Anterior Segment Grand Rounds

Transcription

1 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 blonsberry@pacificu.edu

2 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

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

4 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 cornea Decreased tear prism

5 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

6 Differential Diagnosis of Dry Eye

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

8 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 conjunctiva 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

9 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)

10 SJOGREN S SYNDROME: OLD/NEW CLASSIFICATION Old: 1 o Sjogrens: occurs when sicca complex manifests by itself no systemic disease present 2 o 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.

11 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

12 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.

13 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

14 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

15 Sjö Diagnostic Test

16 Sjö Diagnostic Test

17 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.

18 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

19 Which of the following lid nevi have the greatest chance to convert to a malignant melanoma?

20 Lid Nevi Lid nevi: congenital or acquired occur in the anterior lamella of the eyelid 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

21 Congenital Nevus The nevus is generally well circumscribed and not associated with ulceration. The congenital nevus of the eyelids 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

22 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

23 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

24 CHRPE vs Nevus 24

25 Nevi Trivia 31% of choroidal nevi show slight enlargement over time without the transformation to a melanoma (Ophthalmology 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)

26 TFSOM To Find Small Ocular Melanoma Thickness: lesions >2mm Fluid: any subretinal fluid (suggestive of serous retinal detachment) Symptoms: photopsia, vision loss Orange pigment overlying the lesion Margin touching optic nerve 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.

27 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.

28 From: Enhanced Depth Imaging Optical Coherence Tomography of Small Choroidal Melanoma: Comparison With Choroidal Nevus Arch Ophthalmol. 2012;130(7): doi: /archophthalmol Figure Legend: Date of download: 10/9/2014 Copyright 2014 American Medical Association. All rights reserved.

29 From: Enhanced Depth Imaging Optical Coherence Tomography of Small Choroidal Melanoma: Comparison With Choroidal Nevus Arch Ophthalmol. 2012;130(7): doi: /archophthalmol Figure Legend: Date of download: 10/9/2014 Copyright 2014 American Medical Association. All rights reserved.

30 Case 65 yr old white male Notices spot in vision in his left eye Diabetes 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

31 Ocular Tumors Astrocytic Hamartoma Amelanotic Melanoma Retinoblastoma Metastatic Choroidal Tumor

32 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. Longterm results of proton beam irradiated uveal melanomas. Ophthalmology. 1987;94:

33 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.

34 Preseptal Cellulitis Infection and inflammation 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, ptosis, pain and low grade fever.

35 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

36 Differentiating Orbital vs. Preseptal FINDING ORBITAL PRESEPTAL Visual Acuity Decreased Normal Proptosis Marked Absent Chemosis and Hyperemia Marked Rare/Mild Pupils RAPD Normal Pain and Motility Restricted and Painful Normal IOP Normal Temperature Normal/mild elevation HA and Assoc. Symptoms Common Absent Treatment: Orals for Preseptal, Often IV for Orbital

37 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

38 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 Case: Gonzalez

39 Etiologies of Cotton Wool Spots Vascular Occlusive Disease Hypertension Ocular Ischemic Syndrome Autoimmune Disease e.g. SLE Hyperviscosity syndromes Trauma Pre-eclampsia Radiation Retinopathy Toxic e.g. interferon Neoplastic e.g. leukemia Anterior Ischemic Syndrome Infectious e.g. HIV

40 Patient Update Patient was worked up for lupus and diagnosed with lupus. Patient was already taking Celebrex which was not effective in treating the scleritis 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

41 Treatment and Management: Antimalarials hydroxychloroquine more common and less toxic than more effective chorloquine usual dose is 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 DMARD s 28

42 Treatment and Management: Antimalarial Ocular Complications Have affinity for pigmented structures such as iris, choroid 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.

43 Question Which of the following depicts a retina undergoing hydroxychloroquine toxicity?

44 Question Which of the following depicts a retina undergoing hydroxychloroquine toxicity? ARMD Macular Hole OHS Bull s Eye Maculopathy

45 Question Which OCT goes with a patient undergoing hydroxychloroquine toxicity?

46 Treatment and Management: Antimalarial Ocular Complications Toxicity can lead to whorl keratopathy, bulls eye maculopathy, retinal vessel attenuation, and optic disc 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

47 Treatment and Management: Antimalarials 29 Bulls Eye Maculopathy Whorl Keratopathy

48 Fabry Disease alpha-galactosidase-a deficiency. insufficient breakdown of lipids, which build up to harmful levels in the eyes, 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 stroke. The heart may also become enlarged and the kidneys may become progressively involved. Other signs include decreased sweating, fever, and gastrointestinal difficulties.

49 Revised Recommendations on Screening for Retinopathy 2002 recommendations for screening were published by Ophthalmology Revised recommendations on screening published in Ophthalmology 2011;118: 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

50 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.

51 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

52 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 scotoma

53 Paracentral Scotomas

54 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

55 Normal Retina: VF/OCT/ERG TD-OCT Outer Nuclear Layer PIL SD-OCT Copyright restrictions may apply. Rodriguez-Padilla, J. A. et al. Arch Ophthalmol 2007;125: PIL=PR Integrity Line

56 Mild Maculopathy Normal Foveal Peak Paracentral Scotomas Thinned Outer Nuclear Layer PIL Copyright restrictions may apply. Rodriguez-Padilla, J. A. et al. Arch Ophthalmol 2007;125:

57 Bull s Eye Maculopathy Flattened Foveal Peak Dense Para/Central Defects RPE Atrophy Remnant of PIL Copyright restrictions may apply. Rodriguez-Padilla, J. A. et al. Arch Ophthalmol 2007;125:

58 Revised Recommendations on Screening for Retinopathy Factors Increasing Risk of Retinopathy Duration of use Cumulative Dose Daily Dose Age Systemic Disease Ocular Disease > 5 years > 1000 g (total) > 400 mg/day Elderly Kidney or liver dysfunction Retinal disease or maculopathy

59 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

60 Pre-Malignant Eyelid Lesions: Keratoacanthoma Lesion on the eyelids may produce mechanical problems such as ectropion 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

61 Pre-Malignant Eyelid Lesions: Actinic Keratosis Also known as solar or senile keratosis Most common premalignant skin lesion Develops on sunexposed areas and commonly affect the face, hands and scalp (less commonly the eyelids) Predominately white males

62 Pre-Malignant Eyelid Lesions: Actinic Keratosis Appear as multiple, flattopped papules with an adherent white scale. Development of SCC in untreated lesions as high as 20% Management is surgical excision or cryotherapy (following biopsy)

63 Malignant Eyelid Lesions: Basal Cell 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% Carcinoma (BCC)

64 Malignant Eyelid Lesions: Basal Cell 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 Carcinoma (BCC)

65 Malignant Eyelid Lesions: Squamous Cell 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 Carcinoma (SCC)

66 Malignant Eyelid Lesions: Squamous Cell 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 Carcinoma (SCC)

67 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 lens wearer reports that others in his class have had a similar red eye no seasonal, food or drug allergies has taken Visine 4-5 times/day since eyes became red but hasn t helped much

68 Question Which of the following best represents your patient?

69 Conjunctivitis Bacterial Conjunctivitis Allergic Conjunctivitis Viral Conjunctivitis Blepharo-conjunctivitis

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

71 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)

72 AdenoPlus Have you heard about this?

73 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.

74 Viral Conjunctivitis: Signs and Symptoms Gritty sensation Watery discharge Sticky in mornings Follicular response Chemosis Injection SPK Infiltrates possible Positive lymph nodes Pseudomembranes in severe cases Subconjunctival hemes

75 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 cataract 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

76 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 $ Case of 200 Betadine swabsticks apprx. 45 dollars.

77 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.

78 Orbital Blowout Fracture Signs & Sx s: Enophthalmos Diplopia Impairment of eye movement 2 0 to EOM entrapment, orbital hemorrhage or nerve damage Infraorbital n. anesthesia CT should include axial and coronal cuts

79 Orbital blowout fracture Disposition - If no diplopia, minimal displacement, and no muscle entrapment, discharge with follow up within a week. Consider Surgery - 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.

80 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

81 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 fluorescein angiography.

82 Uveitis 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)

83 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?

84 Helpful Mnemonic Mnemonic for acute forms of nongranulomatous uveitis: BLAIR G B: Behcet s disease L: Lyme disease A: Ankylosing spondilitis I: Irritable bowel syndrome (Crohns) R: Reactive arthritis G: Glaucomatocyclitic crisis

85 Uveitis The clinical features of anterior uveitis are readily recognizable complaints of: photophobia, 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.

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

87 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

88 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

89 Cycloplegics Common cycloplegic agents include: cyclopentolate 1-2% tid for mild-tomoderate, 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

90 Cycloplegics Cycloplegia: used for reduction of pain, break/prevent the formation of posterior synechiae also functions in the reduction of inflammation

91 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

92 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.

93 Treatment NSAIDs: do not play an important role in the treatment of an acute uveitis

94 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 intermediate uveitis

95 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 flareups, when VA affected, or every 3-6 months.

96 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.