should be given when appropriate. Examples include uveitis due to
toxoplasma, syphilis or tuberculosis.
Ocular medication (such as eye drops or subconjunctival injection) is
generally preferred to systemic medication (such as oral or intravenous therapy)
in view of the much lower incidence of systemic side effects from ocular
medication. (1,2,3)
Corticosteroids
Routes of administration of corticosteroid for uveitis include eye
drops, ointment, periocular injection, oral and intravenous. The initial dose
should be proportional to the severity of the inflammation. The dose is tapered
gradually in order to minimize the risk of recurrence; the dose is correlated
with the severity of the inflammation. Systemic corticosteroids can be given for
certain types of posterior uveitis and for severe anterior uveitis unresponsive
to intensive topical therapy. Eye drops are effective for anterior segment
inflammation. Various strengths are available (table 3). Possible side effects
from topical therapy are glaucoma, posterior subcapsular cataract and
exacerbation of infection (particularly herpes simplex).
(1,3)
_______________________________________________________________________
Table Corticosteroid eye drops
(in order of decreasing strength)
Dexamethasone
Betamethasone
Prednisolone
Fluorometholone
(1,3)
________________________________________________________________________
Mydriatic eye drops
Mydriatic eye drops (see table 4) produce pupil dilatation (mydriasis) and paralysis of the ciliary body (cycloplegia). It is important for mydriatic eye drops to be used in anterior uveitis as they provide pain relief, prevent posterior synechiae formation and also break any posterior synechiae that have already formed. Posterior synechiae can cause permanent pupil irregularity and can, if extensive, cause glaucoma. Short acting mydriatic eye drops allow the dilated pupil to remain mobile and possibly less likely to develop posterior synechiae if the inflammation is mild.
_______________________________________________________________________
Table
Mydriatic eye drops (in decreasing order of
strength)
Tropicamide
Cyclopentolate
Homatropine
Atropine
(2)
_______________________________________________________________________
Cytotoxic medication and Immunosupression
These medications are commonly used as steroid sparing agents, patients
will usually not be able to tolerate doses of prednisolone above 20 milligrams
per day for long periods. Cytotoxic medication can cause serious side effects,
such as bone marrow suppression, and is therefore reserved for patients with
potentially blinding uveitis in whom the use of corticosteroid therapy is
effective, poorly tolerated or contraindicated. Cyclosporin, an anti-T-cell
immunosupressive agent, is occasionally used in severe uveitis when
corticosteroids and cytotoxic medication are ineffective. (1)
Table
Cytotoxic and Immunosuppressive medication used in Uveitis Therapy
Cyclosporin-
selectively depresses CD4+ lymphocytes
Azathioprine-
interferes with purine synthesis
Chlorambucil-
alklating agent, used for Bechets Diease
Cyclophosphamide-
alkylating agent used for uveitis in combination with life threatening systemic
disease such as Wegeners Granulomoatosis
Methotrexate
(seldom used) folic acid antagonist
FK
506 ( Tacrolimus), Rapamycin- alkylating agents, originally derived from
streptococcus species (1)
Uveitis may be an important consequence of systemic disease with profound implications for patient morbidity and quality of life. In many cases the morphology of ocular inflammation may be an important guide to the nature of the underlying disease under investigation. (1,3,23) The review encompasses common types of uveitis encountered in assocation with systemic disease in clinical practice and has outlined practical clinical approaches to investigate and treat uveitis .
References
1.
Jones NP, Uveitis an illustrated manual
Oxford ; Butterworth ; Heinemann 1998 1-93
2.
Harvey RB, Practical Ophthalmology- CD ROM
2002 Birmingham; Palmtrees Publishing
3. Nussenblatt RB, Whitcup SM, Palestine AG, Uveitis- Fundamentals and
Clinical Practice 2nd Edition ;
St Louis ; Mosby 1996 3-151
4. Marr JE, Stavrou P, Murray PI, Should we investigate uveitis ?
Invest Ophthalmol Vis Sci 1998 ; 39: S608
5. Murray P, Serum
Autoantibodies and Uveitis Br
J Ophthalmol 1986; 70 :266-8
6. Murray PI, Stavrou P,
Marr JE, Moradi P, Pattern of visual loss in patients with uveitis Invest Ophthalmol
Vis Sci 1998 : 39 : S607
7. Murray PI, Uveitis, When to Investigate ? Focus- Occasional Update from the Royal College of Ophthalmologists
1998 ; 8 : 1-2
8.
Thean LH, Thompson J, Rosenthal AR.
A uveitis register at the Leicester
Royal Infirmary Ophthalmic
Epidemiology 1996 3(3):151-8,
9. Feltkamp TEW. HLA-B27, acute anterior uveitis, and ankylosing
spondylitis. Adv Inflamm Res. 1991;9:211-16.
10. Brewerton DA, Caffrey M, Nicholls A, Walter D, James DCO. Acute
anterior uveitis and HLA-B27. Lancet. 1973;ii:994-6.
11. D'Alessandro LP, Forster DJ, Rao NA. Anterior uveitis and hypopyon.
Am J Ophthalmol. 1991;112:317-21.
12. Evan-Jones G, Ophthalmic Services for Children; Report of a Joint
Working Party Royal College of Ophthalmologists
13. Kanski JJ. Juvenile arthritis and uveitis. Surv Ophthalmol.
1990;34:253-67.
14. International Study Group for Behet's disease. Criteria for
diagnosis of Behet's disease. Lancet. 1990;335:1078-80.
15. Michelson
JB, Chisari FV. Behet's disease. Surv Ophthalmol. 1982;26:190-203.
Barlie GR, Flynn TE Syphilis exposure in patients with uveitis Ophthalmology
1997 ; 104 1605-9
References
16. Yazici H, Pazarli H, Barnes CG, et al. A controlled trial of
azathioprine in Behet's syndrome. N Engl J Med. 1990;322:281-5.
17. Karma A, Hukti E, Poukkula A. Course and outcome of ocular
sarcoidosis. Am J Ophthalmol. 1988;106:467-72.
18. Rothova A, Alberts C, Glasius E, Kijlstra A, Buitenhuis HJ,
Breebaart AC. Risk factors for
ocular sarcoidosis. Doc Ophthalmol. 1989;72:287-96.
19. Bienfait MF,
Hoogstenden HC, Baarsma GS, Adraiaansen HJ, Verheijen-Breemhaar L. Diagnostic
value of bronchoalveolar lavage in ocular sarcoidosis. Acta Ophthalmol.
1987;65:745-8.
20. Selroos O. Treatment of sarcoidosis. Sarcoidosis. 1994;11:80-3.
21. Lower EE, Baughman RP. Prolonged use of methotrexate for
sarcoidosis. Arch Intern Med. 1995;155: 846-51.
22. O'Callaghan CA, Wells AU, Lalvani A, Dhillon PD, Hansell DM,
Mitchell DN. Effective use of cyclosporine in sarcoidosis: A treatment strategy
based on computed tomography scanning. Eur Respir J. 1994;7:2255-6.
23. McCluskey PJ, Towler HM, Susan Lightman, S Management of chronic uveitis BMJ 2000;320:555-558
24. Rosenbaum JT, Wernick R. The utility of routine screening of
patients with uveitis for systemic lupus and tuberculosis: A Bayesian analysis.
Arch Ophthalmol. 1990;108:1291-3.
25. Margo CE, Hamed LM. Ocular syphilis. Surv Ophthalmol.
1992;37:203-20.
26. Tamesis RR, Foster CS. Ocular syphilis. Ophthalmology.
1990;97:1281-7.
27.
Rosenbaum JT. Characterization of uveitis associated with
spondyloarthritis. J Rheum. 1989;16:792-6.