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Glaucoma

Glaucoma. By: Ahmad Al Zu’bi. Definition:. It is a heterogenous group of diseases in which damage to the optic nerve(optic neuropathy) is usually “ not always” caused by raised ocular pressure (normal IOP is 15.5 mmHg) acting on the nerve head.range (11-21). Definition.

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Glaucoma

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  1. Glaucoma By: Ahmad Al Zu’bi

  2. Definition: • It is a heterogenous group of diseases in which damage to the optic nerve(optic neuropathy) is usually “ not always” caused by raised ocular pressure (normal IOP is 15.5 mmHg) acting on the nerve head.range (11-21)

  3. Definition • Its optic neuropathy and visual field defect with or without increase intraocular pressure . • So glaucoma doesn't always equal increase IOP

  4. Basic physiology of aqueous humour: • Conventional pathway • Uveo-scleral pathway IOP: Depends on the balance between production and removal of aqueous humour

  5. 1. Conventional Pathway: • Aqueous humour is secreted by the ciliary processes in the posterior chamber. Then it passes through the pupil into the anterior chamber. • It is drained in anterior chamber through the Trabecular meshwork, Schlemm’s canal, and episcleral veins.

  6. 2. Uveo-scleral pathway choroid Supra-choroidal space • Drains a small proportion of aqueous (4%). • It drains it across the ciliary body into the supra-coroidal space, and into the venous circulation across the sclera.

  7. Mechanism of Optic nerve fiber damage • Mechanical damage To optic nerve axons by the raised IOP • Ischemia of nerve fibers caused by impaired perfusion pressure (reducing blood flow at optic nerve head)

  8. Risk factors of glaucoma • Over age 60 • family member with glaucoma • Are nearsighted • diabetes, high blood pressure, heart disease or hypothyroidism • injury to the eye, certain eye surgeries or chronic eye inflammation • steroids for long periods of time

  9. Classification of Glaucoma: • Primary glaucoma: • Chronic open angle • Acute and chronic closed angle • Congenital glaucoma: • Primary • Rubella • Seconday to other inherited ocular disorders (e.g. an-iridia; absense of iris) • Secondary glaucoma (causes): • trauma • Ocular surgery • Associated with other ocular diseases (uveitis) by { hypopyon , posterior synechea , steriodtt } • Raised episcleral venous pressure • Steroid induced

  10. Primary Glaucoma: Is the iris: NOT covering the Trabecular meshwork Covering the Trabecular meshwork CLOSED angle glaucoma OPEN angle glaucoma

  11. Primary OPEN angle glaucoma • Pathogenesis: • Resistance of drainage of aqueous through the Trabecular meshwok, due to: • Thickening of Trabecular lamellae (reduces pore size). • Reduction in number of lining Trabecular cells. • Increased extracellular material in the Trabecular meshwork spaces.

  12. Open irido-corneal angle (Trabecular meshwork is not covered)

  13. Primary OPEN angle glaucoma: • It is the most common type of glaucoma • It is the 3rd cause of blindness in the UK. • It is also called chronic open angle glaucoma. • It causes SLOW damage to the optic nerve, causing gradual loss of vision.

  14. The patient first loses the peripheral visual field then it progress to total blindness if left untreated.

  15. As fluids accumulates in the anterior chamber due to decreased drainage, intra-ocular pressure increases and cases damage to the optic nerve.

  16. Primary OPEN angle glaucoma • Symptoms: • Because the vision loss is gradual, usu. Bilateral and asymmetrical the patient usually present when severe damage has occurred& Its painless . • Most patients are detected by optometrist routine examination. Other sign is disck cupping . • Visual field defect : Gradual loss of peripheral vision, usually in both eyes, Tunnel vision in the advanced stages • Risk groups: • Affects 1 in 200 of population over the age of 40. • Males and females are equally affected. • There maybe family history but the exact mode of inheritance is not clear. • Myopic patient .

  17. POAG criteria: (you need 2 out of 3) • IOP • Visual field changes • Optic nerve damage (cupping) • Cupping takes place first then the visual field changes. • Visual field changes: 1) nasal step 2) arcuate scotoma 3) tunnel vision 4) blurring in central vision. • C:D(cup:disk) ratio 0.4; visual acuity changes take place after cupping reaches 0.8 { normal is 0.0.-0.8) Note: *visual acuity is the least affected in glaucoma. Don’t mix between v. field and v. acuity.

  18. Optic disc cuppingThe optic disc marks the exit point of the retinal nerve fibers from the eye. With a sustained rise in IOP the nervefibers atrophy, leaving the characteristic sign of chronicglaucoma—the cupped, pale optic disc.

  19. High C:D ratio with smaller disc is more likely to be glaucoma than high C:D ratio with large disc , because the large disc permits higher number of neuron to pass through and achieve good vision . • Rapid progression of C:D ratio even is small increase / time is more significant that higher but steady C:D ratio.

  20. Normal tension glaucoma: • Some open angle glaucoma have normal intra-ocular pressure called low-tension or normal-tension glaucoma.(glucomatous change) • In these cases, there will be damage to the optic nerve even though the intra-ocular pressure is within normal range. • The eyes of the normal tension glaucoma have normal angles, so its features are similar to that of primary open angle glaucoma. • The causes of normal tension glaucoma is still unknown. The optic nerve is susceptible to damage even from normal IOP. • Normal-tension glaucoma is thought to be related, at least in part, to poor blood flow to the optic nerve.

  21. Normal tension glaucoma (cont.): Treatment: • Even though the IOP is normal but medication to decrease IOP as much as possible are used.

  22. TESTS FOR SCREENING AND DIAGNOSIS: • Exclude other systemic diseases. • 1. Tonometer  IOP (<22) • Parameters for referral : IOP > 40 mm Hg: Emergency referral IOP 30 to 40 mm Hg: Urgent referral (within 24 hours) if no symptoms suggesting acute glaucoma • Optic disk : measure vertical ratio (cup to disk) 0.4 (0-0.8) • 2. Gonioscopy  iridocorneal angle to see if its open or closed , not seen in slit lamp . • 3. Pachymetry  corneal thickness , normal corneal thickness is 54o Micrometer , The lower the thickness the higher risk for glaucoma . When corneal thickness is low u overestimate the IOP and vise versa . • 4. Fundus examination : cupping , splinter hemorrhage of nerve fiber • 5. Visual field testing (perimetry)  scotomata

  23. Management: • Aim of treatment is to decrease the IOP • Amount of decrease depends on the level at which no more damage to the optic nerve happens . • This level differs from patient to other . • Modalities : 1- Medical Treatment 2- Laser Treatment 3- Surgical Treatment

  24. Medical treatment Topical eye drops  five families: • Prostaglandins analogues  Latanoprost (1st line of Rx) • B-blocker  Timilol (2nd line of Rx) contraindicated in asthma .we can use bate 1 selective but with caution in asthmatic patient . • Carbonic anhydrase inhibitors  Dorsolamide • Alpha 2 agonist  Brimonidine. • Cholinergic agonist  Pilocarpine Systemic (IV / oral) • CAI (Acetazolamide )  S/E: hypokalemia, metabolic acidosis, renal stones, nephritis, parasthesia (m. common S/E) • Manitol{hyperosmotic} S/E: rebound increased IOP. MOA : 1+4+5 > increase aqueous humor outflow . 2+3+4 > decrease aqueous secretion .

  25. If IOP remains elevated the choice lies between: • Adding additional medical treatment • Laser treatment • Surgical drainage procedures

  26. Laser treatment • laser burns in the trabecular meshwork to improve aqueous flow • Laser trabeculoplastyindications: 1.Failed medical therapy. 2. Avoidance of polypharmacy 3. Avoidance of surgery in elderly 4. As primary therapy in patients who are expected not to comply with medical treatment

  27. Surgery • Drainage surgery ( Trabeculectomy ) by creating a fistula between the anterior chamber and the sub conjunctival space • Conjunctival incision. • Sclerostomy. • Iridectomy.

  28. Ddx of tunnel vision • Open angle glaucoma • Retintis pigmentosa : ( "classic triad" seen on fundoscopic exam of bony spicule pigmentation, vascular narrowing, and abnormal pallor of the optic disc)

  29. Acute angle closure glaucoma: • The condition occurs in small eyes (as in hyperopoia) with shallow anterior chambers. • Normally there is some resistance between the pupil margin when its in the mid-dilated stage and the lens this resistance disturb the drainage of aqueous humor so increase IOP . • But sometimes….

  30. Acute angle closure glaucoma (cont.): Sometimes when the iris is dilated, the lens sticks to the back of the iris causing obstruction of fluid flow from posterior to anterior chambers. Fluid will accumulate behind the iris and pushes it on to the Trabecular meshwork preventing drainage of aqueous from the eye. This causes rapid increase in IOP.

  31. Acute angle closure glaucoma • Symptoms: 1. The eyes becomes red and painful due to rapid increase in IOP & ischemic tissue damage .

  32. Acute angle closure glaucoma 2. Blurred vision; because the cornea becomes edematous.

  33. Acute angle closure glaucoma • Patient may notice haloes (circles of light(rainbow)) around light due to dispersed light in waterlogged cornea. • Headache • Nausea and vomiting dueto vagal stimulation . • Photophobia. DDX : Migraine

  34. Sings • Red eye • Increase IOP . • mid dilated fixed ( reacted poorly to the light) pupil • shallow anterior chamber • Cloudy cornea

  35. Diagnostic tests • Gonioscopy — Gonioscopy is the gold-standard method of diagnosing angle closure. • Slit lamp grading of anterior chamber depth • Ultrasound biomicroscopy

  36. Management • Urgent Treatment is necessary • All efforts to decrease IOP For the acute attack : • IV/oral acetazolamide. If nausea and vomiting are not tolerated switch to manitol. • Topical antiglaucoma Pilocarpine, B-blockers For prevention of subsequent attacks: • Laser  iridotomy • Surgery  iridectomy IS THE MAIN STEP IN TREATMENT . • Prophylactic to the fellow eye. • Note: acetazolamide + B-blocker  reduce aqueous secretion pilocarpine  constricts the pupil and draws the peripheral iris out of the angle

  37. This is an elargement of an optic nerve with glaucoma.

  38. Risk factors • Hypermetropia : closed angle glaucoma • Myopia : open angle

  39. In secondary glaucoma, the rise of intraocular pressure is usually due to trabecular meshwork obstruction. The trabecular meshwork may be blocked by: • • blood ( hyphaema ), following blunt trauma; • • inflammatory cells ( uveitis ); • • pigment from the iris ( pigment dispersion syndrome ); • • deposition in the trabecular meshwork of material produced by the epithelium of the lens, iris and ciliary body ( pseudoexfoliative glaucoma ); • • drugs increasing the resistance of the meshwork ( steroid – induced glaucoma ). • • Abnormal iris blood vessels may obstruct the angle and cause the iris to adhere to the peripheral cornea, closing the angle ( rubeosis iridis ).

  40. Secondary Glaucoma (intro) • Much rarer than Primary Glaucoma • S&S depend on rate at which IOP ↑ • Mostly symptomless.. • Tx : most of underlying cause are not treatable if they are treatable treat them first --Difficult cases : removal of ciliary processes  ↓ aqueous production.. by laser / cryoprobe to d’ sclera overlying d’ processes

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