<Team Rochas> • 90% of aqueous flow • aqueous produced by the ciliary Glaucoma epithelium is secreted into the - Includes a complex of eye diseases which posterior chamber→ anterior have in common an abnormal intraocular chamber passing through the pressure that causes organic changes in the pupil→anterior chamber angle→ optic nerve and produces irreversible fenestrated layers of the trabecular blindness through progressive loss of the meshwork→ Schlemm’s canal→ field of vision - many forms are asymptomatic as they venous tributaries →venous destroy the optic nerve circulation of the eye - if detected and IOP is reduced to normal 2. Unconventional (uveoscleral) route by medication or surgery, the progression of • remaining 10% blindness can be stopped • aqueous passes caross the ciliary body - Pathophysiology, clinical presentation and into the suprachoroidal space and is treatment of the different types of drained by the venous circulation in glaucoma are so varied, there is no single the ciliary body, choroid and sclera definition that adequately encompasses all *some aqueous drains via the iris forms - In the broadest terms, glaucoma involves a study of the following: Pathogenesis of glaucomatous damage 1. IOP 2. optic nerve head damage 1. The Ischemic Theory – compromise of the 3. visual field loss microvasculature of the axons in the optic 4. drainage angle nerve head plays a role in the pathogenesis of glaucomatous damage Aqueous Secretion 1. Active Secretion – 80% of aqueous Possible Mechanisms: production, aqueous secreted by the non- a. loss of capillaries pigmented ciliary epithelium via an active b. alteration of capillary blood flow metabolic process that is dependent on a c. changes that interfere with the number of enzymatic systems delivery of nutrients or removal of 2. Passive secretion – 20% of aqueous metabolic products from the axons production, aqueous produced by passive d. failure of regulation of blood flow process such s ultrafiltration and diffusion e. delivery of injurious vasoactive which are dependen, the on the level of substances to blood vessels of the blood pressure in the ciliary capillaries, the optic nerve head plasma oncotic pressure and the level of IOP 2. The Direct Mechanical Theory Aqueous secretion is diminished by: - elevated IOP directly damages the retinal 1. Drugs – B- blockers, sympathomimetics, nerve fibers as they pass through the lamina carbonic anhydrase inhibitors cribrosa 2. Cyclodestructive procedures 3. Ciliary body shutdown – detachment of Determinatuion of normal IOP is by the ciliary body, inflammation of secretory following factors: ciliary epithelium in iridocyclitis and retinal 1. Rate of aqueous secretion detachment 2. Resistance encountered in outflow channels 3. Level of episcleral venous pressure • The rate of aqueous outflow is as well as though a bandage proportional to the IOP minus the contact lens episcleral venous pressure • The distribution of IOP within the general population has a range of 10 – 12mmHg 2. Gonioscopy • Normal IOP varies with the time of Purposes: the day, heart beat, blood a. Diagnostic – to identify abnormal angle pressure level, and respiration structures and to estimate the width of the • IOP has a tendency to be higher in chamber angle the morning and lower in the b. Surgical- to visualize the angle during afternoon and evening procedures such as laser trabeculoplasty and • Mean range of diurnal IOP goniotomy fluctuations in normal eyes is 5 mmHg Type of Goniolenses: 1. Indirect – provides a mirror image of the Diagnostics: opposite angle and can be used only in 1. Tonometry conjunction with a slitlamp for diagnostic a. Goldmann applanation tonometry purposes gold standard a. Goldmann 3 – mirror goniolens measures the force applied per unit b. Zeiss 4 – mirror goniolens area c. Posner 4 – mirror goniolens IOP is proportional to the pressure 2. Direct – provides a diect view of the angle applied to the radius of curvature of and can be used for both diagnostic and the globe (cornea) and thickness of surgical purposes the globe does not require a slitlamp and used b. Schiotz tonometry with patient in supine position indentation tonometry, a plunger with a. Koeppe – dome-shaped goniolens a preset weight indents the cornea which comes in several sizes handy and cheap b. Swan- Jacob – surgical poniolens c. Perkins tonometry which is held on the cornea by a hand- held applanation tonometer handle which uses a Goldmann prism adapted 3. Perimetry – a method of evaluating the to a small light source visual field d. Air – puff tonometry e.g. Humphrey perimeter, Octopus noncontact tonometer which uses the 4. Other imaging procedures Goldmann applanation principle but, Optical Coherence Tomography (OCT) instead of using a prism the cntral Heidelberg Retinal Tomography (HRT) part of the cornea is flattened by a GDx Nerve Fiber Analyzer jet of air does not require use of anesthetic Grading of Angle Width e. Tono – Pen Grade 4 – (35- 45°), widest angle, ciliary hand- held, self-contained battery body can be visualized with ease powered, miniaturized portable Grade 3 – (25- 35°), open angle in which tonometer the scleral spur can be identified correlate with the Goldmann although Grade 2 – (20°), moderately narrow angle in it slightly overestimates a low which only the trabeculum can be identified IOP and underestimates a high Grade 1 – (10°), very narrow angle in which IOP only the Schwalbe line can be identified can take measurements in an eye with Slit angle – no obvious iridocorneal contact distorted or edematous cornea, but no angle structures can be identified Grade 0- (0°), closed angle due to 3) hemolyzed red cells (e.g. ghost cell iridocorneal contact glaucoma) 4) macrophages (e.g. phacolytic Classification: glaucoma) - According to manner by which aqueous 5) proteins (e.g. acute anterior uveitis) outflow is impaired 6) pseudoexfoliative material (e.g. 1. Open – angle pseudoexfoliation glaucoma) 2. Angle – closure c. Post – trabecular glaucoma- trabeculum is normal but aqueous outflow is impaired - (+)/ (-) of associated factors contributing due to elevated episcleral venous pressure to the rise in IOP 1) Carotid – cavernous fistula and dural 1. Primary shunts 2. Secondary 2) Sturge – Weber Syndrome 3) Obstruction of the superior vena cava - According to onset 1. Congenital Glaucoma Symptoms: 2. Infantile • asymptomatic until a significant visual 3. Juvenile field loss has occurred 4. Adult • initial VF loss – nasal field • rare: eye pain, headache, halos due A. Open – angle Glaucoma to transient corneal epithelial edema 1. Primary Open- angle Glaucoma - generally bilateral, although not generally Signs: symmetrical characterized in at least one • raised IOP, fluctuations IOP, optic disc eye by the following: changes, glaucomatous field changes, a. adult onset open angle on gonioscopy b. an IOP > 21mmHg at some point in the course of the disease Evaluation: c. an open angle of normal ▪ Hx, PE appearance ▪ visual acuity d. glaucomatous optic nerve head ▪ slit lamp biomicroscopy damage ▪ tonometry – note time of day e. visual field loss ▪ gonioscopy ▪ ophthalmoscopy – note appearance of 2. Secondary Open- angle Glaucoma the disc a. Pre- trabecular glaucoma – aqueous ▪ check visual fields perimetry outflow is obstructed by a membrane covering the trabeculum Management: 1) fibrovascular tissue (e.g. neovascular 1. Medical Therapy – topical B blocker, glaucoma) prostaglandin analogue, carbonic anhydrase 2) endothelial cells (e.g. iridocorneal inhibitor, alpha- agonist, miotics endothelial syndrome) 2. Laser trabeculoplasty – application of 3) epithelial cells (e.g. epithelial discrete burns to the trabeculum enhances ingrowth) aqueous outflow and lowers IOP b. Trabecular glaucoma – obstruction occurs a. uncontrolled glaucoma as a result of clogging up of the meshwork b. primary therapy for pxs with poor 1) pigment particles (e.g. pigmentary compliance to medical therapy glaucoma) 2) red blood cells (e.g. red cell glaucoma) c. nocturnal systemic hypotension 3. Trabeculectomy – conventional filtering as well as overtreated systemic (drainage) procedure by creating a new hypertension channel ( fistula) for aqueous outflow d. reduced blood flow velocity in between the anterior chamber and sub- the ophthalmic artery when Tenon space without the use of an artificial measured with transcranial device Doppler ultrasonography e. paraproteinemia and the Indications: presence of serum a. failed medical therapy and laser autoantibodies trabeculoplasty b. lack of stability for laser therapy due Management of NTG: to 1. History • poor patient cooperation 2. Reduction of IOP – indicated only in • inability to adequately patients with documented progressive field visulaize the trabeculum due to loss narrow angle or corneal aim is to reduce IOP by atleast opicification 30 % c. eyes with advanced disease – very low 3. Systemic calcium – channel blockers IOP is required considered in younger patients and in those with early disease NORMAL TENSION GLAUCOMA (NTG) 4. Monitoring of systemic BP (24 hrs) • low- tension glaucoma if a significant nocturnal drop • used to describe a type of POAG is detected, medication for hypertension should be avoided Characteristics: 1. a mean IOP =/< 21mmHg on diurnal B. Angle – Closure Glaucoma testing • glaucoma due to obstruction of 2. glaucomatous optic disc damage and trabecular meshwork by peripheral visual field loss Iris 3. open angle on gonioscopy • may be primary or secondary, with or 4. absence of secondary causes for without papillary block glaucomatous optic disc damage • may be acute, subacute, intermittent, or chronic NTG Risk Factors: 1. Age – elderly 1. Primary Angle- Closure Glaucoma with 2. Gender – females greater risk at 2:1 Pupillary Block ratyion - lens- iris apposition, which interferes 3. Race – more common in Japan than in with aqueous flow and causes the iris either Europe or North America to bow forward and occlude the trabecular meshwork Clinical Features: 2. Primary Angle – Closure Without Pupillary 1. IOP in high teens Block 2. optic nerve head is larger in NTG than in - Plateau iris syndrome POAG and incidence of splinter hges at the 3. Secondary Angle- Closure with Pupillary disc margins is higher in NTG Block 3. visual fields defcts are essentially the - -lens-induced (e.g., phacomorphic, same as in POAG dislocated lens), secclusio pupillae, 4. others aphakic/pseudophakic papillary block, a. peripheral vascular spasm nanopthalmos, ciliary block/ b. migraine headaches malignant glaucoma due to ROP, • IV hyperosmotic agent (Mannitol) trauma, miotic therapy • argon laser trabeculectomy, Nd: YAG 4. Secondary Angle- Closure Without laser iridectomy, laser pupilloplasty, Pupillary Block laser gonioplasty - -due to posterior pushing mechanisms • trabeculectomy with or without use of from tumors, choroidal hemorrhage or antimetabolites effusion, scleral buckle, swelling after • artificial filtering shunts PRP, post-inflammatory with posterior • cyclodestructive procedures, synechiae and iris bombe; or anterior cyclocryotherapy, Nd:YAG pulling mechanism in neovascular cycloablation glaucoma, post- inflammatory peripheral anterior synechiae GLAUCOMA DRUGS 1. Beta-blockers – decrease aqueous Symptoms: secretion with little effect on episcleral AACG- pain, red eye, photophobia, venous pressure decreased/blurred vision, halos around lights, headache, nausea, vomiting 2. Sympathomimetics – alpha and beta *CACG- asymptomatic, may have decreased adrenergics agonists – increase aqueous vision, constricted visual fields outflow
Signs: 3. Miotics – in PAOG, increase aqueous
Decreased VA, increased IOP, ciliary outflow injection, corneal edema, AC cell/flare, - in ACG, opens the angle which results from shallow AC, narrow angles on gonioscopy, the mechanical contraction of the pupil mid-dilated nonreactive pupil, iris bombe; pulling the peripheral iris away from the signs of previous attacks including sector iris trabeculum atrophy, anterior subscapular lens opacities glaucoma/flecken), dilated irregular pupil, 4. Prostaglandins derivatives – enhances and PAS uveoscleral outflow without altering aqueous outflow through the TM Evaluation: • Hx, PE 5. Carbonic anhydrase inhibitor • visual acuity - reduce aqueous secretion through direct • slit lamp biomicroscopy inhibition of carbonic anhydrase • tonometry- note time of day *production of aqueous humor in the ciliary • gonioscopy epithelium is a function of the production of • ophthalmoscopy – note appearance of bicarbonate the disc 6. Hyperosmotic agents • check visual fields/perimetry - increase blood osmolality thereby creating • consider provocative testing (prone an osmotic gradient between the blood and test, prone dark-room test, and vitreous so that water is drawn from the pharmacologic dilation; IOP increase vitreous of > 8mmHg is considered positive