Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 39

CHOROIDITIS

Dr. dr. Fitratul Ilahi, SpM(K)


Anatomy

Uveal Tractus : Iris, Sclera, Choroid


Anatomy of Choroid
• The outer layer of choroidal vessels, known as
the Haller layer, is relatively thick.
• The choroidal vessels : the Sattler layer (smaller
diameter vessels and precapillary arterioles) the
choriocapillaris.
• The choroid has posteriorly ( 0.22 mm ) thick in
the central macular region, thinner anteriorly at
the ora serrata ( 0.1 mm) .
• Normal Subfoveal choroidal thickness : 287 μm.
However, thickness changes with age and disease
states of the eye.
• The presence of thin choroid (leptochoroid) and
thick choroid (pachychoroid) is associated with
ocular disease.
Anatomy of Choroid
• The choroidal circulation supplies 90% of the
oxygen consumed by the retina, primarily by the
photoreceptors The RPE cells, which are
anatomically closely associated with the
choriocapillaris, are exposed to the highest oxygen
tensions of any perfused tissue, increasing the risk
of oxidative damage.
• The rapid flow in the choroid also acts as a heat
sink, removing thermal energy obtained by light
absorption.
INTRODUCTION • Inflammation of
choroid; associated with
severe vision loss.
(Standardization of Uveitis
Nomenclature (SUN) Working
Group)

• Uveitis
• Panuveitis
• Choroiditis
• Chorioretinitis
• Retinochoroiditis
• Neuro-uveitis
SIGN AND SYMPTOMS OF POSTERIOR
UVEITIS
Poor visual acuity Retinal/choroidal inflammatory
Floaters Infiltrates
Photopsia Inflammatory sheating of arteries/vein
Metamorphopsia
Scotoma
(Retinal vasculitis)
Dyschromatopsia Choroidal / retinal exudate
Perivascular inflammatory cuffing
Retinal /choroidal Neovascularization
Optic nerve head/retina/choroid
Swelling or atrophy
Cystoid macula edema
Exudative , tractional or
Rhegmatogenous retinal detachment
RPE atrophy /hypertrophy
CHOROIDITIS
Infectious:
• Toxoplasmic Choroiditis
• Tuberculous Uveitis : Disseminated
Choroiditis

Non-infectious:
• Multifocal Choroiditis
• Punctate Inner Choroidopathy (PIC)
• Serpiginous choroiditis
Ancillary Test
Fluorescein angiography
• Observe Choriocapillaris
• Fluorescein dye ranges from yellow to orange-red in
color.
• Fluorescein is approximately 80% protein-bound in
circulation; the blood–retina barrier prevents it from
diffusing into retinal tissue.
• Leakage can show in areas with new vessel growth,
inflammation or ischemia.
• Fluorescein readily leaks from the choriocapillaris,
staining the surrounding tissue.
• This rapid leakage, as well as the light absorption and
scattering by the pigment in the RPE and choroid,
prevents widespread use of fluorescein in choroidal
imaging.
1. Neovascular Age Macular Degenerative

• The presence of CNV (Choroidal Neovascular)is the


defining characteristic of the neovascular form of
AMD.
• Degenerative changes in Bruch membrane :(eg, the
accumulation of drusen and progressive thickening of
the membrane that characterize nonneovascular
AMD) provide a proangiogenic environment that can
stimulate neovascularization to develop in the
choriocapillaris and perforate the membrane.
• These new vessels, which are accompanied by
fibroblasts, may leak and bleed, disrupting the normal
architecture of the RPE–photoreceptor complex with
a degenerate fibrovascular complex that ultimately
produces a hypertrophic fibrotic disciform scar.
Signs and symptoms of neovascular AMD

• Sudden onset of decreased vision


• Metamorphopsia
• Paracentral scotomas.
• OCT: Subretinal or intraretinal fluid

• Amsler grid : Effective for early detection


Fluorescein Angiography
Management of neovascular AMD
• Laser photocoagulation (“thermal laser”)
Poor outcomes , high recurrence rates
(Macular Photocoagulation Study Trials)
• Photodynamic therapy/PDT(“coldlaser)-.
Intravenous photo sensitizing drug the
application of light of a specific wavelength.
• Antiangiogenic therapi
Angiogenesis is the formation of new blood

vessels that sprout from existing vessels next


comes degradation of extracellular matrix,
facilitating migration and proliferation of
endothelial cells.
2.Polypoidal choroidal vasculopathy
(Posterior uveal bleeding syndrome )
• a variant of CNV (type 1) and presents with
multiple, recurrent serosanguineous RPE
detachments.
• A network of polyps is associated with vessels
that adhere to the RPE monolayer of the
fibrovascular
• PCV was first discovered in hypertensive middle-
aged women of African American or Asian
ancestry,
• it has since been identified in women and men of
all races.
• In Asians, however, 20%–50% of cases of
neovascular AMD are PCV type
3. Pathologic Myopia
• Choroidal Neovascular develop in 5%–10% of
Myopia
• Early manifestations of CNV in pathologic myopia
include decreased or distorted vision.
• The clinical findings include: lacquer
cracks ,chorioretinal degeneration, posterior
staphyloma, subretinal hemorrhage
• Treatment:
laser therapy ( PDT=Photodinamictherapy) )
Intravitreal anti-VEGF , excellent visual
and
anatomical outcomes,
stabilization or improvement of visual acuity
after only 1 or 2 injections.
4.Tuberculosis Uveitis
• Mycobacterium tuberculosis
• Tuberculosis uveitis is uncommon, even in endemic
areas.
• Solitary or multifocal choroiditis,
Serpiginous like chorioretinitis
Eales disease like peripheral nonperfusion in
association with uveitis.
• The patient should be treated for extrapulmonary
tuberculosis ( the US Centers for Disease Control and
Prevention or the World Health Organization).
5.Syphilitic Chorioretinitis
• Uveitis can occur at any stage of the infection.
• Syphilitic uveitis is confirmed through serologic testing :
Specific fluorescent treponemal antibody absorption (FTA-
ABS) test and the nonspecific VDRL or rapid plasma reagin
(RPR) tests,. the Treponema pallidum particle agglutination
assay (TP-PA) and the microhemagglutination assay for T
pallidum antibodies (MHA-TP).
• Patients with uveitis who test positive for syphilis on serologic
tests should also have their cerebrospinal fluid anti
treponemal antibody titers measured
• Many patients with syphilitic uveitis present with panuveitis,
• Specifically suggestive clinical findings include :hypertensive
syndrome, iris roseola, and retinochoroiditis.
• syphilitic outer retinitis termed acute syphilitic posterior
placoid chorioretinitis (ASPPC) is characterized by a placoid,
round or oval, yellow-white lesion near the macula
6. Toxocariasis
• Toxocariasis is infection causeToxocara canis or
Toxocara cati, intestinal parasites of dogs and
cats.
• Humans are infected following ingestion of soil or
vegetables contaminated .
• a systemic infestation : visceral larval migrans,
fever, and eosinophilia.
• Children and young adults are affected
disproportionately.
• Ocular manifestations: decreased vision, floaters.
a peripheral granuloma, a traction band that
extends toward the macula , mimics unilateral
intermediate uveitis
• The condition is unilateral in most cases (1)
• Treatment :local or systemic corticosteroids
Toxocariasis
7. Lyme Disease
• Lyme disease is caused by the spirochete Borrelia burgdorferi,
transmitted to humans from animal reservoirs: primarily
rodents, deer, birds, cats, and dogs.
• Early systemic manifestations consist of myalgias, arthralgias,
fever, headache, malaise, and a characteristic skin lesion known
as erythema migrans or a bull’s-eye rash
• Ocular manifest, is uncommon.
• Ocular findings include keratitis, scleritis, Chronic uveitis, vitritis
, retinal vasculitis, papillitis, or optic neuritis,.
• Initial serologic testing is performed using a sensitive ELISA( IgM
and IgG )
• Treatment for early disease consists of tetracycline, doxycycline,
or penicillin. Advanced disease may require intravenous
ceftriaxone or penicillin.
8. TOXOPLASMIC CHOROIDITIS
• Most common cause of choroiditis in
immuno competent patient.
• Intraocular infection is often accompanied
by CNS involvement in immuno
compromised patient.
• Caused by toxoplasma gondii.
• Ingestion of oocyst from contaminated hand,
food or water.
• Transplacental – 40% of fetus is affected if
mother is infected during pregnancy.
CLINICAL MANIFESTATION OF
TOXOPLASMOSIS
- Congenital toxoplasmosis
- Acquired systemic toxoplasmosis
- Toxoplasmosis in the immunocompromised
host
- Acquired or reactivation of a latent infection
CONGENITAL TOXOPLASMOSIS

⚫ Results from transplacental


transmission of T. gondii.
⚫ Incidence of congenital infection varies
with the trimester during which the
mother becomes infected.
⚫ lowest incidence occurs in the first
trimester (15% to 20%), and highest
incidence in the third
trimester (59%).
⚫ If infection occurs in – 1st trimester →
spontaneou abortion- 3rd trimester →
subclinical infection
COURSE OF DISEASE:-
⚫ Choroidal cicatric surrounded by pigment
proliferation , it may become a
conglomerate or proliferated retinal
pigment cells, or it may be small and
appear as a pigment clump in the retina.
OPTIC NERVE
• Optic neuritis or papillitis associated with edema,
Juxtapapillary Retinochoroiditis , Macular Star

VITREOUS
• Posterior vitreous detachment common
• Inflammatory cells on the posterior vitreous face
ANTERIOR UVEA
• Anterior uveitis (granulomatous or
nongranulomatous) may be associated with
Toxoplasma retinochoroiditis
COMPLICATIONS
• Posterior synaechiae
• Macular edema
• Dragging of macula
• Retinal Detachment
• Choroidal neovascularisation
• BRAO/BRVO
• Optic atrophy
• Cataract
• Glaucoma
• pigmentary retinopathy
DIAGNOSIS
• Classic fundus finding
• Serological testing : IgG , IgM Toxoplasma
• PCR: in vitreous sample. Isolation of organism from
aquous, vitreous
• CNS imaging
• Fluorescein angiographic : a dark hypofluorescent
center of the lesion surrounded by an area of
hyperfluorescence.
• OCT, USG
Management
 Medicamentosa
Pyrimethamine,Sulfadiazine,Oral corticosteroids Folic
acid
Combinations include:
⚫ Clindamycin, Trimethoprim + Sulphamethoxazol (Co-
Trimoxazole), Spiramycin, Azithromycin
⚫ Therapy regimens used during Pregnancy: Spiramycin-2
gr/day in two divided doses
⚫ Standard regimen for newborns- Pyrimethamine +
Sulfadiazine + Folinic acid
 Surgical
• Pars Plana Vitrectomy: to remove Vitreous Opacities
and the persistent Vitreo-Retinal traction.
• Scleral Buckling: in cases complicated with Retinal
Detachment.
 Photocoagulation And Cryotherapy
• Destruction of the Toxoplasma cyst and the tachyzoites in
the retina
8. Punctate Inner Choroidopathy (PIC)

- Subgroup of MCP
- Young, female, myopic
- No inflammation
- Multiple small white spots with
fuzzy boarder at Inner choroid &
retina
9. Serpiginous Choroiditis

• Geographic or helicoid choroidopathy


• Chronic progressive inflammatory condition
affecting adult men and women
• Etiology still unknown, but it is thought to
represent an immune-mediated occlusive
vasculitis
• Manifestation:
- Usually unilateral
- Painless
- Paracentral scotoma
- Decreased vision
- Minimal vitreous involvement and anterior
chamber
• Funduscopy: asymmetric bilateral scarring,
active areas as gray-white lesions at level of
RPE
THANK YOU

You might also like