Medical Management



Medical Management


Malik Y. Kahook

Douglas J. Rhee



INTRODUCTION

Medical treatment of glaucoma began in the late 1800s with the use of eserine and pilocarpine. In the United States, glaucoma treatment is typically begun with topical medications. The short-term goal of medications is to lower intraocular pressure (IOP). The long-term goals are to prevent symptomatic visual loss while minimizing the side effects from the treatments.


DESCRIPTION AND PHYSIOLOGY

Unless there are extreme circumstances, such as an IOP higher than 40 mm Hg or an impending risk to central fixation, treatment is started using a so-called one-eyed therapeutic trial. Typically, one type of drop is started in only one eye with reexamination in 3 to 6 weeks to check for effectiveness. Effectiveness is determined by comparing the difference in IOP in the two eyes before therapy with the difference in IOP after initiating therapy. For example, if IOP is 30 mm Hg OD (oculus dexter; in the right eye) and 33 mm Hg OS (oculus sinister; in the left eye) before treatment, and, following treatment of the right eye, IOP is 20 mm Hg OD and 23 mm Hg OS, the drug is not having any effect. If the IOP after starting treatment is 25 mm Hg OD and 34 mm Hg OS, then the drug is having an effect.

It should be noted that the monocular trial when instituting medical therapy has been the topic of intensive studies over the past few years. Realini has reported that the monocular drug trial is of little clinical value in patients being treated with latanoprost. Bhorade and colleagues came to a similar conclusion in their study of prostaglandin analogues. Regardless, it is common practice to initiate medical therapy once glaucomatous optic neuropathy is diagnosed, and a firm understanding of the limited number of glaucoma therapeutics is necessary to choose the best therapy for each individual patient.

There are several different classes of medications. All medications work to lower IOP through varying pharmacologic mechanisms. IOP is determined by the balance between secretion and drainage of aqueous humor. All medications either decrease secretion or increase outflow. In the subsequent sections, the mechanism of action, common side effects, and contraindications for the different classes of medications are presented. Table 21-1 lists the medications
within each class that are available in the United States as of 2010 to 2011.

The side effects and contraindications described in this chapter are not a complete listing. I recommend that all clinicians read the package insert before prescribing any medication. The figures show sample bottles of medications available in the United States.








TABLE 21-1. Pharmacologic Agents Organized by Pharmacologic Class



















































































































Medication*


Available Strengths


Alpha Agonists


Apraclonidine (Iopidine)


0.5%, 1%


Brimonidine (Alphagan)


0.1% (with purite), 0.15%, 0.2%


Beta-Blockers



Betaxolol (Betoptic)


0.5%


Carteolol (Ocupress)


1%


Levobunolol (Betagan)


0.25%, 0.5%


Metipranolol (OptiPranolol)


0.3%


Timolol hemihydrate (Betimol)


0.25%, 0.5%


Timolol maleate (Timoptic)


0.25%, 0.5%


Carbonic Anhydrase Inhibitors—Oral



Acetazolamide (Diamox)


125-500 mg


Methazolamide (Neptazane, Glauctabs)


25-50 mg


Carbonic Anhydrase Inhibitors—Topical



Brinzolamide (Azopt)


1%


Dorzolamide (Trusopt)


2%


Hyperosmolar Agents



Glycerin (Osmoglyn)


50% solution


Isosorbide (Ismotic)


4% solution


Mannitol (Osmitrol)


5%-20% solution


Miotics



Physostigmine (Eserine)


0.25%


Pilocarpine hydrochloride (Pilocarpine, Pilocar)


0.25%, 0.5%, 1%, 2%, 4%, 6%


Pilocarpine nitrate (Pilagan)


1%, 2%, 4%


Prostaglandins



Bimatoprost (Lumigan)


0.01%, 0.03%


Latanoprost (Xalatan)


0.005%


Travoprost (Travatan)


0.004%


Unoprostone isopropyl (Rescula)


0.15%


Sympathomimetic Agents



Dipivefrin (Propine)


0.1%


Epinephrine (Epifrin)


0.5%, 1%, 2%


Combination Medications


Available Formulations


Dorzolamide/Timolol (Cosopt)


2%/0.5%


Brimonidine/Timolol (Combigan)


0.2%/0.5%


Brinzolamide/Brimonidine (Simbrinza)


1%/0.2%


* Trade names available in the United States are indicated in italics.




ALPHA AGONISTS


Mechanism of Action

• Activation of alpha-2 receptors in the ciliary body inhibits aqueous secretion (Fig. 21-1).


Side Effects

• Local irritation, allergy (Fig. 21-2), mydriasis, dry mouth, dry eye, hypotension, and lethargy



Comments

• Apraclonidine is for short-term use and prophylaxis of postlaser IOP spikes.







FIGURE 21-1. Alpha agonists. All trade-name alpha agonists available in the United States at the time of publication. From left to right: Alphagan (Allergan; Irvine, CA), Alphagan-P (Allergan; Irvine, CA), and Iopidine 0.5% (Alcon; Fort Worth, TX). Note: Iopidine 1% is not shown.






FIGURE 21-2. Allergic reaction from chronic brimonidine. Typical allergic reaction from brimonidine is a follicular conjunctivitis that occurs months to years after chronic use. The prevalence is dose related to the concentration of brimonidine, with lower concentrations having lower prevalence of allergic reactions. This is an extreme case in which an ectropion occurred as a result of periorbital skin excoriation and fibrosis. These findings resolved spontaneously over a few weeks of discontinuing the medication.



BETA-BLOCKERS


Mechanism of Action

• Blockade of the beta receptors in the ciliary body reduces IOP by decreasing aqueous humor production (Fig. 21-3).

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May 4, 2019 | Posted by in OPHTHALMOLOGY | Comments Off on Medical Management

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