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GLAUCOMA Ahmed Hassane, FY2 AQUEOUS HUMOUR PRODUCTION • The ciliary body is made from the pars plicata anteriorly and pars plana posteriorly. • The aqueous humour is formed by the ciliary processes- a double layer of epithelium in the ciliary body pars plicata. • Control of aqueous formation is controlled by the sympathetic (adrenergic innervation) system: • b 2eceptors increases aqueous secretion • a 2eceptors decreases aqueous secretion. • IOP follows a circadian rhythm pattern; IOP is higher in the mornings rather than evenings. THE AQUEOUS OUTFLOW ROUTES • Trabecular outflow (~ 70%): is the conventional aqueous route in the eye going through the trabecular meshwork and Schlemms canal to the episcleral veins. • Uveoscleral outflow: aqueous humour passes through the ciliary muscle to the suprachoroidal space and eventually drained by choroidal veins. OCULAR HYPERTENSION • Eyes having IOP above the normal value (IOP>21 mmHg) without signs of glaucomatous changes. • The Ocular Hypertension Treatment Study (OHTS): • 9.5% of patients with OHT converted to open angle glaucoma in five years. 20% reduction of IOP (treated group)  risk dropped to 4.4%. • Risk factors for conversion: • Older age • Higher IOP (25.75mmHg) • Large cup to disc ratio • Thinner CCT (<555mm) *may lead to underestimation of IOP* • Other risk factors that might contribute (not significant in the OHTS): African-American origin, males, heart disease and myopia.G L A U C O M A T O U S V I S U A L F I E L D D E F E C T S Credit to: David C Broadway, https://www.cehjournal.org/article/visual-field-testing-for-glaucoma-a-practical-guide/ PRIMARY OPEN- ANGLE GLAUCOMA (POAG) • Glaucomatous visual field defects + open angle + IOP >21mmHg • Investigations: • Fundoscopy  high cup to disc ratio and thinning of the neuroretinal rim • Pachymetry  measures CCT • Perimetry: for visual field testing • Management: • Medical treatment: IOP-loweing agents • Laser eg Argon Laser Trabeculoplasty or Selective laser trabeculoplasty. • Surgery eg Trabeculectomy: if failure of other treatments (MIGS) PRIMARY OPEN- ANGLE GLAUCOMA (POAG) Risk factors: 1.Age 2.Ethnicity – common in Afro-Caribbean 3. Family history 4.Myopia 5.Vascular disease (diabetes, HTN) NORMAL TENSION GLAUCOMA (NTG) • Similar to POAG but with normal IOP (IOP 21 mmHg). • More common in far east (e.g. Japanese) • Associations: Raynaud phenomenon, migraines and hypotension. • Untreated, 50% of NTG patients actually show no progression of field defects at 5y • Treatment is similar to POAG and aimed at high risk patients: • Prostaglandin analogue is considered superior to beta-blockers: 1- better IOP control at night 2- beta-blockers can cause a drop in BP PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG) • ‘Angle closure’ refers to occlusion of the TM, causing obstruction of aqueous flow with the potential of causing a rise in IOP and optic nerve damage. • This can be either primary due to an anatomically susceptible eye (see risk factors) or secondary to other ocular conditions. • Terminology: • Primary angle closure suspect (PACS): a narrow angle in which the peripheral iris is almost touching the TM. No peripheral anterior synechiae (PAS) present (PAS- refers to the adherence of the peripheral iris anteriorly in the anterior chamber). • Primary angle closure (PAC): PAS + elevated IOP or presence of PAS. However, no glaucomatous optic nerve changes. • Primary angle closure glaucoma (PACG): PAS + elevated IOP + glaucomatous changes and visual field defects PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG) • Risk factors: • Increasing age. • Far eastern race. • Hyperopia. • Short axial length. • Relative pupillary block (pathophysiology): • Failure of the normal aqueous flow through the pupil results in the anterior bowing of the peripheral iris leading to angle closure. • The risk is highest in a mid-dilated pupil due to maximum contact between iris and lens at this level.• Features • Exacerbated by: watching TV in a dark room, reading, meds. • Symptoms (acute): asymptomatic or haloes, blurring, pain, headache, vomiting and visual loss may occur. • Signs (acute): a fixed mid-dilated pupil, very high IOP, corneal oedema and conjunctival hyperaemia. • Resolved acute attack: can notice Descemet membrane folds, and glaukomflecken anterior cataracts. • Management • Acute: supine position, systemic acetazolamide, topical beta-blockers +/- alpha-2 agonists +/- topical prednisolone. • Bilateral YAG LASER Peripheral Iridotomy after resolution of acute attack. • Cataract extraction  may be effective in lowering IOP Credit to: Jonathan Trobe, M.D, https://en.wikipedia.org/wiki/Glaucoma PSEUDOEXFOLIATION SYNDROME • This is a cause of secondary open angle glaucoma in which grey-white fibrillar deposits blocks the anterior chamber angle • Associations: Hearing loss, Alzheimer’s disease and high plasma homocysteine levels • Features: • Flaky white deposits on the anterior lens capsule. • Sampaolesi line (a band of pigmented anterior to the Schwalbe line on gonioscopy). • Peri-pupillary defect on Transillumination slit lamp. PIGMENT DISPERSION SYNDROME • Cause of secondary open angle glaucoma, characterized by excessive ‘shedding’ of pigmented material of the iris deposited throughout the anterior segment. • AD inheritance • Risk factors: myopia and males • Clinical features • Blurred vision and haloes on exertion. • Mid-peripheral spoke-like defects of the iris on transillumination. • Vertical spindle shaped pigments on the corneal endothelium (Krukenberg spindles). • Trabecular meshwork pigmentation. NEOVASCULAR GLAUCOMA • It is a cause of either secondary open or closed angle glaucoma • Neovascular glaucoma occurs due to proliferation of fibrovascular tissue in the anterior angle and results from rubeosis Iridis (iris neovascularization). • Glaucoma typically occurs 3 months after the occlusive event (‘100-day glaucoma’). • Causes: Ischaemic CRVO, Diabetes mellitus (proliferative), Ocular ischaemic syndrome and CRAO. • Features • Pain • New radially orientated vessels on iris surface and pupillary margins. • Corneal oedema and acute IOP elevation NEOVASCULAR GLAUCOMA • Management: • PRP and/or Anti-VEGF: to reduce neovascularization. • Medical treatment: • Topical steroids and atropine • IOP-lowering agents: similar to POAG; however, pilocarpine (worsens synechial angle closure) and prostaglandin analogues (can increase inflammation) should be avoided • If GOOD visual potential = Glaucoma Drainage Device (Tube) • IF BAD visual potential = Cyclodiode Laser POSNER-SCHLOSSMAN SYNDROME • A rare disorder characterized by recurrent unilateral acute attacks of IOP elevation and may cause secondary open angle glaucoma • Associated with CMV or H. pylori infection and with HLA-BW5 • Clinical features • Discomfort, haloes and blurred vision. • Anterior chamber inflammation (white keratitic precipitates found in anterior chamber on slit lamp). • Mydriasis. • Treatment • Topical beta blockers or CAI + topical steroids. LENS-RELATED GLAUCOMA Phacolytic Glaucoma Phacomorphic Glaucoma • Secondary open angle glaucoma leakage of lens • Secondary angle-closure glaucoma  swelling of protein from a hypermature cataract a cataractous lens potentiating a pupillary block. • Presentation: • Presentation and management is similar to PACG  cataract extraction for definitive treatment • Pain • Decreased vision (cataract) • Corneal oedema / Ant Segment Inflammation • Management: • IOP-lowering agent • Cataract extraction for definitive treatment TRAUMATIC GLAUCOMA Red cell glaucoma Angle-recession glaucoma • The accumulation of red blood cells (hyphaema) • It is a cause of secondary open angle glaucoma due after a blunt trauma, leading to the blockage of tto rupture of the ciliary body caused by a blunt trabecular meshwork  increased IOP. trauma • Visible blood in the anterior chamber on slit lam• The risk of glaucoma occurring is 10% after 10 examination. years following the traumatic incident • Secondary bleed may occurs about 3-7 days post- • Irregular widening of the face of the ciliary body on injury. gonioscopy. OTHER TYPES OF GLAUCOMA Ghost cell glaucoma Schwartz–Matsuo syndrome Blockage of the TM by degenerate RBC typiAnterior Uveitis + high IOP with open angle arising weeks after a vitreous haemorrhage from a rhegmatogenous RD STURGE-WEBER SYNDROME • Congenital neuro-oculocutaneous disorder that can cause secondary open angle glaucoma • Features: • Cutaneous: Port wine stain typically along CNV 1nd CNV .2 • Neurological: Seizures and learning disabilities • Ocular: Ipsilateral choroidal haemangiomas and glaucoma wine-stains-sturge-weber-syndrome/?lp=trueerest.co.uk/sggriffie70/birthmarks-port- PRIMARY CONGENITAL GLAUCOMA (PCG) • PCG is a rare, mostly bilateral disease that usually occur in the first year of life • Epidemiology • Incidence: 1 in 10,000 births. • More common in boys. • Mostly sporadic, however, can have an AR inheritance pattern. • Clinical features • Epiphora, corneal oedema, photophobia, and blepharospasm. • Buphthalmos: large eyes due to elevated IOP. • Increased corneal diameter: >12 mm • Haab striae: Healed breaks in the Descemet membrane due to corneal oedema, best seen on Retroillumination. PRIMARY CONGENITAL GLAUCOMA (PCG) • Investigations • IOP measurements: normal IOP for newborns is 10-12 mm Hg. • Optic disc evaluation for cupping: look for asymmetry or a ratio of > 0.3. • Corneal diameter measurement. Normal range is 10-10.5 mm. • If necessary, the examination can be performed under general anesthetics for uncooperative newborns or infants. • Management: • Angle surgery is the mainstay treatment, Goniotomy or trabeculotomy. • Goniotomy can be performed if the cornea is clear. If the cornea is cloudy then trabeculotomy can be tried. GLAUCOMA PHARMACOLOGY