terminology and guidelines for glaucoma ii - Kwaliteitskoepel

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$Refractiechirurgie - Nederlands Oogheelkundig Gezelschap$

2.2 - PRIMARY OPEN-ANGLE GLAUCOMAS The open-angle glaucomas are chronic, progressive optic neuropathies, that have in common characteristic morphological changes at the optic nerve head and retinal nerve fibre layer in the absence of other ocular disease or congenital anomalies. Progressive retinal ganglion cells death and visual field loss are associated with these changes. The relative risk for POAG rises continuously with the level of the intra-ocular pressure (IOP), and there is no evidence of a threshold IOP for the onset of the condition. It is presumed that risk factors other than IOP have a relatively greater importance if there is glaucomatous optic neuropathy at the lower (statistically ‘normal’) pressure levels. POAG has been arbitrarily subdivided into High Pressure and Normal Pressure disease to reflect this, even though they may represent a spectrum of optic neuropathies variably sensitive to the IOP. Risk Factors associated with increased prevalence of glaucoma damage Glaucomatous damage in the fellow eye Level of intra-ocular pressure, as confirmed in all recent trials (see Ch. Introduction II) Age Race Thin cornea Pseudoexfoliation Myopia > 4 diopters Vascular risk factors: - Local: disc hemorrhage, associated also with worsening of damage peripapillary atrophy, associated also with worsening of damage - Systemic: cerebral disease cardiovascular disease vasospasm: cold hands and feet Raynaud’s phenomena migraine systemic hypotension with nocturnal pressure drops low perfusion pressure hypercholesterolemia / hyperlipidemia. Family history of glaucoma in first degree relatives Diabetes Mellitus: the role is controversial For detailed references a recent review on Evidence - Based glaucoma knowledge is suggested, as well as references in the Introduction Chapter 1 . Supplementary investigations I - If findings do not match, central corneal thickness (CCT) can be useful to evaluate the IOP applanation value (see Ch. 1.1). There is accumulating evidence that a correction factor needs to be incorporated into the readings taken by Goldmann applanation tonometry according to CCT. II - MRI scan of the pituitary gland and ONH indicated if there is an atypical appearance of the optic disc or the visual field defects are suspicious of neurological disease or disc and visual field findings are inconsistent. III - Doppler ultrasound of supra-aortic vessels, particularly when disc and visual field findings are inconsistant with the IOP. Ch. 2 - 5 EGS
2.2.1 - PRIMARY JUVENILE GLAUCOMA Etiology: Unknown Pathomechanism: Decreased aqueous outflow Features: Onset: tenth to 35th year of life Heredity: family history may be present. Genes associated with primary juvenile glaucoma have been identified on chromosome 1 (1q21-q31) and MYOC 2,3 Signs and symptoms: Asymptomatic Peak IOP ≥ 21 mm Hg without treatment (diurnal tension curve) Optic nerve head: Diffuse rim damage typical. Any type of ONH glaucomatos defect is possible Nerve fiber layer: typical diffuse defects Visual field: glaucomatous defects may be present Gonioscopy: wide open anterior chamber angle 2.2.2 - PRIMARY JUVENILE GLAUCOMA SUSPECT Etiology: Unknown Pathomechanism: Unknown Features: Onset: tenth to 35th year of life No structural or functional defects with normal optic disc, nerve fiber layer and visual field Heredity: family history may be present. Genes associated with primary juvenile glaucoma have been identified on chromosome 1 (1q21-q31) and MYOC mutation 2-3 AND Either I: Peak pressure: ≥ 31mm Hg (without treatment) Or II: at least two of the following risk factors: a) peak pressure 22 mm Hg to 30 mm Hg b) IOP difference > 4 mm Hg between the two eyes c) family history of glaucoma d) manifest juvenile glaucoma in the opposite eye 2.2.3 - PRIMARY OPEN-ANGLE GLAUCOMA/High Pressure Glaucoma (POAG/HPG) See Ch. Introduction and 2.2 Etiology: Unknown Pathomechanism: Unknown. TIGR and MYOC mutations may be associated 2,3 Features: Onset: from the 35th year of age onwards Signs and symptoms: Asymptomatic until field loss advanced IOP > 21 mm Hg without treatment (diurnal tension curve) Optic nerve head: acquired characteristic glaucomatous damage and/or retinal nerve fiber layer changes (diffuse or localized defects) Visual field: usually detectable glaucomatous defects corresponding to the optic disc damage may be present Gonioscopy: open anterior chamber angle (not occludable, no goniodysgenesis). See Ch. 1.2 and Ch. 2.4.3. Ch. 2 - 6 EGS
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ISBN: 88-87434-13-1 Editrice DOGMA
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ACKNOWLEDGEMENT This work was made
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2.2.5 - Primary Open-Angle Glaucoma
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Foreword These Definitions and Guid
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INTRODUCTION The aim of the book is
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Since resources are limited worldwi
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II - RANDOMIZED CONTROLLED TRIALS F
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II.3 - COLLABORATIVE NORMAL TENSION
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No stratification for stage of dise
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II. 6. 3 - from CNTG 1. Therapy tha
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References 1) The Ocular Hypertensi
Page 24 and 25: I - QUESTIONS TO ASK TO YOUR GLAUCO
Page 26 and 27: III - ABNORMAL THRESHOLD VISUAL FIE
Page 28 and 29: V - GONIOSCOPIC OPEN ANGLES SOME DI
Page 30 and 31: VII - TREATMENT STEPLADDER JUVENILE
Page 32 and 33: IX - MONOTHERAPY (in alphabetic ord
Page 34 and 35: XI - MANAGEMENT ACUTE ANGLE CLOSURE
Page 36 and 37: XIII - ANTIMETABOLITES FOR WOUND MO
Page 38 and 39: CHAPTER 1 PATIENT EXAMINATION
Page 40 and 41: Other methods 22-25 : Air-puff tono
Page 42 and 43: References 1) Martin XD. Normal int
Page 44 and 45: 1.2 - GONIOSCOPY Gonioscopy is a fu
Page 46 and 47: 1 2 3 4 Fig. 1 Dynamic indentation
Page 48 and 49: The Spaeth classification Insertion
Page 50 and 51: References 1) Palmberg P. Gonioscop
Page 52 and 53: small - size mid - size large - siz
Page 54 and 55: Fig. 5 A) Cirumlinear vessel, B) Ba
Page 56 and 57: 1.3.4.3 - OCT The Optical Coherence
Page 58 and 59: 31) Carpineto P, Ciancaglini M, Zup
Page 60 and 61: central 24 or 30 central degrees re
Page 62 and 63: A retinal sensitivity value worse t
Page 64 and 65: HODAPP CLASSIFICATION 31 EARLY GLAU
Page 66 and 67: References 1) Bengtsson B, Heijl A,
Page 68 and 69: 1.5 - BLOOD FLOW 1.5.1 - VASCULAR F
Page 70 and 71: 28) Flammer J, Orgul S, Costa VP, O
Page 72 and 73: All forms of glaucoma should be cla
Page 76 and 77: 2.2.4 - PRIMARY OPEN-ANGLE GLAUCOMA
Page 78 and 79: 2.3 - SECONDARY OPEN-ANGLE GLAUCOMA
Page 80 and 81: 2.3.1.6 - Glaucoma due to intraocul
Page 82 and 83: 2.4 - PRIMARY ANGLE-CLOSURE Primary
Page 84 and 85: Systemic Risk factors for primary a
Page 86 and 87: OCCLUDABLE ANGLE: “Occludable”
Page 88 and 89: 2.5.3 - SECONDARY ANGLE-CLOSURE GLA
Page 90 and 91: CHAPTER 3 TREATMENT PRINCIPLES and
Page 92 and 93: Furthermore, blindness may occur de
Page 94 and 95: T A R G E T I O P Target IOP range
Page 96 and 97: Practical points for topical medica
Page 98 and 99: 3.3.1.1 - Category: ADRENERGIC AGON
Page 100 and 101: 3.3.1.2 - Category: ADRENERGIC ANTA
Page 102 and 103: 3.3.1.3 - Category: CARBONIC ANHYDR
Page 104 and 105: 3.3.1.4 - Category: PARASYMPATHOMIM
Page 106 and 107: 3.3.1.5 - Category: PROSTAGLANDIN D
Page 108 and 109: Drug interactions Precipitation occ
Page 110 and 111: COMBINATION THERAPY Starting* Addit
Page 112 and 113: 3.3.2.2 - Category: ADRENERGIC ANTA
Page 114 and 115: Pregnancy and nursing mothers Only
Page 116 and 117: 3.5 - LASER SURGERY 3.5.1 - LASER I
Page 118 and 119: 3.5.2 - LASER TRABECULOPLASTY 77-89
Page 120 and 121: 3.5.4 - CYCLOPHOTOCOAGULATION Indic
Page 122 and 123: Although medical therapy is still t
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3.6.4 - COMPLEX CASES Complicated g
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Post-operative use Concentration: 0
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25) Janz NK, Wren PA, Lichter PR, M
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(Rescula TM ) in patients with glau
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in white patients with open-angle g
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CHAPTER 4 TREATMENT GUIDELINES
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4.2 - PRIMARY OPEN-ANGLE GLAUCOMAS
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4.2.7 - OCULAR HYPERTENSION (OH) Al
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4.3.1.7 - Glaucoma associated with
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• Withdrawal of aqueous from vitr
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4.5 - SECONDARY ANGLE-CLOSURE GLAUC
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4.5.3 - SECONDARY ANGLE-CLOSURE GLA
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NOTES
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NOTES
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NOTES
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