Updated: Jul 23, 2008
Aphakia, the absence of the crystalline lens, may occur as a result of trauma, lens subluxation or dislocation, or surgical management of a visually significant cataract. Pupillary block is a complication of cataract surgery with or without lens implantation. Pupillary block in aphakia was a significant complication following round-pupil cataract extraction (without sector iridectomy). This is also possible if an iridectomy was performed but was small and placed in the extreme periphery.
Pupillary block is the most common mechanism of angle closure after cataract extraction. This mechanism can be divided into 2 types, namely, anterior pupillary block and posterior pupillary block. A firm apposition between the pupillary margin and other surfaces anterior or posterior to the iris may lead to a pupillary block. The pupillary aperture may be obstructed by the anterior hyaloid surface, the intraocular lens, or the posterior capsule. A postoperative inflammation following an intracapsular cataract extraction may cause complete posterior synechiae between the iris and the intact anterior hyaloid membrane. A shallow anterior chamber favors formation of these adhesions. Adhesions may occur just between the pupillary margin and the anterior hyaloid surface. Such an occlusion is characterized as anterior pupillary block. The aqueous accumulates between the vitreous and the iris causing the peripheral iris to balloon forward.
A distinct mechanism is seen following extracapsular cataract extraction. A greater amount of postoperative inflammation, due to sensitivity to lenticular cortical material, leads to iridocapsular adhesions. This is seen more frequently after congenital cataract surgery. The aqueous humor accumulates between the iris-capsule diaphragm and the anterior hyaloid face, an area known as the canal of Petit. The pressure from the aqueous trapped in the posterior chamber displaces the iris forward. This is posterior pupillary block. The block impedes the forward movement of the aqueous to the anterior chamber leading to iris bombé, obstruction of the angle, and possible formation of peripheral anterior synechiae.
The absence of an iridectomy facilitates the development of pupillary block. Occasionally, this may also occur in eyes with a visible iridectomy if the iridectomy becomes occluded by iridocapsular adhesions.
A similar mechanism of pupillary block is seen with phacomorphic glaucoma and is referred to as anterior aqueous misdirection perilenticular. The aqueous humor accumulates around and behind the crystalline lens leading to lens-iris contact and the obstruction of anterior aqueous movement.
See related CME at Highlights of the American Glaucoma Society 2008 Annual Meeting.
While no data exist, pupillary block was common during the era of intracapsular cataract extraction. Many cases are asymptomatic and are only recognized during routine examination. The time of presentation is variable. Pupillary block may present in the immediate postoperative period but has been described from weeks to even years after surgery.
Congenital cataracts should be removed early in order to achieve the best possible visual outcome. Pupillary block with secondary angle-closure glaucoma within a few months following surgery has been linked to the cataract extraction. It seems that there is a need to reevaluate the appropriate time for cataract surgery in infants.
According to one study, 11% cases of silicone oil injection in aphakic patients resulted in angle closure and high intraocular pressure (IOP) due to obstruction and tamponade of the trabecular meshwork.
In aphakia, pupillary block impedes the forward movement of the aqueous through the pupillary aperture. With continuous production of aqueous the peripheral iris bows forward (iris bombé). This condition then leads to obstruction of the iridocorneal angle; formation of peripheral anterior synechiae (PAS), further aggravating the passage of aqueous toward the angle; rise in the IOP; and glaucomatous disc damage and associated visual field defects.
In this era of intraocular lenses, pupillary block is seen not only in older individuals who are rendered aphakic but also in infants who undergo surgery for congenital cataracts.
Slit lamp examination
A number of conditions predispose to the development of aphakic pupillary block, to include the following:
Choroidal Detachment
Glaucoma, Malignant
The management of pupillary block involves early recognition, relief of the pupillary block, medical treatment, and surgical treatment.
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.
A glaucoma specialist should be consulted.
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.
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.
500 mg loading dose, then 250 mg q6h PO or 500 mg sequel (sustained-release) bid
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
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Measures that may help reduce side effects include supplemental alkali therapy and taking medication with meals
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.
1 gtt tid in affected eye(s)
Not established
Coadministration with high-dose salicylate therapy may increase toxicity; may have additive systemic effects if patient is already on oral CAIs
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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)
The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous production.
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.
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
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
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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 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.
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.
1-2 g/kg PO and repeat q5h prn
Alternatively, 1 mL/kg PO as a 50% solution in juice
Not established
None reported
Documented hypersensitivity; frank or impending acute pulmonary edema, anuria, severe dehydration, and severe cardiac decompensation
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
Initial dose: 1.5 g/kg (50% solution)
Dose range: 1-3 g/kg bid/qid
Not established
None reported
Documented hypersensitivity; anuria; severe dehydration; frank or impending acute pulmonary edema; severe cardiac decompensation
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Use repetitive doses with caution, particularly in patients with diseases associated with salt retention
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.
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
Not established
May decrease serum lithium levels
Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active intracranial bleeding; progressive heart failure
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
Has a lower molecular weight than mannitol. Diuretic effect is less than that of mannitol.
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
<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
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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
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.
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.
Solution: 1 or 2 gtt tid/qid
Gel: 0.5-inch ribbon in lower conjunctival sac of affected eye(s) hs
Not established
May be ineffective when used concomitantly with nonsteroidal anti-inflammatory agents
Documented hypersensitivity; acute inflammatory disease of anterior chamber
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in acute cardiac failure, peptic ulcer, hyperthyroidism, GI spasm, bronchial asthma, Parkinson disease, recent MI, urinary tract obstruction, and hypertension or hypotension
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].
Shaffer RN. The role of vitreous detachment in aphakic and malignant glaucoma. Trans Am Acad Ophthalmol Otolaryngol. 1954;58:217-231.
Posner A. Postcataract glaucoma associated with shallow anterior chamber. Int Ophthalmol Clin. 1964;4:1029-1043.
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].
Chandler PA. Glaucoma from pupillary block in aphakia. Arch Ophthalmol. 1962;7:44-47.
Chandler PA, Simmons RJ. Gonioscopy during surgery for aphakic eyes with pupillary block. Am J Ophthalmol. Oct 1972;74(4):571-80. [Medline].
Cotlier E. Aphakic flat anterior chamber. IV. Treatment of pupillary block by iridectomy. Arch Ophthalmol. Jul 1972;88(1):22-6. [Medline].
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].
Koc F, Kargi S, Biglan AW, et al. The aetiology in paediatric aphakic glaucoma. Eye. Dec 2006;20(12):1360-5. [Medline].
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].
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].
Tomey KF, Traverso CE. The glaucomas in aphakia and pseudophakia. Surv Ophthalmol. Sep-Oct 1991;36(2):79-112. [Medline].
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].
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
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.
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.
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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