Phacomorphic glaucoma is the term used for secondary angle-closure glaucoma due to lens intumescence. The increase in lens thickness from an advanced cataract, a rapidly intumescent lens, or a traumatic cataract can lead to pupillary block and angle closure.
Phacomorphic glaucoma is shown in the image below.
 View Image | Phacomorphic glaucoma. |
In an eye with advanced cataract formation, the lens is swollen or intumescent. Progressive reduction occurs in the iridocorneal angle. In such eyes, pupillary block glaucoma is caused by changes in the size of the lens and the position of the anterior lens surface. Angle closure may be secondary to an enhanced pupillary block mechanism, or it may be due to forward displacement of the lens-iris diaphragm.
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Although no formal epidemiologic statistics are available, angle closure from hypermature cataracts is more common in countries where cataracts are common and surgery is not readily available.
Phacomorphic glaucoma can occur in any race.
Phacomorphic glaucoma occurs equally in men and women.
Generally, phacomorphic glaucoma is observed in older patients with senile cataracts, but it can occur in younger patients after a traumatic cataract or a rapidly developing intumescent cataract.
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Patients with phacomorphic glaucoma complain of acute pain, blurred vision, rainbow-colored halos around lights, nausea, and vomiting.
Patients generally have decreased vision before the acute episode because of a history of a cataract.
Signs of phacomorphic glaucoma include the following:
Certain factors predispose a patient to phacomorphic glaucoma, as follows:
Phacomorphic glaucoma is more common in smaller hyperopic eyes with a larger lens and a shallower AC.
An angle-closure attack can be precipitated by pupillary dilation in dim light. The dilation to midposition relaxes the peripheral iris so that it may bow forward, coming into contact with the trabecular meshwork, setting the stage for pupillary block. Angle closure also is facilitated by the pressure originating posterior to the lens and the enlargement of the lens itself.
Zonular weakness secondary to exfoliation, trauma, or age can play a part in causing phacomorphic glaucoma.
Optical coherence tomography (OCT) is useful in the visualization of the AC angle. See Medical Care.
Medical treatment of phacomorphic glaucoma is aimed at rapidly reducing the IOP to prevent further damage to the optic nerve, to clear the cornea, and to prevent synechiae formation. The reduction of IOP is necessary to prepare the patient for laser iridotomy, which relieves the pupillary block that is causing the glaucoma.
Initial management should address the acute nature of the angle closure and include beta-blockers, alpha 2-adrenergic agonists, and carbonic anhydrase inhibitors. Miotics can worsen the secondary angle closure attack by increasing iridolenticular contact.
Argon laser peripheral iridoplasty (ALPI) has been studied and has been shown to be safe and effective as a first-line treatment of acute phacomorphic glaucoma.[1] This would still need to be followed by cataract extraction for a definitive treatment.
Secondary management begins with laser iridotomy to relieve the pupillary block. This procedure provides an alternate route for aqueous trapped in the posterior chamber to enter the AC, allowing the iris to recede from occluding the trabecular meshwork. Both the argon laser and the Nd:YAG laser can be used. Laser iridectomy sometimes relieves the acute angle-closure attack, but the AC remains shallow. These eyes are susceptible to repeated attacks of angle closure; therefore, cataract extraction should be performed if the AC does not deepen after laser iridectomy.
Gonioscopy is useful after an iridectomy for retrospective assessment of the angle. If the angle is markedly widened, the pupillary block was the likely main mechanism causing the elevated IOP, and laser iridectomy is sufficient in that case. If the angle does not deepen significantly, lens intumescence or forward displacement of the lens is the causative factor, and the patient needs cataract extraction. If the angle closure is not relieved by a laser iridotomy, plateau iris syndrome also is a differential diagnosis.
OCT may serve as an additional aid in establishing a diagnosis prelaser and postlaser.[2]
Laser iridotomy can temporarily stop an attack of acute pupillary block, but, in most patients with phacomorphic glaucoma, cataract extraction is needed. Laser iridotomy should be performed first as mydriasis before surgery can exacerbate the condition. An extracapsular approach typically is used for cataract extraction. A trabeculectomy often is combined with cataract extraction.
Studies have shown that a shorter time between duration of symptoms to cataract extraction resulted in greater visual improvement.[3]
Surgery in the nanophthalmic eye is not the procedure of choice; laser peripheral iridectomy and iridoplasty with medical therapy are recommended. The nanophthalmic eye is small with a shallow chamber and moderate-to-high hyperopia. In these patients, cataract extraction has a high rate of exudative detachment of the choroid and ciliary body with rhegmatogenous retinal detachment.
On initial puncture of the capsule on an intumescent lens, an increased risk of a tear extending to the equator exists due to increased pressure forces as the liquefied cortex egresses. One method for dealing with this possibility is using a 30-gauge needle on a syringe to aspirate the liquefied cortex as the capsule is punctured. This provides for a controlled lens decompression.
Because of the increased risk of complications during cataract extraction, deepening of the AC with pars plana vitreous tap or small-gauge vitrectomy has been suggested.[4]
Patients should be followed for at least 2 years postoperatively, because 20% of cases may require further glaucoma intervention for IOP control.[3]
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Clinical Context: Inhibits enzyme carbonic anhydrase, reducing the rate of aqueous humor formation, which, in turn, reduces IOP.
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 carbonic anhydrase, reducing hydrogen ion secretion at renal tubule and increasing renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.
Carbonic anhydrase is an enzyme found in many tissues of the body, including the eye. Catalyzes a reversible reaction where carbon dioxide becomes hydrated and carbonic acid becomes dehydrated. By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit carbonic anhydrase in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.
Clinical Context: Reduces elevated and normal IOP whether or not accompanied by glaucoma. Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.
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 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.
Lower IOP by creating an osmotic gradient between ocular fluids and plasma. They are not for long-term use.
Clinical Context: Prostaglandin agonist that selectively mimics effects of naturally occurring substances, prostamides. Exact mechanism of action unknown but believed to reduce IOP by increasing outflow of aqueous humor through trabecular meshwork and uveoscleral routes.
Clinical Context: Prostaglandin F2-alpha analog and selective FP prostanoid receptor agonist. Exact mechanism of action unknown but believed to reduce IOP by increasing uveoscleral outflow.
Clinical Context: May decrease IOP by increasing outflow of aqueous humor.
Clinical Context: Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production.
Clinical Context: May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow.
These agents decrease aqueous production, possibly by blocking adrenergic beta receptors present in the ciliary body. The nonselective medications in this class also interact with the beta receptors in the heart and lungs, causing significant adverse effects.
Clinical Context: Selective alpha-2 adrenergic receptor agonist with a nonselective beta-adrenergic receptor inhibitor. Each of them decrease elevated IOP, whether or not associated with glaucoma damage.
Clinical Context: Brinzolamide catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than 1 topical ophthalmic drug is being used, administer drugs at least 10 min apart.
Brimonidine is a relatively selective alpha2 adrenergic-receptor agonist that decreases IOP by dual mechanisms, reducing aqueous humor production and increasing uveoscleral outflow. Brimonidine has minimal effect on cardiovascular and pulmonary parameters. A moderate risk of allergic response to this drug exists. Caution should be used in individuals who have developed an allergy to Iopidine.
A combination solution that can decrease aqueous humor secretion more than would each solution used as monotherapy, while improving compliance.
Phacomorphic glaucoma.
Phacomorphic glaucoma.
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