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Anatomy of the angle structure (glaucoma)

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This presentation is orginaly uploaded to http://kpkmedicalcolleges.tk by Dr.Suleman

This presentation is orginaly uploaded to http://kpkmedicalcolleges.tk by Dr.Suleman

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  • 1. Recommended Books for Ophthalmology 1. Vaughan & Asbury’s General Ophthalmology 16th Edition 2004 a LANGE medical book • Parsons’ Diseases of the Eye 19th Edition 2003 Butterworth publication 3. Clinical Ophthalmology by Jack J. Kanski 5th Edition 2003 Butterworth publication
  • 2. GLAUCOMA Patho-physiology & Detection Dr. Nasir Saeed
  • 3. Epidemiology of Glaucoma Glaucoma is not a single disease entity,but the result of a group of different mechanisms which cause a loss of retinal ganglion cells. This loss may be acute or episodic, or slowly and relentlessly progressive. Some authors therefore refer to ‘the glaucomas’. The common, connecting feature used to be regarded as the height of the intraocular pressure (IOP), which dominated the understanding of the clinical manifestations to a greater or lesser extent. Although intraocular pressure is frequently raised, it is now regarded as a risk factor, and no longer considered a defining characteristic.
  • 4. Glaucoma prevalence surveys, by racial groups Location Age PACG (%) POAG (%) Secondary glaucoma Congenital/ Developmental European Baltimore, Md. 40+ 0.31 1.29 0.68 No available Origin Beaver Dam, Wisc. 43-84 0.04 2.1 Not stated Not stated Blue Mountains, Australia 49+ 0.27 3.0 0.15 Nil African Jamaica 35-74 Nil 1.4 0.35 Nil Origin Baltimore, Md. 40+ 0.67 4.74 1.42 Not available Asian Umanaq area, Greenland >40 4.8 1.26 1.00 Nil NW Alaska 40+ 2.65 0.24 Nil Nil Beijing, China 40+ 1.4 0.03 Not stated Not stated Hövsgöl, Mongolia 40+ 1.4 0.5 0.3 Nil Origin
  • 5. World estimates of glaucoma prevalence Affected Congenital 300 000 POAG 13.5 million PACG 6 million Secondary 2.7 million Glaucoma suspects 105 million (IOP>21 mmHg) Blind 200 000 3 million 2 million ?
  • 6. RISK FACTORS Age: The prevalence and incidence of PACG increase with age. Although a peak has been claimed, the best evidence suggests that incidence rises continually with age. Attacks of ACG are rare before age 45.
  • 7.  GENDER • POAG • PACG  Race • Chinese • European • Africans • Japanese • Asians  Refraction • ACG • POAG Genetics Equal Females > Males ACG POAG POAG<ACG NTG ACG<=POAG Hypermetopes Myopes
  • 8. • Intra-ocular Pressure • Diabetes • Family History • Hypertension • Vascular Spasm
  • 9. ANATOMY OF THE ANGLE STRUCTURES
  • 10. Aqueous Humour Produced by the ciliary processes into the posterior chamber • Through the pupil it circulates into the anterior chamber • 90% of it is drained through the trabecular meshwork into the Schlemm’s canal and the epi-scleral venous system (conventional pathway) • 10% of it leave the eye through the uveo-scleral route (un-conventional pathway) into the suprachoroidal space and chained by venous circulation of the ciliary body and sclera
  • 11. Functions of Aqueous humour  It maintains the shape and internal structure of the eye by sustaining an intraocular pressure higher then atmospheric pressure and helps in maintaining the optical structure.  It carries oxygen and nutrients to the lens and cornea It carries waste products away from the lens and cornea
  • 12. Aqueous humour production • Produced by the ciliary processes of the ciliary body. Two Mechanisms I- Active secretion • 80% of aqueous is produced by the non pigmented ciliary epithelium as a result of active metabolic process • Involves several enzymatic systems i.e. Na+ - K + ATPase / Carbonic Anhydrase • Na+, K+, Ascrobate, HCO3 • Transported into the posterior chamber • Secretion diminishes by factors which will inhibit active metabolism like drugs, hypoxia, hypothermia • Independent of IOP
  • 13. Aqueous humour production II- Passive Secretions • 20% • Diffusion to maintain equilibrium between the osmotic pressure and electrical balance on the two sides of the ciliary processes • Ultra-filtration • When the diffusion of water and salt is accelerated by blood pressure (hydrostatic pressure) in the ciliary body The passive secretion is dependent on level of blood pressure in the ciliary body, plasma oncotic pressure and intraocular pressure • Blood Aqueous Barrier • Large molecules such as plasma proteins and cells do not get into the aqueous chambers even when the plasma concentration is very high •Sites of the barrier is tight junctions between the non-pigment ciliary epithelium and their basement membrane
  • 14. Intra-ocular pressure (IOP) • The circulation of aqueous humour in the eye maintains the IOP • The equilibrium of aqueous formation and outflow rate is of crucial importance • Normally aqueous humour is secreted at a rate of 0.02µl / minute and same amount is drained •The distribution of IOP in general population : 11-21 mm of Hg •Average = 15 mm of Hg • Diurnal variation – High in morning Low in evening • No sex difference by 5 mm of Hg
  • 15. Determinants of Intraocular Pressure • Rate of aqueous humour formation • Resistance encountered in out flow channels • Level of epi-scleral venous pressure
  • 16. Factors influencing Intra-Ocular Pressure I- Rate of Aqueous Humour formation Increased by a. Inflammation b. Blood Pressure c. Hypo-osmolarity of plasma Decreased by a. Retinal / Choroidal / Ciliary body detachments b. Drugs B-Blocker Carbonic Anhydrase hulibitors c. Anaesthesia
  • 17. II- Out flow Resistance Increased by Age Membrane • Pupillary Block Synechia Lens Vitreous • Trabecular Meshwork block Inflammation Cellular debris Steroids Inflammatory exudates Peripheral Iris bowing Peripheral Anterior Synechia Idiopathic
  • 18. • Outflow Resistance Decreased by • Accommodation • Drugs • Miotics • Prostaglandins • Adrenaline
  • 19. III- Episcleral Venous Pressure Increased by • Increased CVP • Valsalva • Carotid Cavernous fistula • Hypercarbia •Dysthyroid eye disease •Succinyl – choline • Co-contraction of extra-ocular muscles Decreased by • Hypotension • Decreased carotid blood flow • Decrease CVP
  • 20. Applied Anatomy of the optic n. head Retinal Nerve fibre layers
  • 21. Relative positions of nerve fibre layer
  • 22. Cross Section of the Optic N. Head
  • 23. Optic Cup & Neuro-retinal rim
  • 24. Physiological Cup & Neuro-retinal rim
  • 25. Glaucomatous Damage Retinal Nerve fibre layers Normal
  • 26. Glaucomatous Damage Abnormal Nerve fibre layers
  • 27. Abnormal nerve fibre layers
  • 28. Glaucomatous Damage Optic disc cupping
  • 29. Bilateral glaucomatous cupping with inferior notching and ‘bayonetting’
  • 30. Bilateral advanced glaucomatous cupping with nasal displacement of the blood vessels
  • 31. End – Stage glaucomatous cupping
  • 32. Clinical Methods for detection and evaluation of glaucoma • IOP Measurements • Gonioscopy • Perimetry Techniques • Advanced Techniques
  • 33. Measurement of Intraocular Pressure Tonometry Principal • The pressure inside a sphere may be measured directly by canulating it and connecting it to a measuring device. This is called manometry. It is the most accurate method but not practical for routine clinical measurement. • It can also be measured by the • Imbert – Fick Law – Pressure = Force /Area. • The pressure can be measured by measuring the force necessary to flatten a fixed area or by measuring the area flattened by a fixed force. • Also a known force will indent a sphere. In low pressure the indentation will be more and in high pressure the indentation will be less.
  • 34. Goldmann Applanation Tonometer • Applanation tonometry measures the force applied per unit area. The Goldmann tonometry is a variable force tonometer consisting of a double prism with a diameter of 3.06 mm. It is the most popular and accurate tonometer.
  • 35. Goldmann applanation tonometer
  • 36. Fluorescein-stained semicircles seen during tonometry
  • 37. A- Schiotz tonometer B- Principles of indentation tonometry
  • 38. • Checking for diurnal changes= phasing • Demonstrating elevation of IOP after pupillary dilation, water drinking • IOP checking in different direction of gaze • Checking for steroid responsiveness • IOP-measurement digitally
  • 39. Gonioscopy • Visualization of the anterior chamber angle is called Gonioscopy Purposes 1. Diagnostic: to identify abnormal angle structures and to estimate the width of the anterior chamber angle. This is particularly important to classify the open angle and angle closer glaucoma 2. Surgical: to visualize the angle during the procedures such as laser trabeculopasty and goniotomy
  • 40. Optical Principal • In normal circumstances the angle of anterior chamber can not be visualized because of the total internal reflection Lighter Medium a b c d d c b a Critical Angle Denser Medium
  • 41. Optical Principal of Gonioscopy
  • 42. Single Mirror goniolens & Zeiss four mirror goniolens
  • 43. Swan-Jacob surgical goniolens & Koeppe goniolenses
  • 44. Normal Anatomy of Angle structure
  • 45. Schaffer’s Grading System
  • 46. Abnormal Anterior Chamber Angle
  • 47. Perimetry • Visual fields ; • An island of vision surrounded by a sea of darkness
  • 48. • Isopter. An Isopter is a line in the field of vision exhibiting similar visual acuity • Scotoma. Is a defect in the visual field • Absolute • Relative • Positive • Negative • Visible threshold. Is the luminance of the stimulus measured in dB at which it is perceived 50% of times when it is presented statically
  • 49. Perimetric Principals • Perimetry is a method of evaluating the visual fields • Qualitative Perimetry is a method of detecting a visual field defect and is the first screening phases of glaucoma suspects • Quantitative Perimetry
  • 50. Visual Fields defects in glaucoma 1. Arcuate scotomas : develop between 100 and 200 of fixation in areas that constitute downward or more commonly, upward extensions from the blind spot (Bjeerrum area) 2. Isolated paracentral scotomas: superior or inferior scotomas may also be found in early glaucoma. 3. A nasal (Roenne) step 4. Ring scotomas 5. Temporal Wedge 6. End Stage fields defects
  • 51. 1. Arcuate scotomas : develop between 100 and 200 of fixation in areas that constitute downward or more commonly, upward extensions from the blind spot (Bjeerrum area)
  • 52. Isolated paracentral scotomas: superior or inferior scotomas may also be found in early glaucoma
  • 53. A nasal (Roenne) step
  • 54. Temporal Wedge
  • 55. End Stage fields defects
  • 56. Advanced Techniques Quantitative Measurements • Digitalized photogrammetry • Confocal scanning laser ophthalmoscope (HRT) • Measurements of ocular blood flow
  • 57. Digitalized photogrammetry
  • 58. Confocal scanning laser ophthalmoscope (HRT)
  • 59. Glaucoma is the second leading cause of worldwide blindness. Early detection and early onset of treatment are the most important factors for preventing progressive glaucoma damage. A comprehensive evaluation of a glaucoma suspect is the key to diagnosis and management.
  • 60. The aims of assessment are:  To assess the risk factors to determine whether glaucoma is present or likely to develop  To exclude or confirm the alternative diagnosis  To identify the underlying mechanism of damage; so as to select best choice for management  To plan a strategy for management
  • 61. ASSESSMENT
  • 62. Presenting Social HISTORY Family Past
  • 63. VA Gonio OM IOP Exoph EXAMINATION Fundus Ocu surf Cornea Lens Pupils AC
  • 64. Ocular Examination  Record visual functions  Ocular motility  Exclude any proptosis/exophthalmos  Ocular surface for episcleral blood vessels  Conjunctiva for papillae and follicles  Cornea for size, shape and transparency  Check for corneal thickness
  • 65. Ocular Examination  Anterior chamber for inflammation, blood, pigment  Check for AC depth, central and peripheral • Convex iris-lens diaphragm • Shallow anterior chamber • Narrow entrance to chamber angle
  • 66. Ocular Examination Iris for atrophy , rubeosis, trans-illumination defects and pseudoexfoliation Stromal iris atrophy with spiral-like configuration Mid-peripheral iris atrophy Central disc with peripheral band
  • 67. Ocular Examination  Pupil for size, shape and reaction  Lens for presence, transparency, thickness, position and shape
  • 68. Ocular Examination    Record intraocular pressure, look for diurnal variations Evaluate IOP for 24 hours if in doubt Use a Goldmann-style applanation tonometer
  • 69. Ocular Examination Gonioscopy: look for width of the angle, configuration of the iris and chamber, PAS, vessels and iris processes Open angle of normal appearance Schaffer’s grading of angle Trabecular hyperpigmentation - may extend anteriorly (Sampaolesi line) Synechial angle closure Irregular widening of ciliary body band
  • 70. Ocular Examination Fundoscopy: evaluate optic nerve head and retinal nerve fibre layer use slit lamp indirect lenses and a dilated pupil Look for optic disc size, colour, neuro-retinal rim, disc haemorrhage, vascular pattern, peri-papillary atrophy and cup disc ratio Small dimple central cup Larger and deeper punched-out central cup Cup with sloping temporal wall
  • 71. Optic disc evaluation
  • 72. Retinal nerve fibre layer analysis
  • 73. Investigations Order for a visual field examination with a standard automated perimeter
  • 74. Investigations HRT OCT GDx
  • 75. Systemic investigation include Imaging of CNS Evaluation of CVS Haematological profile