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HOW TO DIAGNOSE
UVEITIS
ANDI PUTRA JAYANEGARA
INTRODUCTION
• Uveitis : inflammation of the uvea that may involve surrounding structure
• Associated with systemic disease or infection  careful history and review of systems is
essential first step
• Lab examination help determine etiology but never a substitute for a thorough history
and physical exam
• Most common : anterior uveitis (70 – 80%) > panuveitis > posterior uveitis >
intermediate uveitis
CLASSIFICATION OF UVEITIS
MEDICAL HISTORY
• Key to diagnosis in majority cases of uveitis
• Therapy should be targeted to not only address inflammation, but also to treat
symptoms
• Important for evaluation of therapy
DEVELOPMENT OF DIFFERENTIAL DIAGNOSIS
1.ACUTE OR CHRONIC
2. GRANULOMATOUS OR NON GRANULOMATOUS
• Non granulomatous KPs : fine white (lymphocytes, plasma cells, pigment)  marks
anterior inflammation has occurred
• Granulomatous KPs / ‘mutton-fat’ : large, greasy-appearing (lymphocyte, plasma cells,
giant cels)  useful diagnostic clue (history of chronic disease with insidious onset, and
frequently have posterior segment disease)
• Granulomatous: iris nodules, choroidal granulomas
3. LATERALITY
• Most cases  bilateral but asymetrical
• Unilateral and chronic may help diagnosing condition
4. LOCATION OF INFLAMMATION
Anterior
• Limited predominantly in anterior segment
• Other terms : iritis, iridocyclitis, anterior cyclitis,keratouveitis, sclerouveitis
• Marker: presence of cells and protein (flare) in the COA
• Conjunctival hyperemia, cell and flare in COA, hypopion,KPs, iris abnormalities (change
in pattern & color, posterior synechiae and PAS), mild cellular inflammatory in anterior
vitreus
4. LOCATION OF INFLAMMATION
Intermediate
• Vitreous and peripheral retina
• inflammatory cells in inferior (snowballs)
• inflamatory cells and debris along pars plana and ora serrata (snowbanks)
• vitreous haze, mild anterior uveitis, peripheral retina vasculitis
4. LOCATION OF INFLAMMATION
Intermediate
4. LOCATION OF INFLAMMATION
Posterior
• retina and/or choroid  can affect vitreous, optic nerve head, retinal blood vessels
• Diffuse inflammatory cells throughout vitreous cavity, overlying foci of inflammation, or
on posterior vitreous face
• Focal, multifocal, or diffuse areas of retinitis and/or choroiditis, or retinal vasculitis
4. LOCATION OF INFLAMMATION
Panuveitis
• Involve all segments of the eye, with severe sight-reducing inflammatory response
• No predominantly affected site
5. DEMOGRAPHIC
6. SYMPTOMS
7. SIGNS
• Systemic evaluation
• Epidermal or skin changes : sarcoid granulomas, rashes consistent with lyme disease,
syphilis, kaposi’s sarcoma,VKH, SLE
• Muosal surface ulceration: Bechet (oral genital), SLE (oral), syphilis (genital)
• Joint : signs of inflammation
• Screening neurologic examination :intaocular lymphoma, sarcoidosis, behcet’s disease
8.TIME COURSE OFTHE DISEASE AND RESPONSE
TO PREVIOUSTHERAPY
• Infectious disease: initially improve with anti-inflammatory therapy  later worsen
• Postoperative endophthalmitis caused by P. acnes improves temporarily with topical or
systemic corticosteroid but then recurs
• Temporary and partial response to therapy also suggest that ocular inflammation may be
associated with chronic systemic disease (sarcoidosis, malignancy-like lymphoma)
• Long history of intermittent response to therapy suggest chronic non infectious and
nonmalignant disease
LABORATORY EVALUATION
• only to discern among likely diagnoses
• all patient with uveitis should be tested for syphilis
• Intraocular specimen (aqueous humor, vitreous) and extraophthalmologic examinations
• Routine blood investigation
- May not yield specific diagnosis but should be done in al patients
- Eosinophilia : sarcoidosis, parasitic infections
- Raised WBC : bacterial infections
- Lymphocytosis : viral infections, TB
- Liver & renal function test
- Also important when planning immunosuppressive treatment
CONCLUSION
• Diagnostic approach to uveitis should be adapted to demographic epidemiology data
• Ophthalmologic and systemic signs and symptom are very crucial in diagnosing uveitis
• Diagnostic strategy based on clinical examination, further investigations referred to
anatomic location type of uveitis
TERIMA KASIH

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IIM- How to diagnose Uveitis.pptx

  • 1. HOW TO DIAGNOSE UVEITIS ANDI PUTRA JAYANEGARA
  • 2. INTRODUCTION • Uveitis : inflammation of the uvea that may involve surrounding structure • Associated with systemic disease or infection  careful history and review of systems is essential first step • Lab examination help determine etiology but never a substitute for a thorough history and physical exam • Most common : anterior uveitis (70 – 80%) > panuveitis > posterior uveitis > intermediate uveitis
  • 4.
  • 5. MEDICAL HISTORY • Key to diagnosis in majority cases of uveitis • Therapy should be targeted to not only address inflammation, but also to treat symptoms • Important for evaluation of therapy
  • 6.
  • 7.
  • 10. 2. GRANULOMATOUS OR NON GRANULOMATOUS • Non granulomatous KPs : fine white (lymphocytes, plasma cells, pigment)  marks anterior inflammation has occurred • Granulomatous KPs / ‘mutton-fat’ : large, greasy-appearing (lymphocyte, plasma cells, giant cels)  useful diagnostic clue (history of chronic disease with insidious onset, and frequently have posterior segment disease) • Granulomatous: iris nodules, choroidal granulomas
  • 11.
  • 12. 3. LATERALITY • Most cases  bilateral but asymetrical • Unilateral and chronic may help diagnosing condition
  • 13. 4. LOCATION OF INFLAMMATION Anterior • Limited predominantly in anterior segment • Other terms : iritis, iridocyclitis, anterior cyclitis,keratouveitis, sclerouveitis • Marker: presence of cells and protein (flare) in the COA • Conjunctival hyperemia, cell and flare in COA, hypopion,KPs, iris abnormalities (change in pattern & color, posterior synechiae and PAS), mild cellular inflammatory in anterior vitreus
  • 14.
  • 15.
  • 16.
  • 17.
  • 18. 4. LOCATION OF INFLAMMATION Intermediate • Vitreous and peripheral retina • inflammatory cells in inferior (snowballs) • inflamatory cells and debris along pars plana and ora serrata (snowbanks) • vitreous haze, mild anterior uveitis, peripheral retina vasculitis
  • 19. 4. LOCATION OF INFLAMMATION Intermediate
  • 20.
  • 21. 4. LOCATION OF INFLAMMATION Posterior • retina and/or choroid  can affect vitreous, optic nerve head, retinal blood vessels • Diffuse inflammatory cells throughout vitreous cavity, overlying foci of inflammation, or on posterior vitreous face • Focal, multifocal, or diffuse areas of retinitis and/or choroiditis, or retinal vasculitis
  • 22.
  • 23. 4. LOCATION OF INFLAMMATION Panuveitis • Involve all segments of the eye, with severe sight-reducing inflammatory response • No predominantly affected site
  • 24.
  • 27. 7. SIGNS • Systemic evaluation • Epidermal or skin changes : sarcoid granulomas, rashes consistent with lyme disease, syphilis, kaposi’s sarcoma,VKH, SLE • Muosal surface ulceration: Bechet (oral genital), SLE (oral), syphilis (genital) • Joint : signs of inflammation • Screening neurologic examination :intaocular lymphoma, sarcoidosis, behcet’s disease
  • 28. 8.TIME COURSE OFTHE DISEASE AND RESPONSE TO PREVIOUSTHERAPY • Infectious disease: initially improve with anti-inflammatory therapy  later worsen • Postoperative endophthalmitis caused by P. acnes improves temporarily with topical or systemic corticosteroid but then recurs • Temporary and partial response to therapy also suggest that ocular inflammation may be associated with chronic systemic disease (sarcoidosis, malignancy-like lymphoma) • Long history of intermittent response to therapy suggest chronic non infectious and nonmalignant disease
  • 29. LABORATORY EVALUATION • only to discern among likely diagnoses • all patient with uveitis should be tested for syphilis • Intraocular specimen (aqueous humor, vitreous) and extraophthalmologic examinations • Routine blood investigation - May not yield specific diagnosis but should be done in al patients - Eosinophilia : sarcoidosis, parasitic infections - Raised WBC : bacterial infections - Lymphocytosis : viral infections, TB - Liver & renal function test - Also important when planning immunosuppressive treatment
  • 30.
  • 31.
  • 32. CONCLUSION • Diagnostic approach to uveitis should be adapted to demographic epidemiology data • Ophthalmologic and systemic signs and symptom are very crucial in diagnosing uveitis • Diagnostic strategy based on clinical examination, further investigations referred to anatomic location type of uveitis

Editor's Notes

  1. Uvea (vascular coat of the eye composed of iris, ciliary body, choroid other structure (retina, sclera, cornea, vitreous, optic nerve)
  2. SUN system  anatomic location and specific duration of onset, duration, and course
  3. Detailed medical history is the key to diagnosis in majority cases of uveitis Therapy should be targeted to not only address inflammation, but also to treat sympotms that affect patient function or quality of life Important in assessing response to therapy and side effects of medication
  4. Nussenbalt
  5. KPs : helps classify inflammatory process as granulomatous and non granulomatous Non granulomatous  does not help tremendously in the formulation of differential diagnosis clinical appearance of uveitis as granulomatous or nongranulomatous may not necessarily correlate with the histologic description and can instead be related to the disease stage, the amount of antigen at presentation, or the patient’s state of immunocompromise (eg, a patient being treated with corticosteroids).
  6. Non granulomatous KPs : fine white (lymphocytes, plasma cells, pigment)  marks anterior inflammation has occurred Granulomatous KPs / ‘mutton-fat’ : large, greasy-appearing (lymphocyte, plasma cells, giant cels)  useful diagnostic clue (history of chronic disease with insidious onset, and frequently have posterior segment disease) Granulomatous: iris nodules, choroidal granulomas KPs : helps classify inflammatory process as granulomatous and non granulomatous Non granulomatous  does not help tremendously in the formulation of differential diagnosis clinical appearance of uveitis as granulomatous or nongranulomatous may not necessarily correlate with the histologic description and can instead be related to the disease stage, the amount of antigen at presentation, or the patient’s state of immunocompromise (eg, a patient being treated with corticosteroids).
  7. Although one eye may be affected first, uvetis resulting from most causes involves both eyes within the first several months. Therefore, the history that the disease is both chronical and unilateral can help diagnosing the condition Box 4-4 listed diseases that frequently involve a single eye, even after months or years Parasitic typically involve one eye, although may occur bilaterally Behcet  single eye esp in asian decent
  8. Severe / chronic  uveitic macular edema, optic disc sweling, cataract, corneal edema, band keratopathy Newly formed KPs tend to be white and smoothly rounded, later transitioning to crenated (shrunken), pigmented, or glassy in nature Type of KP’s Mutton fat KP’s Granulomatous iridocyclitis Large, thick, fuffy, greasy or waxy appearance Usually few (10 – 15) in number 2. Small and medium KP’s (granular KPs) Pthognomic of non-granulomatous uveitis Small, discrete dirty white KPs, arranged irregularly at back of cornea Numerous in number 3. Fine (Stellate) KPs Cover entire corneal endothelium and form endothelial dusting Seen in fuchs heterochromic iridocyclitis, herpetic irits, and CMV retinitis 4. Old KP’s All KPs, with healing process, shrink, fade become pigmented and irregular in shape Have ground glass appearance due to hyalinization Hypoipion Dense mobile hypopyion : slow to absorb due to high fibri content, seen in HLA-B27 Hypopyin in Behcet syndrome has minimal fibrin and hence shifts with head position and is quick to absorb Hemorrhagic hypopion associated with herpetic infection, trauma, and rubeosis iridis Rubeosis iridis  in chronic iridocyclitis and Fuch’s heterochromic iridocyclitis
  9. Complication : macular edema, peripheral exudative/tractional detachments, retinal neovascularization, cataract, retrolental membrane formation Pars planitis  subset of intermediate uveitis in which there are peripheral preretinal collections of exudative and inflammatory debris in the absence of an associated infection or systemic disease Intermediate uveitis is a T-cell-mediated disase Lymphocytic infiltration of the retinal venules leads to clinical picture of vasculitis Histological studies : condenses vitreous, fibroblast, spindle cells, lymphocytes, and blood vessels and prominent lymphocyte cuffing of retinal veins Pars plana exudates appear to consist of loose fibrovascular layer containing scattered mononuclear inflamatory cels and a few fibrocyte-like cells adjacent to hyperplastic nonpigmented epithelium of pars plana
  10. Complication : macular edema, peripheral exudative/tractional detachments, retinal neovascularization, cataract, retrolental membrane formation Pars planitis  subset of intermediate uveitis in which there are peripheral preretinal collections of exudative and inflammatory debris in the absence of an associated infection or systemic disease Intermediate uveitis is a T-cell-mediated disase Lymphocytic infiltration of the retinal venules leads to clinical picture of vasculitis Histological studies : condenses vitreous, fibroblast, spindle cells, lymphocytes, and blood vessels and prominent lymphocyte cuffing of retinal veins Pars plana exudates appear to consist of loose fibrovascular layer containing scattered mononuclear inflamatory cels and a few fibrocyte-like cells adjacent to hyperplastic nonpigmented epithelium of pars plana
  11. Characteristic mobile, globular, yellow-white “snowballs”seein in the inferior peripheral vitreous Inflammatory exudates accumulate over pars plana form snowbank Later vitreous shows degenerative changes with fibre-like cylindrical condensations of coarse vitrous strands PVD is common Retinal changes in IU include tortousity in arteriorels and venules, sheating of peripheral veins, neovascularizations, and retinal detachments Cystoid macular edema
  12. Panuveitis Esssential to rule out infectious etiology, especialy in acute, unilateral PU Do not hesitate to repeat work up (even if negative before) in cases of strictly, unilteral disease; in case of chronic, long standi ng, nd recalcitrant uveitis; and in case of resistance to therapy
  13. VKH: whitening of hair eyebrow lashes it is almost unheard of for a detailed physical examination to be performed in the office. Unless you are prepared to do a thorough physical examination, it is probably more practical to refer patients to their primary care physician for this part of the evaluation. Nevertheless, it is fruitful for the ophthalmologist to examine a few things before making the referral.
  14. Is the disease responsive to antiinflammatory therapy? Does it require continued corticosteroid therapy? If so, how much corticosteroid is needed? Is the disease resistant to corticosteroid therapy? These questions can help the clinician determine the correct diagnosis.
  15. Syphilis remain a common cause of uveitis and is easily treatable Patients with untreated ocular syphilis often have devastating visual outcomes Importantly, the fluorescent treponemal antibody absorption (FTA-ABS) test for syphilis is both extremely sensitive and specific. For patient with late syphilis, the sensitivity and specificity of thr FTA-ABS are both 99% With this combination of a treatable and common disease; poor outcome in untreated patients; and a highly sensitive and specific diagnostic test with little risk and moderate cost, screening become useful. But not all as good for screening for late syphilis. VDRL test has sensitivity oly 70% for late syphilis. Therefore clinician should insist on FTA-ABS test in uveitis patient Also, the incidence of syphilis in patients with AIDS is increasing. As a result, all patients with syhilis who have uveitis should also be testes for HIV infection, and vice versa consequences of treating with steroid in the presence of untreated occult syphilis infection can be disastrous for patient outcomes. A number of test are used for research purposes but are commercially available. Many practitioners order these test but do not know wha to do with the resuls when they come back.