2. Epidemiology
• ~15 per 100,000 in U.S. each year
• Causes 10% of blindness in U.S.
• Third leading cause of blindness in developed countries
• Prevalence varies by location, age, and date of study
• Highest among >65 years of age
• Females
• Chronic and unilateral
• Anterior Uveitis most common
3. Pathophysiology
• Inflammation of the uvea
• Infectious, traumatic,
neoplastic, autoimmune,
idiopathic
• Inflammatory response:
chemical mediators result
in vasodilation, increased
vascular permeability, and
chemotaxis of
inflammatory cells in eye.
23. HLA-B27 DISEASES
•
Class 1 surface antigen
•
Seronegative spondyloarthropathies are strongly associated with acute
anterior uveitis and HLA-B27
•
spondylitis and sacroiliitis
Include:
•
Ankylosing spondylitis
•
Reactive arthritis syndrome
•
Inflammatory bowel disease
•
Psoriatic arthritis
24. Ankylosing
Spondylitis
•
lower back pain and
stiffness
•
men, 20-40‟s
•
HLA-B27: 90%
•
dx: sacroiliac imaging
studies - “bamboo spine”
Ocular findings (40%):
•
acute anterior uveitis - fibrin
and hypopon not
uncommon
25. Reactive Arthritis Syndrome
•
Triad: nonspecific urethritis,
polyarthritis, and conjunctivitis
often accompanied by iritis
•
HLA-B27: 95%, young adult men
•
arthritis in knees, ankles, feet,
sacroiliitis in 70% of pts
Ocular findings:
•
Mucopurulent and papillary
conjunctivits, acute
nongranulomatous iritis in 10%
Keratoderma blennorrhagicum
26. Psoriatic Arthritis
•
Inflammatory arthritis occurs in 30% of
pts with chronic psoriasis
Inflammatory Bowel Disease
•
cutaneous changes, distal phalangeal
joint inflammation, ungula involvement
•
•
20% may have sacroiliitis
•
25% develop iritis
12% of ulcerative colitis pts
and 2.4% of Chrons
disease pts develop acute
anterior
•
20% have sacroiliitis
•
60% HLA-B27 positive
27. Glaucomatocyclitic Crisis
•
Recurrent unilateral mild
acute iritis
•
Elevated IOP, corneal edema,
fine KPs, low-grade cell and
flare, slightly dilated pupil
•
Duration: hours to days
•
Associated with HLA-B54
28. Lens-associated
Uveitis
•
•
Immune reaction to lens
material: granulomatous or
nongranulmatous
KPs can be small or large,
cells mild to severe, hypopon,
PS, elevated IOP, vitritis
Postoperative
inflammation:
IOL-associated
Mild inflammation to UGH syndrome
(uveitis-glaucoma-hyphema)
IOL implantation can activate
complement cascade, cellular deposits
on IOL, synechiae formation, capsular
opacification
•
Retained lens material
•
Phthisis bulbi, persistent uveitis,
or glaucoma often occurs in
these eyes
•
iris chafing caused by the edges or
loops of IOL – mechanical irritation and
inflammation
31. •
most common systemic disorder
associated with iridocyclitis in
children
•
iritis develops within 5-7 yrs of
onset of joint disease
•
RF: female, pauciarticular onset,
ANA
•
negative RF
•
eye is usually white and uninflamed, some pts do not have
pain
•
Ocular findings: fine KPS, flare and
cells, posterior synechiae, cataract,
glaucoma, band keratopathy,
vitreous debris, ME, chronic
hypotony, phthisis
Juvenile Idiopathic
Arthritis
35. •
absence of infection and systemic
disease
•
85-90% of intermediate uveitis
cases
•
5-40 yrs, healthy individuals
•
associated with HLA-DR15 and HLADR51 alleles
Pars Planitis
Clinical Characteristics:
•
80% bilateral
•
Ocular manifestations: spillover into
anterior chamber, vitreous cells,
snowballs, peripheral phlebitis and
retinal venous sheathing
•
Ddx: Syphilis, lyme, sarcoidosis, MS,
toxicarasis, lymphoma
36. Multiple Sclerosis
•
30% of MS pts will get
uveitis
•
15% of pts with pars planitis
will eventually develop MS
•
women, 20-50 yrs
•
HLA-DR2 and DR15
•
Granulomatous anterior
uveitis, intermediate uveitis,
panuveitis
39. Systemic Lupus
Erythematosus
•
Multisystem autoimmune
connective tissue disorder
•
Type 3 hypersensitivity reaction:
Antibody-immune complexes
precipitate and cause further
immune response
•
Affects heart, nervous system,
joints, skin, lungs, blood vessels,
liver, and kidney
•
Women, 15-45 years
•
Labs: ANA
•
Malar “butterfly” rash -70-80%
40. Clinical findings
Ocular manifestations in 50%
•
Keratoconjunctivitis sicca
(20%)
•
Lupus retinopathy -CWS
•
Cutaneous lesions on the
eyelids
•
Scleral inflammatory
disease
•
Neuro-ophthalmic disorders
•
Retinal vasculopathy
•
In rare cases uveitis
41. Polyarteritis nodosa
and microscopic
polyangiitis
•
Systemic vasculitis –
necrotizing inflammation of
medium and small sized
arteries
•
40-60 yrs, men, hepatitis B
•
Ocular involvement in 20%
•
Mortality rate of untreated
PAN is 90% by 5 yrs
•
Labs: p-ANCA, ESR, CRP,
tissue biopsy
42. Wegener‟s
Granulomatosis
•
Triad: necrotizing granulomatous vasculitis of upper and lower respiratory
tract, glomerulonephritis, necrotizing vasculitis of small arteries and veins
•
Involvement of paranasal sinuses is most characteristic feature
•
Ocular involvement in 50%:
-- orbital involvement: pseudotumor, cellulitis, dacryocystitis
-- anterior, intermediate, or posterior uveitis
--scleritis (necrotizing), uveitis, retinal vascular involvement
Dx: tissue biopsy, chest x-ray, CRP, ESR, c-ANCA
43. White Dot Syndromes
• Group of chorioretinopathies that are inflammatory in
nature presenting with discrete, multiple, yellow-white
lesions
• Symptoms: photopsia, blurred vision, floaters,
nyctalopia, enlarged blind spot
• Young females
46. Sarcoidoses
•
Multisystem non-caseating
granulomatous disorder of
unknown etiology
•
Intrathoracic : 90%, intraocular:
50%
•
Affect lymph nodes, skin, eyes,
CNS, bones and joints, liver, and
heart
•
African American, females, 20-50
years
•
Dx: chest x-ray, lymph node biopsy,
elevated ACE and lysozyme levels
47. Ocular Findings
•
can involve any ocular tissue
•
most common: Anterior
granulomatous uveitis
–mutton fat KP‟s, koeppe and
busacca iris nodules, synechiae
•
Posterior segment in 20% of
ocular sarcoidosis
--vitreous infiltration “string of
pearls” or “snow balls”
--granulomas seen in retinal,
choroid
--perivascular sheathing,
occlusive vascular disease
•
Eyelid granulomas
•
Conjunctival nodules
•
Lacrimal gland infiltration
48. Sympathetic Ophthalmia
•
Bilateral, diffuse granulomatous, non-necrotizing
panuveitis
•
Autoimmune inflammatory response toward ocular
antigens – delayed hypersensitivity to melanin
containing structures?
•
Occurs after surgery or trauma to an eye
•
2% of uveitis cases
•
Anterior Uveitis: mutton fat KPs, PS, thickening of
iris from lymphocytic infiltration
•
Posterior vitritis, dalen-fuchs nodules,
peripapillary choroidal lesions, exudative RD
49. •
Cell-mediated autoimmune process
driven by T lymphocyctes directed
against self-antigens associated with
melanocytes of all organ systems
•
Higher association in darkly pigmented
ethnic groups
•
4% of uveitis referrals in US
•
Chronic, bilateral, diffuse,
granulomatous panuveitis with
integumentary, neurologic, and auditory
involvement
Vogt-KoyanagiHarada Syndrome
50. Stages
Acute: bilateral granulomatous
anterior uveitis, vitritis,
thickening of choroid, edema
and hyperemia of optic nerve,
multiple serous retinal
detachments
Convalescent: “sunset glow”
fundus, skin changes: vitiligo,
alopecia, poliosis
Chronic recurrent: repeated
bouts of uveitis
51. Behcet Disease
• chronic, relapsing,
occlusive systemic
nongranulomatous
vasculitis of unknown
etiology
• recurrent oral ulcers,
skin lesions, genital
ulcers, ocular
inflammatory disease
(70%)
• can affect all portions
of uveal tract
52. Ocular Findings
80% bilateral
• Anterior uveitis:
hypopyon in 25% of
cases
• Posterior segment:
necrotizing retinal
vasculitis affects both
veins and arteries
• Optic nerve affected in
25% of pts
• Visual prognosis is
guarded -25% VA <
20/200
54. Viral
• Herpes Simplex:
• Usually iritis is a keratouveitis but can be: corneal,
cutaneous, retinal
• arborized
• +/- KPs, +/- Hypopyon
• HSV-1 is generally oral-labial HSV-2 generally genital
infections, although crossover does occur.
Image: C. Blake Perry. Source: http://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/HSV-epithelial-keratitis.htm
55. Viral
• Herpes Zoster
•
•
•
•
72 hours PHN
¼ ocular involvement
Infiltrative pseudodendrites (negative stain)
Typically elderly and immunocompromised
Image:Yanoff, Myron, and Jay Duker. Ophthalmology. 3rdrd ed. N.p.: Mosby Elsevier, 2009. 223. Print.
56. •
Viral
ARN
•
•
•
•
•
•
VZV>HSV>CMV
Immunocompetent
Starts unilateral but 36%Fellow eye
Within 6 weeks of onset
Painful, Floaters, LOV
Peripheral „creamy‟ necrosis that spread,
occlusive vascular involvement, Panuveitis
• Poor Prognosis, RD in 75%
• PORN
• VZV mainly
• Immunocompromised
• Posterior pole involved early
• Patchy confluent necrosis, weak or
absent uveitis, no vascular involvement
• Poor Prognosis, RD in 70%
Images: Baumal, Caroline et al. Duane‟s Ophthalmology ,2006.‟Acute Retinal
Necrosis and Progresive Outer Retinal Necrosis Syndromes Accessed online:
http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v3/v3c028.html#ref
57. Viral
• CMV
•
•
•
•
•
•
•
CD4 <50-100
Most common opportunistic infection in AIDS
In congenital cases + birth defects
Before HAART ~30% of CD4<50
After HAART incidence decreased 75-80%
May start by looking like CWS (small infiltrates)
Perivascular hemorrhages, white necrotic retina, frosted
branches /vasculitis
Image: Yanoff, Myron, and Jay Duker. Ophthalmology. 3rdrd ed. N.p.: Mosby Elsevier, 2009. 796. Print.
58. Protozoal
• Toxoplasmosis
• Toxoplasma gondii
• Undercooked meat /cat feces
• Most common posterior uveitis in immunocompetent
individuals
• Often acquired in utero (0.2-1% of pregnancies)
• Further Trimester = increased chance of exposure, worst if
acquired early (spontaneous abortion)
• Majority do not develop ocular manifestations
Image: Tabbara. Khalid. „Toxoplasmosis‟. Duane‟s Ophthalmology 2006. Accessed online:
http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html
59. Protozoal
• Toxoplasmosis
• „Headlights in the fog‟
• Focal chorioretinal scar with adjacent necrosis and dense
vitritis
• With AIDS may have multiple lesions
• Often self-resolving over months
• May use sulfadiazine, pyramethamine, steroids.
Image: Tabbara. Khalid. „Toxoplasmosis‟. Duane‟s Ophthalmology 2006. Accessed online:
http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html
60. Helminthic Parasites
• Toxocaraisis
• Ingesting eggs of Toxocara
• Dogs >cats
• Acquired through soil, or uncooked food
• Particularly affects kids with pica
• Yellow white mass with tractional component, may have
vitritis.
• Often leads to TRD
• Treat uveitis, consider anti-helminthics (albendazole)
Image: Yanoff, Myron, and Jay Duker. Ophthalmology. 3rdrd ed. N.p.: Mosby Elsevier, 2009. 834. Print.
61. Bacterial
• Syphilis
•
•
•
•
•
•
Treponema pallidum
„Great Mimicker/Masquerader/Imitator‟
Enters through intact mucosa
Ocular Syphilis in 2‟ and 3‟ stages (2-6 mo after)
Uveitis most common ocular manifestation (up to 10%)
Affects immunocompetent or immunocompromised
Image: „Syphilis‟. WebMD. Accessed Online: http://www.webmd.com/sexual-conditions/guide/syphilis
64. Bacterial
• Lyme
•
•
•
•
•
Borrelia burgdorferi
1: rash (e. migrans)
2: dermatologic, neurologic, cardiac
3: Late arthritis, cranial and peripheral nerves
50% reported no hx of tick bite
Image: Sources for Rashes: Poster: "Looking for a Bull's-Eye Rash? Look again - erythema migrans can take many
forms. A collaborative effort between the Maryland Department of Health and Mental Hygeine and the Lyme
Disease Research Foundation of Maryland Maryland.http://www.bayarealyme.org/get-help/lymes-many-symptoms
65. Bacterial
• Lyme
1. Conjunctivitis early
2.Motility / CN palsies, optic neuropathy, PTC,
chorioretinitis, uveitis
3. Stromal keratitis, symblepharon
ELISA, Western Immuoblot
Tx: Doxycycline, amoxicillin, if needed ceftriaxone
Image: Pediatric Associates of Connecticut. „Tick Bites and Lyme Disease, Accessed Online:
http://www.pediatricdoc.com/newsletter.cfm?nid=625
66. Bacterial
• Tuberculosis
•
•
•
•
•
•
•
•
•
•
Mycobacterium tuberculosis
Incidence: Annually ~9.3 million patients worldwide
Communicable: inhaled aerosolized droplets
Primarily involves the lungs
Uveitis is common
Cough, fever, night sweats
Caseating necrotic granulomas
CXR
PPD / Mantoux testing
TB blood tests: interferon-gamma release assays (IGRAs)
Images taken from wikipedia . Accessed online: http://en.wikipedia.org/wiki/Tuberculosis_diagnosis
67. Bacterial
• Tuberculosis
•
•
•
•
Granulomatous anterior, intermediate or posterior uveitis
Vasculitis with choroiditis, or choroidal tubercles
Phlyctenular conjunctivitis
Tx: Rifampin, Isoniazid, Pyrazinamide, Ethambutol
Image: Yanoff, Myron, and Jay Duker. Ophthalmology. 3rdrd ed. N.p.: Mosby Elsevier, 2009. 808. Print.
68. Infectious
Endophthalmitis
• Endogenous (<10%)
• Systemic via blood stream
• Organisms causing endocarditis and GI tract are primary sources,
usually with sepsis, immunocompromise, IV drug abuse,
catheders.
• Typically less pain and inflammation, and can be bilateral
• Exogenous
•
•
•
•
Trauma, Surgery, Infection
Acutely is usually gram + (normal flora)
Decrease in occurrence over the last 30 years.
Bleb-associated may occur at any time.
• Acute 0.061-0.3%
• Delayed 0.2-18% (variable reports)
Image taken from „Endophthalmitis‟ by the American Academy of Ophthalmology 2013. Accessed Online:
http://www.aao.org/theeyeshaveit/red-eye/endophthalmitis.cfm
69. Infectious
Endophthalmitis
• EVS
• used <6 weeks, for cataract PO (Acute Onset)
• Blur (94%), red eye (82%), pain (74%), hypopyon
(86%)
• No view of retinal vessels in 79%
• Red reflex present in only 32%
• Immediate vitrectomy if LP or worse.
• B scan
• Tx: culture, Vancomycin/Amikacin/Ceftazidime +/Dexamethasone
70. Masquerade
Syndromes
Accounts for nearly 5% of all patients with uveitis at tertiary referral.
Neoplastic Masquerade
• Lymphoma
• Uveal melanoma
• Retinoblastoma
• Juvenile xanthrogranuloma
• Metastatic tumors
Nonneoplastic Masquerade
• Retinitis Pigmentosa
• Ocular Ischemic Syndrome
• Retinal detachment
• Intraocular Foreign Bodies
• Pigment Dispersion Syndrome
71. Lymphoma
• 5th to 7th decade of life
• 25% ocular involvement
• 15% ocular as initial presentation
• 56% with ocular involvement develop
CNS involvement
• Variable uveitic presentations
unresponsive to therapy
• Can mimic chronic uveitis
82. Cycloplegics
Mydriatics
• These opthalmic
preparations block the
responses of the iris
sphincter and the
accommodative muscle of
the ciliary body to
cholinergic stimulation,
producing pupillary dilation
(mydriasis) and paralysis of
accommodation
(cycloplegia)
• Tropicamide 1%,
cyclopentolate and atropine
have both properties
• Phenylephrine has only
mydriasis.
www.lookfordiagnosis.com/mesh_info.php?term=
83. Cycloplegics
Purpose:
•To break or prevent posterior
synechiae and to relieve ciliary
spasm induced photophobia.
•Short acting vs. long acting
cycloplegics
•Dosing depends on the extent
of inflammation
•(1-2xdaily atropine, 3xdaily
tropicamide and
phenylephrine)
85. Antigen-dependent lymphocyte activation and STEROID/NSAID
activation sites
Cunningham, Emmett. Practical approach to the use of corticosteroids in patients
with uveitis. Can J Opthalmol 2010; 45:352-8
87. Common uses of
corticosteroids
-Mainstay of initial therapy
Cunningham, Emmett. Practical approach to the use of corticosteroids in patients with
uveitis. Can J Opthalmol 2010; 45:352-8
100. Indications for IMT
inadequate response of uveitis to corticosteroid therapy for greater than 3
months with doses exceeding 5-10mg/day.
contraindications to corticosteroid use:
1. (diabetes, hypertension, peptic ulcer, GERD, immunocompromised
state, psychiatric conditions)
2. exacerbated side effects
3.chronic corticosteroid dependence
www.fortiusfitness.com/blog/steroi
d-side-effects
101. Precautions
No infection present
No hepatic or hematologic contraindications
Close physician follow up
Teratogenic
mamaprayed.blogspot.com/2012/08/if-you-give-m
102. Antimetabolites
•
Azathioprine, methotrexate, mycophenolate mofetil
•
Azathioprine (purine nucleoside analogue)
-interferes with DNA replication and RNA transcription
-found beneficial in VKHsyndrome, int. uveitis, Behcet uveitis, sympathetic
opthalmia and necrotizing scleritis
-GI side effects (nausea, upset stomach) are cause for D/C.
-CBC, LFT every 4-6 weeks.
-Thiopurine S-methyltransferase (TPMT) testing (metabolizes 6mercaptopurine,ie 6-MP)
www.lookfordiagnosis.com/mesh_info.php?term
103. Methotrexate
•
Folic Acid analogue
•
Inhibitor of dihydrofolate
reductase and it’s DNA
replication
•
Causes extracellular
accumulation of adenosine to
create an anti-inflammatory
effect.
•
Useful for JIA (first line choice
IMT treatment for
children), sarcoidosis, panuveiti
s, various other types of uveitis
•
Prospective study for IV inj. for
refractory uveitis and uveitic
CME.
www.humira.com/jia/what-is-jia.aspx
104. Mycophenolate Mofetil
• Inhibits inosine monophosphate dehydrogenase
and DNA replication
• Side effects: reversible GI distress, diarrhea;
20%pt. pop.
• CBC monthly
• 85% effectivity in chronic uveitis patients and a
good second choice IMT for children.
105. T Cell Signaling Inhibitors
Cyclosporine and tacrolimus:
•
Calcineurin inhibitors- disrupt
T-cell receptor signal
transduction and down regulate
IL-2 transcription and CD4 T
lymphocyte receptor expression.
Sirolimus:
•
Non-calcineurin inhibitordisrupts T cell signaling that
inhibits Ab production and Blymphocytes.
www.bdbiosciences.com/research/tcell/reg
106. Cyclosporine
• SE: Nephrotoxicity and systemic hypertension;
paresthesia,hypertrichosis.
• BP, CBC, serum creatinine monthly.
• Used for int. uveitis and posterior uveitis cases from
Behcets and VKH.
• Used in combination with corticosteroids for modest
improvement
107. Tacrolimus
• AE: nephrotoxicity
• Low dose and increased potency to cyclosporine
• Less risk of hypertension and hyperlipidemia
• Useful for chronic int. and posterior uveitis.
108. Sirolimus
• One open-label, prospective study it was found useful in
treatment for refractory noninfectious uveitis
• GI side effects
• Under active investigation for use in treating uveitis
109. Alkylating Agents
Cyclophosphamide
• Active metabolites alkylate purines in DNA and RNA, creating
impaired DNA replication and cell death
• Cytotoxic to dividing and resting lymphocytes
• AE:myelosuppression, hemorrhagic cystitis, sterility
Chlorambucil
• Interferes with DNA replication
• AE:myelosuppression, sterility
Treatment for int. uveitis, VKH, SO, Behcet
Significant AE: increased risk for malignancy (leukemia, various cancers)
110. Infliximab
Biologic Response
Modifiers
• Chimeric, monoclonal IgG1k antibody against TNFalpha
• Treatment for Behcet, sarcoidosis and VKH. Some HLA
B27 ant. uveitis
• Drug induced toxicity (lupus, systemic vascular
thrombosis, CHF, malignancy, demyelinating disease and
vitreous hemorrhage)
• +PPD, contraindication
• Adalimumab, less AE, same effectiveness
111. Alternative Therapy Under
FDA Investigation
• Rituximab:chimeric monoclonal antibody against CD20
positive cells (B lymphocytes)
• Daclizumab: monoclonal Ab to IL-2
• IFNalpha2a: antiviral, immunomodulatory and
antiangiogenic effects (leukopenia and thrombocytopenia
side effects)
112. Management/Follow up
• Encounter visit determines
extent of ocular inflammation
(ant., int., panuveitis, etc).
• Make a differential list and
send out for further pertinent
lab work to confirm/rule out
differentials.
super-trainer.com/fitness-business-becoming-a-bu
113. Anterior Uveitis
• Cycloplegic
• Steroid
• Dosage depends on severity
• Follow up in 2-3 days
• If 2-3 additional follow up
appt. prove no
improvement, referral to
uveitis specialist
medlibes.com/entry/anterior-uveitis
114. Intermediate/Posterior Uveitis
• Determine extent of
inflammation, if anterior
involvement, start on
cycloplegic and steroid.
• Refer to retinal specialist for
periocular steroid injections (if
deemed non-infectious)
• Intravitreal injections for
chronic anterior uveitis or
inflammation not responsive
to periocular injection
www.retinaeye.com/uveitis.html
115. Uveitic Treatment
Adverse Effects
• Steroid responders:
Need to lower IOP by utilizing beta blockers, alpha2
agonists,CAI, prostaglandins and their combinations
where appropriate.
116. Case #1
• 70+ yr old cauc. male
• Redness, mild pain, blurry
vision in the right eye.
• Slit lamp: 2+ AC WBC
reaction; florrid NVI,NVA,
corneal edema with descemet
folds; IOP 16mmHg OD
118. OIS!
• DFE: mid-peripheral blot hemorrhages
• No CME, NVD, NVE
• Tx: Prednisolone Forte q2hrs, Atropine BID OD
• Referral to retinal consult for PRP and possible injections of anti-vegf
• Contact PCP for carotid doppler, echocardiogram, EKG
119. Case #2
• 17 yr cauc. female
• CC:
redness, pain, photophobia, bl
urry vision
• Review of systems was
unremarkable
• Second episode, first episode
two years ago in GA.
120. Review of Systems
• General - Weight loss, fatigue, fever Skin - Rash, nodules, changes in
nails
• Neck - Lymphadenopathy
• Respiratory - Cough, wheezing
• Cardiac - Chest pain/discomfort, dyspnea
• Gastrointestinal - Hepatomegaly, diarrhea, frequent bowel movements
• Genitourinary - Delayed secondary sexual characteristics
• Musculoskeletal - Muscle or joint pain, arthritis, back pain, limitation
of motion
(refer to uveitis.org for more information and questionnaire)
121. Differentials?
• JIA, lyme disease, lupus, sarcoid
• ?????
• Ran pertinent lab tests for her age (CBC c diff.,ANA, ACE,
Lyme titer,ESR,RF, HLA B27)
• Durezol q2hrs, Atropine BID OD. Pledget of 10%
phenylephrine to break posterior synechiae
• CBC with diff., lyme titre, RF, ANA, ACE, serum lysozyme
• Blood results…negative. Consult with uveitis specialist.
123. Chief Complaint
• 46 year old WM
• Redness OS x 5 days, gradually getting worse
that is constant throughout the day
• (+) photophobia, epiphora
• ( - ) eye pain, flashes, floaters, cold sores
• He was seen at Patient First 3 days ago where
they diagnosed him with shingles over the left
eyelid, noting ocular involvement
• Treated with 20 mg Pred, mild pred taper and 1
gm of Valtrex tid x 10 days
124. History
• Medical History
• Hypertension, GERD
• Treated with Omeprazole and Diovan
• Family Medical History
• Unremarkable
125. Examination
• VA sc 20/25 OD, OS, OU
• OD unremarkable findings
• OS
• Lid: vesicles along upper
forehead & nose, lid
erythema, small hordeolum
• Conj: nasal injection
128. Assessment
1. Redness/Discharge of
Eye OS
1. Educated patient on
findings
2. H. Zoster
Keratoconjunctivitis OS
2. Neomycin ung on
vesicles, BID
3. H. Zoster Iridocyclitis, OS
3. Pred Forte TID, OS
4. H. Zoster of Eyelid
4. Cool compresses and
antibiotic ung on vesicles
129. Follow Up: 2 days later
• Patient now complains
of eye pain in the
morning
• Thinks it is getting
worse
• Currently taking pred
forte tid OS and will
finish Valtrex the
following week
130. Examination: 2 days
•
VA sc 20/25 OD; 20/40 OS PHNI
•
OD unremarkable
•
OS Lid: Vesicles along upper
forehead & nose with lid
erythema, hordeolum on superior
lid
•
Cornea
• Prominent pseudodendrites
•
Anterior Chamber
• 2+ WBC
•
IOP 16, 27
•
Fundus: Unremarkable OU
131. Assessment: 2 days
1. Zoster, Eyelid OS
1. Continue ointment
2. Zoster Iridocyclitis, OS
2. Continue pred forte tid,
atropine instilled in office
Due to increased IOP:
Combigan OS bid
RTO 1 week
132. Follow up: 1 week later
• Currently on pred forte TID, Combigan BID, OS
only
• Finished Valtrex
• Feels improvement
133. Examination: 1 week
• VA sc 20/25 OD, 20/40-2
PH 20/25-, OS
• OD unremarkable
• OS
• Lids: healed vesicles, mild
ptosis
• Conjunctiva: Trace injection
• Cornea: Pseudodendrites
with endothelialitis inferiorly
• Anterior Chamber: 2+ WBC
• IOP 17, 20
134. Assessment: 1 week
1. Redness/discharge of
eye OS
1. Injection improved, less
tearing
2. H. Zoster of eyelid OS
2. Complete resolution
3. Zoster iridocyclitis
3. Durezol QID, atropine in
office (increased IOP);
continue combigan BID
OS
4. H Zoster
keratoconjunctivis
4. Pseudodendrites stable
135. Follow up 2 weeks later
• Patient reports improvement
• VA sc 20/30 PH 20/25 OD, OS
• OD unremarkable
• OS
•
•
•
•
Lid: no vesicles
Conjunctiva: trace injection
Cornea: punctate staining
Anterior chamber: KP‟s less
evident
• IOP 16, 18 mm Hg
136. Assessment: 2 weeks
1. H Zoster Iridocyclitis, OS
1. Improvement with quiet
A/C, IOP stable
--Continue Combigan BID OS
--Taper durezol over 2 weeks,
then D/C
--RTO 5 weeks
137. Follow up 5 weeks later
• Patient currently on
Combigan BID OS only
• VA sc 20/25 OD; 20/30
• OD unremarkable
• OS
• Conjunctiva: tr injection
• Cornea: punctate staining
• Anterior chamber: NO cells
• IOP 16, 18 mm Hg
• Assessment
• H. Zoster Iridicyclitis
• No signs of recurrent
inflammation; IOP well
• D/C combigan
• Follow up 1 month for IOP
check
138.
139. References
• Cunningham, Emmett. Practical approach to the use of corticosteroids
in patients with uveitis. Can J Opthalmol 2010; 45:352-8
• Moorthy, Ramana. Intraocular Inflammation and Uveitis.American
Academy of Opthalmology. Section 9. pgs 98-116.
• http://www.uveitis.org/uveitis-questionnaire
• http://emedicine.medscape.com/article/1209891-clinical
• “Care of the Patient with Anterior Uveitis,” Optometric Clinical Practice
Guideline. American Optometric Association.
Hinweis der Redaktion
To help manage and treat uveitis, especially bilateral, recurrent, or recalcitrant uveitis, it is imperative that the underlying cause is found. Here is a brief overview on different disease and conditions that have been associated with uveitis.
Most common form of uveitis
Negative RFClass 1 surface antigen that presents to T suppressor cellsDisease are sometimes clinically indistinguishable5% of population, about ½ of pts with acute iritis
--improves with exertion, bamboo spine is conplete fusion of the spineis a chronic inflammatory disease of the axial skeleton with variable involvement of peripheral joints and nonarticular structuresNot all HLA-B27 develop the disease, only 1 in 4 will develop spondyloarthritis or eye diseaseShould be referred to rheumotologist, NSAIDs are mainstay of tx of AS, anti-TNF are gaining popularity-physical therapy and smoking cessation can slow down disease progression
triggered by an infection in another part of your body — most often your intestines, genitals or urinary tract.--in addition to classic triad they can have scaly, erythematous disorder of the palms and soles of feetConjunctivitis most common, uveitis -10% can become bilateral and chronic b/c of permanent breakdown of blood-aqueous barrier
IBD: may also develop slerouveitis, these pts are usually HLAB27 –ve compared to those with acute iritisPA: dx based on typicl cutaneous changes -erythematous hyperkeratotic rash
Symptoms are vague: discomfort,blurred vision, halos--recurrences are very common over many years--rare, dx of exclusion, other syndromes must be r/o such as herpetic uveitis
can occur following disruption of the lens capsule (traumatic or surgical) or leakage of lens protein in hypermature cataracts--other names include phacoanaphylacticendopthalmitis, phacotoxic uveitis and phacolytic glaucoma--unsure of mechanism but thought due to immune rxn to lens protein--now with modern IOL’s less complications
relatively rare occurrence and is reported to represent less than 0.5 % of cases in a tertiary referral uveitis clinic (1). The time between medication use and occurrence of symptoms varies, ranging from a few days to months.. The cause for drug-induced inflammation is not well known. Postulates include direct and indirect mechanisms. Direct mechanisms are typically seen soon after medication use, typically occurring with topical or intracamerally instilled drugs. Indirect mechanisms include immune complex deposition in uveal tissues, immune reactions to antigens released from antibiotic-induced death of microorganisms, or an alteration of melanin’s ability to scavenge free radicals (2).
Inflammation of the anterior segment persistent and relapses less than 3 months after d/c of therapy
--pauciarticular onset 85=90% of JIA that have uveitis: 4 or fewer joints are involved in 1st 6 months or disease, may have no joint symptoms--because of freq. asymptomatic nature of uveitis in these pts profound silent ocular damage can occur, long term prognosis often depends on extent of damage at time of dx--pts should be evaluated by rheumatologist and undergo ANA testing--joint pain can be minimal or absent at time of uveitis diagnosesDdx: fuchs, sarcoid, behcet, seronegativespondy., herpetic and lyme disease
Usually overlooked, 3% of cases referred to uveitis clinics are dx w fuchs--usually vague symptomsdx: made due to distribution of KP’s, lack of synechiae, lack of symptoms, and heterochromiafew require therapy, topical steroids can lessen inflammation but do not resolve itLighter colored eye indicated involved, although in blue eyed the darker b/c stromal atrophty and darker iris pig epith shows
15% of all cases of uveitis’--inflammation in ant vitreous and the vitreous base overlying ciliary body and peripheral retina-pars plana complex--may aggregate in the vitreous “snow balls”, accumulate on inf pars plana –”snowbanking”
In older main complaint is floatersComplications: cataract (60%), glauc, CME(5)%), retinal neovas. (15%), VH, tractional or rhegmatogenous RD-- CME develops and becomes chronic and refractory in 10% of pts--ischemia from phlebitis with angiogenic stimuli from intraocular inflammation can lead to neovascularization 10% of casesthought to be autoimmune reaction against vitreous, peripheral retinal and CB
Can preceed dx of MS in 25% of pts and by 5-10yrs15% of pts with pars planitis may eventually develop MSME less common then pars planitis, also less mild interm. uveitis
SUN: Inflammation involving the retina and or choroid. Inflammatory cells may be observed diffusely throughout the vitreous cavity overlying foci of active inflammation
B lymphocyte hyperactivity, polyconal B-lymphocyte activation, hypergammaglobulinemia, autoantibody formation, and T-lymphocyte autoreactivity with immune complex deposition
KCS most common symptomLupus retinopathy is most well recognized post. Segment manifestation and is considered and important marker of systemic disease -3% to 29% in severe –w or w/o hemesVascular occlusiveLupus choroidopathy- choroidal infarction, CNV, serous elevations of RPE and retina
Consequence of Underlying vascular disease: Post pole: may manifest as HTN retinopathy, retinal arteriolar occlusive disease, choroidal infarcts, choroidaliscehmia, neuro-ophthmanifestions, scleritis, optic atrophy, peripheral ulcerative keratitis
15% ocularinvolv. At presentation, 50% during course of disease
Level of retinal, RPE , choriocapillaris and choriodDdx: syphilis, DUSN (diffuse unilateral subacuteneuroretinitis, OHS, as well as non infectios: sarcoidosis, sympathetic ophthalmia, VKH, intraocular lymphoma
Many of these have viral or autoimmune component--Serpiginouschoroiditis is associated with HLA B-27
Involvement of all anatomical compartments of the eye –AC, vitreous, retina and choroidUsually bilateral
abnormal collections of chronic inflammatory cellsgranulomas) that can form as nodules in multiple organs.[1] The granulomas that appear are usually not of the caseating variety and are most often located in the lungs or the lymph nodes, but virtually any organ can be affected. uveitis being most frequent manifestation
Cutaneous invovment –orbital and eyelid granuloma’s, conj. Nodules, lacrimal gland infiltration -KCS2/3 pts with ocular sarcoidosis have ant. Uveitis-
Usually occurs 3 months after injury (80%) to 1 year (90%)--characteristic white, midequatorialchoridal lesions (Dalen nodules) that may become confluent, peripapillarychoridal lesionslymphocytic infiltration and the formation of granulomas. Deposition of these granulomas between Bruch's membrane and the RPE is termed a Dalen-Fuchs' nodule--injured eye “exciting eye” and noninjured is “sympathizing” eye--dx: clinical, ddx VKH
The prodromal stage is marked by flu-like symptoms. Patients present with headache, nauseadysacusia and tinnitus.
Sunset glow –resolution of exudative detachments,depigmentation of the choroid
Oral ulcers are the most frequent finding BD –recurrent mucosal ulcers the produce sign discomfort and pain (round white ulcerations with red rims, occur every 5-10 days or every month)
AO and VO’s, combination, vascular sheathing with variable amounts of vitirtis –becomes very ischemic--can look like ARN due to ischemic nature of vasculitis and accompanying retinitis.--can have papillitis, ischemic optic neuropathiesHLA associations: HLAB12, HLA B27, HLA B51IMT is essential due to chronic inflamm.
Based on maryland 2011 data from the CDC:Maryland ranked 3rd in the US in reports of primary and secondary syphilisMD reported 452 cases of primary and seconday syphilis in 201124 cases of congenital syphilis in 2011.
Short acting agents like tropicamide are useful for acute non-granulomatous anterior uveitis. Chronic uveitis and moderate flare anterior chamber reactions for disease like juvenile idiopathic arthritis (JIA) require chronic use of short acting agents to prevent further complications like synechiae. If there is a significant uveitic reaction like granulomatous inflammation, the use of long acting agents like atropine are useful to prevent the accumulation of inflammatory cells by stabilizing the ciliary body vascular system.Long acting agents like atropine are useful for
Corticosteroids have both direct and indirect inhibitory effects on the potent pro-inflammatory transcription factor NF-kB.
Periocular injections (either transseptal or sub-tenon approach) of triamcinolone acetonide or methylprednisolone should not be used in infectious uveitis cases such as toxoplasmosis. Also these injections can cause high IOP spikes with increased duration.
Suspension needs to be shaken, emulsion does not.
Higher concentration does not mean higher potency, only high corneal permeability or penetration into the anterior chamber,can yield higher potencies
COX1 and 2 inhibitors-commonly used in ocular inflammationCOX 2 only inhibitors (celecoxib,rofecoxib,valdecoxib)-increased risk of adverse cardiovascular events, therefore these are not used for ocular inflammation or are limited in scope-Systemic NSAIDS: useful for chronic iridocyclitis (ie. JIA-associated iridocyclitis) and potentially for CME to allow maintenance on a lower dose of topical NSAIDS.Topical NSAIDS: limited role in ocular inflammation, not used in the treatment of anterior uveitis, but only implicated in postoperative pseudophakic CME and episcleritis.
These medications take 2-4months for successful control of ocular inflammation. Therefore, it is necessary to start these medications while the corticosteroids are being tapered to not further delay of successful treatment.
Corticosteroid-induced side effects:pars planitis (int. uveitis), retinal vasculitis, panuveitis, and chronic iridocyclitis.
Low/no TPMT activitiy: do not use aziothioprineInt.:reduced dosage <50mg/dayNormal/High: higher doses