Medscape is available in 5 Language Editions – Choose your Edition here.


Aphakic Pupillary Block Medication

  • Author: Mitchell V Gossman, MD; Chief Editor: Hampton Roy, Sr, MD  more...
Updated: May 02, 2014

Medication Summary

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


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.


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.


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.


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.

Contributor Information and Disclosures

Mitchell V Gossman, MD Partner and Vice President, Eye Surgeons and Physicians, PA; Medical Director, Central Minnesota Surgical Center; Clinical Associate Professor, University of Minnesota Medical School

Mitchell V Gossman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, Minnesota Medical Association, North American Neuro-Ophthalmology Society, Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

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

Disclosure: Nothing to disclose.

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

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, Sigma Xi, Southern Medical Association, Pan-American Association of Ophthalmology

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, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

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, Association for Research in Vision and Ophthalmology, American Glaucoma Society, California Medical Association

Disclosure: Nothing to disclose.


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.

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.

  1. Kumar A, Kedar S, Garodia VK. Angle closure glaucoma following pupillary block in an aphakic perfluoropropane gas-filled eye. Indian J Ophthalmol. 2002 Sep. 50(3):220-1. [Medline].

  2. Shaffer RN. The role of vitreous detachment in aphakic and malignant glaucoma. Trans Am Acad Ophthalmol Otolaryngol. 1954. 58:217-231.

  3. Posner A. Postcataract glaucoma associated with shallow anterior chamber. Int Ophthalmol Clin. 1964. 4:1029-1043.

  4. Beekhuis WH, Ando F, Zivojnovic R, et al. Basal iridectomy at 6 o'clock in the aphakic eye treated with silicone oil: prevention of keratopathy and secondary glaucoma. Br J Ophthalmol. 1987 Mar. 71(3):197-200. [Medline].

  5. Chandler PA. Glaucoma from pupillary block in aphakia. Arch Ophthalmol. 1962. 7:44-47.

  6. Chandler PA, Simmons RJ. Gonioscopy during surgery for aphakic eyes with pupillary block. Am J Ophthalmol. 1972 Oct. 74(4):571-80. [Medline].

  7. Cotlier E. Aphakic flat anterior chamber. IV. Treatment of pupillary block by iridectomy. Arch Ophthalmol. 1972 Jul. 88(1):22-6. [Medline].

  8. Jaffe NS, Light DS. The danger of air pupillary block glaucoma in cataract surgery with osmotic hypotonia. Arch Ophthalmol. 1966 Nov. 76(5):633-4. [Medline].

  9. Koc F, Kargi S, Biglan AW, et al. The aetiology in paediatric aphakic glaucoma. Eye. 2006 Dec. 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. 2003 Jan. 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. 1987 Nov 15. 104(5):502-7. [Medline].

  12. Tomey KF, Traverso CE. The glaucomas in aphakia and pseudophakia. Surv Ophthalmol. 1991 Sep-Oct. 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. 1987 Dec. 71(12):903-6. [Medline].

All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.