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Anatomy of the angle structure (glaucoma)
This document provides an overview of glaucoma including epidemiology, risk factors, anatomy, pathophysiology, clinical evaluation methods, and assessment process. Some key points include: - Glaucoma prevalence varies by race and ethnicity with higher rates in African, Asian, Inuit, and Hispanic populations. - Risk factors include increased age, elevated intraocular pressure, family history, myopia, and diabetes. - The anatomy of angle structures and pathways of aqueous humor outflow are described. - Clinical evaluation involves assessment of visual acuity, intraocular pressure, gonioscopy, optic nerve examination, retinal nerve fiber layer analysis, and visual field testing. - A comprehensive glaucoma assessment aims to determine
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Anatomy of the angle structure (glaucoma)
- 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 Glaucomais 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 ofglaucoma 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 prevalenceand 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 THEANGLE STRUCTURES
- 10. Aqueous Humour Produced bythe 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 Aqueoushumour 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 IntraocularPressure • Rate of aqueous humour formation • Resistance encountered in out flow channels • Level of epi-scleral venous pressure
- 16. Factors influencing Intra-OcularPressure 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 flowResistance 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 ResistanceDecreased by • Accommodation • Drugs • Miotics • Prostaglandins • Adrenaline
- 19. III- Episcleral VenousPressure 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 ofthe optic n. head Retinal Nerve fibre layers
- 21. Relative positions ofnerve fibre layer
- 22. Cross Section ofthe Optic N. Head
- 23. Optic Cup &Neuro-retinal rim
- 24. Physiological Cup &Neuro-retinal rim
- 25. Glaucomatous Damage RetinalNerve fibre layers Normal
- 26. Glaucomatous Damage AbnormalNerve fibre layers
- 27. Abnormal nerve fibrelayers
- 28.
- 29. Bilateral glaucomatous cuppingwith inferior notching and ‘bayonetting’
- 30. Bilateral advanced glaucomatouscupping with nasal displacement of the blood vessels
- 31. End – Stageglaucomatous cupping
- 32. Clinical Methods fordetection and evaluation of glaucoma • IOP Measurements • Gonioscopy • Perimetry Techniques • Advanced Techniques
- 33. Measurement of IntraocularPressure 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.
- 36. Fluorescein-stained semicircles seenduring tonometry
- 37. A- Schiotz tonometer B-Principles of indentation tonometry
- 38. • Checking for diurnalchanges= 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 theanterior 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 • Innormal 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 ofGonioscopy
- 42. Single Mirror goniolens& Zeiss four mirror goniolens
- 43. Swan-Jacob surgical goniolens& Koeppe goniolenses
- 45. Normal Anatomy ofAngle structure
- 46.
- 47.
- 48. Perimetry • Visual fields; • An island of vision surrounded by a sea of darkness
- 49. • Isopter. An Isopteris 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
- 50. Perimetric Principals • Perimetryis 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
- 51. Visual Fields defectsin 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
- 52. 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)
- 53. Isolated paracentral scotomas:superior or inferior scotomas may also be found in early glaucoma
- 54. A nasal (Roenne)step
- 55.
- 56. End Stage fieldsdefects
- 57. Advanced Techniques Quantitative Measurements •Digitalized photogrammetry • Confocal scanning laser ophthalmoscope (HRT) • Measurements of ocular blood flow
- 58.
- 59.
- 60. Glaucoma is thesecond 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.
- 61. The aims ofassessment 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
- 62.
- 63.
- 64.
- 65. Ocular Examination Recordvisual 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
- 66. Ocular Examination Anterior chamberfor inflammation, blood, pigment Check for AC depth, central and peripheral • Convex iris-lens diaphragm • Shallow anterior chamber • Narrow entrance to chamber angle
- 67. Ocular Examination Iris foratrophy , rubeosis, trans-illumination defects and pseudoexfoliation Stromal iris atrophy with spiral-like configuration Mid-peripheral iris atrophy Central disc with peripheral band
- 68. Ocular Examination Pupilfor size, shape and reaction Lens for presence, transparency, thickness, position and shape
- 69. Ocular Examination Record intraocularpressure, look for diurnal variations Evaluate IOP for 24 hours if in doubt Use a Goldmann-style applanation tonometer
- 70. Ocular Examination Gonioscopy: lookfor 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
- 71. Ocular Examination Fundoscopy: evaluateoptic 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
- 72.
- 73. Retinal nerve fibrelayer analysis
- 74. Investigations Order for avisual field examination with a standard automated perimeter
- 75.
- 76. Systemic investigation include Imagingof CNS Evaluation of CVS Haematological profile