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1 Disclosure Statement: Jeffrey R. Varanelli, OD, FAAO, Dipl ABO, ABCMO Nicholas Colatrella, OD, FAAO, Dipl AAO, ABO, ABCMO Allergan Pharmaceuticals Speaker s Bureau Bio-Tissue BioD Logics, LLC Katena / IOP Ophthalmics Seed Biotech Johnson and Johnson Vision Care, Inc Minnesota Optometric Association Board of Trustees AAO Anterior Segment Section Board Text NICHOLASCOLA090 to to join Live Text Poll Nicholas Colatrella, OD, FAAO, Dipl AAO, ABO, ABCMO Jeffrey Varanelli, OD, FAAO, Dipl ABO, ABCMO Health care decisions have substantial consequences, and involve important uncertainties and trade-offs Uncertainties may be about diagnosis, accuracy of available diagnostic tests or treatments, history of disease or the effects of treatment in an individual patient or group Decision analysis should be broken down into its components, so they can be analyzed individually and then recombine them systematically to help guide your treatment by way of: Development of differential diagnoses Literature based treatment studies Evidence based treatment strategies 76 year old Caucasian male Uncomplicated cataract surgery 3 days prior OS Woke up with complaint of redness, pain, and decreased VA 1

2 BCVA: Hand Motion at 3 Corneal edema / central folds Epithelium intact IOP: 21 mm Hg 3-4+ cell / fibrin in chamber No view of fundus Diagnosis and plan? TASS Acute, sterile postoperative anterior segment inflammation that develops following anterior segment sx Monson et al. first used the term TASS in 1992 received greater attention because of a national outbreak in 2005 that affected 112 patients treated at seven sites in six states linked to endotoxins in Advanced Medical Optics Endosol balanced salt solution (BSS). Caused by any substance that enters the anterior segment of the eye either during or immediately after surgery, causing toxic damage of the intraocular tissues. Careful history and exam help differentiate between TASS and endophthalmitis intraocular cultures and intravitreal AB must be utilized when interpretation difficult Most common clinical symptom is significantly blurred vision Most common clinical finding is corneal edema Limbus to limbus Indicative of widespread endothelial damage Marked anterior segment inflammation Hypopyon Fibrin from surface of iris onto surface to IOL, to wound and side ports Can create significant iris damage Permanently dilated Transillumination Damage to TM leading to 2 nd Glaucoma Treatment Immediate high dose topical corticosteroid Follow closely Same day Daily IOP monitoring Usually low to start but can rise rapidly Acute trabeculitis PAS development gonio Specular Microscopy Monitor for permanent endo damage No help to wash out the AC 2

3 Epithelial edema often associated with elevated IOP Pressure elevation Retained viscoelastic Inflammation Hyphema Ciliary or pupillary block Mechanical angle closure Treatment Time Ocular hypotensives Wound burp Cystoid Macular Edema Most common cause of decreased vision after cataract surgery Incidence? Higher risk patients? Presents 4-12 weeks after uncomplicated surgery with reduced VA ocular inflammation leakage of FL from optic nerve and macula Results from retinal leakage in perifoveal region and accum. of fluid in the outer plexiform layer of the retina Major contributing factors intraocular inflammation vitreous traction (wound, iris, or macula) pre-existing microvascular disease yellowish spot in fovea Courtesy of Steven Silverstein, MD What are differentials? Toxic Anterior Segment Syndrome (TASS) Increased IOP CME Corneal abrasion Endophthalmitis Acute Bacterial Endophthalmitis Usually manifests 2-7 days after surgery, most within 6 weeks Pain, injection, significant decrease in VA, purulent discharge Incidence 1:1000 Most acute cases due to S.aureus and S.epidermidis Key to diagnosis is culturing aqueous and vitreous 3

4 Acute Endophthalmitis Clinical Appearance Cells in anterior chamber Hypopyon Fibrin Focal corneal edema Eyelid edema Chemosis Hyperemia Vitreal Involvement Pain 21% with underlying DM Endophthalmitis Vitrectomy Study (EVS) Multicenter randomized trial carried out at 24 centers in U.S. ( ) Looked at 420 patients with clinical evidence To determine the role of IV and systemic antibiotics To determine role of immediate PP Vitrectomy Results No difference in final visual acuity or media clarity with or without use of systemic / IV antibiotics Therefore recommend intravitreal injection of AB Arch Ophthalmol Dec;113(12): Results of the Endophthalmitis Vitrectomy Study. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Endophthalmitis Vitrectomy Study Group. Endophthalmitis Vitrectomy Study (EVS) Patients with LP vision or worse with an early vitrectomy did favorably with final VA 20/40 or better was achieved 3x more often following PPV than needle tap Patients with better than LP VA, do not require a vitrectomy only required tap/biopsy Overall 53-60% achieved >20/40 following AB therapy Spring white male 1 day uncomplicated Cataract Post Op evaluation Pt reports slept well and in no acute distress No real pain or discomfort but blurry 20/200 SLE 2-3+ Diffuse limbus to limbus corneal edema 3+ Fibrin in AC emanating from pupil to wound + Hypopyon Pupil mid-dilated Ta 18 mmhg Ant Vitreous difficult to view but appeared clear 4

5 CLINICAL FEATURES TASS INFECTIOUS Onset Clinical of symptoms Features Relatively immediate TASS (12-48 Somewhat Infectious delayed hours) Relatively (2-7 Somewhat days) delayed Onset of symptoms immediate (12 48h) (2 to 7d) Pain Most patients do not >75% of patients have pain experience Most patients do >75% of patients Pain not experience have pain Corneal Edema Diffuse limbus-to-limbus Focal corneal edema Diffuse limbus-tolimbus cell/flare, hypopyon, Increased cell/flare, hypopyon, Focal corneal edema Corneal Edema Anterior Segment Inflammation Increased marked fibrin reaction moderate to severe fibrin Ant Seg inflamm Increased cell flare, Increased cell/flare, hypopyon, marked hypopyon, moderate Iris/pupil Iris fibrin atrophy, reaction with dilated, nonreactive pupil Changes to severe relatively fibrin uncommon Iris / pupil iris atrophy with changes relatively dilated nonreactive uncommon Vitreous Usually clear, rare spillover Opacified Usually clear, rare Opacified spillover Sandra, 75 years old Medical Hx: HTN, Osteoporosis Ocular History Successful cataract surgery 2012 OU Longstanding dry eye syndrome Medications Lotrel Fosamax Restasis FreshKote as needed Ophthalmic Exam Decreased TBUT Dense and diffuse SPK Patient very photophobic 5

6 Mild Mild 10/16/2015 Dry eye is a disorder of the tear film due to tear deficiency or excessive evaporation, which causes damage to the inter-palpebral ocular surface and is associated with symptoms of ocular discomfort NEI, 1995 Dry eye is a multi-factorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface Tear Film and Ocular Surface Society, 2007 Severity Level 1 to moderate symptoms and no signs to moderate conjunctival signs Severity Level 2 Moderate to severe symptoms Tear film signs Mild corneal punctate staining Conjunctival staining Visual signs Severity Level 3 Severe symptoms Marked corneal punctate staining Central corneal staining Filamentary keratitis Severity Level 4 Severe symptoms Severe corneal staining, erosions Conjunctival scarring Behrens A, Doyle JJ, Stern L, et al; Dysfunctional Tear Syndrome Study Group. Dysfunctional Tear syndrome: a Delphi approach to treatment recommendations. Cornea 2006;25 (8): Severity Level 1 Education and counseling Environmental modifications Control systemic meds Preserved tears Allergy control Severity Level 2 No inflammation non-preserved tears, gel / ointment qpm Inflammation Steroids, Cyclosporine A Secretagogues, nutritional supplements Severity Level 3 Tetracyclines Autologous Serum Punctal Plugs Severity Level 4 Topical Vitamin A Contact Lens Acetylcysteine Moisture goggles Oral cyclosporine Surgery December practitioners from around the country met to see if there was a better way to disseminate information to OD s 0summit%20results.pdf?dl=0 1. Do your eyes ever feel dry or uncomfortable? 2. Are you bothered by changes in your vision throughout the day? 3. Are you ever bothered by red eyes? 4. Do you ever feel the need to use eye drops? 6

7 Options? 1. For all DED Patients a) Ocular Lubrication b) Lid Hygiene c) Nutrition 2. Topical Anti-inflammatories Options? Promotes Epithelialization Suppresses Inflammation Inhibits Scarring Inhibits Angiogenesis Neurotrophic Factors Anti-Microbial Agent All without the harmful side effects found in topical and oral medications 17 yo white male, Logan K c/o red, painful, irritated left eye Been going on for almost a month 2 weeks ago went to ER and given Polytrim. Since then no real improvement Wearing Biofinity DW, reports good compliance, no EW, but wearing them today (with the red eye) Vacc 20/20 OD, 20/30 OS (-4.00 OU) Also had infection on forehead just prior, Dx as dermatitis or impetigo which had oral AB He is also a wrestler and routinely has face smeared into mat And after each match usually goes into hot tub to relax muscles, etc, while wearing CL s (May have gone under) Dec 25 7

8 Cultured everything Performed corneal sensitivity Was reduced objectively and subjectively OS Presumptive Dx of Herpes Simplex Keratitis (dendrite and marginal keratitis) Started Zirgan 5x/day Besivance q2h Debride vs no debridement Also started on Oral Acyclovir 400mg 5x/day But had notes in chart saying Concerned about Acanthamoeba. Also worried about NTM due to face in mat and possibly even Nocardia. If not improved in next couple of days switch to fortified Amikacin and consider PHMB Most common form of HSV keratitis Dendrite is derivative of dendron Greek word for tree Linear, branching lesion, swollen epithelial borders, terminal bulbs Stains positively w FL along length Rose Bengal or Lissamine Green at epi borders Do cultures prior to RB Contains live virus Central ulceration through basement membrane Ulcerated and not raised as VZV pseudodendrites & healing Epi defects 8

9 Dendritic ulcer may result in abnormal-appearing epi for several weeks after ulcer heals i.e. HSV Dendritic Epitheliopathy Lesion is dendritic in shape, but not ulcerated Stains negatively along length of lesion Represents healing epi and no antiviral is needed Enlarged or expanding dendritic ulcer True ulcer that has live virus and extends through basement membrane Typically has swollen scalloped epithelial borders Differentiates from smooth borders of neurotrophic ulcer and healing abrasions Wilhelmus et al 22% of all initial infections Assoc w longer duration and topical corticosteroids Uncommon and often confused with Staph Marginal disease Result of active live virus in close proximity to limbus Unique clinical features Epi lesion (perhaps dendrite) with underlying anterior stromal infiltrate and adjacent limbal injection Pt extremely symptomatic due to inflammatory nature More difficult to tx If inappropriately tx with corticosteroids, will progress centrally w ulceration and subepithelial infiltration (takes on dendrite pattern) Ways to help differentiate Features HSV Marginal Ulcer Staph Marginal Infiltrate Etiology Active HSV Immune response to staph antigen Epithelial Defect Always Absent (unless late) Neovascularization Often Never Progression Centrally Circumferentially Blepharitis Unrelated Usually Location Any meridian Typically 2,4,8,10 O clock meridians 9

10 Physical debridement of dendrite w cotton tip applicator with topical or oral Tx: Topical Trifluiridine (Viroptic) q2h until epithelium is healed, then qid x 7 days Gancyclovir (Zirgan) 5x daily until epithelium is healed, then tid x 7 days Oral Zovirax (acyclovir) 400mg five times daily for 10 days Valtrex (valacylovir) 500mg three times daily 10 days Famvir (famciclovir) 250mg three times daily 10 days. Prophylaxis with broad spectrum AB prudent, esp when treating large geographic ulcers 56 yo WF originally reported Dec 2009 for self reported Ulcer Noted when woke up in AM Red, pain, photophobia (had occurred previously) Epithelial defect w stain RCE? Tx w AB, BSCL and followed w Lub ung QHS Reported in May 2010 c/o pain and redness again New Dx Immune Stromal Keratitis Tx w Pred Forte Made me re-think prev Dx of RCE Gave Oral Acyclovir 400 mo BID PO Successfully avoided recurrence x 3 years Had stomach upset thought was from Acyclovir so stopped 3 mo later recurrence Switched to Restasis BID 10

11 Stromal disease accounts for 2% of initial episodes but 20-48% of recurrent disease Commonly confused and poorly categorized Stroma can be affected either primarily or secondarily Secondary causes such as infectious epithelial keratitis, neurotrophic keratopathy or endotheliitis should direct its tx towards those layers Primary involvement includes Necrotizing Stromal keratitis and Immune Stromal keratitis Rare manifestation of direct live viral invasion to stroma Along with severe host inflammatory response Necrosis, ulceration and dense infiltration of stroma w overlying epi defect Severe inflammation can lead to thinning and perforation in short period of time Mimics microbial invasion Must culture to rule out bacterial and fungal Treatment High dose anti-inflammatory and antivirals Combo of replicating virus and severe host inflammatory response leads to destructive intrastromal inflamm that is often refractory to tx Synonymous with interstitial keratitis Confusing terminology Stromal neovascularization w inflammation?? Posterior neovascularization only?? Syphilitic keratitis?? Refers to any inflammatory condition of the stroma that has an immunologic etiology not restricted to: Presence or absence of neo Depth of stromal inflammation Etiology of inflammation Common chronic recurrent manifestation 20% of all Ocular HSV After infectious epithelial keratitis 21% within 2 years 26-48% within 7 years Not live virus but retained viral antigen within stroma Triggers an antigen-antibody-complement (AAC) cascade resulting in stromal inflamm T-cell mediated autoimmune response Underlying stromal inflammation with intact epithelium Can lead to severe scarring and dec vision Vision loss from immune stromal keratitis scarring accounts for 3% of all PK s performed Patients present in pain and discomfort Can take on several forms Punctate stromal opacities and haze Pattern may be focal, multifocal or diffuse Often has AC rxn and ciliary flush Stromal edema 11

12 Immune ring or Wessely ring AAC precipitate that forms full or incomplete ring found in mid stroma May have one or multiple rings Stromal Neovascularization May occur at any level Can occur rapidly w multiple fronds Sectoral or diffuse Aggressive tx of inflammation can result in complete resolution of vessels Ghost vessels common Lipid Keratopathy can follow neovascularization Neo leaks lipid into stroma Leads to further scarring and loss of vision Permanent neovascularization decreases the success rate of PK due to inc risk of rejection Corticosteroids needed in tx pt with immune mediated disease High initial dose, q2h, to control inflamm Avoid rapid taper Customize to the amount of inflammation Controversy with HEDS Tx longer then 10 weeks Flare Dose Match one to one dosing with concurrent antiviral Prophylaxis 400mg Acyclovir BID PO long term Newer Tx options Topical Cyclosporine A (CsA) Supported by several studies over last decade Resolution of stromal inflammation in 83% 4.5 weeks 2 lines of VA improvement in 75% Resolved neovascularization in 64% Topical CsA alone or in conjunction w corticosteroid provides alternate therapeutic option Works by inhibiting activation of CD4 T-helper cell pathways Steroid sparing agent May exacerbate epithelial keratitis if active Amniotic Membrane Transplantation (AMT) Possesses several anti-inflammatory factors such as IL-10, IL-1 receptor antagonist, activin, protease inhibitors Supernatants inhibit neovascularization Inhibit keratocytes into myofibroblasts and pv scarring 12

13 First reported in 1985 (Robin) Corneal endothelium primary site of inflammation Characterized by corneal edema, KP, mild to moderate AC reaction Exact pathogenesis unknown Immunologic due to KP and iritis Possibly live virus as well Inflammatory reaction at level of endothelium No stromal infiltrate or neovascularization May cause permanent loss of endothelial cells w subsequent intractable edema Photophobia and mild to mod ocular discomfort Limbal injection w accompanying iritis Visual acuity can be reduced depending on location of edema Holland and Schwartz classified into 3 distinct forms (1999) Disciform Diffuse Linear Most common form Round disc shaped area of stromal edema Central or paracentral Spans entire stromal thickness Void of infiltrate or neo Striking demarcation bet involved / uninvolved cornea Epithelial microcystic edema? bullae Disciform edema or disciform keratitis Overlying KP? hidden Mild to mod iritis Elevated IOP common Rare Scattered KP over entire cornea w overlying diffuse stromal edema Mild to mod iritis? Detect Epithelial edema common Retrocorneal plaque of inflammatory cells w hypopyon Very Rare Can follow unilaterally after Cat Sx Peripheral corneal nerve trauma leads to recrudescence of latent virus Bilateral involvement commonplace Line of KP on endothelium Progress from limbus to central cornea Sectoral or circumferential May be straight or serpiginous KP mark the area of edematous and non-edematous Peripheral stromal and epithelial edema If not treated promptly leads to decompensation Tx w both corticosteroid and antiviral 13

14 Corticosteroids needed in tx pt with immune mediated disease High initial dose, q2h, to control inflamm Avoid rapid taper Customize to the amount of inflammation Flare Dose Match one to one dosing with concurrent antiviral Oral Corticosertoid Disciform endotheliitis Diffuse endotheliitis All cases of linear endotheliitis JM, 68 year old female Initial visit April 16, 2014 Presented with complaint of: Redness, discharge, swelling OD x 2 days Ocular/Medical Hx: Non-contributory Initial Diagnosis Epidemic Keratoconjunctivitis Slit lamp exam OD Chemosis, lid swelling, faint SEI inferior, subconj hemorrhage Slit lamp exam OS Unremarkable Viral conjunctivitis caused by adenoviruses 8, 19 Highly contagious Typically unilateral No sore throat / fever Redness Discomfort SEI Chemosis Photophobia 14

15 Helpful to Tx EKC There are no FDA-approved medicines to kill adenoviruses But, an excellent off-label application of an FDA-approved drug is readily and inexpensive: 5% Betadine Sterile Ophthalmic Prep Solution Decreases the viral load Prevents entry into the anterior stroma stopping SEI Video courtesy Atlantic Eye Physicians Topical Antimicrobial OTC Used to apply and clean wound or prep for surgery MOA Oxidizes cell constituents Iodinates proteins and inactivates them Side Effects Severe pain on application Irritation Pruritic Erythema Edematous erythema Melton-Thomas EKC Betadine Protocol 1. By history, rule out any allergy or sensitivity to iodine 2. Instill a drop of 0.5% proparacaine 3. Instill a drop or two of a topical NSAID. 4. Instill four to five drops of 5% Betadine onto the eye. 5. Ask the patient to gently close the eyes and roll them around to ensure thorough distribution of the Betadine across the ocular surfaces. 6. After 1-2 minutes, lavage out the Betadine 7. Instill another drop or two of the NSAID (or even proparacaine if the patient has any discomfort). Betadine For EKC study / betadineforekc.com Trinavarat A, Atchaneeyasakul LO. Treatment of epidemic keratoconjunctivitis with 2% povidone-iodine: a pilot study. J Ocul Pharmacol Ther Feb;28(1):53-8. Approved 2009 for treatment of acute HSK or dendritic epitheliopathy Has been avail in Europe since 1995 First FDA approval for this class in 3 decades to help treat one of the 60k (29k pts) new cases of HSK each yr 1 drop 5x/d (Q3H) until ulcer heals then TID for 7 d no toxicity, very quick resolution, very comfortable Selectively inhibits synthesis of viral DNA Competitive inhibition of viral DNA polymerase direct incorporation into DNA primer strand SE s Blurred Vision (60%) Irritation (20%) SPK (5%) Conj Hyperemia (5%) Off label Tx of EKC Safety not established below age of 2 15

16 Research presented at ARVO 2001 by Tabarra et al 18 patients with EKC Compared topical ganciclovir to preservative free tears Clinical Exam (4/22/14) Patient much more comfortable Minimal injection No photophobia Recovery Time Presence of subepithelial opacities Topical ganciclovir 0.15% 7.7 days 22% Preservative free artificial tears 18.5 days 77% Pre-Betadine Post-Betadine Pre-Betadine Post-Betadine 58 yo WM Dennis L. Day 1 OS blurry and painful but more comfortable today ph = 7 VA cc 20/100 PH 20/40 L/L erythema and edema Conj 2-3+ inj Defect inferior Cornea OS- 95% Epithelial defect w sloughed tissue along edges Approx ¼ limbal involvement OD clear A/C view hazy but appreciable cell Iris details somewhat visible Fundus difficult views appears intact T(a) 14 16

17 Involves corneal epithelium only Limbal stem cells spared Cornea remains clear Epithelium denuded No opacity No limbal ischemia Prognosis: Excellent for full recovery of normal corneal appearance and function Grade 1 ocular surface burn. Large corneal burn following accidental exposure to ammonia. There is no limbal or conjunctival involvement. Fluorescein stained diffuse view of the cornea. Partial loss of limbal stem cells Focal limbal ischemia < 1/3 of limbus Cornea is hazy, but anterior segment structures are visible Prognosis: Good Concerns: Persistent epithelial dysfunction Conjunctivalization Haze Neovascularization Extensive limbal ischemia 1/3 to 1/2 of limbus Loss of most limbal stem cells Stromal haze limits visualization of iris and lens Prognosis: Guarded Surgery needed for visual rehabilitation Complete loss of corneal epithelium and limbal stem cells Loss of proximal conjunctival epithelium Opaque cornea No view of iris or pupil Porcelainization Limbal ischemia (more than 50%) Ischemic necrosis of proximal conjunctiva and sclera Prognosis: Extremely poor High risk for sterile ulceration and corneal melt Even with most aggressive tx limbal stem cell death most likely too advanced First Wave occurs hours after chem injury with infiltration of peripheral cornea with PMN and mononuclear leukocytes. Resulting from: Blood elements from injured vessels in conj and uvea Necrotic tissue of bulbar and tarsal conj Chemotactically attracted byproducts of epi and stromal tissue Second, more aggressive wave of inflammatory cell infiltration begins at 7 days and peaks when corneal repair and degradation are maximal (bet day) Medical Management Topical Pred Forte Q1h or Durezol Q2h x 7 d then taper & switch to 1% topical medroxyprogesterone QID 1% Atropine QD Zymaxid / Moxeza / Besivance QID Amniotic Membrane by day 3 Non Preserved artificial tears q1h 100mg Doxycycline BID PO 500 mg Diamox BID PO Ultram 100mg PO q4-6h Topical 10% ascorbate and 10% Citrate Q2h 17

18 58 yo WM Dennis L. Dx Grade II Alkali burn of cornea and conjunctiva Plan debride loose tissue Vigamox Q4h OS Pred Forte Q1h OS Atropine BID OS Ciloxan ung QHS OS NP Art Tears Q1h OS NO topical NSAID or BSCL Rx topical citrate and ascorbate through compounding pharm 58 yo WM Dennis L. Day 8 Unable to come in at last visit Eye bothers pt more in AM than PM Certain moments it will hurt. VA cc 20/50 PH 20/40 Ta = 9mmHg Corneal defect closed in 360 leaving residual central defect. Descemet fold and haze noted in stroma CPM. Cut Pred to BID RTO 2 day 58 yo WM Dennis L. Day 16 Went out of town. Unable to come in last week. Vision seems to be improving VA cc 20/80 PH 20/50 Ta = 20mmHg Corneal defect finally resolved. Haze noted in stroma D/C Atropine, D/C Vigamox Cont Ciloxan ung TID, tears q1h, inc PF QID RTO 7 day Antibiotic ointment QID Cycloplegia for comfort Preservative free tears Topical corticosteroids when epithelium healed prednisolone acetate 1% QID with taper Follow up every 1-2 days Supportive therapy to ocular surface Control inflammation Intensive topical corticosteroids x 1wk then hold off x 1 mo prednisolone acetate 1% hourly/ Durezol q2h Other considerations Cycloplegia Do not use phenylepherine and other adrenergic drugs should not be used, owing to their vasocostrictive action leading to the worsening of limbal ischemia Oral narcotics Oral NSAID 4 th generation FQ Topical sodium ascorbate 10% and Citrate oral vitamin C? Limited value Oral tetracycline Preservative free tears Glaucoma meds as needed Systemic Diamox / Neptazane 18

19 Most sight threatening of interface disorders Rare but potentially devastating Incidence: Solomon et al % Moshirfar et al % Llovet et al % (72 eyes of 204,586 from ) Variety of organisms have been implicated (bacteria and viruses) Staphylococcus Pseudomonas Atypical mycobacteria Fungi Acanthamoeba HSV Adenovirus Two dense infiltrates caused by Staphylococcus aureus Most common non-viral cause of IK has evolved over time Prior to 2005 Nontuberculosis (Atypical) Mycobacterium Reduced incidence attributed to routine use of 4 th gen fluoroquinolones Mozayan A. Madu A. Channa P. Laser in-situ keratomileusis infection: review and update of current practices. Curr Opin Ophthalmol. 2011:22: Clinical picture of bilateral Mycobacterium chelonae keratitis 5 weeks after laser keratomileusis Most common non-viral cause of IK has evolved over time More recently Methicillinresistant S. aureus has become more common in early postoperative period Due to potential to develop resistance to fluororquinolones Mozayan A. Madu A. Channa P. Laser in-situ keratomileusis infection: review and update of current practices. Curr Opin Ophthalmol. 2011:22:

20 Risk factors for IK Blepharitis Dry eye Intraoperative epithelial defects Excessive manipulation Intraoperative contamination Delayed postoperative re-epithelialization Use of topical corticosteroids Patients in health profession IK divided into two groups Early onset (first 2 weeks) Symptoms usually appear 2.7days +/- 4.2d Staph and strep species Late onset (2 weeks to 3 months) Symptoms will appear 27.4 days +/- 3.6d Non-tuberculosis mycobacteria and fungi Note the focal infiltrates interspersed within the somewhat diffuse inflammatory reaction. The causative organism was Mycobacterium J. Randleman; R Shah. LASIK Interface Complications: Etiology, Management, and Outcomes. J Ref Surg. 2012;28: Staphylococcus aureus typically presents within 3-7 d Mycobacterial infections from 3wk-4 months Many occur in clusters Mycobacterium chelonae linked to CL used during surgery to mask portion of laser Mycobacterium szulgai linked to ice used to chill BSS on surgical field Acanthamoeba 70 days Management All Flap lift Culture and scrape Flap bed irrigated w fortified antibiotics Early onset Topical 4 th gen FQ alternating q30min with fortified Cefazolin 50mg/ml If health care worker substitute cefazolin with vancomycin 50mg/ml Besivance Q1-2 hour Late onset Topical 4 th gen FQ alternating q30min with Amikacin (beneficial in tx atypical mycobacteria) If non-responsive flap amputation may be necessary to facilitate anitbiotic penetration Prevention Infectious lid disease and dry eye treated preoperatively Intraoperative, strict adherence to aseptic techniques Lid scrub with povidone-iodine solution Use of different set of instruments and microkeratome blades in cases of bilateral procedure Ensure sterile water being used to clean instruments When deciding on the correct treatment Differential diagnoses Literature based treatment studies Evidence based treatment strategies Most resolve with mild to mod loss of VA, but rarely PK required 20

21 Please feel free to contact us: Nicholas Colatrella, OD, FAAO, Dipl ABO, ABCMO Jeffrey Varanelli, OD, FAAO, Dipl ABO, ABCMO 21