eMedicine Specialties > Ophthalmology > Pupil

Pupillary Block, Aphakic: Treatment & Medication

Author: Deborah R Eezzuduemhoi, MD, Assistant Professor, Department of Ophthalmology and Visual Sciences, Texas Tech University, Health Sciences Center School of Medicine
Coauthor(s): Deborah Wilson, MD, Director of Glaucoma Service, Assistant Professor, Department of Ophthalmology, Georgetown University Medical Center
Contributor Information and Disclosures

Updated: Jul 23, 2008

Treatment

Medical Care

The management of pupillary block involves early recognition, relief of the pupillary block, medical treatment, and surgical treatment.

  • Medical treatment consists of intensive cycloplegia, mydriasis, and aqueous suppressants.
  • If the eye is inflamed, if the cornea is hazy, or if a peripheral iridotomy cannot be performed immediately, then the following agents are recommended:
    • Mydriatic agents (eg, cyclopentolate 2% and phenylephrine 2.5% q15min for 4 doses)
    • Carbonic anhydrase inhibitors (eg, acetazolamide, two 250-mg tab PO or 500 mg IV)
    • Topical beta-blockers (eg, timolol 0.5%), 1 dose
    • Topical alpha-agonists (eg, brimonidine 0.15% or apraclonidine 1%), 1 dose
  • In very early cases, relieving the block may be possible by the vigorous use of strong mydriatics alone or with hyperosmotic agents (glycerol 3 mL/kg PO, mannitol 1-2 g/kg IV). Posterior synechiae may be broken and herniation of a mushroomlike plug of vitreous may be relieved.

Surgical Care

Surgical care consists of peripheral iridotomy, peripheral iridectomy, or incision of the hyaloid membrane. The length of time that the angle had remained closed is crucial in deciding the appropriate treatment.

  • Less than 2 weeks
    • Usually, a peripheral iridotomy or incision of the hyaloid membrane is adequate to relieve the block. Sometimes multiple iridotomies are needed because of loculation by vitreous to the posterior surface of the iris, resulting in multiple pockets of trapped aqueous.
    • Argon laser iridotomy can promptly relieve pure pupillary block by vitreous or other causes.
    • Photomydriasis (pupilloplasty) using argon laser is another modality of treatment.
      • Radial rows of contraction burns can be applied for 360 degrees to create symmetric pupillary dilation or just in one quadrant to create focal dilation. This mode of treatment is used when creating an iridotomy is impeded by corneal edema.
      • Laser peripheral iridoplasty using low energy contraction burns may also be used to deepen the anterior chamber angle. This may be combined with a pupilloplasty.
    • The Nd:YAG laser can be used to perform peripheral iridotomy, especially in an inflamed eye.
    • A thick brown iris may require treatment with both argon laser and Nd:YAG laser. If laser treatment is not successful, one may proceed as in the treatment of pupillary block greater than 2 weeks' duration.
    • Nd:YAG laser posterior capsulotomy is an alternative to laser iridotomy in selected cases of pupillary block following extracapsular cataract extraction without an intraocular lens.
    • A smaller than optical capsulotomy is recommended to lyse the adhesions. This may not be the treatment of choice because of the possibility of subsequent pupillary block by the vitreous.
    • Iris sphincterectomies may be performed with the Nd:YAG laser.
  • Greater than 2 weeks
    • Laser treatment is often not successful. Surgical iridectomy is the classic treatment of pupillary block in aphakic eyes.
    • Pars plana vitrectomy is another modality that may be performed.
    • If the angle has closed, a trabeculectomy with antimetabolites or a tube shunt procedure might be required.
    • Aphakic eyes with silicone oil or expansile gas placement require a large inferior iridotomy in the 6-o'clock position to decrease the risk of aphakic pupillary block.

Consultations

A glaucoma specialist should be consulted.

Medication

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

Carbonic anhydrase inhibitors (CAIs)

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.

Adult

500 mg loading dose, then 250 mg q6h PO or 500 mg sequel (sustained-release) bid

Pediatric

10-15 mg/kg PO q6-8h
Alternatively, 5-10 mg/kg IV/IM q4-6h

Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Measures that may help reduce side effects include supplemental alkali therapy and taking medication with meals


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.

Adult

1 gtt tid in affected eye(s)

Pediatric

Not established

Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CAIs

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Local ocular adverse effects, primarily conjunctivitis and lid reactions, may occur with long-term administration of dorzolamide (discontinue therapy and evaluate patient before restarting therapy)

Beta-adrenergic antagonists

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


Timolol (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.

Adult

1 gtt of 0.25% or 0.5% in affected eye(s) bid; if IOP is maintained at satisfactory levels, change dosage to 1 gtt in affected eye(s) qd

Pediatric

Not established

May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects)

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second-degree and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, chronic obstructive pulmonary disease, mental changes (especially in the elderly)

Oral hyperosmotic agents

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.

Adult

1-2 g/kg PO and repeat q5h prn
Alternatively, 1 mL/kg PO as a 50% solution in juice

Pediatric

Not established

Documented hypersensitivity; frank or impending acute pulmonary edema, anuria, severe dehydration, and severe cardiac decompensation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Administer orally, never parenterally; for oral use only; avoid in acute urinary retention in preoperative period; continued use may result in weight gain; caution in hypervolemia, diabetes, individuals who are severely dehydrated, confused mental states, congestive heart disease, and cardiac, renal, or hepatic disease


Isosorbide (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.

Adult

Initial dose: 1.5 g/kg (50% solution)
Dose range: 1-3 g/kg bid/qid

Pediatric

Not established

Documented hypersensitivity; anuria; severe dehydration; frank or impending acute pulmonary edema; severe cardiac decompensation

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use repetitive doses with caution, particularly in patients with diseases associated with salt retention


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.

Adult

1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over a period as short as 30 min

Pediatric

Not established

May decrease serum lithium levels

Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active intracranial bleeding; progressive heart failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Carefully evaluate cardiovascular status before rapid administration of mannitol since a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood


Urea (Ureaphil)

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

Adult

1-1.5 g/kg; 0.45-0.68 g/lb (30% solution) by slow infusion; not to exceed 4 mL/min or 120 g/d

Pediatric

<2 years: 0.1 g/kg may be adequate
>2 years: 0.5-1.5 g/kg

May decrease effects of lithium

Documented hypersensitivity; severely impaired renal function, active intracranial bleeding, marked dehydration, frank liver failure; infusion into veins of lower extremities in elderly persons may cause phlebitis and thrombosis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use if intracranial bleeding present, unless prior to surgical intervention to control hemorrhage (reduction of brain edema by urea may result in reactivation of intracranial bleeding); may increase risk of venous thrombosis and hemoglobinuria in patients who are hypothermic; caution in renal impairment

Cholinergic agents

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 (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.

Adult

Solution: 1 or 2 gtt tid/qid
Gel: 0.5-inch ribbon in lower conjunctival sac of affected eye(s) hs

Pediatric

Not established

May be ineffective when used concomitantly with nonsteroidal anti-inflammatory agents

Documented hypersensitivity; acute inflammatory disease of anterior chamber

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in acute cardiac failure, peptic ulcer, hyperthyroidism, GI spasm, bronchial asthma, Parkinson disease, recent MI, urinary tract obstruction, and hypertension or hypotension

More on Pupillary Block, Aphakic

Overview: Pupillary Block, Aphakic
Differential Diagnoses & Workup: Pupillary Block, Aphakic
Treatment & Medication: Pupillary Block, Aphakic
Follow-up: Pupillary Block, Aphakic
References

References

  1. Kumar A, Kedar S, Garodia VK. Angle closure glaucoma following pupillary block in an aphakic perfluoropropane gas-filled eye. Indian J Ophthalmol. Sep 2002;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. Mar 1987;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. Oct 1972;74(4):571-80. [Medline].

  7. Cotlier E. Aphakic flat anterior chamber. IV. Treatment of pupillary block by iridectomy. Arch Ophthalmol. Jul 1972;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. Nov 1966;76(5):633-4. [Medline].

  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].

Further Reading

Keywords

pupillary block, aphakic pupillary block, aphakia, pupillary block glaucoma, angle closure, cataract surgery, cataracts, cataract extraction, crystalline lens, lens implantation, lens subluxation, anterior pupillary block, posterior pupillary block, intraocular trauma

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.

Medical Editor

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.

Pharmacy Editor

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.

Managing Editor

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.

CME Editor

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.

 
 
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