Glaucoma, Angle Closure, Acute Medication
- Author: Robert J Noecker, MD, MBA; Chief Editor: Hampton Roy, Sr, MD more...
The medical therapy for acute ACG is directed toward preparing the patient for laser or incisional iridotomy, which will create passage through the iris from the posterior to anterior chamber and will break an acute attack. IOP must be returned to normal, and the cornea must be cleared before a definitive procedure can be undertaken. In acute ACG, several drugs from different classes are used simultaneously to accelerate and maximize their pressure-lowering effects.
Topical adrenergic agonists, or sympathomimetics, decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and allergenicity.
Selective alpha2-receptor that reduces aqueous humor formation and possibly increases uveoscleral outflow.
Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Reduces IOP whether or not accompanied by glaucoma. Selective alpha-adrenergic agonist without significant local anesthetic activity. Has minimal cardiovascular effect.
Topical beta-adrenergic receptor antagonists decrease aqueous humor production by the ciliary body. Adverse effects of the beta-blockers are due to systemic absorption of the drug and include decreased cardiac output and bronchial constriction. In susceptible patients, this may cause bronchospasm, bradycardia, heart block, or hypotension. Pulse rate and blood pressure should be monitored in patients receiving topical beta-blocker therapy, and punctal occlusion may be performed after administration of the drops.
Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production
Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor.
May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor.
Miotic agents (parasympathomimetics)
Contract ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous. Miosis results from action of these drugs on pupillary sphincter. Adverse effects include brow ache, induced myopia, and decreased vision in low light.
A naturally occurring alkaloid, pilocarpine mimics muscarinic effects of acetylcholine at postganglionic parasympathetic nerves. Directly stimulates cholinergic receptors in the eye, decreasing resistance to aqueous humor outflow.
Instillation frequency and concentration are determined by patient's response. Individuals with heavily pigmented irides may require higher strengths. If other glaucoma medication also is being used, at bedtime, use gtt at least 5 min before gel. May use alone, or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.
Increase uveoscleral outflow of the aqueous. One mechanism of action may be through induction of metalloproteinases in ciliary body, which breaks down extracellular matrix, thereby reducing resistance to outflow through ciliary body.
Decreases IOP by increasing outflow of aqueous humor.
Carbonic anhydrase inhibitors
Reduce secretion of aqueous humor by inhibiting carbonic anhydrase in ciliary body. In acute ACG, may be given systemically but are used topically in patients with refractory open-angle glaucoma. Topical formulations are less effective, and their duration of action is shorter than many other classes of drugs. Adverse effects of topical carbonic anhydrase inhibitors are relatively rare, but they include superficial punctate keratitis, acidosis, paresthesias, nausea, depression, and lassitude.
Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute ACG when delay of surgery desired to lower IOP.
Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.
Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.
Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than one topical ophthalmic drug is being used, administer drugs at least 10 min apart.
CA inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.
Timolol is a nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion and may slightly increase outflow facility. Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly.
Shields MB. Textbook of Glaucoma. 4th ed. 1998.
Cantor L, et al. Glaucoma. Basic and Clinical Science Course. Section 10. 1996-7.
Epstein DL, Allingham RR, Schuman JS. Chandler and Grant's Glaucoma. 4th ed. 1997.
Hitchings RA. Glaucoma: current thinking. Br J Hosp Med. 1996 Mar 20-Apr 2. 55(6):312-4. [Medline].
Wang BS, Narayanaswamy A, Amerasinghe N, Zheng C, He M, Chan YH, et al. Increased iris thickness and association with primary angle closure glaucoma. Br J Ophthalmol. 2011 Jan. 95(1):46-50. [Medline].
Tan SZ, Sampat K, Rasool S, Nolan D. Unilateral acute angle closure glaucoma. BMJ Case Rep. 2013 Feb 25. 2013:[Medline].
Xu L, Cao WF, Wang YX, Chen CX, Jonas JB. Anterior chamber depth and chamber angle and their associations with ocular and general parameters: the Beijing Eye Study. Am J Ophthalmol. 2008 May. 145(5):929-36. [Medline].
Ah-Kee EY, Egong E, Shafi A, Lim LT, Yim JL. A review of drug-induced acute angle closure glaucoma for non-ophthalmologists. Qatar Med J. 2015. 2015 (1):6. [Medline].
Czyz CN, Clark CM, Justice JD, Pokabla MJ, Weber PA. Delayed Topiramate-induced Bilateral Angle-Closure Glaucoma. J Glaucoma. 2013 Apr 29. [Medline].
Nolan W. Anterior segment imaging: ultrasound biomicroscopy and anterior segment optical coherence tomography. Curr Opin Ophthalmol. 2008 Mar. 19(2):115-21. [Medline].
Sihota R, Dada T, Gupta R, et al. Ultrasound biomicroscopy in the subtypes of primary angle closure glaucoma. J Glaucoma. 2005 Oct. 14(5):387-91. [Medline].
Marchini G, Chemello F, Berzaghi D, Zampieri A. New findings in the diagnosis and treatment of primary angle-closure glaucoma. Prog Brain Res. 2015. 221:191-212. [Medline].
Sng CC, Aquino MC, Liao J, Zheng C, Ang M, Chew PT. Anterior segment morphology after acute primary angle closure treatment: a randomised study comparing iridoplasty and medical therapy. Br J Ophthalmol. 2015 Aug 20. [Medline].
Liesegang TJ. Glaucoma: changing concepts and future directions. Mayo Clinic Proceedings. 1996. 71:689-694.
Lai JS, Tham CC, Chan JC. The clinical outcomes of cataract extraction by phacoemulsification in eyes with primary angle-closure glaucoma (PACG) and co-existing cataract: a prospective case series. J Glaucoma. 2006 Feb. 15(1):47-52. [Medline].
Yao J, Chen Y, Shao T, Ling Z, Wang W, Qian S. Bilateral Acute Angle Closure Glaucoma as a Presentation of Vogt-Koyanagi-Harada Syndrome in Four Chinese Patients: A Small Case Series. Ocul Immunol Inflamm. 2013 May 29. [Medline].