Transcript PITFALLS IN MANAGEMENT OF UVEITIS

UVEITIS
Inflammation of the uveal tract
ANATOMICAL CLASSIFICATION
Anterior uveitis : inflammation of iris.
Intermediate uveitis : inflammation of the ciliary
body and vitreous.
pars planitis ( idiopathic ).
Posterior uveitis : inflammation of the choroid.
Panuveitis : inflammation of the whole uveal tract.
ETIOLOGIC CLASSIFICATION
 Infectious uveitis: viral, bacterial, parasitic.
 Noninfectious uveitis: Autoimmune
HISTOLOGIC CLASSIFICATION
Nongranulomatous uveitis ( NGU ) is more
common, often acute and involves anterior segment
of the eye with lymphocyte and plasmocyte
infiltration and a tendency to develop hypopyon
and keratic precipitates K.Ps.
NGU is often noninfectious and develops as a
hypersensitivity reaction.
GRANULOMATOUS UVEITIS
Often chronic, painless and insidious, can involve
any part of the uveal tract but has a tendency for
posterior segment involvement.
Pathologically it has infiltration of epithelioid and
giant cells surrounded by lymphocytes.
Large mutton fat keratic precipitates K.Ps are seen
on slit lamp examination.
GRANULOMATOUS UVEITIS
Common infectious etiologies are toxoplasmosis
and tuberculosis.
Noninfectious causes are sarcoidosis, vogt koyanagi
harada and sympathetic ophthalmia.
UVEITIS
Although the term UVEITIS refers primarily to
inflammation of the uveal tissue,adjacent sructures
such as the retina,vitreous,sclera and cornea are
also frequently involved secondarily in the
innflammatory process.
UVEITIS
UVEITIS is responsible for 10% of blindness.
Among patients with UVEITIS
about 75% have anterior uveitis ( iritis,
iridocyclitis )
8% intermediate uveitis (pars-planitis )
17% posterior or panuveitis.
UVEITIS SIGNS
 Autoimmune uveitis tends to be bilateral.
 Unilateral uveitis is often infectious.
 However both etiologies can be unilateral or
bilateral.
CLINICAL FINDINGS IN
ANTERIOR UVEITIS
 Pain
 Photophobia
 Lacrimation
 Congestion
 Reduced vision
 Systemic symptoms may be present if there is
association with systemic disease.
CLINICAL FINDINGS IN POSTERIR
UVEITIS
Reduced vision.
 Floaters.
 Pain and congestion usualy are not seen.
 Systemic findings may be present if there is
association with systemic disease.
SIGNS in ANTERIOR UVEITIS
Reduced corrected vision
Pupillary constriction
Perilimbal congestion
Cornea: keratic precipitates, edema
Anterior chamber: aqueous flare, cell
Iris: nodules, posterior synechia
Crystalline lens: pigment deposits, cataract
ANTERIOR UVEITIS SIGNS
 CELLS seen in anterior chamber are seen in
anterior uveitis and iridocyclitis.
 FLARE seen in anterior uveitis and iridocyclitis is
the result of increased permeability of iris vessels
and protein leak in anterior chamber.
SIGNS IN UVEITIS
Iris nodules usually seen in granulomatous uveitis can be
present in different locations of the eye.
BERLIN nodules are inflammatory nodules of the iris and are
located in anterior chamber angle.
BUSSACA nodules are seen in iris stroma.
KOEPPE nodules are inflammatory nodules located in
pupillary margin.
ANTERIR UVEITIS:
(AUTOIMMUNE )
 IS THE MOST COMMON FORM OF UVEITIS.
 BECAUSE UVEITIS MAY OCCUR
SECONDARILY TO INFLAMMATION OF THE
CORNEA AND SCLERA, THE PHYSICIAN
SHOULD EVALUATE THESE STRUCTURES
CAREFULLY TO RULE OUT A PRIMARY
KERATITIS OR SCLERITIS.
ANTERIOR UVEITIS
HLA-B27 ASSOCIATED UVEITIS.
JUVENILE IDIOPATHIC ARTHRITIS( chronic).
FUCH’S HETEROCHROMIC IRIDOCYCLITIS.
PHACOGENIC UVEITIS( lens-induced ).
TUBULOINTERSTITIAL NEPHRITIS and
UVEITIS SYNDROME.
HLA-B27 ASSOCIATED UVEITIS
ANKYLOSING SPONDYLITIS
REITER SYNDROME( REACTIVE ARTHRITIS SYNDROME ) IS SECONDARY TO
INFECTION BY : UREAPLASMA UREALYTICUN, CHLAMYDIA, SHIGELLA, SALMONELLA,
YERSINIA ORGANISMS,
INFLAMMATORY BOWEL DISEASE
PSORIATIC ARTHRITIS
INTERMEDIATE UVEITIS
Idiopathic :( Pars planitis ) is the most commom
form that constituting 85%-90% of cases.
Secondary :
Lyme disease
Syphilis
Tuberculosis
Multiple sclerosis
Sarcoidosis
Toxocariasis
POSTERIOR UVEITIS
Toxoplasmosis
Toxocariasis
Tuberculosis
Sarcoidosis
Vogt-Koyanagi-Harada Syndrome
Sympathetic Ophthalmia
AIDS related
Bird shot Retinochoroiditis
Behcet Syndrome,
Lymphoma
AIDS RELATED UVEITIS
 Cytomegalovirus
 HSV
 HZV
 Treponema pallidum
 Tuberculosis
 Cryptococcus neoformans
POSTERIOR UVEITIS SIGNS
 Funduscopic examination :
 Optic nerve congestion.
 Macular edema.
 Vascular sheathing ( vasculitis)
 Retinal infiltration,pigmentary
changes,exudation,snow balls and snow banking,
intravitreal bands ,retinal detachment,retinal and
macular scars and optic atrophy in chronic cases.
LOW VISION IN ANTERIOR
UVEITIS
 CORNEA :
 Epithelial lesions and defects, particularly in some
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cases like herpes virus and herpes zoster infection
Edema: increased intraocular pressure,ocular
hypotension.
Keratic precipitates: deposits of inflammatory cells on
corneal endothelium
Corneal opacities and scars: in chronic cases
Band keratopathy: seen in chronic cases such as cases
associated with pauciarticular juvenile idiopathic
arthritis
UVEITIS: ( LOW VISION )
 Retinal infiltrations can be infectious as in:
 Toxoplasmosis, tuberculosis, Toxocariasis, and
varicella-zoster virus infection ( Acute retinal
necrosis ).
 They can also be noninfectious and immune
related as in: Behcet disease,
sarcoidosis and white dot syndromes.
UVEITIS: ( LOW VISION )
 Retinal vasculitis is seen in sarcoidosis, wegner
granulomatosis,lupus,polyarteritis
nodosa,multiple sclerosis and numerous
fungal,parasitic,bacterial,viral and rickettsial
diseases
UVEITIS: (LOW VISION )
Reduced vision is noticeable in posterior uveitis
only if macula is involved in the process of
infiltration,ischemia, exudation and edema in active
uveitic syndromes.
Macular traction, pigmentary changes,macular scar
and macular hole are permanent changes that are
seen in chronic cases of posterior uveitis.
UVEITIS: ( LOW VISION )
Optic nerve involvement may also contribute to
reduced vision in uveitic syndromes.
Optic neuropathy can present as papillitis,
papilledema,optic nerve infiltration and ischemia.
Optic atrophy may be seen as a sequela of any of the
above conditions in posterior uveitis.
UVEITIS: ( LOW VISION )
Attacks of anterior uveitis and iridocyclitis if
associated with prolonged periods of poorly
controlled high intraocular pressure may leave the
optic nerve atrophic and pale and lead to
permanent vision loss.
Optic nerve atrophy is often detectable in
funduscopic examination and perimetry is only
required to confirm doubtful cases.
UVEITIS: ( LOW VISION )
Clinical examination including slit lamp
biomicroscopy and funduscopy recognize the
cause of low vision in uveitis.
In some cases special diagnostic tests such as
fluorescein angiography, perimetry,
ultrasonography and optical coherence
tomography are needed to determine the cause
of low vision as well as the degree of
contribution of each structure in reducing
vision.
UVEITIS
IN ABOUT HALF OF CASES OF UVEITIS NO
SPECIFIC ASSOCIATION IS FOUND AND
UVEITIS IS PRESUMED TO BE IDIOPATHIC
BACTERIAL UVEITIS
 SYPHILIS: treponema pallidum
 LYME DISEASE: borrelia burgdorferi
 LEPTOSPIROSIS:gram-negative spirochete
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Leptospira interrogans
OCULAR NOCARDIOSIS: Nocardia asteroides
TUBERCULOSIS: Mycobacterium tuberculosis
OCULAR BARTONELLOSIS: Bartonella henselae
is the principal etiologic agent of cat-scratch
disease
WHIPPLE DISEASE: Tropheryma whipplei
SYPHILITIC UVEITIS
SYPHILIS : is caused by spirochete TREPONEMA
PALLIDUM
Congenital : transplacental infection of the fetus
after tenth week of gestation.
Acquired : sexual contact.
Diagnosis is important because syphilis can mimic
any kind of intraocular inflammation that is curable
and has definitive antibacterial treatment.
Uveitis can occur at any stage of the disease
including tertiary syphilis
SYPHILITIC UVEITIS
 Ocular manifestations of syphilis are protean and
affect all structures including the conjunctiva,
sclera, cornea, lens, uveal tract, retina, retinal
vasculature, optic nerve, cranial nerves, and
pupillomotor pathways.
 Intraocular inflammation may granulomatous or
nongranulomatous, unilateral or bilateral, and it
may affect the anterior, intermediate, posterior
segment.
SYPHILITIC UVEITIS
 Primary syphilis may be diagnosed by direct
visualization of the spirochete with dark- field
microscopy.
 Serodiagnosis is performed by VDRL, RPR and
FTA ABS test.
 Testing for HIV should be performed in all
patients with syphilis.
TUBERCULOUS UVEITIS
 Ocular manifestations of TB may result from
active infection or an immunologic reaction to the
organism.
 Tuberculous uveitis is classically a chronic
granulomatous disease that may affect the
anterior and/ or posterior segments withmutton
fat K.Ps, although a nongranulomatous uveitis
may occur.
 Disseminated choroiditis is the most common
presentation of TB and is characterized as
multiple, deep, yellowish lesions as tubercles.
TB UVEITIS
 Definitive diagnosis of TB requires the findjng of
mycobacteria in body fluids and tissues.
 This approach is not often possible, and the
diagnosis is instead presumptive, based on
indirect evidence.
 A positive result on the PPD test or intrferon
gamma release assays such as the QuantiFERONTB Gold test is indicative of prior exposure to TB.
AUTOIMMUNE PANUVEITIS
Sarcoidosis
Sympathetic Ophthalmia
Vogt-Koyanagi-Harada Syndrome
Behcet Disease
SARCOIDOSIS
 A multisystem granulomatous disorder of
unknown etiology with protean systemic and
ocular manifestations.
 Although intrathoracic manifestations are most
common (90%), other organs frequently involved
include the lymph nodes, skin, eyes, CNS, bones
and joints, liver and heart.
 Ocular involvement may be seen in up to 50% of
patients with systemic disease, with uveitis being
the most frequent manifestation.
SARCOIDOSIS
 In most large series sarcoidosis acccouts for up to
10% of all cases of uveitis.
 Both sexes are affected, albeit with a slight female
predominance, onset usually occurs between the
ages of 20 and 50 years.
 Pediatric involvement is uncommon and the
clinical course is atypical.
 Sarcoidosis can present as any kind of uveitis.
SARCOIDOSIS
 Anterior uveitis presenting as granulomatous
iridocyclitis is the most common ocular lesion.
 Although cornea is infrequently involved, corneal
infiltrates may be seen, band keratopathy may
develop either due to chronic uveitis or
hypercalcemia.
 Posterior segment lesions occur in up to 20% of
patients with ocular sarcoidosis.
SARCOIDOSIS
 Vitreous involvement manifests as inflammation
with snowballs appearing as intermediate uveitis.
 Perivascular sheathing apperas as periphlebitis.
 Irregular nodular granulomas along venules have
been termed candle-wax drippings, or taches de
bougie.
 Occlusive retinal vascular disease, especially
branch retinal vein occlusion, and less commonly
central retinal vein occlusion and peripheral
retinal capillary nonperfusion may lead to retinal
neovascularization and vitreous hemorrhage.
FORMS of SARCOIDOSIS
 LOFGREN SYNDROME:uveitis plus erythema
nodosum, febrile arthropathy, bilateral hilar
adenopathy.
 HEERFORDT SYNDROME (uveoparotid fever):
uveitis, parotitis, fever and facial nerve palsy.
 MIKULICZ SYNDROME: sarcoidosis plus
lacrimal gland involvement.
VOGT- KOYANAGI-HARADA
SYNDROME
 VKH syndrome is an uncommon multisystem
disease of presumed autoimmune etiology.
 VKH starts with prodromal stage of flulike
symptoms.
 VKH UVEITIS is marked by bilateral
granulommatous anterior uveitis, vitritis,
choroiditis, optic disc edema and serous retinal
detachment.
NON OCULAR SIGNS of VKH
SYNDROME
Acute disease manifests as flulike symptoms with
orbital pain, headache, meningismus, dysacusia,
tinnitus, fever, photophobia and rarely cranial
neuropathies, hemiparesis, transverse myelitis
associated with CSF lymphocytic pleocytosis.
Chronic stage is marked by resolution of retinal
detachment, fundus depigmentation, perilimbal
vitiligo (sugiura sign), alopecia, vitiligo and poliosis.
SYMPATHETIC OPHTHALMIA
 SO is a rare diffuse bilateral granulomatous
uveitis that may develop after a surgical or
accidental trauma to one eye( the exciting eye),
followed after a latent period by the appearance of
uveitis in the uninjured fellow eye(sympathizing
eye).
 Until recently, accidental penetrating ocular
trauma was the most common cause but ocular
surgery particularly vitreoretinal surgey has now
emerged as the main risk factor.
SYMPATHETIC OPHTHALMIA
 Severe anterior granulomatous uveitis with
mutton-fat KPs, posterior synechia, elevation of
IOP may be seen.
 Posterior segment uveitis presents with vitritis,
yellowish white choroidal lesions (DALENFUCHS nodules) and exudative RD.
 Structural complications include cataract,CME,
choroidal neovascularization and optic atrophy.
SYMPATHETIC OPHTHALMIA
 History of trauma helps differentiate SO from
other diseases with granulomatous uveitis and
uveitis starts and is more severe in the exciting
eye.
 The precise etiology of SO is unknown and in
majority of patients there is a history of
penetrating ocular trauma complicated by
incarceration of the uveal tissue.
BEHCET DISEASE
 A chronic, relapsing, occlusive systemic vasculitis
of unknown etiology that is characterized by a
uveitis that can affect the anterior and posterior
segments of the eye, often simultaneously.
 The typical age of onset is between 25 and 35
years, but can al o develop as early as 10-15.
NONOCULAR BEHCET
 ORAL.
 DERMATOLOGIC.
 GENITAL ULCERS.
 SYSTEMIC VASCULITIS.
 NEUROLOGIC
Oral manifestations of BEHCET
DISEASE
Oral aphthae are the most frequent finding in
Behcet disease.These are recurrent mucosal ulcers
of the lips, gums, palate, pharynx and tongue that
produce significant discomfort and pain.
They are discrete, round or oval, white ulcerations
with red rims.
Genital ulcers are quite similar to oral lesions.
BEHCET DISEASE
Gastrointestinal involvement occurs as ulcers of the
esoghagus, stomach and intestines.
Pulmonary disease manifests as pulmonary arteritis
with aneurysms.
Arthritis occurs 50% of cases, the knee is most
affected.
NEUROLOGIC BEHCET
CNS vasculitis is the most serious manifestation of
BEHCET and occurs in 10% of cases.
CNS BEHCET creates headache, strokes, palsies
and confusional states.
Cranial nerve palsies, papillitis and papilledema are
sometimes seen.
OCULAR BEHCET
Anterior uveitis is nongranulomatous with transient
hypopyon.
Posterior uveitis is a sight threatening necrotizing
retinal vasculitis.
Branch retinal artery and vein occlusion, vitritis and
CME may be seen.
Retinitis as retinal infiltrates and optic neuropathy
as optic papillitis leading to optic atrophy may be
seen.
MANAGEMENT OF
UVEITIS
THE FIRST STEP IN THE MANAGEMENT OF
UVEITIS IS TO DETERMINE WHETHER
UVEITIS IS INFECTIOUS OR NONINFECTIOUS ( AUTOIMMUNE ) AND IS SIGHT
THREATENING OR NOT
ANY MISTAKE IN THIS APPROACH IS NOT
FORGIVEABLE AND COULD BE DISASTEROUS
TO THE FINAL VISUAL PROGNOSIS.
UVEITIS THERAPY
MOST PATIENTS WITH ACTIVE UVEITIS AND
ALL THOSE WITH ACUTE ANTRIOR UVEITIS
REQUIRE TREATMENT.
TREATMENT IS NOT RECOMMENDED FOR
SOME FORMS OF UVEITIS IF THE
INFLAMMATION IS NEIGHTER PROGRESSIVE
NOR SIGHT THREATENING.
UVEITIS THERAPY
THE GOAL OF TREATMENT OF UVEITIS IS
RAPID RESOLUTION OF OCULAR
INFLAMMATION, PREVENTION OF
SEQUELAE FORMATION AND RESTORATION
OF VISION.
DIAGNOSIS OF PROBABLE UNDERLYING
DISEASE NOT ONLY DIRECTS THE
PHYSICIAN TO START PROPER TREATMENT
BUT ALSO PREVENTS FURTURE
RECURRENCES THAT COULD BE SIGHT
THREATENING WITH EACH ATTACK.
UVEITIS THERAPY
TREATMENT IS CURRENTLY BASED ON BOTH
EVIDENCE AND PROTOCOLS AND ALSO BY
EXPERIENCE OF THE PHYSICIAN OR THE
OPHTHALMOLOGY CENTER INVOLVED IN
UVEITIS MANAGEMENT
IN AUTOIMMUNE UVEITIS, IT IS NOT ALWAYS A
RULE TO WAIT FOR ACHIEVEMENT OF
SPECIFIC DIAGNOSIS AS UNJUSTIFIED DELAY
IN TREATMENT MAY SOMETIMES CREATE
IRREPARABLE DAMAGE TO THE OCULAR
STRUCTURES AND PERMANENT VISION LOSS.
UVEITIS THERAPY
TREATMENT OF AUTOIMMUNE UVEITIS
CONSTITUTES THE FOLLOWING APPROACHES :
MEDICAL :
CORTICOSTEROIDS .
IMMUNOSUPPRESSIVES.
BIOLOGIC AGENTS.
OCULAR SURGERY :
CATARACT SURGERY
GLAUCOMA SURGEY
VITREORETINAL SURGERY.
CORTICOSTEROID
IT SHOULD BE EMPHESIZED THAT STEROIDS ARE THE
MAINSTAY OF THERAPY PARTICULARLY WHEN UVEITIS
IS ASSOCIATED WITH SYSTEMIC DISEASE
IN INFECTIOUS UVEITIS STEROIDS USE IN COMBINATION
WITH SPECIFIC ANTIMICROBIAL THERAPY MAY REDUCE
THE INFLAMMATORY RESPONSE AND THE
ACCOMPANYING TISSUE DAMAGE
IF NECESSARY AND BASED ON CLINICAL JUDGEMENT , IN
INFECTIOUS UVEITIS SYSTEMIC STEROIDS SHOULD BE
STARTED 48 HOURS AFTER COMMENCEMENT OF
ANTIMICROBIAL THERAP
DISCONTINUATION OF STEROIDS SHOULD BE MADE 7
DAYS BEFORE ANTIMICROBIAL THERAPY IS
TERMINATED
IMMUNOMODULATION
ALKYLATING AGENTS : CHLORAMBUCIL,
CYCLOPHOSPHAMIDE.
ANTIMETABOLITES: AZATHIOPRINE,
METHOTREXATE, MYCOPHENOLATE MOFETIL
T CELL INHIBITORS: CYCLOSPORINE, FK-506
(TACROLIMUS )
COMPLICATIONS :
MYELOSUPPRESSION, NEPHROPATHY,
HEPATOTOXICITY, SUPERINFECTION, GI UPSET,
MALIGNANCY. GONADAL ATROPHY
IMMUNOMODULATION
UNLIKE SYSTEMIC STEROIDS , CONTROL OF
INFLAMMATION IS NOT ACHIEVED BY THE
APPLICATION OF IMMUNOSUPPRESSIVES IN
INFECTIOUS UVEITIS,
SO IMMUNOSUPPRESSIVES ARE ABSOLUTELY
CONTRAINDICATED IN INFECTIOUS UVEITIS
AND THEIR USE LEADS TO DETERIORATION AND
POGRESSION OF THE INFECTIOUS PROCESS.
BIOLOGIC AGENTS
TUMOR NECROSIS FACTOR INHIBITORS:
 INFLIXIMAB ( REMICADE ) IS THE FIRST DRUG, I.V
ROUTE IS USED. VERY EFFECTIVE
 ETANERCEPT( ENBREL ) : SUBCUTANEOUS ROUTE,
LESS EFFECTIVE.
 ADALIMUMAB( HUMIRA ), SUBCUTANEOUS ROUTE
WITH PROMISING RESULTS.
 CETROLIZUMAB PEGOL( CIMZIA ): IS THE NEWEST
DRUG IN THIS GROUP WITH SUBCUTANEOUS ROUTE
BUT NO PUBLISHED DATA ARE AVAILABLE ON ITS
EFFECTIVENESS IN UVEITIS.
ROUTES OF DRUG
ADMINISTRATION IN UVEITIS
 TOPICAL TREATMENT FOR ANTERIOR UVEITIS:
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DROPS , OINTMENTS
SYSTEMIC ADMINISTRATION: PARTICULARLY WHEN
UVEITIS IS ASSOCIATED WITH SYSTEMIC DISEASE
PERIOCULAR INJECTIONS: TRIAMCINOLONE
INTRAVITREAL INJECTIONS: TRIAMCINOLONE,
DEXAMETHASONE, METHOTREXATE, ANTI- VEGFS
INTRAVITREAL IMPLANTS: FLUOCINOLONE
ACETONIDE ( RETISERT), DEXAMETHASONE
(OZURDEX ).
DEXAMETHAZONE IMPLANT MAY BE LONGER
LASTING THAN TRIAMCINOLONE .
PITFALLS OF INTRAVITREAL
INJECTIONS & IMPLANTS
FLUOCINOLONE ACETONIDE ( RETISERT )
IMPLANT RELEASES THE DRUG OVER A PERIOD
OF 30 MONTHS BUT IN CONTRAST TO OZURDEX
REQUIRES SURGICAL PLACEMENT.
EXPERIENCE IS LIMITED OVER THE
APPLICATION OF INTRAOCULAR BIOLOGIC
AGENTS AND THEIR USE IS NOT CURRENTLY
PROMISING
PITFALLS IN INTRAVITREAL
DRUG THERAPY
INTRAVITREAL METHOTREXATE REDUCES
INFLAMMATION, VITREITIS AND MACULAR
EDEMA WITHOUT RISING IOP IN PATIENTS
WITH A HISTORY OF STEROID RESPONSE.
UVEITIS THERAPY
SIMILAR TO METHOTREXATE, ANTI- VEGF
AGENTS HAVE THE ADVANTAGE OVER
TRIAMCINOLONE ACETONIDE OF BEING
MUCH LESS LIKELY TO CAUSE CATARACT
PROGRESSION OR A RISE IN IOP
HOWEVER ANTI-VEGF AGENTS HAVE LESS
ANTIINFLAMMATORY EFFECT MAKING
THEM LESS SUITABLE FOR THE TREATMENT
OF CME IN UVEITIS.
SYSTEMIC STEROID PITFALLS
DIABETES MELLITUS.
OSTEOPOROSIS.
HYPERTENSION.
MENTAL DISORDER
INCREASE IN BODY WEIGHT
CUSHINGOID APPEARANCE
INTRAVITREAL INJECTION
PITFALLS
CATARACT FORMATION
GLAUCOMA
ENDOPHTHALMITIS
RETINAL DETACHMENT
NEED FOR REPEATED INJECTIONS
INTRAVITREAL IMPLANT
PITFALLS
 CATARACT FORMATION.
 IOP RISE.
 HYPOTONY.
 IMPLANT MULFUNCTION.
 RETINAL DETACHMENT.
 ENDOPHTHALMITIS.
 SCLERAL THINNING.
 GLOBE PERFORATION
 OPPORTUNISTIC INFECTIONS: CMV AND
HERPETIC RETINITIS
INFECTIOUS UVEITIS
 TOXOPLASMOSIS: THE MOST COMMON
ETIOLOGY OF INFECTIOUS UVEITIS IN ALL
AGE GROUPS, SELF LIMITED IN
IMMUNOCOMPETENT INDIVIDUALS.
 STANDARD RX: PYRIMETHAMINE +
SULFADIAZINE.
 CLINDAMYCIN IS AN OPTION.
 AZITHROMYCIN.
TOXOPLASMOSIS
 SULFAMETHOXAZOLE + TRIMETHOPRIM IS
AN OPTION TO STANDARD RX.
 ORAL STEROIDS CAN BE ADDED 2 DAYS
AFTER SYSTEMIC THERAPY IF OCULAR
INFLAMMATION IS SEVERE AND
DESTRUCTIVE.
OCULAR TOXOCARIASIS
 PERIOCULAR AND SYSTEMIC STEROIDS ARE
EFFECTIVE IN OCULAR TOXOCARIASIS.
 ANTIHELMINTHIC AGENTS LIKE
THIABENDAZOLE, ALBENDAZOLE AND
MEBENDAZOLE ARE HELPFUL IN SYSTEMIC
TOXOCARIASIS BUT MAY WORSEN OCULAR
INFLAMMATION.
SYPHILIS
 OCULAR SYPHILIS CAN OCCUR DURING ANY
STAGE OF DISEASE AND CAN AFFECT ALL
STRUCTURES OF THE EYE :
 PARETERAL PENICILLIN G IS THE DRUG OF
CHOICE IN THE TREATMENT OF ALL STAGES OF
SYPHILIS.
 JARISCH-HERXHEIMER REACTION SOMETIMES
DEVELOPS DURING TREATMENT AND IS
MANIFESTED AS : MALAISE, FEVER, SWEATING,
ANXIETY AND TEMPORARY EXACERBATION OF
SYPHLITIC LESIONS: THE MECHANISM NOT
UNDERSTOOD
ACUTE RETINAL NECROSIS (
ARN)
 ARN TYPICALLY CAUSED BY HERPES
SIMPLEX VIRUS 1, 2 AND VARICELLA ZOSTER
VIRUS :
 TREATMENT : I.V ACYCLOVIR, ORAL
VALACYCLOVIR, ORAL FAMCYCLOVIR.
 INTRAVITREAL GANCYCLOVIR.
 INTRAVITREAL FOSCARNET.
ARN
 SYSTEMIC CORTICOSTEROIDS ARE
TYPICALLY USED AFTER ANTIVIRAL
TREATMENT TO HELP DECREASE
INFLAMMATION:
 PROPHYLACTIC LASER
PHOTOCOAGULATION TO THE BORDER OF
NECROTIC RETINA IS CONTROVERCIAL AND
HAS BEEN ADVOCATED TO REDUCE THE
RISK OF RETINAL DETACHMENT.
ARN
RETINAL DETACHMENT OFTEN REQUIRES
VITRECTOMY AND SILICONE INJECTION.
LOW VISION IS DUE TO RETINAL
DETACHMENT OR OPTIC NERVE
INVOLVEMENT
CMV RETINITIS
 CMV IS A HERPES VIRAL INFECTION IN
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IMMUNOCOMPROMISED PATIENTS.
PARENTERAL THERAPY WITH GANCYCLOVIR
OR FOSCARNET.
ORAL VALACYCLOVIR EQUALLY EFFECTIVE
TO I.V THERAPY.
INTRAVITREAL GANCYCLOVIR 2mg AND
FOSCARNET 2.4 mg.
GANCYCLOVIR INTRVITREAL IMPLANT.
DIFFUSE UNILATERAL SUBACUTE
NEURETINITIS ( DUSN )
CAUSED BY ANCYLOSTOMA CANIUM AND
BAILISACARIS PROCYONIS.
TREATMENT BY ANTIHELMINTHIC AGENTS:
ALBENDAZOLE AND THIABENDAZOLE.
DIRECT LASER PHOTOCOAGULATION OF THE
INTRARETINAL PARASITE.
LYME DISEASE
 MULTISYSTEM INFECTIOUS DISEASE
CAUSED BY SPIROCHETE ( BORRELIA
BURGDORFERI ).
 IT IS TRANSMITTED TO HUMANS BY TICK:
IXODES SCAPULARIS AND IXODES
PACIFICUS.
 ORAL ANTIBIOTIC AT EARLY STAGE
 I.V ANTIBIOTICS IN LATER STAGES:
CEFTRIAXONE, PENICILLIN, TETRACYCLINE,
DOXYCYCLINE, ERYTHROMYCIN.
TUBERCULOSIS
 INTRAOCULAR T.B CAN PRESENT AS ACUTE
OR CHRONIC GRANULOMATOUS UVEITIS.
 IZONIAZID, RIFAMPIN, PYRAZINAMIDE FOR
6-9 MONTHS.
 ETHANBUTOL OR STREPTOMYCIN CAN BE
ADDED IN CASE OF DRUG RESISTANCE.
 ORAL STEROIDS REDUCE THE
INFLAMMATORY COMPONENT OF T.B.
BRUCELLOSIS
 DOXYCYCLINE AND RIFAMPIN.
 DOXYCYCLINE AND STREPTOMYCIN.
 IN CHILDREN RIFAMPIN AND
TRIMETHOPRIM +SULFAMETHOXAZOLE