Essential Topical Formulary. Carlo J. Pelino, OD, FAAO Joseph J. Pizzimenti, OD, FAAO.

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1 Essential Topical Formulary Carlo J. Pelino, OD, FAAO Joseph J. Pizzimenti, OD, FAAO Course Description The ability to use pharmaceutical agents has enabled optometrists to become true primary health care providers. This includes the use of drugs that are topically applied. Clinical cases are used to illustrate indications, mechanism of action, contraindications, adverse effects, and dosage of these therapeutic agents. Goal The goal of this course is to provide current and accurate information about key drugs that are used to treat eye diseases. Learning Objectives After completion of this course, the participant will be able to: 1. Apply the principles of pharmacotherapy to clinical cases in ocular disease. 2. Discuss indications, mechanism of action, contraindications, adverse effects, and dosage of ocular therapeutic agents. 3. Understand the proper diagnosis and management of ocular infection, inflammation, and itch. 4. Properly diagnose and medically manage the glaucomas.

2 Essential Topical Formulary: My Go-to Drops Joseph J. Pizzimenti, OD, FAAO Course Goal The goal of this course is to provide current and accurate information about key drugs that are used to treat eye diseases. Learning Objectives After completion of this course, the participant will be able to: Apply the principles of pharmacotherapy to clinical cases in ocular disease. Discuss indications, mechanism of action, contraindications, adverse effects, and dosage of ocular therapeutic agents. Understand the proper diagnosis and management of ocular infection, inflammation, and itch. Properly diagnose and medically manage the glaucomas. Introduction to Ocular Pharmacology Diagnostic Pharmaceutical Agents Antibiotics Corticosteroids Combination Medications Non-Steroidal Anti-Inflammatory Medications Anti-Viral Medications Glaucoma Medications Decongestants Ocular Allergy Medications Dry Eye Treatment Local Side Effects of Topical Medications Eyelids allergic reaction (redness and chemosis) Conjunctiva allergic reaction (redness and chemosis) Irritation (burning and stinging) Cornea punctate epithelial keratitis medicamentosa Uveal tissue (iris and ciliary body) change in pupillary diameter change in accommodation inflammation color change Lens opacification

3 Intraocular Pressure (IOP) Increase in IOP Retina cystoid macular edema (CME) Systemic Side Effects of Topical Medications Since topical ocular medications are mostly absorbed directly into the bloodstream, they are not broken down or weakened by the GI system or the liver absorbed through conjunctival capillaries absorbed through the nasal mucosa absorbed by the pharynx or GI system after swallowing To decrease systemic side effects use lowest concentration and dose possible use punctal occlusion keep the eyes closed and apply pressure to the inner corner of the eye with your finger for 1 or 2 minutes to allow the medicine to be absorbed by the eye Keep in mind the patient s medical history and current medications Keep in mind special populations pregnant or lactating women geriatric population pediatric population immuno-compromised patients exceptional patients visually impaired patients Corticosteroids Topical steroids are used to treat ocular inflammatory conditions Choosing which medication to use depends on the severity and location of the ocular inflammation Possible ocular side effects glaucoma prolonged use (3-5 weeks) may cause an increase in intraocular pressure cataract formation decreased wound healing promotion of certain viral and fungal infections Herpes Simplex Virus Moderate to Severe Inflammation Prednisolone acetate 1% Ophthalmic suspension greatest ant-inflammatory efficacy the acetate suspension facilitates corneal penetration to provide increased concentrations in the anterior chamber effective for treating a host of ocular inflammations especially anterior uveitis or iritis and severe episcleritis Loteprednol etabonate 0.5% Ophthalmic suspension

4 effective against almost all ocular inflammations except uveitis and severe episcleritis effective in treating post-operative inflammation decreased tendency to increase IOP Steroid-Antibiotic Combinations These medications are steroids and therefore cause the same side effects Primary use is for control of inflammation Provides antibacterial prophylaxis while treating the ocular inflammation May cause increased IOP and cataract formation with prolonged use Dexamethasone alcohol.1% with tobramycin.3% moderate to severe conditions PHLYCTENULOSIS Small, white limbal nodules with surrounding redness as response to Staph. Associated with tuberculosis Good response to topical AB/steroid such as tobramycin/dexamethasone QID x 5-7 days Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Effective against mild inflammation and used post-surgically diclofenac ketorolac tromethamine flurbiprofen suprofen Ocular side effects redness, burning, stinging, dryness Conventional NSAIDs Diclofenac 0.1% and ketorolac 0.5% have been shown to be equally effective in: Treating postoperative CME Treating postoperative inflammation Ketorolac 0.5% is indicated for postcataract inflammation Ketorolac 0.4% is indicated for postrefractive pain NSAID Mechanism of Action 1. Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the cyclooxygenase (COX) athway, limiting prostaglandin formation. Goals of NSAID Prophylaxis Inhibition and treatment of cystoid macular edema (CME) following cataract surgery Management of postoperative inflammation Prevention of intraoperative miosis during cataract surgery Reduction of pain and discomfort following surgery or injury

5 Advantages of NSAID Therapy Reduction of inflammation NSAIDs work alone or with steroid therapy to minimize inflammation following ocular surgery Decreased intraoperative miosis When dosed preoperatively, NSAIDs play a significant role in decreasing intraoperative miosis Prevention of CME CME development is due in part to a prostaglandin-mediated breach of the bloodretinal barrier Risk Factors for CME Pre-existing ocular inflammation Epiretinal or vitreoretinal interface membrane problems Diabetic retinopathy Patients suffering from ocular vascular or cardiovascular disease Patients with history of retinitis pigmentosa Prophylaxis treatment should be started earlier and extended longer for high-risk patients Hypothesis on Mechanism of CME Formation Following Cataract Surgery Role of Ophthalmic NSAIDs in Prevention of CME Topical NSAIDs are effective in preventing postsurgical CME NSAID therapy has also been shown to have beneficial effect on visual function It is critical to achieve therapeutic concentrations in the posterior chamber to maximize the effect of NSAID therapy on target tissue/retina Adverse Events Associated With Conventional NSAID Therapy NSAIDs are frequently associated with unwelcome corneal effects: Burning and irritation Superficial punctate keratitis Delayed wound healing Severe corneal issues also reported with all conventional NSAIDs Thinning Perforation due to melts NSAID Therapy: A Novel Prodrug Target-specific efficacy Nepafenac demonstrates 6-fold greater tissue permeation compared with diclofenac Tissue and intraocular accumulation of active amfenac is greater than that of conventional NSAIDs Suppresses prostaglandin production longer than diclofenac in iris/ciliary body and

6 retina/choroid tissues Minimizes toxicity Ocular surface complications associated with conventional NSAID therapies may be minimized Drug rapidly distributes into anterior and posterior segments Cornea and anterior and posterior chamber safety demonstrated in vivo via slitlamp examination Antibiotics First-line agents for Bacterial Infections Fluoroquinolones eradicate a wide variety of ocular pathogens Aminoglycosides provide broad spectrum coverage, slightly more effective against gram-negative bacteria Polymyxin B Combinations provide broad spectrum coverage, except for Pseudomonas Fluoroquinolones The bactericidal action results from interference with the enzyme DNA gyrase which is needed for the synthesis of bacterial DNA ciprofloxacin 0.3% ofloxacin 0.3% levofloxacin 0.5% moxifloxacin 0.5% gatifloxacin 0.3% Corneal ulcers May be bacterial, viral, fungal, other bugs Edema: accumulation of fluid within the tissue, can be diffuse or microcystic Ulceration: epithelial break accompanied by infiltration, may involve deeper corneal layers Contact lens wearers at higher risk, specially extended-wear patients Neovascularization: new blood vessels as response to hypoxia Infiltrate formation: immune response If culturing, do not use any eyedrops, may interfere with process If bacterial, must be treated agressively with topical AB ie. moxifloxacin 0.5%: Dosing for corneal ulcer: loading dose, then 1 gt q 15min- 1hr x 1 d If viral (herpetic, use topical antivirals) If fungal or acanthoameba, refer ASAP to corneal specialist Fluoroquinolones DNA gyrase inhibitor Ciprofloxacin, ofloxacin, levofloxacin, norfloxacin, gatifloxacin, moxifloxacin Extremely potent bacteriocidal drugs with broad spectrum Aminoglycosides Inhibit bacterial protein synthesis by binding to the bacterial ribosome Neomycin, gentamicin, tobramycin, amikacin

7 Good against gram-negative bacilli Dissadvantages: extensive side effect profile, may create resistance The bactericidal action results from inhibiting protein synthesis Gentamicin 0.3% Tobramycin 0.3% Neomycin (increased allergic reactions) Available in generic forms Good for short term use (cytotoxic) Case A 25 year old male presents for a routine physical. He states that he has hayfever in the spring and has been congested recently. He complains of itchy, red, watery eyes. DVA OD: 20/20 OS: 20/20 Ocular assessment of the conjunctiva is remarkable for mild redness and a watery discharge, no corneal staining Allergies Common symptoms: Itching, mucous discharge, occasional swelling and redness. Patients often report a history of allergies and concurrent rhinitis. Common signs: chemosis, hyperemia, papillae, mucous. Allergic Conjunctivitis TREATMENT Reassurance No rubbing!!! Avoidance Cold compresses Artificial tears Olopatadine Ketotifen fumarate Loteprednol Ocular Allergy Medications Provide relief from itching, redness and chemosis due to acute or chronic ocular allergies Acute care medications Antihistamines (safe and effective) NSAIDS Corticosteroids Chronic care medications Mast cell stabilizers degranulation of the mast cell occurs in the presence of the allergen releasing histamine causing allergic symptoms Antihistamine with some mast cell stabilizing properties azelastine hydrochloride 0.1% also has anti-inflammatory activity olopatadine hydrochloride 0.1%

8 olopatadine hydrochloride 0.2% ketotifen fumarate 0.025% Olopatadine.1 % Combo drug: Antihistamine/Mast Cell Stabilizer Very safe Very comfortable BID dosing or qd Chronic Care Medications pemirolast potassium 0.1% nedocromil sodium 2% lodoxamide tromethamine 0.1% cromolyn sodium 4% Glaucoma Glaucoma is a group of ocular conditions in which the level of ocular pressure damages the optic nerve causing a loss of visual function Medications for glaucoma either increase fluid outflow (via trabecular meshwork or uveoscleral) or decrease aqueous production A SLOW PROGRESSIVE DEATH OF RETINAL GANGLION CELLS WITH CHARACTERISTIC EXCAVATION OF THE OPTIC DISC AND SEQUENTIAL VISUAL FIELD LOSS THAT STARTS IN THE MID-PERIPHERY. HARRY A. QUIGLEY, MD Johns Hopkins University s Wilmer Eye Institute, 1997 Risk Factors Increased iop Increased age Thin cornea Enlarged c/d ratio Increased psd on visual field Diabetes? Race African americans, hispanics First degree relative with glaucoma Other High myopia, hypertension, eye trauma, topical steroids, migraines, vasospasm, sleep apnea Diagnosing Glaucoma Recognize the risk factors Establish a baseline Intraocular pressure (minimum of 3 readings) Central corneal thickness Evaluate the optic nerve

9 A big cup does not necessarily mean glaucoma Remember the isnt rule Evaluate the nerve fiber layer At the slit-lamp with red free filter Evaluate the visual field Must match the optic nerve Photograph the optic nerve Better than a drawing Advanced optic nerve testing Gdx, oct, hrt Not necessary for diagnosis May help monitor for change Glaucoma Medications Beta Adrenergic Receptor Antagonists Beta-Blockers Prostaglandin Analogs Alpha Adrenergic Receptor Agonist Alpha Agonist Adrenergic Stimulating Agents Cholinergic Stimulating Agents Carbonic Anhydrase Inhibitors (CAI s) Treating glaucoma Iop reduction Remains the mainstay of treatment Possibly prevents optic nerve damage Possibly preserves the visual field Possibly prevents the loss of visual function Mechanism Decrease aqueous production Increase aqueous outflow (tm / uveoscleral) Methods Medication (topical / oral) Laser Surgical Lowering the IOP Not as easy as you might think Not as simple as just going low Keep in mind Balance between iop and blood pressure Ocular perfusion pressure Proper balance may sustain the optic nerve Problems Iop peaks in the morning Blood pressure bottoms out in the morning

10 Iop can spike at any time Target pressure Set target iop based on Highest iop Amount of optic nerve damage Extent of visual field loss Consider Age Progression Monocular status Family hx Modify as needed 20-30% reduction (oc htn / ntg / mild) 1-2 medications 30-40% reduction (moderate - advanced) 2 medications Possibly alt / slt, oral cai 40-50% reduction (advanced) 2-3 medications Alt / slt, oral cai Trabeculectomy or tube / shunt Cyclodestructive procedure Choosing a medication Consider Efficacy Ability to flatten the diurnal curve Safety Convenience Cost When treating ocular htn or glaucoma, What is your preferred first line agent? 1. Prostaglandin 2. Non-selective beta-blocker 3. Cardioselective beta-blocker 4. Alpha-agonist 5. Topical carbonic anhydrase inhibitor 6. Miotics Prostaglandins Increase uveoscleral aqueous outflow Reduces iop about 30% Can cause darkening of the iris and lengthening of eyelashes Can cause iridocyclitis or cme Relative contraindication for patients with: History of uveitis or cme

11 Aphakia or yag posterior capsulotomy History of herpes simplex keratitis Latanoprost Travoprost Bimatoprost Mechanism Enhances uveoscleral outflow Lumigan may aid conventional tm outflow Efficacy 27-34% reduction of iop Iop reduction starts in 3-4 hours Maximum iop effect after 8-12 hours Dosing Once a day Side effects Ocular side effects Hyperemia Spk Longer / thicker lashes Iris color changes (melanin) Periocular pigmentary changes Uveitis, cme 3-4% Hsk reactivation Systemic side effects Muscle / joint pain, gi distress, skin rash Contraindications Uveitis Aphakia, ac/iol, torn posterior lens capsule H/o herpes simplex Pregnancy / nursing Category c, use with caution Benefit must outweigh risk Animal studies show teratogenic effects on fetus Caution to those lactating Children Safety and effectiveness not established Is there a difference? Additional information Cost: $50-60 / month hour duration of effect Once a day = compliance / persistence 4% latanaprost users are nonresponders Rosetti l et al, j of glaucoma, 2006 Bimataprost more effective in blacks

12 Noecker, 2006, 2004, 2003 What s new? Travoprost-z.004% (2006) No benzalkonium chloride (bak) Less hyperemia Less corneal toxicity Statistically equivalent iop Instillation aids Future use in combinations Monocular treatment trial Pros and cons + allows for determining agent efficacy - assumes spontaneous iop is symmetrical - assumes efficacy is equal between two eyes - there is a crossover effect What if not at target? Change within class? Change to a different class? Add a medication? What is your preferred class to use as adjunctive therapy when the target iop is not reached or progression is noted? 1. Prostaglandin 2. Non-selective beta-blocker 3. Cardioselective beta-blocker 4. Alpha-agonist 5. Topical carbonic anhydrase inhibitor 6. Miotics Considering all possible regimens Different preparations Formulations Percentages Concentrations There are 56,000 potential combinations! Realini t, fechtner r. Ophthalmology 2002; 109; What to add? Consider Safety / tolerability Efficacy 15% additional iop lowering is the goal Complementary mechanism of action Convenient dosing

13 Non-selective beta-blockers Options Timoptic (1978) Betagan (1985) Optipranolol (1989) Ocupress (1990) Timoptic xe (1993) Betimol (1995) Istalol (2004) Beta adrenergic receptor antagonists (betablockers) Decrease aqueous production Reduce iop about 25% Selective vs. Non-selective beta-blockers Selective effect mainly the beta 1 adrenergic receptors (cardioselective) Non-selective effect the beta 1 and 2 adrenergic receptors (cardiac and pulmonary) Nonselective beta-blockers: Timolols Timolol hemi-hydrate 0.25% or 0.5% Levobunolol 0.25% or 0.5% 0.25 vs 0.5 timolol and qd vs bid Depends upon iris color? Recommendation Lowest concentration once a day Check for efficacy If no or minimal response, change class If some response, increase concentration If still not at target Go to twice a day If still not at target Change class Add a medication or go to alt / slt / trab / tube Mechanism B1 (blood vessels / heart), b2 (bronchial) B receptors on nonpigmented ciliary epithel Decrease aqueous production Efficacy 10-25% reduction of iop Dosing Qd or bid depending upon the agent Ocular side effects Blurred vision Stinging, burning, dry eyes, punctate keratitis, corneal anesthesia Systemic side effects

14 Shortness of breath, reduced pulse, fatigue Decreased libido, confusion Headaches, dizziness, hallucinations Depression? May mask hypoglycemia Bronchospasm Contraindicated in patients with asthma or chronic obstructive pulmonary disease (copd) Bradycardia (check pulse) Shortness of breath Systemic hypotension Depression May cause blood sugar levels to rise or mask symptoms of low blood sugar (dm) Signs of hypoglycemia Rapid heart beat Anxious Sweaty Weak, dizzy, drowsy, faint Changes in vision Headache Chills Tremors Increased hunger Contraindications Asthma, copd Bradycardia, chf High cholesterol, uncontrolled diabetes? Pregnancy / nursing Category c Use with caution, animal studies have shown teratogenic effects on the developing fetus Benefit must outweigh risk Caution to those lactating Children Safety and effectiveness not established Additional information: Non-selective betablockers Long track record Cost effective $13 for 5 ml, $19 for 15 ml of tim 0.5% 15% non-responders Not as effective if on systemic bb Systemic bb reduces iop up to 30%

15 Negative effect on hdl Not as bad for carteolol What s new? No increased risk of depression Kaiserman i, et al. Ophthalmology. July Future use in combinations Dry eye treatment Artificial tears is the mainstay of initial topical treatment Preservative free Low viscosity (thinner consistency) Medium viscosity (medium consistency) High viscosity (thick consistency) Ointments Preservative free Low viscosity Medium viscosity High viscosity Ointments Dry Eye Treatment Cyclosporine 0.05% Ophthalmic emulsion Provides anti-inflammatory effects for ocular surface tissues and lacrimal glands Requires 3-4 months of continuous use to reach clinically significant effects and up to 6 months to achieve full therapeutic effects Nutrition and Dietary Supplements Omega-3 and Omega 6 fatty acids are fats your body needs but can t produce Omega-3 s-flaxseed oil and fish oil TheraTears Nutrition (4 capsules BID by mouth) Omega-6 s vegetable oil/shortening, dairy, beef Studies show a decreased risk of dry eye Higher dietary intake of omega-3 s Lower dietary ratio of omega-6 s vs. omega-3 s <4:1 (average in American diet 10:1) THANK YOU!

Managing the Patient with POAG

Managing the Patient with POAG Vision Institute Annual Fall Conference Mitchell W. Dul, OD, MS, FAAO mdul@sunyopt.edu Richard J. Madonna, MA, OD, FAAO rmadonna@sunyopt.edu Ocular Hypertension (OHT) Most