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  • 2020–2021 BCSC Basic and Clinical Science Course™

    Go to Academy Store Learn more and Purchase.

    10 Glaucoma

    Chapter 12: Medical Management of Glaucoma and Ocular Hypertension

    Adrenergic Drugs

    β-Adrenergic Antagonists

    Mechanism of action

    Topical β-adrenergic antagonists, or β-blockers, lower IOP by inhibiting cyclic adenosine monophosphate (cAMP) production in the ciliary epithelium, thereby reducing aqueous humor secretion by 20%–50%, with a corresponding IOP reduction of 20%–30%. In healthy eyes, β-blocker administration reduces aqueous secretion and lowers IOP; interestingly, however, there is a compensatory reduction in aqueous outflow facility that dampens the magnitude of IOP reduction. The effect on aqueous production occurs within 1 hour of instillation and can last for up to 4 weeks after discontinuation of the medication. Because systemic absorption occurs, an IOP-lowering effect may also be observed in the untreated contralateral eye. β-Blockers have much less effect on aqueous production during sleep, as aqueous production is already reduced during the nocturnal period; thus, they are ineffective in lowering IOP during sleep.

    Available agents and dosing frequency

    In the United States and Europe, 5 topical β-adrenergic antagonists are approved for the treatment of glaucoma: (1) betaxolol, (2) carteolol, (3) levobunolol, (4) metipranolol, and (5) timolol. Betaxolol, the only topical β1-selective antagonist, is less effective in lowering IOP than the others, which are nonselective β-adrenergic antagonists. Most β-blockers are approved for twice-daily therapy. In many cases, the nonselective agents can be used once daily. Generally, dosing first thing in the morning is preferred in order to effectively blunt an early-morning pressure rise while minimizing the risk of systemic hypotension during sleep. Many nonselective β-blockers are available in more than 1 concentration. Clinical experience has shown that in many patients, timolol maleate 0.25% is as effective as timolol maleate 0.5% in lowering IOP.

    In approximately 10%–20% of patients treated with topical β-blockers, IOP is not significantly lowered. Patients already taking a moderate or high dose of a systemic β-blocker may experience little additional IOP lowering from the addition of a topical ophthalmic β-blocker. Extended use of β-blockers may result in tachyphylaxis due to receptor upregulation. Physiologic changes in the trabecular meshwork may occur in response to decreased IOP and aqueous humor flow rate, resulting in decreased outflow facility. The underlying disease process responsible for decreased outflow facility and IOP elevation may also worsen during the course of therapy.

    Adverse effects

    Topical β-blockers are generally very well tolerated when administered to individuals without specific contraindications. The ocular and systemic adverse effects of β-adrenergic antagonists are listed in Table 12-2. Plasma drug levels from topical medications can approach those achieved with systemic administration because of their absorption in the nasolacrimal drainage system and lack of first-pass hepatic metabolism. However, administering topical medications in a gel vehicle results in reduced systemic absorption and decreased plasma concentrations of β-blockers compared with the equivalent solution. Punctal occlusion also reduces systemic absorption.

    Systemic adverse effects of β-adrenergic antagonists include bronchospasm, bradycardia, increased heart block, systemic hypotension, reduced exercise tolerance, and central nervous system (CNS) depression. Patients with diabetes mellitus may experience reduced glucose tolerance and masking of hypoglycemic signs and symptoms. In addition, abrupt withdrawal of ophthalmic β-blockers can exacerbate symptoms of hyperthyroidism.

    Before a β-blocker is prescribed, the clinician should ask whether the patient has a history of asthma, because β-blockers may induce severe, life-threatening bronchospasm in susceptible patients. β2-Receptors are present in bronchial smooth muscle cells, and their inhibition results in bronchospasm in susceptible individuals. Because betaxolol is a β1-selective antagonist, it is safer than the nonselective β-blockers for use in patients with asthma. In addition, betaxolol may be less likely to cause depression. However, β-blocker–related adverse effects can still occur with its use.

    Prior to initiation of therapy with a topical β-blocker, the patient’s pulse should be measured; the β-blocker should be withheld if the pulse rate is slow or if more than first-degree heart block is present. Administration of topical β-blockers has been associated with the development of signs and symptoms of myasthenia gravis in patients without a preexisting diagnosis and can exacerbate the condition in patients already known to have the disease. The mechanism by which this occurs is unclear.

    Other adverse effects of β-blockers include lethargy, mood changes, depression, altered mentation, light-headedness, syncope, visual disturbance, corneal anesthesia, punctate keratitis, allergy, impotence, reduced libido, and alteration of serum lipids (reduction in high-density lipoprotein). In children, β-blockers should be used with caution, because of the relatively high systemic levels achieved.

    Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.

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