eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Angle Recession: Treatment & Medication

Author: Brian R Sullivan, MD, Associate Professor, Department of Ophthalmology, University of Texas Southwestern Medical Center
Contributor Information and Disclosures

Updated: Jan 21, 2009

Treatment

Medical Care

The necessity of initiating treatment of angle-recession glaucoma depends on the severity of the initial injury and the somewhat variable clinical course as healing progresses. Normotensive eyes with angle recession of more than 180° should be routinely reexamined for an indefinite period to monitor for the development of late glaucoma.

• In patients with an abnormal elevation of IOP, the decision to begin therapy is based on the clinician's overall assessment of the risk of vision loss.
  • The severity of IOP elevation, optic nerve appearance, and visual field findings contribute to the decision-making process.
  • Treatment almost always is indicated when the IOP is greater than an arbitrary range of 25-28 mm Hg and/or when glaucomatous optic nerve or visual field changes are documented over time.
• After the diagnosis of angle recession is established, its management is similar to that of POAG, with a few special considerations.
  • Use of topical aqueous suppressants in the initial medical treatment is preferred; these include beta-antagonists, alpha-agonists, and carbonic anhydrase inhibitors.
  • Prostaglandin analogs, which increase uveoscleral outflow, have a theoretical benefit in angle recession because the trabecular meshwork is thought to be dysfunctional in such cases.
  • Use caution in administering miotic agents because pilocarpine has been reported to cause a paradoxical elevation of IOP in angle recession, presumably due to a reduction of uveoscleral outflow.
  • Atropine has been reported to reduce IOP in angle-recession glaucoma; therefore, cycloplegic agents may have a role in treatment.
  • A trial of a cycloplegic agent should be reserved either for cases involving failure of conventional glaucoma therapy or for cases with other indications for cycloplegia (eg, inflammation).
• The response to medical therapy in angle-recession glaucoma is variable.
  • Topical medical treatment may be effective in cases of mild-to-moderate angle recession, while elevated IOP of eyes with extensive angle injury eventually may become refractory to medications.
  • Severe early cases may fail to show an initial response to aggressive medical treatment, indicating a poorer overall prognosis.

Surgical Care

Surgical intervention in angle-recession glaucoma is usually indicated when maximally tolerated medical treatment has failed and when the risk of progressive visual loss outweighs the estimated risk of the planned surgical management. In general, outcomes of surgical treatment are less favorable than those of POAG.

• Argon laser trabeculoplasty
  • Argon laser trabeculoplasty (ALT) has been associated with short-term success, though the procedure has been reported to have poor long-term effectiveness, particularly in eyes with more than 180° of angle recession.
  • IOP elevation may become worse in response to ALT.
  • In eyes with less than 180° of angle recession, ALT may be beneficial if applied to only the trabecular meshwork of the nonrecessed portions of the anterior-chamber angle.
• Alternative laser procedures
  • Nd:YAG laser trabeculopuncture (YLT) has been used with variable success. A 1992 study demonstrated a 100% failure rate in eyes with 360° angle recession.²⁴
  • Currently, YLT is not recommended for the routine management of angle-recession glaucoma.
  • Other laser procedures that have shown promise are transscleral krypton laser cyclophotocoagulation, transpupillary argon laser cyclophotocoagulation, and endoscopic cyclophotocoagulation.
• Filtration surgery
  • Filtration surgery has a success rate lower than that of POAG.
  • Trabeculectomy in eyes with angle recession is associated with decreased postoperative reduction in IOP, increased rates of bleb fibrosis and bleb failure, and increased dependence on postoperative medical treatment of glaucoma.²⁵
  • The adjunctive use of antimetabolites, particularly mitomycin C, can improve the success of trabeculectomy. This finding suggests that an antimetabolite should be used during the initial filtering procedure. A 2001 report described effective results with an acceptable complication rate in such cases.²⁶
• Tube shunt devices
  • Benefits with the implantation of tube shunt devices have been demonstrated, but outcomes are reportedly less successful in angle recession than in other types of refractory glaucoma.
  • A 1993 study showed the superior results of trabeculectomy with antimetabolite over Molteno implantation in cases of posttraumatic angle-recession glaucoma.

Consultations

• Consultation with a glaucoma specialist should be considered in cases with an uncertain diagnosis, with early severe IOP elevation, with a poor response to treatment, or with advanced visual field loss.
• Depending on the presence of other posttraumatic ocular or orbital abnormalities, consider referring the patient to subspecialists in corneal and/or external disease, oculoplastics retinal disease, or neuro-ophthalmology.

Medication

The preferred drugs have the pharmacologic action of aqueous suppression. A beta-antagonist is the common first choice, with subsequent additions of an alpha-agonist and/or a carbonic anhydrase inhibitor, as necessary. Prostaglandin analogs probably have a useful role, but the use of miotic agents is controversial and not routinely recommended.

The goal of therapy is IOP reduction. Medications must often be used long term. IOP should be monitored whenever medications are discontinued or changed, and therapy should be restarted, if necessary.

Beta-agonists

Topical beta-adrenergic receptor antagonists decrease the production of aqueous humor by the ciliary body. Adverse effects are due to systemic absorption of the drug, which causes decreased cardiac output and bronchoconstriction. These agents may cause bronchospasm, bradycardia, heart block, or hypotension. Monitor the patient's pulse rate and blood pressure. Patients may be instructed to perform punctal occlusion after administering the drops. Some patients may have depression or anxiety, and sexual dysfunction may occur or worsen.

Timolol maleate (Timoptic, Timoptic XE) 0.25%, 0.5%

May reduce elevated or normal IOP, with or without glaucoma, by reducing aqueous humor production.

Levobunolol (Betagan, AKBeta) 0.25%, 0.5%

Nonselective beta-adrenergic blocking agent. Lowers IOP by reducing aqueous humor production.

Carteolol HCl (Ocupress) 1%

Blocks beta1- and beta2-receptors. Has mild intrinsic sympathomimetic effects.

Betaxolol (Betoptic) 0.25%, 0.5%

Selectively blocks beta1-adrenergic receptors. Reduces IOP by reducing aqueous humor production.

Adrenergic agonists

Topical adrenergic agonists (sympathomimetics) decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and hypersensitivity.

Apraclonidine (Iopidine) 0.5%, 1%

Selective alpha-adrenergic agonist that suppresses aqueous production. Minimal cardiovascular effect.

Brimonidine (Alphagan)

Selective alpha2-receptor agonist. Reduces aqueous humor formation. Possibly increases uveoscleral outflow.

Carbonic anhydrase inhibitors

These drugs reduce secretion of the aqueous humor by inhibiting carbonic anhydrase in the ciliary body. These agents are less effective than many other classes of drugs and have a shorter duration of action. Adverse effects are relatively rare but include superficial punctate keratitis, acidosis, paresthesias, nausea, depression, and lassitude. Corneal decompensation has been reported when this class of drugs is used in patients with corneal endothelial dysfunction.

Dorzolamide HCl (Trusopt) 2%

Used concomitantly with other topical ophthalmic drugs to lower IOP. If > 1 ophthalmic drug used, administer >10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule. Increases renal excretion of sodium, potassium bicarbonate, and water to decrease aqueous humor production.

Brinzolamide (Azopt) 1%

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 >1 topical ophthalmic drug used, administer >10 min apart.

Dorzolamide HCl/timolol maleate (Cosopt)

Dorzolamide is carbonic anhydrase inhibitor that may decrease aqueous humor secretion, decreasing IOP; presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport. Timolol is nonselective beta-adrenergic receptor blocker; decreases IOP by decreasing aqueous humor secretion. Administered together bid may reduce IOP more than either alone, but reduction not as much as that with concomitant dorzolamide tid and timolol bid.

Acetazolamide (Diamox, Diamox Sequels)

Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, decreasing IOP.

Methazolamide (Neptazane, GlaucTabs)

Reduces aqueous humor formation by inhibiting carbonic anhydrase, decreasing IOP.

Prostaglandin analogs

These selective agonists act on prostaglandin receptors in the eye to lower IOP by increasing uveoscleral outflow.

Latanoprost (Xalatan)

Decreases IOP by increasing outflow of aqueous humor.

Bimatoprost ophthalmic solution (Lumigan)

Prostamide analog with ocular hypotensive activity. Mimics IOP-lowering activity via the prostamide pathway. Used to reduce IOP in open-angle glaucoma or ocular hypertension.

Travoprost ophthalmic solution (Travatan)

Prostaglandin F2-alpha analog. Selective prostaglandin F2 receptors prostanoid receptor agonist; may reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

Unoprostone ophthalmic (Rescula)

Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist; may reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

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