terminology and guidelines for glaucoma ii - Kwaliteitskoepel

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$Refractiechirurgie - Nederlands Oogheelkundig Gezelschap$

2.3 - SECONDARY OPEN-ANGLE GLAUCOMAS Elevated IOP causing progressive typical glaucomatous optic neuropathy and visual field loss, caused by ophthalmological or extraocular disease(s), drugs and treatments. Assessment of the glaucomatous damage to visual function, including visual field staging, may be difficult because of the underlying ophthalmological diseases or complex clinical picture. The following classification is primarily based on pathophysiologic mechanisms. Distinct clinical glaucoma types are discussed at the corresponding point of the mechanistic classification. When no etiology and pathomechanism are evident, a primary glaucoma should be considered. In secondary Open-angle Glaucomas the anterior chamber-angle is open for over 270°. In several forms of secondary glaucoma pathomechanisms leading to both secondary open-angle and angle-closure glaucoma are combined. Since the number of the combinations is very high, in each case individual evaluation is necessary. 2.3.1 - SECONDARY OPEN-ANGLE GLAUCOMAS CAUSED BY OPHTHALMOLOGICAL CONDITIONS 2.3.1.1 - Pseudoexfoliation Glaucoma (PEX) 4,5 Etiology: Pseudoexfoliative material, an abnormal fibrillo-granular protein, and pigment accumulate in the trabecular meshwork, where TM function decreases. Similar material has been identified in the conjuntiva and body parts outside the eye. Why many eyes with pseudoexfoliation do not have glaucoma is not known. Pathomechanism: Reduction of the trabecular outflow owing to the pseudoexfoliative material. Features: Onset: usually older than 60 years Frequency: large racial variations Asymptomatic until visual field loss advanced One or both eyes affected, often bilateral and asymmetrical Sign and symptoms: IOP: > 21 mm Hg, frequently higher than in average POAG cases Visual field loss as in POAG; frequently severe at least in one eye Slit lamp examination: dandruff-like exfoliation material on the pupil border and on the surface of the anterior lens capsule except the central zone, better visualized after pupillary dilation. The pupillary collarette is irregular and typically has a moth-eaten appearance. Frequently associated with nuclear cataract, pigmentary loss from the central or mid-iris, pigment granules in the angle. When pigment accumulates along an ondulating line on or anterior to Schwalbe’s line, it is called Sampaolesi’s line. Loose zonules are frequent with occasional phacodonesis and lens subluxation. Narrow or closed-angle is relatively common. 2.3.1.2 - Pigmentary Glaucoma 5,6 Etiology: Melanin granules accumulate in the trabecular meshwork, where TM function decreases. Pathomechanism: Reduction of the trabecular outflow owing to melanin granules. According to the theory of ‘reverse pupillary block’ the iris works as a valve resulting in IOP higher in the anterior chamber than in the posterior chamber, causing peripheral posterior bowing of the iris. Melanin granules are released from the iris as a result of rubbing between the zonules and the posterior surface of the iris. Ch. 2 - 9 EGS
Features: Onset: typically third to fifth decades Frequency: 1-1.5 % of the total glaucoma cases, mostly Caucasians, more in myopic males One or both eyes Sign and symptoms: Uncommonly mild to moderate pain during acute episodes of IOP rise. Haloes around lights. IOP: > 21 mm Hg, characteristically with large variations. Significant increase may occur after exercise, pupillary dilation or blinking. Gradual decrease of IOP with age over 60 years has been reported. Slit lamp examination: deep anterior chamber, midperipheral iris pigment epithelial atrophy with radial pattern especially well visible with retroillumination. Pigment dispersed on the trabecular meshwork, Schwalbe’s line, the iris surface, the lens equator and on the corneal endothelium, where often shapes itself as a central, vertical spindle (Krukenberg’s spindle). Dim light in the examination room is recommended, in order to enhance the observation of the peripheral iris shape. UBM examination is often helpful to diagnose reverse pupillary block. 2.3.1.3 - Lens-induced Secondary Open-Angle Glaucoma Etiology: Obstruction of the trabecular meshwork by lens proteins and/or inflammatory cells induced by lens proteins. Pathomechanism: • Lens proteins from a mature or hypermature cataract with intact capsule (phacolytic glaucoma) • Lens particles from a traumatically or surgically injured lens (lens particle glaucoma) • Granulomatous inflammation of the TM after uneventful ECCE when the fellow eye was already operated and its lens proteins sensitized the immune system (phacoanaphylactic glaucoma) Features: Age of onset and acute or chronic course depend on the pathomechanism Sign and symptoms: Often painful with redness and inflammation IOP > 21 mm Hg Slit lamp examination: injured lens and/or cataract or after ECCE, with or without iritis 2.3.1.4 - Glaucoma associated with intraocular haemorrhage Etiology: Obstruction of the trabecular meshwork by rigid red blood cells (ghost cell glaucoma, Sickle cell disease) or by a large quantity of normal red blood cells (hyphaema). Pathomechanism: Red blood cells (ghost cells) from an old vitreous hemorrhage, via a ruptured anterior hyaloid face, or from the iris (for example trauma, intraocular surgery) obstruct the trabecular meshwork Features: Sign and symptoms: Pain, redness, recurrences possible IOP > 21 mm Hg 2.3.1.5 - Uveitic Glaucoma Etiology: Several forms of anterior and intermediate uveitis can cause unilateral or bilateral obstruction of the trabecular meshwork. The most frequent conditions are juvenile rheumatoid arthritis, Fuchs’ heterochromic iridocyclitis, Posner- Schlossman syndrome (glaucomatocyclitic crisis), herpes simplex, herpes zoster, syphilis, sarcoidosis, Behçet disease, sympathetic ophthalmia, pars planitis. Pathomechanism: Obstruction and edema of the trabecular meshwork caused by inflammatory cells, precipitates, debris, secondary scarring and neovascularization of the chamber angle. Secondary angle-closure glaucoma due to synechiae can also develop. Features: Onset depends on underlying condition. Any age Sign and symptoms: Pain, redness, photophobia, decreased vision are possible. IOP > 21 mm Hg. Some forms are associated with wide oscillations or periodic rise of IOP. Ch. 2 - 10 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
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I - QUESTIONS TO ASK TO YOUR GLAUCO
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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 74 and 75: 2.2 - PRIMARY OPEN-ANGLE GLAUCOMAS
Page 76 and 77: 2.2.4 - PRIMARY 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
Page 124 and 125: 3.6.4 - COMPLEX CASES Complicated g
Page 126 and 127: 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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