1. Glaucoma.

2. Glaucoma Glaucoma describes a number of ocular conditions characterized by: 1-Raised intraocular pressure (IOP). 2-Optic nerve head damage. 3-Corresponding loss of visual field (VF). IOP depends on the relationship between aqueous production and outflow. The normal ocular tension is between 10-21mm.Hg. There is a normal fluctuation in ocular tension of up to 3- 5mm.Hg. during the course of the day called diurnal variation. Glaucoma remains one of the principal causes of blindness throughout the world 3. Anatomy of the drainage angle The anterior chamber of the eye is that space, containing aqueous humor, which is bounded in front by the cornea and part of the sclera, and behind by the iris and part of the ciliary body. Its normal depth in adults varies from 2.5-3.5mm. The angle of the anterior chamber refers to that peripheral recess bounded posteriorly by the root of the iris and the ciliary body and anteriorly by the corneo- scleral junction or the limbus. Among the deeper lamellae of the limbus, there is an annular channel, called the canal of Schlemm. The canal is separated from the aqueous in the anterior chamber by the trabecular meshwork. 4. ANATOMY 5. The trabecular meshwork is made up of circumferentially disposed flattened collagenous bands which criss-cross, leaving numerous tortuous passages through which the aqueous humor drains from the anterior chamber to the canal of Schlemm. The aqueous humor is a transparent colorless fluid which fills the anterior and posterior chambers of the eye. Its chief site of formation is the processes of the ciliary body. The volume of aqueous in the anterior chamber of the human eye is 0.25 ml. 6. Classification of glaucoma. according to three principal parameters: Angle configuration 1-open(POAG=primary open angle glaucoma). 2- Narrow/closed.(PACG=primary angle closure) Onset 1- acute(acute congestive glaucoma)red eye differential diagnosis. 2- Chronic(primary open angle glaucoma) Causes 1-congenital glaucoma. 2-primary glaucoma 3- secondary glaucoma(secondary open angle and secondary close angle) Secondary to other ocular diseases 7. Primary open angle glaucoma (POAG). 8. PRIMARY OPEN-ANGLE GLAUCOMA(POAG). Primary open-angle glaucoma (POAG) is characterized by the development of glaucomatous optic neuropathy in an eye with a normal-appearing mechanically opened anterior chamber angle and absence of other ocular or systemic disorders which may account for the optic nerve damage. Most cases of primary open-angle glaucoma are associated with statistically elevated intraocular pressure. Primary open-angle glaucoma is also called chronic open-angle glaucoma or simple open-angle glaucoma. POAG is the most common form of glaucoma. It is typically a bilateral disease but may be asymmetric. 9. Risk factors: age(>40 y): positive family history; diabetes; myopia. Aetiology: Unknown. Theories suggest: functional inadequacy of TM drainage; hypoperfusion of optic N. head; and weakness of structural collagen in the angle and disc. Symptoms: usually asymptomatic until late, when considerable field loss has already occurred; not associated with pain, discomfort or redness; new cases are usually identified by screening. Signs: IOP: usually elevated, even sometimes double the normal value, may be up to 40 mm hg. Visual field (VF): up to 50% of ganglion cell axons entering the disc may be lost before disc and field changes are evident. Peripheral field is progressively lost, but central acuity is affected late. 10. Glaucomatous Optic nerve disc cupping 11. Pathophysiology: Even today, much remains unknown about this disease. Elevated IOP almost certainly plays a significant role, but the process is poorly understood. According to the mechanical theory of POAG, chronically elevated IOP distorts the lamina cribrosa, crimping the axons of retinal ganglion cells as they pass through the lamina cribrosa and eventually killing the cells. The vascular theory suggests that with elevated IOP, reduced blood flow to the optic nerve starves the cells of oxygen and nutrients 12. Clinical Testing and Examination Techniques in Glaucoma TONOMETRY Indentation Tonometry The Schiotz tonometer is the primary indentation tonometer used to measure intraocular pressure. Applanation Tonometry applanation tonometry uses a variable amount of force to produce a fixed amount of flattening of the corneal surface. Applanation tonometry is based on the Imbert-Fick principle, which states that the external force (F) exerted to a sphere, equals the pressure inside this sphere (P) times the area (A) which is flattened or "applanated" by the external force. Gonioscopy is an examination technique used to visualize the structures of the anterior chamber angle. Mastering the various techniques of gonioscopy is crucial in the evaluation of the pathophysiology of aqueous humor outflow obstruction and the diagnosis of the various 13. Disc: damage usually begins as an upper or lower temporal notch, giving rise to a nasal arcuate scotoma. Management; disc cupping and field loss in POAG progress at a variable rate, leading in the most severe cases to profound field constriction and ultimately blindness. The aim of management is to lower IOP sufficiently to arrest progressive VF loss. Medical treatment: topical beta-blocker (Timolol, carteolol,betaxolol) and pilocarpine. Surgical treatment: Trabeculectomy provides a definitive and permanent reduction of IOP to within safe limits in the majority of cases. 14. Angle-Closure Glaucoma 15. PRIMARY ANGLE-CLOSURE GLAUCOMA WITH PUPILLARY BLOCK 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 (acute angle-closure glaucoma), slowly over time (chronic angle-closure glaucoma), or intermittently (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. 16. Eyes with short axial lengths, small corneal diameters, and increased thickness of the crystalline lens are predisposed to increased pupillary block and angle-closure glaucoma. 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. 17. 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. 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. 18. Clinical features: Visual reduction: due to corneal oedema and posterior segment ischaemia. Raised IOP: usually 40-70 mmHg. Coloured haloes around lights, due to diffraction of light through the oedematous corneal epithelium. Pain: may be severe, and associated with vomiting. Ciliary injection. Mid-dilated pupil, due to ischaemic iris atrophy. Corneal oedema: due to decopensation of the corneal endothelial pump. Anterior chamber cell and flare due to anterior uveitis. 19. Treatment; The IOP must be reduced medically as quickly as possible, using: Diuretic: Acetazolamide to reduce aqueous production: 500 mg i.v immediately, 250-500 mg orally,t.d.s.,if the pressure remain high, give an i.v mannitol infusion( 200 ml 20% i.v over 1-2 hr.). Miotic: Intensive pilocarpine therapy (every 10 min for 1 hr, then hourly for 6hr). Then maintain on pilocarpin 2% q.d.s. Steroid: Topical steroid q.d.s during acute phase to reduce the accompanying inflammatory response. Analgesia: Parentral analgesia and antiemetic may be needed. Surgical treatment: Peripheral iridectomy or iridotomy(YAG laser). 20. Chronic, primary angle-closure glaucoma with pupillary block 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 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. 21. The diagnosis of acute angle-closure glaucoma is often self-evident; increased elevations 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. 22. 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 bomb. The peripheral iris appears to balloon into the anterior chamber causing angle-closure glaucoma. This typically follows chronic uveitis. Iris bomb 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. 23. 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. 24. CHEMICAL BURNS Chemical burns to the eye may lead to extreme intraocular inflammation, collagenous contracture of the sclera, and disruption of the intrascleral aqueous outflow pathways. All are potential causes of acute or continual elevated intraocular pressures. 25. LENS-ASSOCIATED GLAUCOMA 1. 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 26. 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, photophobia, and blepharospasm. 27. 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. 28. These drugs are subcategorized as cholingeric agonists, adrenergic agonists, and adrenergic antagonists. Many ocular topical medications were originally derived from systemic cardiovascular medications. Systemic antiglaucomatous medications are also available. Oral carbonic anhydrase inhibitors form the mainstay of systemic therapy for the control of intraocular pressure. 29. TOPICAL MEDICATIONS 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 cholingeric agonists stimulate the motor endplates . while indirect agents inhibit acetylcholinesterase 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. 30. 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. Intraocular pressure reduction of up to 50% is seen with these agents. 31. SYSTEMIC MEDICATIONS Carbonic Anhydrase Inhibitors Carbonic anhydrase inhibitors are systemically administered medications which reduce aqueous humor formation to decrease the intraocular pressure (acetazolamid) 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 32. Laser Surgical Procedures ARGON LASER TRABECULOPLASTY Laser Iridotomy LASER IRIDOPLASTY Incisional Surgical Procedures TRABECULECTOMY 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.