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.
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.[1, 2]
Mortality/Morbidity
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.
Age
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.
If the pupillary block is treated promptly, IOP will return to the reference range, ocular symptoms will be ameliorated, and the visual acuity will improve.
Slit lamp examination findings for aphakic pupillary block may include the following:
Cornea: Epithelial and stromal edema may be seen.
Anterior chamber
Overall shallowing of the anterior chamber with a normal or elevated IOP is the usual presenting sign of pupillary block. However, iris bombé is the classic presentation.
The disparity between the central and the peripheral anterior chamber depth, with a deeper central depth is a result of posterior synechiae.
The presence of inflammatory debris or blood may cause an unevenness in the anterior chamber depth.
Pupil
Seclusio pupillae or posterior synechiae may be seen.
A mushroomlike plug of vitreous protruding through the pupil may be seen.
Gonioscopy
Forward bowing and convexity of the iris periphery is seen on gonioscopic evaluation.
Shallowing and then flattening of the anterior chamber results in the loss of view of the iridocorneal angle structures.
Initially, an appositional closure can be present, which may lead to permanent angle closure at a later stage.
A number of conditions predispose to the development of aphakic pupillary block, to include the following:
Wound leakage can result in shallowing of the anterior chamber and can be associated with hypotony. This may be exaggerated by the rotation of the ciliary body and displacement of the vitreous, which can promote blockage of the pupillary aperture.
Complete adhesion along the pupillary margin (seclusio pupillae) may result from any cause of severe postoperative inflammation (eg, retained lens material).
Inadequate postoperative mydriasis
Air bubble
Injection of air into the anterior chamber of a hypotonic eye following cataract extraction has been shown to be potentially hazardous.
Preoperatively, some eyes are rendered hypotonus by osmotic agents (eg, mannitol, glycerol), and these eyes may accept a considerable amount of air at the end of the surgery.
With resumption of normal fluid volume, the air will be compressed and forced into the posterior chamber, causing the iris to move forward leading to pupillary block. This condition is usually self-limited with resorption of the air bubble.
Gas bubble
In an aphakic eye, a gas bubble anterior or posterior to the iris may interfere temporarily with the passage of aqueous humor across the pupil and predispose to pupillary block.
Pupillary block arises if the volume is of substantial amount as in the case of expanding gases (eg, sulfur hexafluoride [SF6], octafluoropropane [C3 F8]) used in retinal reattachment surgery. Following expansion, these gases may occupy the entire vitreous cavity and displace the iris forward, subsequently blocking the pupil.
Kumar et al described a case of aphakic pupillary block following the use of perfluoropropane (or octafluoropropane) (C3 F8) at a nonexpansile concentration of 14%.[3]
Vitreous plugging
Vitreous gel has been recognized as an etiology of pupillary block by many authors. After intracapsular cataract extraction without sector iridectomy, the intact anterior hyaloid molds itself into the pupillary aperture leading to a secondary angle closure.
In some cases, even in the presence of small peripheral iridectomy, the vitreous can plug the openings and lead to angle closure. Shaffer observed that posterior vitreous detachment predisposed to such pupillary block.[4]
Pupillary block by the vitreous has been described following surgical discission of posterior capsule as well as Nd:YAG laser posterior capsulotomy.
Posner has described 3 stages of pupillary block by the vitreous, as follows:[5] (1) An early stage characterized by relative block due to decreased permeability of the hyaloid face. (2) A moderate stage with adhesions between the vitreous and sphincter pupillae referred to as sphincteric pupillary block. (3) The irido-hyloidal stage with extensive adhesions between the anterior hyaloid face and the entire posterior iris surface.
Silicone oil
Pupillary block has been described in aphakic eyes after retinal reattachment surgery with silicone oil injection, both in the immediate and long-term postoperative periods.
Pars plana vitrectomy with silicone oil injection is being performed with increasing frequency in proliferative vitreoretinopathy. Because of the cohesive forces, the silicone oil takes a smooth spherical form within the aqueous in the vitrectomized posterior segment. Since silicone oil is lighter than aqueous humor, it settles superiorly behind the iris. Thus, a superiorly placed peripheral iridectomy may become blocked. In addition, if the silicone oil fills the vitreous cavity as the aqueous is being produced, it may force the silicone oil through the pupil. If the silicone oil completely fills the vitreous cavity, the pupillary space, and the entire anterior chamber, the IOP may rise further as aqueous humor may have no access to the trabecular meshwork.
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 consists of peripheral iridotomy, peripheral iridectomy, or incision of the hyaloid membrane.[6] 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.
More 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.
Clinical Context:
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.
Clinical Context:
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.
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
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.
Clinical Context:
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.
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.
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
Disclosure: Nothing to disclose.
Specialty Editors
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
Disclosure: Nothing to disclose.
J James Rowsey, MD, Former Director of Corneal Services, St Luke's Cataract and Laser Institute
Disclosure: Nothing to disclose.
Chief Editor
Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
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
Disclosure: Nothing to disclose.
Acknowledgements
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
