Glaucoma 1

glaucoma ppt

1. Glaucoma

2. GLAUCOMA Definition The term glaucoma refers to the group of diseases that have in common a characteristic optic neuropathy with associated visual function loss. Although IOP is one of the primary risk factors , it’s presence or absence doesn’t have a role in the definition of the disease. Glaucoma leads to a characteristic appearance of the optic nerve head and a specific pattern of irreversible visual field defects.

3. Why glaucoma is important? Second leading cause of global blindness Leading cause of irreversible visual loss. Visual impairment from glaucoma affects adults more than children and women more than men. By the year 2020 : 80.5 million people in the world with glaucoma

4. ANATOMY AND PHYSIOLOGY APPLIED ANATOMY Pathophysiology of glaucoma revolves around the aqueous humour dynamics It is essential to understand the production and drainage of aqueous humour as well as the anatomy of the angle of the anterior chamber The principal ocular structures concerned with it are Ciliary body Angle of anterior chamber Aqueous outflow system

5. CILIARY BODY Ciliary body is forward continuation of the choroid at ora serrata T riangular in shape The anterior side of the triangle forms the part of the angle of anterior and posterior chambers The anterior part (about 2 mm) having finger-like ciliary processes is called pars plicata and the posterior smooth part (about 4 mm) is called pars plana

6. Angle of anterior chamber Angle of anterior chamber plays an important role in the process of aqueous drainage Formed by root of iris, anterior-most part of ciliary body, scleral spur, trabecular meshwork and Schwalbe’s line (prominent end of Descemet’s membrane of cornea) Fig. Section of the anterior ocular structures showing region of the anterior chamber

7. Clinically the angle structures can be visualised by gonioscopic examination Gonioscopic grading of the angle width The most commonly used is Shaffer’s system Diagrammatic depiction of various angle structures (SL, Schwalbe's line; TM, trabecular meshwork; SS, scleral spur; CBB, ciliary body band; ROI, root of iris) as seen in different grades of angle width (Schaffer's gradingsystem ): A, Gonioscopic view; B, Configuration of the angle in cross section of the anterior chamber

8. Aqueous outflow system IT includes Trabecular meshwork sieve-like structure through which aqueous humour leaves the eye consists of three layers,which from inside out are Uveal meshwork Corneoscleral meshwork Juxtacanalicular (endothelial) meshwork Schlemm’s canal Collector channels Direct( aqueous veins) Indirect Episcleral veins The aqueous outflow system

9. APPLIED PHYSIOLOGY Concerned with the dynamics of aqueous humour are its production, drainage and maintenance of intraocular pressure Aqueous humour and its production Functions and compostion of aqueous humour Volume : A nterior chamber (0.25 ml) and posterior chamber (0.06 ml ) Functions of aqueous humour are M aintains a proper intraocular pressure Metabolic and nutritional role Optical function Clearing function

10. Functions and compostion of aqueous humour cont. Refractive index of aqueous humour is 1.336 Composition Water 99.9% , solids 0.1% Proteins (colloid content )(5-6 mg%) Amino acid 5 mg/kg water Non-colloid constituents Oxygen Aqueous humour : anterior chamber versus posterior chamber main differences are : HCO3 and Ascorbate in posterior chamber Cl in posterior chamber

11. Aqueous humour formation Ultrafiltration Secretion Diffusion Control of aqueous formation Drainage of aqueous humour Trabecular (conventional) outflow Uveoscleral (unconventional) outlow Flow chart depicting drainage of aqueous humour

12. Mechanism of aqueous transport across inner wall of Schlemm’s canal Passive filter mechanism Leaky pores in endothelial cells Contraction microfilaments Sondermann’channels Vacuolation theory-it was one of the most accepted view till recent past Aqueous outflow active pump mechanism

13. Vacuolation theory of aqueous transport across the inner wall of the Schlemm's canal: 1. Non-vacuolated stage; 2. Stage of early infolding of basal surface of the endothelial cell; 3. Stage of macrovacuolar structure formation; 4. Stage of vacuolar transcellular channel formation;5.Stage of occlusion of the basal infolding .

14. Aqueous outflow pump mechanism, a part of muscular circulatory loop: (A) during diastole; (B) during systole

15. Intraocular pressure The intraocular pressure (IOP) refers to the pressure exerted by the intraocular fluids on the coats of the eyeball. Normal IOP = 10-21 mmHg It is determined by the rate of aqueous secretion and rate of outflow.

16. Factors influencing intraocular pressure Local factors Rate of aqueous formation which in turn is influenced by permeability of ciliary capillaries and osmotic pressure of the blood. Resistance to aqueous outflow Increased episcleral venous pressure may result in rise of IOP Dilatation of pupil in patients with narrow angle can cause rise in IOP Refractive errors

17. General factors Hereditary Age - increases after 40 years Sex- mean IOP is greater in females in the older age group Diurnal variation- usually the IOP is greater in the morning than evening ( normal <5mmHg) Postural variation- increases from sitting to supine Blood pressure- glaucoma is more prevalent in hypertensives Osmotic pressure of blood- increase in plasma osmolarity is associated with decrease in IOP and vice versa General anaesthetics and drugs

18. CLASSIFICATION OF GLAUCOMA Classification Clinico -etiologically glaucoma may be classified as follows : (A) Congenital and developmental glaucomas 1. Primary congenital glaucoma (without associated anomalies ). 2. Developmental glaucoma (with associated anomalies). ( B) Primary adult glaucomas 1. Primary open angle glaucomas (POAG) 2. Primary angle closure glaucoma (PACG) 3. Primary mixed mechanism glaucoma (C) Secondary glaucomas Depending upon etiology Depending upon mechanism of raised IOP

19. Epidemiology Global prevalence of glaucomas 2% of those over the age of 40 years , and 10% of those over 80 years of age POAG versus PACG in different ethnic groups Glaucoma blindness Global : 8% India : 12.8%

20. Glaucoma – what is happening ? Either: the drain blocks here Or poor blood supply here Damages the optic nerve..looks ‘caved in’, called ‘cupped’

21. Pathogenesis of ocular damage Death of retinal ganglion cells(RGCs) caused by : Primary insults M echanical theory( r aised IOP) Neurotrophins are unable to reach the RGCs due to axonal deformation and ischaemia caused by mechanical stretch on lamina cribrosa . Vascular insufficiency theory Failure of autoregulatory mechanism Vasospasm Systemic hypotension Secondary insults Toxic factors like glutamate, oxygen free radicals, nitric oxide released when RGCs undergo apoptosis due to primary insults

22. What happens in glaucoma

23. CONGENITAL / DEVELOPMENTAL GLAUCOMAS TERMINOLOGY Types 1 . Primary developmental/congenital glaucoma 2 . Developmental glaucoma with associated ocular anomalies 3. developmental glaucoma with associated systemic anomalies

24. PRIMARY DEVELOPMENTAL/CONGENITAL GLAUCOMA Newborn glaucoma Infantile glaucoma Juvenile glau coma Prevalence and genetic pattern Pathogenesis Maldevelopment of trabeculum including the iridotrabecular junction ( trabeculodysgenesis ) is responsible for impaired aqueous outflow resulting in raised IOP Flat iris insertion is more common than the concave iris insertion Concave iris insertion is less common

25. Clinical features:- 1. Blephrospasm 2.Photophobia 3.Lacrimation Triad Blephrospasm and Photophobia

26. Clinical features Photophobia, blepharospasm , lacrimation ( classic triad) Corneal signs Corneal oedema Corneal enlargement Tears and breaks in Descemet’s membrane ( Haab’s striae ) Sclera Anterior chamber becomes deep Iris may show iridodonesis and atrophic patchesin late stage Lens becomes flat due to stretching of zonules and may even subluxate Optic disc may show variable cupping and atrophy especially after third year IOP is raised which is neither marked nor acute Axial myopia

27. Haab Striae

28. Corneal Haze

29. Examination ( Evaluation) A complete examination under general anaesthesia (EUA) should be performed on each child suspected of having congenital glaucoma The examination should include following Measurement of IOP Measurement of corneal diameter SLIT LAMP EXAMINATION Gonioscopic examination of angle of anterior chamber Ophthalmoscopy Differential diagnosis I t is to be considered for different presenting signs as follows Cloudy cornea, Large cornea, Lacrimation, Photophobia, Raised IOP, Optic disc changes

30. Cloudy Cornea - STUMPED S clerocornea T ears (e.g. tears in Descemets due to forceps delivery) U lcers M ucopolysaccharidoses P eters anomaly E ndothelial dystrophy D ermoids

31. Treatment Medical treatment Surgical procedures for congenital glaucoma Incisional angle surgery Goniotomy Trabeculotomy Filteration surgery Trabeculectomy with antimetabolites Combined trabeculotomy and trabeculectomy with antimetabolites Glaucoma drainage devices(GDD) Technique of goniotomy : A, showing position of goniotomy knife in the angle under direct visualization; B, showing procedure of sweeping the knife in the angle

32. Technique of trabeculotomy

33. Follow-Up Patient should be reviewed 1 month after initial surgery. IOP & Corneal diameters should be monitored at regular interval. Cycloplegic refraction should be done at 6 monthly interval.

34. DEVELOPMENTAL GLAUCOMAS WITH ASSOCIATED OCULAR ANOMALIES Glaucoma associated with iridodysgenesis ANIRIDIA FAMILIAL IRIS HYPOPLASIA CONGENITAL ECTROPION UVEA WITH CONGENITAL MICROCORNEA CONGENITAL NANOPHTHALMOS Glaucoma associated with iridocornealdysgenesis POSTERIOR EMBRYOTOXON AXENFELD-RIEGER SYNDROME PETER’S ANOMOLY COMBINED REIGER’S SYNDROME AND PEYERS ANOMALY

35. DEVELOPMENTAL GLAUCOMAS WITH ASSOCIATED SYSTEMIC ANOMALIES Chromosomal disorders Ectopic lentis syndromes which include Marfan’s syndrome, Weil- Marchesani syndrome and homocystinuria . Glaucoma associated with phakomatosis is seen in Sturge -Weber syndrome ( 50% cases) and Von Recklinghausen’s neurofibromatosis (25% cases) Metabolic syndromes