Glaucoma PDF

Glaucoma Dr khosro senyar Fellowship of Vitreo-Retina Anterior Chamber (AC): The anterior chamber is bordered anteriorly by the cornea and posteriorly by the iris diaphragm and the pupil. Anterior chamber angle (iridocorneal angle): lies at the junction of the cornea and the iris, con...

Glaucoma Dr khosro senyar Fellowship of Vitreo-Retina Anterior Chamber (AC): The anterior chamber is bordered anteriorly by the cornea and posteriorly by the iris diaphragm and the pupil. Anterior chamber angle (iridocorneal angle): lies at the junction of the cornea and the iris, consist of the following structures: ‣ Schwalbe`s line* ‣ Trabecular meshwork and Schlemm`s canal** ‣ Scleral spur ‣ Anterior border of ciliary body ‣ Iris * Schwalbe`s line is termination of Descemet`s membrane and it is white in gonioscopy (measures the angle). ** Schlemm`s canal is a large channel that closely resembles a lymphatic vessel, formed by a continuous monolayer of nonfenestrated endothelium and a thin connective tissue wall. Aqueous humor formation: Aqueous humor is produced by 3 processes at an average rate of 2 µL/min: Active secretion by double-layered non-pigmented ciliary epithelium. Ultrafiltration Simple diffusion Aqueous humor outflow: occurs by 2 major mechanisms: Trabecular outflow (pressure dependent): most of the aqueous humor exits the eye by way of the trabecular meshwork - schlemm`s canal - venous system. Aqueous moves both across and between the endothelial cells lining the inner wall of schlemm`s canal. The juxtacanalicular meshwork is thought to be the major site of outflow resistance. Uveoscleral outflow (pressure independent): in the normal eye, any nontrabecular outflow is termed uveoscleral outflow. A variety of mechanisms are involved, predominantly aqueous passage from the anterior chamber into the ciliary muscle then into the supraciliary and suprachoroidal space. Accounts for 15-45% (even wider range, influenced by age) of total outflow. This outflow is increased by cycloplegia, adrenergic agent, prostaglandin analogue and certain form of surgery (e.g cyclodialysis) and is decrease by miotics. The anterior chamber is filled with aqueous humor, which is produced by the non pigmented ciliary epithelium in the posterior chamber, the fluid passes through the pupillary aperture and drains chiefly through the trabecular into schlemm`s canal. Accessory drainage pathways are, uveoscleral, diffusion into the iris, cornea and posterior segment.  Arrah did Glaucoma Optic neuropathy visual Refers to a group of diseases that have characteristic optic neuropathy with associated visual field loss for which elevated intraocular pressure (IOP) is one of the primary risk factors. IOP mutts Normal IOP 9-21 mmHg determined by: normal a 21 The rate of aqueous humor production by the ciliary body. Resistance to outflow through the trabecular meshwork. The level of episcleral venous pressure. In most cases increased IOP is caused by increased resistance to aqueous humor outflow. The different type of glaucoma were theoretically calculated to be responsible for 15% of blindness, placing glaucoma as the second leading cause of blindness worldwide superseded only by cataract.  Classification of Glaucomas Primary vs secondary (cause) Open vs Closed (angle) Congenital vs Acquired (onset)  Primary glaucoma: Is not associated with known ocular or systemic disorders that cause increased resistance to aqueous outflow. Secondary glaucoma: Is associated with ocular or systemic disorders responsible for decrease aqueous outflow. Open angle glaucoma (OAG): Tresistance ‣ primary open angle glaucoma ‣ normal tension glaucoma ‣ juvenile open angle glaucoma Angle closure glaucoma (ACG): ‣ Primary (Acute, Subacute, Chronic) ‣ Secondary with pupillary block (e.g swollen lens, secluded pupil) without papillary block esterseyes Primary congenital / infantile glaucoma (triad of epiphora, photophobia, and blepharospasm) Angle closure glaucoma (ACG): ACG is characterized by apposition of the iris against the trabecular meshwork, resulting in obstruction of aqueous outflow. Risk factors: Iris against Age: prevalence increases with each decade after 40. Sex: 2-4 times more in women. transition Family history. Hyperopia (shallow anterior chamber).hyperopic Others: shallow anterior chamber depth (< 2.5 mm), thick lens, short axial length, small corneal diameter. The depth of anterior chamber is variable, it is about 3 mm deep at its centre in normal adult emmetropic eye. It tends to be deeper in aphakia (no lens) & myopia but shallower in hyperopia. Mechanisms of ACG: 1. Mechanisms that push the iris forward from behind (with or without pupillary block) 2. Mechanisms that pull the iris forward (without pupillary block) Mid dilated pupil relaxes the peripheral iris so that it may bow forward & backwards → apposition of iris with trabecular meshwork (forward) & with anterior surface of the lens (backward) → pupillary block → ↑ fluid pressure in the posterior chamber → more forward shift of the iris → closure of the anterior chamber angle → ↑ IOP → ACG. Secluded pupil (360° posterior synechiae) also causes pupillary block. ACG is most frequently caused by pupillary block but may also occur without pupillary block as in: ciliary body swelling aqueous misdirection (to vitreous chamber) posterior segment tumors scleral buckling procedures Clinical Features of Acute ACG: Symptoms: Ocular pain, headache, blurred vision, rainbow-colored halos around light, nausea, vomiting, bradycardia, sweating. The rise in IOP causes corneal epithelial edema which is responsible for the visual symptoms. Signs: Corneal epithelial edema, congested episcleral and conjunctival blood vessels, a mild amount of aqueous flare and cells, mid-dilated sluggish and often irregular pupil (no or poor constriction to light reflex), shallow anterior chamber, high IOP. Definitive diagnosis depend on the gonioscopic finding. The pupillary change is thought to resulted from paralysis of the sphincter pupillae, which is caused by reduction in blood supply induced by the elevated IOP and possibly by degeneration of the ciliary ganglion. PAACG is a bilateral disease and the fellow eye has a 40%-80% chance of developing an acute attack of angle closure over the next 5-10 years. Chronic angle closure glaucoma is asymptomatic disease until late of the disease when the visual field constricted. 0 Shallow anterior chamber O  Treatment Mild attacks may be broken by cholinergic agents (pilocarpine 1-2%), which d induce miosis that pulls the peripheral iris away from the trabecular meshwork, however when the IOP is quite elevated (e.g > 40-50 mmHg), the pupillary sphincter may be ischemic and unresponsive to miotic agents alone so patient should be treated with some combination of a topical β2 blockers (Timolol 0.5%), oral, topical, or IV carbonic anhydrase inhibitor (Acetazolamide 500 mg IV, dorzolamide) and when necessary, a hyperosmotic agent (e.g oral glycerol 1-1.5 g/kg of 50% solution in lemon o juice, Intravenous mannitol 2g/kg of 20% solution) and topical steroid or glycerin to decrease corneal inflammation and edema. Laser iridotomy with YAG laser is the treatment of choice for angle closure glaucoma secondary to pupillary block, and prophylactic iridotomy should be o performed in the contralateral eye (because it is a bilateral disease) unless the angle clearly appears to be non-occludable (these operations are done when cornea is clear). Surgical iridectomy is indicated if laser iridectomy cannot be accomplished.  0 Laser peripheral iridotomy Laser peripheral iridotomy Surgical peripheral iridectomy  Secondary Glaucoma 1. Lens-induced glaucoma: Phacolytic glaucoma (lens protein glaucoma): hypermature cataract 8 → shrinkage of lens → leakage of lens material through intact capsule → trabecular obstruction is caused by high molecular weight proteins or microphages laden (engulfed) with these proteins. Rx: control IOP medically, then sugery (cataract extraction). e Phacomorphic (Intumescent) glaucoma: Intumescent (swelling) of lens → pupillary block → secondary acute ACG. Presentation is the same like that of PACG but with cataract. Rx: cataract extraction. e Phacoanaphylactic (phacoantigenic) glaucoma: Is an autoimmune reaction to lens proteins occurring in an eye with a traumatic ruptured anterior capsule (large lens matter passing through a rupture in capsule, this matter is regarded as foreign body and antibodies against it is produced). Therefore, there will be occlusion of the pores of trabecular meshwork by immune complexes and cells. Rx: control IOP or anterior chamber washout. Lens particle glaucoma: pieces of lens particle (after trauma or surgery) will physically block the trabecular meshwork. 2. Neovascular glaucoma (NVG): Is a relatively common and serious condition, which occurs as a result of iris neovascularization (Rubeosis iridis). The common aetiopathogenic factor is severe, diffuse and chronic retinal ischaemia which can be caused by: Central retinal vein occlusion. (CRVO, commonest cause), or branch retinal vein occlusion (BRVO). Proliferative diabetic retinopathy (PDR). Central retinal artery occlusion (CRAO). Carotid obstructive disease (Ocular ischemic syndrome, OIS) Intraocular tumours. Long standing retinal detachment. Chronic intraocular inflammation. 3. Inflammatory (uveitic) glaucomas: uveitis  Neovascular glaucoma (NVG) 00  Primary open angle glaucoma FEET POAG is a chronic, slowly progressive optic neuropathy characterized d by atrophy and cupping of the optic nerve head and associated with characteristic patterns of visual field loss. Increase IOP is an important risk factor for POAG. o POAG is usually insidious inteonset , slowly progressive, and painless. While usually bilateral, it can be quite asymmetric. Because central visual acuity is relatively unaffected until late in the disease, visual loss generally progress without symptoms. POAG is diagnosed by assessing a combination of finding including IOP levels, optic disc appearance, and visual field loss. Prevalence of POAG shows a strong racial disparity, among whites 40 years of age and older, a prevalence of between 1.1% and 2.1% was reported, the prevalence among blacks is 3 to 4 times higher, The prevalence of POAG increases with age, and estimates among persons in their seventies have generally been 3 to 8 times higher compared with persons in their forties. Risk factors for POAG: Increased IOP 10P Race (black population) Blue Age Family history rise Association with myopia has been reported Diabetes. Decreased corneal thickness (central thickness 0.52 mm paracentral zone 0.52 mm inferior, 0.57 superior). F The following are typical glaucomatous defects that seen in perimetry (used to asses visual field) of patients with POAG: Paracentral scotoma Arcuate or Bjerrum scotoma Nasal step Altitudinal defect Temporal wedge Ophthalmoscopic signs of glaucoma: Generalized: Large optic cup Asymmetry of the cups Progressive enlargement of the cup Focal: Narrowing of the rim Vertical elongation of the cup Cupping to the rim Regional pallor F Splinter hemorrhage Nerve fiber layer loss Less specific: Exposed lamina cribrosa Nasal displacement of vessels Baring of circumlinear vessels Prepapillary crescent  20s (lamina cribrosa) w Peripapillary crescent ! Splinter hemorrhage 0 Vertical elongation of the cup Nasal displacement of vessels  1 Large optic cup RNFLD: Retinal nerve fibrer layer defect Open Angle a Closed Angle Normal ↑ optic cup with progression of glaucoma  Treatment POAG is treated when damage to the optic nerve has been demonstrated in the form of progressive pathologic cupping and\or characteristic visual field loss defects, or when IOP is elevated to an extent that it is likely to cause damage to the optic nerve. The goal of currently available glaucoma therapy is to preserve visual function by lowering IOP below a level that is likely to produce further damage to the nerve. Initial treatment of primary open angle glaucoma has commonly be medical, and surgical therapy of glaucoma is undertaken when medical therapy is not appropriate, not tolerated, not effective, or not properly utilized by a patient, and the glaucoma remain uncontrolled with either progressive damage or a very high risk of further damage.  Medical agents We can decrease IOP by decreasing aqueous secretion or by increasing aqueous out flow. Ocular hypotensive agents divided into several groups based on chemical structure and site of action. β blockers (Timolol 0.25% and 0.50% bid, Betaxolol tid). these agents lower IOP by inhibiting cAMP production in ciliary epithelium, thereby reducing aqueous humor secretion 20-50% , with a corresponding IOP reduction of 20-30%. Parasympathomimetic agents, including cholinergic and anticholinesterase agents (pilocarpine E\D 2%, 3%, 4%, 1% qid and carbachol]. Both direct and indirect acting agents reduce IOP by causing contraction of the ciliary muscle, which pulls the scleral spur to tighten the trabecular meshwork, increasing the outflow of aqueous humor. These agents can reduce IOP by 10-20%. Prostaglandin analogues (Latanoprost 005% qid). These agents increase uveoscleral aqueous outflow and reduce IOP by 25-30%.  Carbonic anhydrase inhibitors: IM, IV, oral and topical (oral acetazolamide tab 10-15 mg\kg\day and topical dorzolamide 2% bid or tid). These agents decrease aqueous humor formation by direct antagonist activity upon ciliary epithelial carbonic anhydrase and reduce IOP by 15-20%. Adrenergic agonist (like epinephrine and dipivefrin) These agents increase outflow of aqueous humor. α2 adrenergic agents (Apraclonidine 0.5%, 1% bid or tid and Brimonidine 0.2% bid or tid). These agents decrease aqueous production and increase uveoscleral outflow (brimonidine) and decrease episcleral venous pressure (apraclonidine) and reduce IOP by 20-30%. Hyperosmotic agents: like IV mannitol 1-2g\kg, oral glycerin 50%. These agents work by dehydrating vitreous. Subdural and subarachnoid hemorrhages have been reported after treatment with these agents. Glycerin can produce hyperglycemia or even ketoacidosis in diabetic patients, since it metabolized into sugar and ketone body so it is contraindicated in DM. Other treatment are argon laser trabeculoplasty and filtering surgery (with or without glaucoma tube shunt e.g Ahmed valve) Ahmed valve  Optic Neuropathy in Glaucoma There are two hypothesis for optic nerve damage in glaucoma: 1. Mechanical hypothesis: trophic factors including brain derived neurotrophic factor is retrogradely transported from the retinal ganglion cell axonal terminal to the cell bodies of the neurons and that trophic factors are essential to RGC survival. Thus RGC compression was shown to reduce axonal transport of trophic factors that causing RGC death by trophic insufficiency. 2. Vascular hypothesis: in which chronic hypoxia or ischemia is thought to contribute to glaucomatous optic neuropathy. Factors associated with IOP elevation include: postural change, valsalva maneuver, hard blinking, use of general anesthesia with ketamin and succinylcholine, tobacco, corticosteroid, elevated episcleral venous pressure. Factors associated with IOP reduction include :prolonged exercise, intake of alcohol, marijuana, pregnancy, metabolic acidosis and general anesthesia. Factors that may increase IOP: Factors that may decrease IOP: + Elevated episcleral venous pressure - Aerobic exercise Valsalva maneuver - Anaesthesia Breath holding - Metabolic or respiratory acidosis: decreases Playing a wind instrument aqueous humor production Wearing a tight collar or tight necktie - Hormonal influences (pregnancy) Bending over or being in a supine position - Drugs unrelated to therapy Elevated central venous pressure Alcohol consumption Orbital venous outflow obstruction Heroin Intubation Marijuana (cannabis) + Pressure on the eye Blepharospasm Squeezing and crying, especially in young children + Elevated body temperature: associated with increased aqueous humor production + Hormonal influences Hypothyroidism Thyroid ophthalmitis + Drugs unrelated to therapy Lysergic acid diethylamide (LSD) Topirarnate (Topamax) Corticosteroids Antichoiinergics: may precipitate angle closure Anesthetic drugs: Ketamine, succinylcholine Peripheral ganglion cells has longer axons so they are more likely to be affected so glaucoma initially leads to peripheral optic neuropathy → peripheral vision loss → delayed presentation.