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Dr.Ali.A.Taqi.Fifth year students 2012.

Glaucoma.lecture 2

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Angle-Closure Glaucoma

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PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG). Primary angle-closure glaucoma refers to an increase in intraocular pressure secondary to iris apposition to the trabecular meshwork .This apposition prevents aqueous humor outflow from the anterior chamber and may

occur suddenly …1-acute angle-closure glaucoma.

slowly over time …2-chronic angle-closure glaucoma. intermittently …3-subacute angle-closure glaucoma.

Primary angle-closure glaucoma derives from relative pupillary block. Relative pupillary block is an increased resistance to aqueous humor flow from the posterior chamber into the anterior chamber, through the pupil. Relative pupillary block is dependent on the contact between the lens and iris and is increased in eyes with narrow anterior segments, such as hyperopic eyes.

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Diagramshowing the differencebetween open and closedangle glaucoma.

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•RISK FACTORS:-1/Eyes with short axial lengths, 2/small corneal diameters, and

3/increased thickness of the crystalline lens are predisposed to increased pupillary block and angle-closure glaucoma.

4/Relative pupillary block also increases with age as the lens thickens and the pupil becomes more miotic. Maximal pupillary block occurs in the middilated position; therefore, angle-closure may be exacerbated by pupillary dilation. In the middilated eye, the apposition between the lens and iris is substantial, and the peripheral iris is lax enough to be anteriorly displaced.

•EPIDEMIOLOGY:-Primary angle closure glaucoma affects 1 in 1000 subjects over 40 years.

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•Eyes in which the pupil has been pharmacologically dilated are most prone to increased pupillary block and acute angle-closure glaucoma as the medications begin to wear off and the pupil is in the mid dilated position.(atropine 1% eye drops).

• In the normal eye, there is apposition between the posterior surface of the iris and the anterior surface of the lens, but the resistance to aqueous humor flow into the anterior chamber is minimal.

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1-In acute angle closure glaucoma, there is an abrupt increase in pressureand the 2-eye becomes very painful and photophobic. 3-There is watering of the eye and4- loss of vision. The patient may be systemically unwell withnausea and abdominal pain, symptoms which may take them to a generalcasualty department.Intermittent primary angle closure glaucoma occurs when an acuteattack spontaneously resolves.The patient may complain of pain, blurringof vision and seeing haloes around lights.

Acute primary angle closure glaucoma.History.

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Clinical features: signs and symptoms

•Visual acuity reduction: due to corneal edema and posterior segment ischemia.•Raised IOP: usually 40-70 mmHg.•Colored haloes around lights, due to diffraction of light through the edematous corneal epithelium.•Pain: may be severe, and associated with vomiting.•Ciliary injection.•Mid-dilated pupil, due to ischemic iris atrophy.•Corneal edema: due to decompensation of the corneal endothelial pump.•Anterior chamber cell and flare due to anterior Uveitis.

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The diagnosis of acute angle-closure glaucoma is often self-evident:-•elevation of intraocular pressure and •a closed anterior chamber angle are present. •When extensive corneal edema prohibits gonioscopic examination of the anterior chamber angle, acutely lowering the intraocular pressure often clears the corneal edema.• Examination may also be enhanced by the application of glycerin to the anterior surface of the cornea after topical anesthesia. •This will temporarily osmotically dehydrate and clear the cornea, enhancing the view of the anterior segment.

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The appearanceof the eye in angle closure glaucoma.Note the cloudycornea and dilated pupil.

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Medical management :Patient must be(admission ,check vital signs ,with I-V line).The IOP must be reduced medically as quickly as possible, using:1/Diuretic:Acetazolamide to reduce aqueous production: 500 mg in 10 ml normal saline i.v over 10 minutes immediately, 250-500 mg orally, three times daily if the pressure remain high or give an intravenous(i.v )Mannitol infusion(1-2 g/kg, 200 ml-350 ml 20% i.v over ½-1 hour).2/Miotic:Intensive pilocarpine therapy (every 10 min for 1 hr, then hourly for 6hr). Then maintain on pilocarpine 2% ,4 times daily.3/Steroid:Topical steroid during acute phase to reduce the accompanying inflammatory response.4/Analgesia:Parenteral analgesia and antiemetic may be needed.

Surgical and Laser treatment: Peripheral surgical iridectomy or laser peripheral Iridotomy (YAG laser PI).

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(Chronic) primary angle-closure glaucoma

• Is also known as "creeping angle-closure.•Patients are usually asymptomatic with this disorder, although they may have other stigmata of glaucoma, including glaucomatous optic neuropathy and visual field loss. •Intraocular pressures (IOP)range from normal to highly elevated and are the result of prolonged narrowing of the anterior chamber angle with formation of peripheral anterior Synechiae. •This results from prolonged apposition of the iris to the trabecular meshwork, and the amount of pressure elevation depends on the extent of angle- closure.

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Angle-closure glaucoma may also occur secondary to posterior Synechiae. Total Synechiae formation between the iris and the anterior lens surface may create obstruction of aqueous flow into the anterior chamber resulting in an iris configuration, known as iris bombé. The peripheral iris appears to balloon into the anterior chamber causing angle-closure glaucoma. This typically follows chronic Uveitis. Iris bombé configuration is also seen in primary angle-closure glaucoma if the relative pupillary block results in a large pressure differential between the anterior and posterior chambers. Secondary angle-closure glaucomas, such as angle-closure after a central retinal vein occlusion or angle-closure secondary to a posterior segment intraocular tumor, should be ruled out in all cases of angle-closure glaucoma.Examination of the fellow eye with Gonioscopy should be done in all patients presenting with angle-closure glaucoma. Patients with a marked difference in the depth of the anterior chamber and the configuration of the anterior chamber angle between the two eyes should be suspected of having a secondary cause of angle-closure glaucoma.

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SECONDARY GLAUCOMASLENS-ASSOCIATED GLAUCOMA1. Even in the healthy eye, cataractous change and enlargement of the

lens(intumescent cataract), with increase in irido-lenticular touch and relative pupillary block, may result in angle-closure glaucoma(phacomorphic glaucoma).

2. Dislocated or subluxed lenses also may migrate forward to become entrapped in the pupil, leading to angle-closure glaucoma.

3. A spectrum of glaucomas associated with a permeable or "leaky" lens capsule have been described These include (phacolytic glaucoma), which is a lens-induced Uveitis with secondary glaucoma, and obstruction of the trabecular meshwork by lens protein or particles of lens material. Phacoanaphylactic endophthalmitis GLAUCOMA AFTER CATARACT EXTRACTION Virtually any of the varieties of glaucoma previously discussed may develop in an eye that has had cataract surgery

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•Pigment from the iris (pigment dispersion syndrome).•Deposition of material produced by the epithelium of the lens, iris andciliary body in the trabecular meshwork (pseudoexfoliative glaucoma).•Drugs increasing the resistance of the meshwork (steroid-induced glaucoma).•Secondary glaucoma may also result from blunt trauma to the eyedamaging the angle (angle recession).•Angle closure may also account for some cases of secondary glaucoma:•Abnormal iris blood vessels may obstruct the angle and cause the iristo adhere to the peripheral cornea, closing the angle (rubeosis iridis). Thismay accompany proliferative diabetic retinopathy or central retinal veinocclusion •A cataract may swell, pushing the iris forward and closing the drainageangle.•Uveitis may cause the iris to adhere to the trabecular meshwork.

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Congenital, Infantile, Juvenile and Developmental Glaucoma• Primary congenital glaucoma occurs at birth or within the first several months of life. •.It is characterized by severe elevations of intraocular pressure, which when left untreated will cause stretching of the various support tissues of the eye and enlargement of the globe (buphthalmos).•The classic presentation of a child with primary congenital or infantile glaucoma is the triad of •excessive Epiphora(watery eye) •Photophobia(inability to open eye in light) •and blepharospasm(eyelids tight closure).

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Glaucoma Therapy.

Medical therapy for glaucoma has been greatly expanded during the past several decades. Currently, the clinician has a variety of topical and systemic agents with which to lower intraocular pressure. These agents include drugs which:-• enhance aqueous humor outflow from the eye and drugs which suppress aqueous humor formation. •All currently available topical medications exert their effect by changes in the autonomic nervous system. •These drugs are subcategorized as cholinergic agonists, •adrenergic agonists•adrenergic antagonists. •Systemic antiglaucomatous medication as Oral carbonic Anhydrase inhibitors form the mainstay of systemic therapy for the control of intraocular pressure.

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TOPICAL MEDICATIONS. 1/Cholinergic Agonists.• Cholinergic agonists (parasympathomimetic agents) were the first class of drugs used in the therapy of glaucoma .•These medications, called "miotics" for their pupillary action, may be either direct-acting or indirect-acting agents. •Direct-acting cholinergic agonists stimulate the motor endplates .• while indirect agents inhibit acetyl cholinesterase and potentiate the effects of acetylcholine by preventing its degradation. •Pilocarpine is a direct-acting agent.• Carbachol has both direct and indirect cholinergic actions. •All miotics lower intraocular pressure by enhancing aqueous humor outflow from the anterior chamber.

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2/Adrenergic Antagonists• Beta-adrenergic inhibitors are the most commonly prescribed medications in the treatment of glaucoma .Beta-adrenergic antagonists, or "beta blockers," were originally used as a systemic treatment of cardiac arrhythmias and systemic hypertension.• Most of these medications nonselectively block both beta1 (heart) and beta2 (pulmonary smooth muscle) adrenergic receptors (timolol maleate, metipranolol hydrochloride, carteolol, and levobunolol hydrochloride).• A relatively cardioselective, beta1-adrenergic antagonist is also available (betaxolol hydrochloride) which has less effect on pulmonary smooth muscle. •All beta blockers reduce intraocular pressure by decreasing the aqueous humor production.

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SYSTEMIC MEDICATIONS• Carbonic Anhydrase Inhibitors. Carbonic Anhydrase inhibitors are systemically administered medications which reduce aqueous humor formation to decrease the intraocular pressure (acetazolamide 250/500 mg vial ) Hyperosmotic Agents.• Hyperosmotic agents are systemically administered medications which lower intraocular pressure by increasing the plasma osmolality, resulting in vitreous dehydration .•Fluid is osmotically drawn from the vitreous cavity into the circulation.•Mannitol, glycerin, and isosorbide are the most frequently used hyperosmotic agents.• Hyperosmotic agents are only used as a short-term therapy. Glycerin and isosorbide are administered orally, while mannitol is administered intravenously.

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Laser and surgical procedures for glaucoma.A/Laser Surgical Procedures• Argon laser trabeculoplasty (ALT).for POAG• YAG Laser peripheral Iridotomy(laser PI). For PACG.• Laser iridoplasty.

B/Incisional Surgical Procedures Trabeculectomy (filtering operation)• Trabeculectomy is the most frequently performed Incisional operation for the control of elevated intraocular pressure in adult glaucoma .•Various filtering procedures have been developed to shunt the aqueous humor from the anterior chamber to a subconjunctival reservoir. •These procedures provide an alternative pathway of less resistance for aqueous humor egress from the eye. •It is believed that the aqueous humor either filters through the conjunctiva from the reservoir mixing with the tears, or it is absorbed by the vascular tissue of the episclera and conjunctiva.

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References .• 1-Parson’s disease of the eye

2003.2-Lecture notes on ophthalmology, Bruce James, Chris Chew, ninth edition, Blackwell scientific 20033-Atlas of ocular pathology, ocular trauma, on CD.

• 2-Clinical ophthalmology Kanski J 2007

• 3-ophthalmology.a short textbook.Gerhard.k.Lang.Thieme publications.2000.