sign in sign up
<<
Home , Ocular ischemic syndrome, Photopsia

Anterior Segment Grand Rounds

Blair B Lonsberry, MS, OD, MEd., FAAO Diplomate, American Board of Optometry Professor of Optometry Pacific University College of Optometry Portland, OR [email protected] Disclosures and Special Request Paid consultant for: • Alcon Pharmaceuticals, Bausch and Lomb, Carl Zeiss Meditec, NiCox, Special Request: Interactive remotes don’t work on your TV, so please don’t take them home!  Commitment to change: - write down three things that you “learned” from this presentation that you can incorporate into your practice to improve patient care

Case

• 55 yr white female complains of fluctuating vision – Worse at near – Spends 8-10 hours/day on the computer • Medical Hx: – for 10 years – Joint • Medications: – HCTZ for HTN – Celebrex for her joint pain Exam Data

• VA (corrected): OD: 20/25, OS: 20/25 • PERRL • EOM’s: FROM • CVF: FTFC • SLE: – TBUT 5 sec OD, OS – Positive NaFl staining and Lissamine green staining of conj and – Decreased tear prism Additional Testing/Questions

• Schirmer: < 5 mm of wetting in 5 minutes OD, OS • RF and ANA: normal for patients age • SS-A: 2.0 (normal < 1.0), SS-B: 1.9 (normal <1.0) • Additional symptoms reported: – Patient experiences dry mouth and taking Salagen

• Diagnosis: Sjogren’s Syndrome

Differential Diagnosis of Dry of Dry Eye

Signs: Symptoms: – Ocular Surface Damage – Grittiness • Corneal Staining (Fluorescein and/or Rose Bengal) – Burning • Conjunctival Staining (Lissamine Green ) – Irritation – Decreased Tear Quantity – Stringy discharge • Schirmer Score – Blurring of vision • Phenol Red Thread Test – Ocular Surface Disease Index (OSDI) • Tear Meniscus Height – Decreased Tear Quality • Tear Break Up Time (TBUT) • Tear Osmolarity Treatment

• We initiated: – Omega-3 supplements (3-4 grams per day) – Recommended warm compresses and lid washes qhs – Testosterone cream 3% applied to upper lid bid

• Patient had significant improvement in symptoms with the use of the topical testosterone cream. – However, she was still symptomatic at the end of the day and she still had significant staining on her cornea and – Initiated FML tid for 1 month, restasis bid after 2 weeks • 2 months later patient reported further improvement in her symptoms • No conjunctival staining was noted and only slight SPK • Schirmer values improved to OD: 9 mm, OS: 10 mm

Role of Androgens?

• Recent studies have suggested that androgen deficiency may be the main cause of the meibomian gland dysfunction, tear-film instability and evaporative dry eye seen in Sjogren patients • Transdermal testosterone 3% promotes increased tear production and meibomian gland secretion, thereby reducing dry eye symptoms (Dr. Charles Connor). • Progesterone 0.05%/Testosterone 0.05% Ophthalmic Solution BID (available from Leiter’s Pharmacy) SJOGREN’S SYNDROME: OLD/NEW CLASSIFICATION • Old: – 1o Sjogrens: occurs when sicca complex manifests by itself • no systemic disease present – 2o Sjogrens: occurs in association with collagen vascular disease such as • RA and SLE • significant ocular/systemic manifestations • New: – The diagnosis of SS should be given to all who fulfill the new criteria while also diagnosing any concurrent organ-specific or multiorgan autoimmune diseases, without distinguishing as primary or secondary. Diagnosis: New Criteria

• Sjogren’s International Collaborative Clinical Alliance (SICCA) was funded by the National Institutes of Health to develop new classification criteria for SS • New diagnostic criteria requires at least 2 of the following 3: – 1) positive serum anti-SSA and/or anti-SSB or (positive rheumatoid factor and antinuclear antibody titer >1:320), – 2) ocular staining score >3, or – 3) presence of focal lymphocytic sialadenitis with a focus score >1 focus/4 mm2 in labial salivary gland biopsy samples Ocular Surface Score (OSS)

• The ocular surface score (OSS) is the sum of: – 0-6 score for fluorescein staining of the cornea and – 0-3 score for lissamine green staining of both the nasal and temporal bulbar conjunctiva, – yielding a total score ranging from 0-12. Antibodies to SS-A and SS-B

• Sjogren’s syndrome A and B • Typically tested by ELISA and immunoblot • Associated Conditions: – Uncommon in the normal population and in patients with rheumatic diseases other than Sjogren’s syndrome and SLE – Present in 75% of patients with “primart” Sjogren’s but only 10-15% of patients with RA and secondary Sjogren’s syndrome Antibodies to SS-A and SS-B

• Indications: – Should be measured in patients with a clinical suspicion of Sjogren’s or SLE • Interpretation: – Presence of AB’s is a strong argument for the diagnosis of Sjogren’s Syndrome in a patient with sicca syndrome Sjö Diagnostic Test

Sjö Diagnostic Test

Sjo: new diagnostic test for Sjogrens

• SP-1 (salivary gland protein-1), CA-6 (carbonic anhydrase-6) and PSP (parotid secretory protein). • Traditional tests use ANA, SS-A and SS-B and RF antibodies which have significant limitations of sensitivity and/or specificity and are associated with later-stage disease. • During studies, these novel antibodies were found in 45% of patients meeting the criteria for Sjögren’s Syndrome who lacked the traditional antibodies for SS-A and SS-B. Dry Eye and Lid Disease?

• It is estimated that 67-75% of patients who have dry eye have some form of lid disease – it is often the most overlooked cause for dry eye symptoms

• Important to address the lids in any treatment plans for patients with dry eye Which of the following lid nevi have the greatest chance to convert to a malignant melanoma?

1 2

3 4 Lid Nevi • Lid nevi: – congenital or acquired – occur in the anterior lamella of the and can be visualized at the eyelid margin. • The congenital eyelid nevus is a special category with implications for malignant transformation. • With time, slow increased pigmentation and slight enlargement can occur. • An acquired nevus generally becomes apparent between the ages of 5 and 10 years as a small, flat, lightly pigmented lesion

Congenital Nevus • The nevus is generally well circumscribed and not associated with ulceration. • The congenital nevus of the may present as a "kissing nevus" in which the melanocytes are present symmetrically on the upper and lower eyelids. – Presumably this nevus was present prior to eyelid separation Congenital Nevus • Most nevi of the skin are not considered to be at increased risk of malignancy. – However, the large congenital melanocytic nevus appears to have an increased risk of malignant transformation of 4.6% during a 30 year period

Acquired Lid Nevi • Acquired nevi are classified as: – junctional (involving the basal epidermis/dermis junction), typically flat in appearance – intradermal (involving only the dermis), tend to be dome shaped or pedunculated – compound (involving both dermis and epidermis) tend to be dome shaped CHRPE vs Nevus

24 Nevi Trivia

• 31% of choroidal nevi show slight enlargement over time without the transformation to a melanoma ( 2011) • The prevalence of choroidal nevi in the white U.S. population ranges from 4.6% to 7.9% – If it is assumed that all choroidal melanomas arise from preexisting nevi, then the published data suggest a low rate (1/8845) of malignant transformation of a choroidal nevus in the U.S. white population. (Ophthalmology 2005) • Choroidal melanoma risk for metastasis, ranging from 16% to 53% (at 5 years of follow-up) depending on the size of the tumor at the time of diagnosis. (Arch Ophthalmol 1992) TFSOM—“To Find Small Ocular Melanoma” Thickness: lesions >2mm Fluid: any subretinal fluid (suggestive of serous ) Symptoms: photopsia, vision loss Orange pigment overlying the lesion Margin touching head

• None of these factors = 3% risk of a nevus converting to melanoma in five years. One of these factors = 8% risk of conversion in five years. Two or more factors = 50% risk of conversion in five years. For any changes noted during the course of follow-up, refer the patient to a retinal practice or an ocular oncology service.

Melanoma Size and Mortality

• 5-year mortality after enucleation: – 16% for small melanoma, – 32% for medium melanoma, and – 53% for large melanoma. • the prognostic importance of tumor size: – each 1-mm increase in melanoma thickness adds approximately 5% increased risk for metastatic disease at 10 years. From: Enhanced Depth Imaging Optical Coherence Tomography of Small Choroidal Melanoma: Comparison With Choroidal Nevus

Arch Ophthalmol. 2012;130(7):850-856. doi:10.1001/archophthalmol.2012.1135

Figure Legend:

Copyright © 2014 American Medical Date of download: 10/9/2014 Association. All rights reserved. From: Enhanced Depth Imaging Optical Coherence Tomography of Small Choroidal Melanoma: Comparison With Choroidal Nevus

Arch Ophthalmol. 2012;130(7):850-856. doi:10.1001/archophthalmol.2012.1135

Figure Legend:

Copyright © 2014 American Medical Date of download: 10/9/2014 Association. All rights reserved. Case

• 65 yr old white male – Notices spot in vision in his left eye – for 15 years • Vision:20/20 (6/6) and 20/40 (6/12 ) • Dilated exam: – Large lesion noted in left eye (not noted in exam 6 months previously – See photo and B-scan Ocular Tumors Astrocytic Hamartoma Amelanotic Melanoma

Retinoblastoma Metastatic Choroidal Tumor Choroidal Melanoma Metastases

• 80 to 90% of metastases from uveal melanoma occurred in the liver, less common sites being the skin and lung. – Gragoudas ES, Seddon JM, Egan KM, et al. Long- term results of proton beam irradiated uveal melanomas. Ophthalmology. 1987;94:349–53. Latest Development

• September 4, 2014, the US FDA approved a new therapy for patients with advanced melanoma. • The treatment, Keytruda (pembrolizumab), proved so successful in a large Phase 1 clinical trial that the drug was granted breakthrough therapy designation by the FDA, meaning that it was fast tracked for approval. Preseptal Cellulitis

 Infection and located anterior to the orbital septum and limited to the superficial periorbital tissues and eyelids.  Usually follows sinus infection or internal hordeolum (possibly trauma)  Eyelid swelling, redness, , pain and low grade fever. Preseptal Cellulitis

 Tx:  Augmentin 500 mg TID or 875 mg BID for 5-7 days  Keflex 500 mg QID 5-7 days  or if moderate to severe IV Fortaz (ceftazidime) 1-2 g q8h.  If MRSA possible, consider Bactrim/Septra Differentiating Orbital vs. Preseptal

FINDING ORBITAL PRESEPTAL Visual Acuity Decreased Normal Proptosis Marked Absent Chemosis and Marked Rare/Mild Hyperemia RAPD Normal Pain and Motility Restricted and Painful Normal IOP Normal Temperature 102 - 104 Normal/mild elevation HA and Assoc. Common Absent Symptoms

Treatment: Orals for Preseptal, Often IV for Orbital Case: Gonzalez

• 33 HF presents with a painful, red right eye – Started a couple of days ago, deep boring pain – Has tried Visine but hasn’t helped the redness • PMHx: patient reports she has been diagnosed with rheumatoid arthritis 3 years ago – Takes Celebrex for the joint pain – Patient reports she occasionally gets a skin rash when she is outdoors in the sun • POHx: unremarkable • PMHx: mother has rheumatoid arthritis Case: Gonzalez

• VA: 20/30 OD, 20/20 OS • Pupils: PERRL –APD • VF: FTFC OH • EOM’s: FROM OU • BP: 130/85 mm Hg RAS • SLE: see picture – 2+ cells, mild flare • IOP’s: 16, 16 mm HG • DFE: see fundus photo Etiologies of Cotton Wool Spots

Vascular Occlusive Disease Hypertension Ocular Ischemic Syndrome

Autoimmune Disease e.g. Hyperviscosity syndromes Trauma SLE

Pre-eclampsia Radiation Toxic e.g. interferon

Neoplastic e.g. leukemia Anterior Ischemic Infectious e.g. HIV Syndrome Patient Update

• Patient was worked up for lupus and diagnosed with lupus. • Patient was already taking Celebrex which was not effective in treating the she presented with – upon referral to rheumatology it was discovered that she had several organs already being affected by the lupus – she was put on immunosuppressive agents to treat the systemic and ocular manifestations • Patient was taken off of Celebrex and put on plaquenil (hydroxychloroquine) 400 mg po qd Treatment and Management: Antimalarials • hydroxychloroquine more common and less toxic than more effective chorloquine • usual dose is 200-400 mg/d @night with onset of action after a period of 2-4 months • has mild DMARD effect, does not slow radiographic progression and has relatively slow

onset of action, useful with other DMARD28 ’s Treatment and Management: Antimalarial Ocular Complications • Have affinity for pigmented structures such as , and RPE • Toxic affect on the RPE and photoreceptors leading to rod and cone loss. • Have slow excretion rate out of body with toxicity and functional loss continuing to occur despite drug discontinuation. Question

Which of the following depicts a undergoing hydroxychloroquine toxicity?

1 2 3 4 Question

Which of the following depicts a retina undergoing hydroxychloroquine toxicity?

’ ARMD Macular OHS Bull s Eye Hole Question Which OCT goes with a patient undergoing hydroxychloroquine toxicity?

1 2

4 3 Treatment and Management: Antimalarial Ocular Complications • Toxicity can lead to whorl keratopathy, “bulls eye” maculopathy, retinal vessel attenuation, and pallor. • Early stages of maculopathy are seen as mild stippling or mottling and reversible loss of foveal light reflex • “Classic” maculopathy is in form of a “bulls eye” and is seen in later stages of toxicity – this is an irreversible damage to the retina despite discontinuation of medication Treatment and Management: Antimalarials

29

Bulls Eye Maculopathy Whorl Keratopathy Fabry Disease

• alpha-galactosidase-A deficiency. – insufficient breakdown of lipids, which build up to harmful levels in the , kidneys, autonomic nervous system, and cardiovascular system. • Fabry disease is one of several lipid storage disorders and the only X-linked lipid storage disease. • Lipid storage may lead to impaired arterial circulation and increased risk of heart attack or . – The heart may also become enlarged and the kidneys may become progressively involved. • Other signs include decreased sweating, fever, and gastrointestinal difficulties. Revised Recommendations on Screening for Retinopathy • 2002 recommendations for screening were published by Ophthalmology • Revised recommendations on screening published in Ophthalmology 2011;118:415-42 – Significant changes in light of new data on the prevalence of retinal toxicity and sensitivity of new diagnostic techniques – Risk of toxicity after years of use is higher than previously believed • Risk of toxicity approaches 1% for patients who exceed 5 years of exposure

Revised Recommendations on Screening for Chloroquine and Hydroxychloroquine Retinopathy • Screening Tests: Newer objective tests, such as multifocal electroretinogram (mfERG), spectral domain optical coherence tomography (SD-OCT), and fundus autofluorescence (FAF), can be more sensitive than visual fields. It is now recommended that along with 10-2 automated fields, at least one of these procedures be used for routine screening where available. When fields are performed independently, even the most subtle 10-2 field changes should be taken seriously and are an indication for evaluation by objective testing. Because mfERG testing is an objective test that evaluates function, it may be used in place of visual fields. Amsler grid testing isno longer recommended. Fundus examinations are advised for documentation, but visible bull’s-eye maculopathy is a late change, and the goal of screening is to recognize toxicity at an earlier stage. Revised Recommendations on Screening for Retinopathy • Amsler grid testing removed as an acceptable screening technique – NOT equivalent to threshold VF testing • Strongly advised that 10-2 VF screening be supplemented with sensitive objective tests such as: – Multifocal ERG – Spectral domain OCT – Fundus autofluorescence Revised Recommendations on Screening for Retinopathy • Parafoveal loss of visual sensitivity may appear before changes are seen on fundus evaluation • Many instances where retinopathy was unrecognized for years as field changes were dismissed as “non-specific” until the damage was severe • 10-2 VF should always be repeated promptly when central or parafoveal changes are observed to determine if they are repeatable • Advanced toxicity shows well-developed paracentral Paracentral Revised Recommendations on Screening for Retinopathy • SD-OCT can show localized thinning of the parafoveal retinal layers confirming toxicity – not appreciable with time-domain OCT – changes maybe visible prior to VF defects • Fundus autofluorescence may reveal subtle RPE defects with reduced autoFL or show areas of early photoreceptor damage • MF-ERG can objectively document localized paracentral ERG depression in early retinopathy Normal Retina: VF/OCT/ERG

TD-OCT

Outer Nuclear Layer

PIL

SD-OCT

Rodriguez-Padilla, J. A. et al. Arch Ophthalmol 2007;125:775-

Copyright restrictions may780. apply. PIL=PR Integrity Line Mild Maculopathy

Normal Paracentral Scotomas Foveal Peak

Thinned Outer Nuclear Layer PIL

Rodriguez-Padilla, J. A. et al. Arch Ophthalmol 2007;125:775-

Copyright restrictions may780. apply. Bull’s Eye Maculopathy Flattened Foveal Dense Para/Central Defects Peak

RPE Atrophy Remnant of PIL

Rodriguez-Padilla, J. A. et al. Arch Ophthalmol 2007;125:775- 780. Copyright restrictions may apply. Revised Recommendations on Screening for Retinopathy

Factors Increasing Risk of Retinopathy Duration of use > 5 years Cumulative Dose > 1000 g (total) Daily Dose > 400 mg/day Age Elderly Systemic Disease Kidney or liver dysfunction Ocular Disease Retinal disease or maculopathy Pre-Malignant Eyelid Lesions: Keratoacanthoma • Appears as a solitary, rapidly growing nodule on sun exposed areas of middle-aged and older individuals • Nodule is usually umbilicated with a distinctive crater filled with keratin • Lesion develops over weeks and undergoes spontaneous involution within 6 mo to leave an atrophic scar Pre-Malignant Eyelid Lesions: Keratoacanthoma • Lesion on the eyelids may produce mechanical problems such as or ptosis. • Differential SCC, BCC, verruca vulgaris and molluscum • Many pathologists consider it a type of low grade SCC • Complete excision is recommended as there are invasive variants Pre-Malignant Eyelid Lesions: Actinic Keratosis • Also known as solar or senile keratosis • Most common pre- malignant skin lesion • Develops on sun- exposed areas and commonly affect the face, hands and scalp (less commonly the eyelids) – Predominately white males Pre-Malignant Eyelid Lesions: Actinic Keratosis • Appear as multiple, flat- topped papules with an adherent white scale. • Development of SCC in untreated lesions as high as 20% • Management is surgical excision or cryotherapy (following biopsy) Malignant Eyelid Lesions: Basal Cell Carcinoma (BCC) • Most common malignant lesion of the lids (85-90% of all malignant epi eyelid tumors) • 50-60% of BCC affect the lower lid followed by medial canthus 25- 30% and upper lid 15% Malignant Eyelid Lesions: Basal Cell Carcinoma (BCC) • Etiology is linked to excessive UV exposure in fair-skinned, ionizing radiation, arsenic exposure and scars • Metastases is rare but local invasion is common and can be very destructive Malignant Eyelid Lesions: Squamous Cell Carcinoma (SCC) • Much less common than BCC on the eyelid but has much higher potential for metastatic spread • Typically affects elderly, fair-skinned and usually found on the lower lid Malignant Eyelid Lesions: Squamous Cell Carcinoma (SCC) • Presents as a erythematous, indurated, hyperkeratotic plaque or nodule with irregular margins • Lesions have a high tendency towards ulceration and tend to affect lid margin and medial canthus Case

• 27 year old pharmacy student presents to the clinic on emergent basis – complains about red/painful eyes for the past 2 days – started OD then transferred to OS – reports a watery discharge, no itching, and is not a contact wearer – reports that others in his class have had a similar – no seasonal, food or drug allergies – has taken Visine 4-5 times/day since eyes became red but hasn’t helped much

Question Which of the following best represents your patient?

1 2

3 4

Bacterial Conjunctivitis

Viral Conjunctivitis Blepharo-conjunctivitis Viral Conjunctivitis

• Most common infectious presenting on emergent basis • 62% caused by adenovirus • Two major types: – Pharyngoconjunctival fever (PCF) – Epidemic (EKC) Viral Conjunctivitis

• PCF: history of recent/current upper respiratory infection • EKC: highly contagious with a history of coming in contact with someone having a red eye. • Can stay viable on surfaces for up to 30 days – Adenovirus 8 common variant leading to “rule of 8’s” • First 8 days red eye with fine SPK • Next 8 days deeper focal epithelial lesions • Following 8 potential development of infiltrates • Resolution • AdenoPlus available to use for adenoviral confirmation – AdenoPlus is currently being marketed and distributed by RPS (as of August 2014) AdenoPlus

• Have you heard about this? Interpreting the results

NEGATIVE RESULT • Only a BLUE line appears in the control zone. – A negative result is indicative of an absence of Adenovirus Antigens.

POSITIVE RESULT • The presence of both a BLUE line in the control zone and a RED line in the result zone indicates a positive result. • Even if the RED line is faint in color, incomplete over the width of the test strip, or uneven in color, it must be interpreted as positive. • A positive result indicates the presence of Adenovirus antigens. Viral Conjunctivitis: Signs and Symptoms

• Gritty sensation • Watery discharge  Pseudomembranes in severe cases • Sticky in mornings  Subconjunctival hemes • Follicular response • Chemosis • Injection • SPK • Infiltrates possible • Positive lymph nodes Management

• Consider the use of anti-inflammatory treatment to relieve patient symptoms and improve comfort – Alrex QID OU – Lotemax QID OU • New: Lotemax gel (indicated for post-op but has longer contact time than standard lotemax) • EKC patients are typically very uncomfortable and would benefit from anti-inflammatory treatment – especially if infiltrates or pseudomembrane present Management • Betadine (Melton-Thomas Protocol): – Proparacaine – 4-5 drops of Betadine 5% • Get patient to close eye and gently roll them around – After one minute, lavage the eye – Lotemax 4 times a day for 4 days • Alternative: Betadine swabsticks. – 5% Betadine solution only comes in 30 ml bottles cost $14.00. – Case of 200 Betadine swabsticks apprx. 45 dollars. Management

• Antivirals used in HSV keratitis are ineffective in treatment of viral conjunctivitis – New Update: in conversation with several colleagues, Zirgan 4-5 times/day has shown significant improvement in patients over a 7- 10 time period. • Important to stress limited contact with others, frequent hand washing, not sharing of towels, etc. Orbital Blowout Fracture • Signs & Sx’s: – – – Impairment of eye movement 20 to EOM entrapment, orbital hemorrhage or nerve damage – Infraorbital n. anesthesia • CT should include axial and coronal cuts Orbital blowout fracture

Disposition - If no diplopia, minimal displacement, and no muscle entrapment, discharge with follow up within a week. Consider - For enophthalmos, muscle entrapment, or visual loss. Management: – Ice packs beginning in clinic and for 48 hrs will help decrease swelling associated with injury. – Elevate head of bed (decrease swelling). – If sinuses have been injured, give prophylactic antibiotics and instruct patient not to blow nose. – Treat nausea/vomiting with antiemetics. Case

• 30 BF presents with eye pain in both eyes for the past several days – Severe pain (8/10) – Never had eye exam before • PMHx: – Has chronic bronchitis – Rash on legs – Has recently lost weight and has a fever – Taking aspirin for pain

Ocular Health Assessment • VA: 20/30 OD, OS • PERRL • FTFC • EOM”s: FROM with eye pain in all quadrants • SLE: – 3+ injection, – 3+ cells and trace flare, – deposits on endo (see photo) • IOP: 18, 18 mmHg • DFE: – see attached fundus image and .

• Uveitis frequently is nonspecific but can be associated with: – systemic disease, – occur following trauma, or – be the result of a primary ocular disorder such as: • Fuchs's heterochromic iridocyclitis or • glaucomatocyclitic crisis (ie, Possner-Schlossman syndrome) Classification of Uveitis

• 4 main questions we need answered – Where is the inflammation located? – Is disease acute or chronic? – Granulomatous or non-granulomatous? – Unilateral or bilateral? Helpful Mnemonic

• Mnemonic for acute forms of non- granulomatous uveitis: BLAIR G – B: Behcet’s disease – L: Lyme disease – A: Ankylosing spondilitis – I: Irritable bowel syndrome (Crohns) – R: Reactive arthritis

– G: Glaucomatocyclitic crisis Uveitis

• The clinical features of anterior uveitis are readily recognizable – complaints of: • , • pain, • blurred or variable vision • A change in the blood-aqueous barrier results in the liberation of protein and cellular matter into the anterior chamber and the vitreous. Uveitis

• Clinical findings of: – circumlimbal hyperemia, – cells and flare in the aqueous and anterior vitreous, and – keratic and trabecular precipitates Uveitis: Treatment

– “Classical treatment”: • Pred forte: every 1-2 hours, ensure taper –Pred forte: prednisolone acetate formulation which allows penetration through cornea to anterior chamber – Newer treatment option: • Durezol Treatment Options

• Durezol: – Difluprednate • only difluorinated steroid – Steroid emulsion – BAK free – Increased “potency” so dosing needs to be less than “classical treatment” with Pred Forte • rough recommendation is 1/2 dosing of Pred Forte Cycloplegics

• Common cycloplegic agents include: – cyclopentolate 1-2% tid for mild-to- moderate, – homatropine 5% BID – scopolamine 0.25% – atropine 1% bid-tid for moderate-to-severe inflammation • most common is the use of Homatropine 5% bid • be careful using atropine as there is potential for severe systemic side effects – also makes the iris essentially immobile Cycloplegics

• : – used for reduction of pain, – break/prevent the formation of posterior synechiae – also functions in the reduction of inflammation Treatment

• Topical administration is most common though periocular injections and systemic meds are useful for posterior uveitis and difficult cases • Dosing is dependent upon severity of the inflammation – typically you want to hit the uveitis hard and fast! • E.g 1 gtt q 2hrs until the inflammation is gone! • If you have a minimal anterior chamber reaction then steroid may not be necessary at all Treatment

• NOTE: it is crucial to taper your steroid treatment! – You will have a rebound inflammation if you simply remove your patient from their steroids… – The taper will be dependent upon how long you have had them on the steroid to get rid of the inflammation! – Typically, a slow taper is better in order to prevent rebound inflammation – If the patient has been on the steroid for less than a week a faster taper can be considered. Treatment

• NSAIDs: – do not play an important role in the treatment of an acute uveitis Treatment: Additional Therapies

• Immunosuppressive agents (cytotoxic) – reserved for sight-threatening uveitis that have not responded to conventional treatment • e.g. cyclophosphamide • Antimetabolites (e.g. methotrexate) have been found useful in JIA related iridocyclitis and scleromalacia • Cyclosporin has a very specific effect on the immune system and has been found useful in posterior and Follow-up

• Every 1-7 days in acute phase depending upon severity and every 1-6 months when stable. • On each f/u visit the AC reaction and IOP should be evaluated – DFE should be performed for flare- ups, when VA affected, or every 3-6 months. Follow Up

• If AC reaction improving, then steroid drops can be slowly tapered. – cycloplegia can also be tapered as the AC reaction improves. – slow taper recommended for chronic granulomatous uveitis.