Uveitis Flashcards
(51 cards)
Iris nodules
Location:
Koeppe
Busacca
Berlin
KOEPPE: located at pupil margin; occur in granulomatous and nongranulomatous uveitis
BUSACCA: located on anterior iris surface; occur only in granulomatous uveitis BERLIN: located in anterior chamber angle; occur in granulomatous uveitis
Granulomatous Uveitis
Granulomatous
INFECTIOUS: syphilis, TB, leprosy, brucellosis, toxoplasmosis, P. acnes, fungal (Cryptococcus, Aspergillus), HIV
IMMUNE-MEDIATED: sarcoidosis, VKH, sympathetic ophthalmia, phacoanaphylactic
Non-granulomatous uveitis
Acute:
idiopathic
HLA-B27 asso (Ankylosing spondylitis, Reiter’s, psoriatic arthritis, inflammatory bowl dis)
Behcet’s dis
Posner-Schlossman syn (glaucomatocyclitic crisis)
HSV
Kawasaki’s
Lyme
Traumatic
Postop
other autoimmune: lupus, relapsing polychondritis, Wegener’s granulomatosis, interstitial nephritis)
Chronic (>6 weeks):
JIA
Fuchs’ heterochromic iridocyclitis
D/D
Uveitic glaucoma
HSV, HZV Fuchs' Posner-Schlossman Sarcoid Rarely: Toxo, syphilis, S.O.
D/D
hypotony
HLA-B27 a/w Infection (keratitis, endophthalmitis) Foreign body JIA Behcet's VKH malignancy (leukemia, lymphoma, retinoblastoma) Toxi (rifabutin)
D/D
diffuse KP
Fuchs' Sarcoidosis syphilis keratouveitis toxo (rarely)
NONGRANULOMATOUS
GRANULOMATOUS
composed of what cells?
Nongranulomatous:
lymphocytes
PMNs
Granulomatous: macrophages lymphocytes epithelioid cells multinucleated giant cells
Expanded w/u for:
recurrent ant uveitis >3
granulomatous
Pos of review of sys
post involvement
ESR, ACE, ANA, ANCA, IL-10, PPD plus anergy panel, CXR or chest CT
consider Lyme test in endemic areas, HLA typing (25% with HLA-B27 develop sacroiliac disease, so obtain sacroiliac X-ray), HIV Ab test
Targeted w/u for
CHILD WITH RECURRENT OR CHRONIC IRIDOCYCLITIS:
rule out JIA (usually ANA-positive, RF-negative)
ANA
RF
HLA-B8
Targeted w/u for
RETINAL VASCULITIS
RECURRENT APHTHOUS ULCERS
PRETIBIAL SKIN LESIONS
rule out Behçet’s disease
Skin lesion biopsy
HLA-B51 and -B27
Targeted w/u for:
PARS PLANITIS AND EPISODIC PARESTHESIAS:
rule out multiple sclerosis (MS)
Brain MRI Lumbar puncture
D/D
iris heterochromia
trauma (intraocular metallic foreign body), inflammation, congenital Horner’s syndrome, iris melanoma, Waardenburg’s syndrome (iris heterochromia, telecanthus, white forelock, congenital deafness), Parry-Romberg syndrome (iris heterochromia, Horner’s syndrome, ocular motor palsies, nystagmus, facial hemiatrophy), glaucomatocyclitic crisis, medication (topical prostaglandin analogues [Xalatan, Lumigan, Travatan]), nevus of Ota
Tx for toxo
-pyrimethamine + sulfadiazine and folinic acid; add prednisone 48 hr later
OR:
-oral or invitravitreal clindamycin and dexamethasone
-azithromycin +/- pyrimethamine
Onchocerciasis treatment
ivermectin + doxycycline (for Wolbachia crucial for worn fertility and survival)
CMV retinitis
does not require testing and a primarily clinical dx.
serology least helpful due to positivity in general population
Retisert
fluocinolone acetonide
release for 30 months
CMV retinitis
- response to treatment is indicated by lesion size and activity at the border of lesion
- Activity reflected by the new retinal hemorrhage and whitening at the border.
- Vitritis is uncommon
Uveitides benefit from eary immunomodulatory tx
Behcet’s (azathioprine 1st preferred line; CSA or infliximab 2nd; Chlorambucil most effective in achieving durable remission)
Necrotizing scleritis
VKH
S.O.
ibopamine
non-selective dopaminergic med increase aqueous production 4-fold
alkylating agents SE
pneumocystis carinii tx by Bactrim DS
Sterility
Malignancy
Hemorrhagic cystitis-cyclophosphamide
AZOOR (Acute Zonal Occult Outer Retinopathy)
vs
MEWDS (Multiple Evanescent White-Dot Syndrome)
photopsia
prodromal flu-like illness
AZOOR bil (esp. male) vs MEWDS unil
MEWDS: complete resolve w/i 3 months w/o visual damage.
AZOOR: acute visual and visual field loss followed by stabilization for 6 months, RPE atrophy and hyperpigmentation (bone spicules resemble RP and syphilitic chorioritinits) gradually develop.
So D/D for AZOOR:
other WDS esp MEWDS, RP, syphilis, diffuse unilateral subacute neuroretinitis, CAR
PIC (punctate inner choriodopathy) vs MFC (multifocal choroiditis) vs POHS(presumed ocular histoplasmosis syndrome)
both PIC and MFC young myopic healthy women
PIC: small focal atrophy and hyperpigmentation chorioretinal scar confined to posterior pole with minimal vitritis
MFC in contrast with more diffuse larger lesion with vitritis
POHS: mid-peripheral punch-out lesion, peripapillary atrophy, absence of vitritis
A common cause of visual loss of all due to CNV
VKH
The B-scan demonstrates thickening of the posterior choroid which is commonly found during the acute uveftic phase of Vogt-Koyanagi-Harada (VKH) disease.
VKH is more common in Asians, Asian Indians, and Hispanics and rare m Caucasians and Africans.
The djnical steges of VKH are:
• Prodromal stage - flu-like symptoms, meningitis-like symptoms (e.g. headache, neck pain), tinnitus, dysacusis, fever, nausea
• Acute uveitic stage (a few days after pmdromal stage) “- blurry vision, bilateral granutomatous anterior uveitis, vitritis, thickening ofchoroid, optic disc hyperemia/edema, multiple serous RDs
• Convalescent stage (several weeks later) -‘ resolution of serous RDs, sunset-glow fundus, perilimbal vitiligo (Sugiura sign), vitiliQO, alopecia, poliosis
• Chronic recurrent stage (if not treated adequately) - recurrent episodes of granulomatous anterior uveitis, iris depigmentation, posterior synechiae, cataract, glaucoma, CNV, subretinal fibrosjs
Lyme disease
Stage one - local, erythema migrans – follicular conjunctivitis
Stage 2 - several wks to mos after – large joint pain – uveitis
Stage 3 – CNS manifestation (meningitis, encephalitis, Bell’s palsy) – keratitis