Glaucoma

1. Glaucoma By: noor majeed rehani

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 posterior 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 • Asian-American descent – this puts you at increased risk for angle-closure glaucoma

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 dick 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 0.9 { normal is 0.0.-0.9) Note: *if IOP reaches 30 mmHg then its enough to diagnose POAG. If IOP <30 with no v. field changes or optic nerve damage its considered ocular hypertension. *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 fibersfrom the eye. With a sustained rise in IOP the nervefibers atrophy, leaving the characteristic sign of chronicglaucoma—the cupped, pale optic disc.

19. Normal disc diameter is 1.5 • 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.

21. Normal tension glaucoma: • Some (dr said 60%)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.

22. Normal tension glaucoma (cont.): • Risk factors: • Family history of glaucoma. • Cardiovascular diseases(migraine , raynaud’s phenomena ) • F>M (dr said that ) Treatment: • Even though the IOP is normal but medication to decrease IOP as much as possible are used.

23. TESTS FOR SCREENING AND DIAGNOSIS: • Exclude other systemic diseases. • 1. Tonometer  IOP (20 – 44 mmHg) • 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 IOP 25 to 29 mm Hg: Evaluation within one week IOP 23-24 warrants repeat measurement to confirm and/or referral for comprehensive eye examination • 5. Visual field testing (perimetry)  scotomata • 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

24. 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

25. Medical treatment Topical eye drops  five families: • Prostaglandins analogues  Latanoprost (1st line of Rx) • B-blocker  Timilol (2nd line of Rx) contraindicated in asthma . • 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 .

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

27. 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

28. Surgery • Drainage surgery ( Trabeculectomy ) by creating a fistula between the anterior chamber and the subconjunctival space • Conjenctival incision. • Sclerostomy. • Iridectomy. • Ahmed valve implant: The device works by bypassing the trabecular meshwork and redirecting the outflow of aqueous humour through a small tube into an outlet chamber or bleb. The IOP generally decreases from around 33 to 10 mmHg by removing aqueous on average 2.75 microliters/min

29. Ddx of tunnel vision • Open angle glaucoma • Retintis pigmentosa

30. 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….

31. 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.

32. Risk factors • Hypermetropia : small eye, big lens • Age 55 – 70 yrs • Female ( have smaller anterior chamber) • Common in asians • Family history of glaucoma • Mature cataracts • Shallow anterior chamber • Pupil dilation ( topical and systemic anticholinergics, stress, darkness)

33. Types of angle-closure glaucoma: • Primary angle closure — Patients are anatomically predisposed to this type of glaucoma; there is no identifiable secondary cause. • Secondary angle closure — A secondary process is responsible for narrowing or closure of the anterior chamber angle. Same causes of synecia  uvietis , NVD. (at first lead to 2ry open then progresses to 2ry closed). • Examples of secondary causes are a fibrovascular membrane that grows over the angle to pull it closed, as in neovascular glaucoma, or a mass or hemorrhage in the posterior segment of the eyeball that pushes the angle closed 

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

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

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

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

38. Acute angle closure glaucoma • They may have similar symptoms in the past that are aborted by going to sleep, because sleeping constricts the pupils pulling it from the lens. • Most common mechanism by which glaucoma happens is when susceptible patient awakes from sleep and gets exposed to faint light.

40. Diagnostic tests • Gonioscopy — Gonioscopy is the gold-standard method of diagnosing angle closure. This technique involves using a special lens for the slit lamp, which allows the ophthalmologist to visualize the angle and diagnose angle closure • Slit lamp grading of anterior chamber depth — In this technique, the width of the angle is estimated by shining a light beam from the slit lamp on the peripheral anterior chamber. It is not as reliable as gonioscopy for diagnosing angle closure. • Ultrasound biomicroscopy — Specialized ultrasound of the anterior chamber can show angle closure and help to define the mechanism. The ultrasound biomicroscope instrument is costly and thus not widely available. This technique also requires specialized interpretation of the results.

41. 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. • Incase of occludable angle or 2ry closed angle glaucoma perform trabeculectomy or Ahmed valve implant. • Note: acetazolamide + B-blocker  reduce aqueous secretion pilocarpine  constricts the pupil and draws the peripheral iris out of the angle

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

43. ENLARGED OPTIC NERVENotice the large cupping or large white area within the nerve

44. The red vessel located at about 11 o'clock should not be there.  This is called a Drance Hemorrhage and shows up in glaucoma.

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

46. Congenital glaucoma

47. Congenital glaucoma • By definition, primary congenital glaucoma is present at birth; however, its manifestations may not be recognized until infancy or early childhood. • It is characterized by improper development of the eye's aqueous outflow system, leading to increased intraocular pressure (IOP), with consequent damage to ocular structures, resulting in loss of vision.. Early recognition and appropriate therapy of the glaucoma can significantly improve the child's visual future.

48. Congenital glaucoma • This type of glaucoma is due to the abnormal development of the anterior chamber angle before birth. • This causes a decrease in aqueous outflow through the trabecular meshwork. • Congenital glaucoma may be found in association with congenital cataract extraction, inflammation, injury, or in conjunction with other syndromes or diseases.

49. Congenital glaucoma History:  This 15-day-old infant was presented with a history of having cloudy corneas since birth.  The child is fussy and her eyes watery.  Two older siblings are normal and there is no family history of a similar eye condition.  Intraocular pressure is 50 in each eye and the corneal diameters are 12.5 mm in each eyeDiagnosis:  congenital glaucoma

50. Congenital glaucoma Symptoms • Tearing • Light sensitivity • Bupthalmusdue to epithelial oedema.(increase corneal diameter ). • Cloudy cornea. • Spilts in descement’s membrane ( habbsstria = horizontal stretch marks )