Pupillary Block, Aphakic Medication

  • Author: Deborah R Eezzuduemhoi, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: May 21, 2010
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Carbonic anhydrase inhibitors (CAIs)

Class Summary

By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, they may inhibit CA in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.

Acetazolamide (Diamox)

 

Reduces the formation of aqueous humor by direct inhibition of CA on secretory ciliary epithelium. More than 90% of CA must be inhibited before IOP reduction can occur. May reduce IOP by 40-60%. Effects are seen in about an hour, they peak in 4 h, and trough in about 12 h. Inhibits enzyme CA, reducing rate of aqueous humor formation, which in turn reduces IOP. Derived chemically from sulfa drugs. If one form is not well tolerated, another form may be better or lower dose of the drug may better tolerated.

Dorzolamide (Trusopt)

 

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 CA, reducing hydrogen ion secretion at renal tubule and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.

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Beta-adrenergic antagonists

Class Summary

The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous production.

Timolol ophthalmic (Timoptic, Blocadren)

 

Competes with catecholamines for beta2-adrenergic receptor sites, which results in a reduction of aqueous production. Maximal effect achieved in 1-2 h and lasts up to 24 h. Available in 0.25 and 0.5% concentrations.

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Oral hyperosmotic agents

Class Summary

Oral hyperosmotic agents reduce the IOP by drawing water out of the eye. Intravenous hyperosmotic agents cause marked diuresis and thereby reduce the IOP. The maximal effect is seen within 30 min and lasts for up to 4-6 h.

Glycerin (Ophthalgan, Osmoglyn)

 

Oral osmotic agent for reducing IOP. Able to increase tonicity of blood until finally metabolized and eliminated by the kidneys. Maximum reduction of IOP usually occurs 1 h after glycerin administration. Effect usually lasts approximately 5 h. Given as a solution in water or lemon juice. Strong diuretic. May cause nausea and vomiting. Not preferred in diabetics because it is metabolized to glucose. Maximum effect is seen in 1 h and lasts for 3 h.

Isosorbide dinitrate (Ismotic)

 

May be used to abort an acute attack of glaucoma. In the eyes, it may create an osmotic gradient between the plasma and ocular fluids and induce diuresis by elevating the osmolarity of the glomerular filtrate. These effects may in turn inhibit the tubular reabsorption of water. This treatment is preferred when less risk of nausea and vomiting than that posed by other oral hyperosmotic agents is desired.

Mannitol (Osmitrol, Resectisol)

 

Reduces elevated IOP when the pressure cannot be lowered by other means. Initially, assess for adequate renal function in adults by administering a test dose of 200 mg/kg, given IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h. In children, assess for adequate renal function by administering a test dose of 200 mg/kg, given IV over 3-5 min. Should produce a urine flow of at least 1 mL/h over 1-3 h.

Urea (Ureaphil)

 

Has a lower molecular weight than mannitol. Diuretic effect is less than that of mannitol.

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Cholinergic agents

Class Summary

Both direct and indirect-acting agents contract the longitudinal fibers of the ciliary muscle, which pulls scleral spur to open the trabecular meshwork with a resultant increase of the aqueous humor outflow.

Pilocarpine ophthalmic (Akarpine, Adsorbocarpine, Pilagan, Pilocar)

 

Direct acting parasympathomimetic, only on muscarinic sites. Low concentration leads to miosis. High concentration leads to pupillary block. Increases facility of outflow through the trabecular meshwork. Decreases uveoscleral outflow. Induces myopia. Not effective with very high IOP (eg, 40 mm Hg) due to ischemia. The pressure-lowering effect begins within 20 min, peaks in 1.5 h, and lasts up to 4 h. Continued therapy with this agent is only indicated in older patients who cannot tolerate a peripheral iridectomy or where iridotomy is not possible (eg, argon laser is not available).

The available concentrations are 1-4%. Once an initial reduction of IOP has been achieved with acetazolamide or timolol, a single drop of pilocarpine, preferably a 2% concentration, will break the angle closure associated with pupillary block.

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Contributor Information and Disclosures
Author

Deborah R Eezzuduemhoi, MD  Assistant Professor, Department of Ophthalmology and Visual Sciences, Texas Tech University, Health Sciences Center School of Medicine

Deborah R Eezzuduemhoi, MD is a member of the following medical societies: American Academy of Ophthalmology, American Academy of Pediatrics, and Women in Ophthalmology, Inc

Disclosure: Nothing to disclose.

Coauthor(s)

Deborah Wilson, MD  Director of Glaucoma Service, Assistant Professor, Department of Ophthalmology, Georgetown University Medical Center

Deborah Wilson, MD is a member of the following medical societies: American Academy of Ophthalmology and American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Neil T Choplin, MD  Adjunct Clinical Professor, Department of Surgery, Section of Ophthalmology, Uniformed Services University of Health Sciences

Neil T Choplin, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Association for Research in Vision and Ophthalmology, and California Medical Association

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

J James Rowsey, MD  Former Director of Corneal Services, St Luke's Cataract and Laser Institute, Florida

J James Rowsey, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for the Advancement of Science, American Medical Association, Association for Research in Vision and Ophthalmology, Florida Medical Association, Pan-American Association of Ophthalmology, Sigma Xi, and Southern Medical Association

Disclosure: Nothing to disclose.

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

References
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  9. Koc F, Kargi S, Biglan AW, et al. The aetiology in paediatric aphakic glaucoma. Eye. Dec 2006;20(12):1360-5. [Medline].

  10. Mandal AK, Bagga H, Nutheti R. Trabeculectomy with or without mitomycin-C for paediatric glaucoma in aphakia and pseudophakia following congenital cataract surgery. Eye. Jan 2003;17(1):53-62. [Medline].

  11. Tomey KF, Traverso CE. Neodymium-YAG laser posterior capsulotomy for the treatment of aphakic and pseudophakic pupillary block. Am J Ophthalmol. Nov 15 1987;104(5):502-7. [Medline].

  12. Tomey KF, Traverso CE. The glaucomas in aphakia and pseudophakia. Surv Ophthalmol. Sep-Oct 1991;36(2):79-112. [Medline].

  13. Zborowski-Gutman L, Treister G, Naveh N, et al. Acute glaucoma following vitrectomy and silicone oil injection. Br J Ophthalmol. Dec 1987;71(12):903-6. [Medline].

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