ophthalmology.Glaucoma 2nd lect.(dr.ali)


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ophthalmology.Glaucoma 2nd lect.(dr.ali)

  1. 1. Glaucoma. lecture 2 Dr.Ali.A.Taqi. Fifth year students 2012. 1
  2. 2. Angle-Closure Glaucoma 2
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  4. 4. PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG). Primary angle-closure glaucoma refers to an increase in intraocular pressuresecondary 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. Relativepupillary block is an increased resistance to aqueous humor flow from the posteriorchamber into the anterior chamber, through the pupil. Relative pupillary block isdependent on the contact between the lens and iris and is increased in eyes withnarrow anterior segments, such as hyperopic eyes. 4
  5. 5. Diagramshowing the differencebetween open and closedangle glaucoma. 5
  6. 6. •RISK FACTORS:-1/Eyes with short axial lengths,2/small corneal diameters, and3/increased thickness of the crystalline lens are predisposed to increased pupillaryblock and angle-closure glaucoma.4/Relative pupillary block also increases with age as the lens thickens and the pupilbecomes more miotic.Maximal pupillary block occurs in the middilated position; therefore, angle-closuremay be exacerbated by pupillary dilation.In the middilated eye, the apposition between the lens and iris is substantial, and theperipheral iris is lax enough to be anteriorly displaced.•EPIDEMIOLOGY:-Primary angle closure glaucoma affects 1 in 1000 subjects over 40 years. 6
  7. 7. •Eyes in which the pupil has been pharmacologically dilated are most prone toincreased pupillary block and acute angle-closure glaucoma as the medications beginto 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 andthe anterior surface of the lens, but the resistance to aqueous humor flow into theanterior chamber is minimal. 7
  8. 8. Acute primary angle closure glaucoma. History.1-In acute angle closure glaucoma, there is an abrupt increase in pressureand the2-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. 8
  9. 9. Clinical features: signs and symptoms•Visual acuity reduction: due to corneal edema andposterior segment ischemia.•Raised IOP: usually 40-70 mmHg.•Colored haloes around lights, due to diffraction of lightthrough 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 cornealendothelial pump.•Anterior chamber cell and flare due to anterior Uveitis. 9
  10. 10. The diagnosis of acute angle-closure glaucoma is oftenself-evident:-•elevation of intraocular pressure and•a closed anterior chamber angle are present.•When extensive corneal edema prohibits gonioscopicexamination of the anterior chamber angle, acutelylowering the intraocular pressure often clears thecorneal edema.• Examination may also be enhanced by the applicationof glycerin to the anterior surface of the cornea aftertopical anesthesia.•This will temporarily osmotically dehydrate and clearthe cornea, enhancing the view of the anteriorsegment. 10
  11. 11. The appearanceof the eye in angle closure glaucoma.Note the cloudycornea and dilated pupil. 11
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  13. 13. 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 salinei.v over 10 minutes immediately, 250-500 mg orally, three times daily if thepressure 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). Thenmaintain on pilocarpine 2% ,4 times daily.3/Steroid:Topical steroid during acute phase to reduce the accompanying inflammatoryresponse.4/Analgesia:Parenteral analgesia and antiemetic may be needed.Surgical and Laser treatment:Peripheral surgical iridectomy or laser peripheral Iridotomy (YAG laser PI). 13
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  15. 15. (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 fieldloss.•Intraocular pressures (IOP)range from normal to highlyelevated and are the result of prolonged narrowing of theanterior chamber angle with formation of peripheral anteriorSynechiae.•This results from prolonged apposition of the iris to thetrabecular meshwork, and the amount of pressure elevationdepends on the extent of angle- closure. 15
  16. 16. Angle-closure glaucoma may also occur secondary to posterior Synechiae.Total Synechiae formation between the iris and the anterior lens surface may createobstruction of aqueous flow into the anterior chamber resulting in an irisconfiguration, 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 therelative pupillary block results in a large pressure differential between the anterior andposterior chambers. Secondary angle-closure glaucomas, such as angle-closure after a central retinalvein occlusion or angle-closure secondary to a posterior segment intraoculartumor, should be ruled out in all cases of angle-closure glaucoma.Examination of the fellow eye with Gonioscopy should be done in all patientspresenting with angle-closure glaucoma.Patients with a marked difference in the depth of the anterior chamber and theconfiguration of the anterior chamber angle between the two eyes should besuspected of having a secondary cause of angle-closure glaucoma. 16
  17. 17. 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 (phacolyticglaucoma), which is a lens-induced Uveitis with secondaryglaucoma, and obstruction of the trabecular meshwork by lens proteinor particles of lens material. Phacoanaphylactic endophthalmitisGLAUCOMA AFTER CATARACT EXTRACTION Virtually any of the varieties of glaucoma previously discussed maydevelop in an eye that has had cataract surgery 17
  18. 18. •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-inducedglaucoma).•Secondary glaucoma may also result from blunt trauma to the eyedamaging the angle (angle recession).•Angle closure may also account for some cases of secondaryglaucoma:•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. 18
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  21. 21. Congenital, Infantile, Juvenile and DevelopmentalGlaucoma• Primary congenital glaucoma occurs at birth or within thefirst several months of life.•.It is characterized by severe elevations of intraocularpressure, which when left untreated will cause stretching ofthe various support tissues of the eye and enlargement of theglobe (buphthalmos).•The classic presentation of a child with primary congenital orinfantile glaucoma is the triad of•excessive Epiphora(watery eye)•Photophobia(inability to open eye in light)•and blepharospasm(eyelids tight closure). 21
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  23. 23. Glaucoma Therapy.Medical therapy for glaucoma has been greatly expanded during the past severaldecades. Currently, the clinician has a variety of topical and systemic agents withwhich to lower intraocular pressure. These agents include drugs which:-• enhance aqueous humor outflow from the eye and drugs which suppress aqueoushumor formation.•All currently available topical medications exert their effect by changes in theautonomic nervous system.•These drugs are subcategorized as cholinergic agonists,•adrenergic agonists•adrenergic antagonists.•Systemic antiglaucomatous medication as Oral carbonic Anhydrase inhibitors form themainstay of systemic therapy for the control of intraocular pressure. 23
  24. 24. TOPICAL MEDICATIONS. 1/Cholinergic Agonists.• Cholinergic agonists (parasympathomimetic agents) werethe 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 motorendplates .• while indirect agents inhibit acetyl cholinesterase andpotentiate the effects of acetylcholine by preventing itsdegradation.•Pilocarpine is a direct-acting agent.• Carbachol has both direct and indirect cholinergic actions.•All miotics lower intraocular pressure by enhancing aqueoushumor outflow from the anterior chamber. 24
  25. 25. 2/Adrenergic Antagonists• Beta-adrenergic inhibitors are the most commonly prescribedmedications in the treatment of glaucoma .Beta-adrenergicantagonists, or "beta blockers," were originally used as a systemictreatment of cardiac arrhythmias and systemic hypertension.• Most of these medications nonselectively block both beta1 (heart) andbeta2 (pulmonary smooth muscle) adrenergic receptors (timololmaleate, metipranolol hydrochloride, carteolol, and levobunololhydrochloride).• A relatively cardioselective, beta1-adrenergic antagonist is alsoavailable (betaxolol hydrochloride) which has less effect on pulmonarysmooth muscle.•All beta blockers reduce intraocular pressure by decreasing theaqueous humor production. 25
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  28. 28. SYSTEMIC MEDICATIONS• Carbonic Anhydrase Inhibitors. Carbonic Anhydrase inhibitors are systemically administeredmedications which reduce aqueous humor formation to decrease theintraocular pressure (acetazolamide 250/500 mg vial ) Hyperosmotic Agents.• Hyperosmotic agents are systemically administered medications whichlower intraocular pressure by increasing the plasma osmolality, resultingin vitreous dehydration .•Fluid is osmotically drawn from the vitreous cavity into the circulation.•Mannitol, glycerin, and isosorbide are the most frequently usedhyperosmotic agents.• Hyperosmotic agents are only used as a short-term therapy. Glycerinand isosorbide are administered orally, while mannitol is administeredintravenously. 28
  29. 29. 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 operationfor the control of elevated intraocular pressure in adult glaucoma .•Various filtering procedures have been developed to shunt the aqueoushumor from the anterior chamber to a subconjunctival reservoir.•These procedures provide an alternative pathway of less resistance foraqueous humor egress from the eye.•It is believed that the aqueous humor either filters through theconjunctiva from the reservoir mixing with the tears, or it is absorbed bythe vascular tissue of the episclera and conjunctiva. 29
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  33. 33. References .• 1-Parson’s disease of the eye 2003. 2-Lecture notes on ophthalmology, Bruce James, Chris Chew, ninth edition, Blackwell scientific 2003 3-Atlas of ocular pathology, ocular trauma, on CD.• 2-Clinical ophthalmology Kanski J 2007• 3-ophthalmology.a short textbook.Gerhard.k.Lang.Thi eme publications.2000. 33