terminology and guidelines for glaucoma ii - Kwaliteitskoepel

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$Refractiechirurgie - Nederlands Oogheelkundig Gezelschap$

2.3.1.6 - Glaucoma due to intraocular tumors Etiology: Reduced aqueous humour outflow due to primary or secondary intraocular (anterior segment) tumors Pathomechanism: Compression or tumor extension to the trabecular meshwork and/or outflow channels. Trabecular meshwork obstruction due to tumor related inflammation, tumor necrosis, hemorrhage and pigment dispersion. (Secondary angle-closure glaucoma may also develop) Features: Sign and symptoms: IOP > 21 mm Hg Onset and clinical picture highly variable, combining evidence for both the tumor and the glaucoma 2.3.1.7 - Glaucoma associated with retinal detachment Etiology: Although retinal detachment is usually associated with lower than normal IOP, the same disease processes can also cause both reduced trabecular outflow and retinal detachment Pathomechanism: Neovascularization, proliferative retinopathy, scarring, pigment dispersion and inflammation (e.g. photoreceptor sensitization). Cases in which surgery for retinal detachment causes glaucoma are discussed in part 2.5. See also Ch. 2.3.1.8 Features: Sign and symptoms: IOP > 21 mm Hg Redness, pain are possible Retinal detachment is present Note In general, retinal detachment is associated with lower than normal IOP. Surgery for retinal detachment repair can cause glaucoma. See also Ch. 2.3.2.2. 2.3.1.8 - Open-Angle Glaucoma due to ocular trauma Ocular trauma leads to glaucoma by several different mechanisms. The secondary traumatic glaucomas can be caused by both open-angle and angle-closure pathomechanisms. To identify the etiology one must carefully evaluate all traumatic damage to the eye. Etiology: Reduced trabecular outflow due to traumatic changes of the trabecular meshwork Pathomechanism: Scarring and inflammation of the trabecular meshwork, obstruction by red blood cells and debris, lens induced glaucoma, angle recession. Positive steroid responsiveness to be also considered (see Ch. 2.3.2.1). Features: Highly variable Signs and symptoms: Redness, pain, decreased vision, or no symptoms IOP > 21 mm Hg. Elevated intraocular pressure can be present immediately, but slow elevation occuring months, or up to decades later are also possible. Slit lamp examination: chemical burns, hyphema, traumatic cataract, swollen lens, uveitis, angle recession, ruptured iris sphincter. 2.3.2 - IATROGENIC SECONDARY OPEN-ANGLE GLAUCOMAs 2.3.2.1 - Glaucoma due to corticosteroid treatment Etiology: Reduced trabecular outflow due to trabecular changes caused by corticosteroids (TIGR/MYOC protein) 2-3 Pathomechanism: Topical as well as high dose and long-term systemic corticosteroid therapy induces changes in the trabecular extracellular material (glycoproteins) which leads to decreased outflow facility. Usually pressure elevation is reversible if the corticosteroid is stopped. A modification of the TIGR gene was demonstrated. Features: Individual, hereditary susceptibility can occur. Myopic, diabetic subjects and POAG Patients may be more susceptible Ch. 2 - 11 EGS
Signs and symptoms: No pain, no redness, corneal edema is possible IOP > 21 mm Hg Typical glaucomatous optic nerve head and visual field damage if the disease is long-standing 2.3.2.2 - Secondary Open-Angle Glaucoma due to ocular surgery and laser Ocular surgery can cause secondary open-angle glaucoma by some of the mechanisms discussed above: pigmentary loss from uveal tissue, lens material, haemorrhage, uveitis and trauma. See also ch.s 2.3.1.1 to 2.3.2.1 Etiology: Reduced trabecular outflow Pathomechanism: • Viscoelastic materials, inflammatory debris, intra-operative application of alpha-chymotrypsin, lens particles, vitreous in the anterior chamber after cataract surgery, prostaglandin release. IOP elevation is usually transient. • Acute onset secondary IOP elevation after Nd:YAG laser iridotomy, capsulotomy and argon laser trabeculoplasty. Usually transient, within the first 24 hours, most frequent in the first 4 hours after treatment. • Emulsion of silicone oil implanted intravitreally enters the anterior chamber and is partially phagocytosed by macrophages and accumulates in the trabecular meshwork (especially in the upper quadrant). • Uveitis -glaucoma- hyphema (UGH) syndrome. Episodic onset, associated with anterior chamber pseudophakia. IOP elevation is induced by recurrent iris root bleeding and anterior uveitis. Features: Sign and symptoms: Pain, redness, corneal edema are possible IOP > 21 mm Hg Visual field loss when IOP elevation is sufficient/prolonged 2.3.3 - SECONDARY OPEN-ANGLE GLAUCOMA CAUSED BY EXTRAOCULAR CONDITIONS 2.3.3.1 - Glaucoma caused by increased episcleral venous pressure Etiology: Increase of the episcleral venous pressure which causes reduced trabecular outflow and elevated intraocular pressure Pathomechanism: Episcleral, orbital or general causes for reduced episcleral venous outflow: * Dural shunts * Chemical burn, radiation damage of the episcleral veins * Endocrine orbitopathy * Orbital (retrobulbar) tumour, pseudotumour, * Orbital phlebitis * Orbital or intracranial arteriovenous fistula * Sturge-Weber syndrome * Nevus of Ota * Cavernous sinus thrombosis * Jugular vein obstruction (radical neck dissections) * Superior vena cava obstruction * Pulmonary venous obstruction * Idiopathic forms Features: Onset can be acute Signs and symptoms: Wide variations of clinical features IOP > 21 mm Hg Dilated, congested episcleral veins, chemosis, facial lymphoedema, orbital bruit Vascular bruits in case of A/V fistulae Ch. 2 - 12 EGS
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ISBN: 88-87434-13-1 Editrice DOGMA
Page 4 and 5:
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
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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 78 and 79: 2.3 - SECONDARY OPEN-ANGLE GLAUCOMA
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
Page 128 and 129: 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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