11/30/2009. Glaukosis: ancient greek term meaning sparkling or shining appearance of pupil

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1 Normal Ocular Anatomy Glaucoma Dr Sunil Deokule, MD Asst. Prof and Glaucoma Specialist University of Kentucky Definition Glaukosis: ancient greek term meaning sparkling or shining appearance of pupil Optic nerve damage and visual field loss caused by high intraocular pressure Characteristic optic neuropathy associated with loss of retinal ganglion cells presenting as specific optic nerve changes and/or visual field damage Glaucoma Characteristic optic nerve damage Characteristic visual field damage Associated with high intraocular pressure in 2/3 rd Can occur with normal intraocular pressure Glaucoma Prevalence Glaucoma Impact Worldwide 60 million increasing to 79.6 million in million blind from glaucoma, 2 nd most common cause Projected Blindness: 8.1 million in 2010, 11 million in million US Nearly half unaware 200,000 blind from glaucoma accounting for 9-12% of blindness Leading cause of blindness in African- Americans Quigley et al. BJO 2006;90:253 Causes for blindness worldwide 1

2 Glaucoma and Quality of Life Classification Glaucoma OAG patients have significantly poorer QOL than controls Activities involving gg glare and dark adaptation most problematic Primary Secondary QOL correlated with severity 41% of patients with bilateral VF loss stopped driving versus 15% controls. Congenital/Childhood Open Angle Narrow Angle Congenital/Childhood Open Angle Inflammation, steroid, trauma Ramulu et al. Ophthalmology 2009;116:1846 Goldberg et al. J Glaucoma 2009;18:6 Open Angle Glaucoma Visual Impairment Silent Progressive Irreversible Preventable Open Angle Glaucoma Normal Optic Nerve Age Nonocular risk factors Family history Hypertension Diabetes Race Steroid use Myopia (minus power glasses) Ocular risk factors Intraocular pressure Central corneal thickness Optic nerve structure Disc Hemorrhage Other ocular disorders 2

3 Glaucomatous Optic Nerve Obvious Optic Disc Change Subtle Normal Abnormal RIM CUP Enlarged optic disc cup Loss of neuro-retinal rim Visual Field Loss Superior Arcuate Normal Abnormal 3

4 IOP and OAG Age and OAG IOP is one of the strongest and the only modifiable risk factor Everybody over the age of 60 years and blacks over 40 years are at increased risk Race and OAG Glaucoma 3-4 times more likely in blacks compared to whites Blacks 6 times more likely to go blind from glaucoma than whites Hispanic Between whites and blacks Greater effect of age compared to other ethnicities Chinese descent have preponderance for narrow angle glaucoma Vascular Diseases and OAG Normal-tension glaucoma HT, atherosclerosis and vasospasm For every 10 mm Hg rise in systolic and diastolic blood pressure IOP increases by 0.24 mm Hg and 0.40 mm Hg Diastolic perfusion pressure more important DPP=DBP-IOP Family History and OAG Diabetes and OAG Glaucoma 4 times more likely in individuals with siblings with OAG Risk of having gg glaucoma was 9.2 fold in individual with family history of glaucoma Multifactorial 3% ascribed to single gene abnormality Association is unclear Bias as diabetics much more likely to have fundus examination for retinaopathy Greater prevalence of OAG in subjects with DM in black and hispanic population Worse outcome of treatment Individual with Juvenile glaucoma more likely to have gene defect 4

5 Risk Factors Myopia 2-3 fold risk of glaucoma Confounding factor Confusing visual field changes Myopic optic disc changes Sleep Apnea Large swings in blood pressure and hypoxic episodes Greater prevalence of glaucoma Reports of stabilization of glaucoma progression with treatment of sleep apnea Medical Treatment Beta Blocker Alpha agonist Carbonic anhydrase inhibitors Prostaglandin Analogues Laser Trabeculoplasty Filtration Surgery Nocturnal BP and OAG <10% to >20% 10% to 20% Significantly greater progression in nonphysiologic dippers compared to physiologic dippers Jpn J Ophthalmol 2004;48: Exercise Aerobic Avoid head inversion Exercise Aerobic Avoid head inversion Diet 5

6 Diet Exercise Aerobic Avoid head inversion Diet Manage sleep apnea Sleep Apnea Treatment Exercise Aerobic Avoid head inversion Diet Manage sleep apnea Avoid medication that may compromise blood flow Treatments for erectile dysfunction Angle Closure Glaucoma Risk Factors Angle Closure Glaucoma Increasing age Female gender Ethnicity Inuit and East Asian Less common in African-american american Ocular Biometry Hypermetropia (+ power glasses) Narrow Angle 6

7 Systemic Medications Patient Presentation Sulfa derivatives Sulfonamide Hydrochlorothiazide Antiepileptics Topiramate F > M Sudden onset Antidepressants Venlafaxine Paroxetine Fluvoxamine Maprotiline Imipramine Amitriptyline Nebulized agents Ipratropium Anticoagulants Warfarin Anticholinergics Tropicamide Atropine Tricyclic and tetracyclic antidepressants Pilocarpine 6-7th decade History of transient headaches, blurred vision, haloes Family history Ocular pain, headache, nausea, vomiting Blurred vision, haloes Examination Findings D/D Reduced visual acuity Circumlimbal injection Hazy cornea Shallow anterior chamber Semi-dilated fixed pupil Nausea/vomiting Acute Conjunctivitis Watery or purulent discharge, lack of circumlimbal injection Iritis Miosed pupil Relatively clear cornea Deep anterior chamber Migraine Subacute Giant cell arteritis Congenital Glaucoma Congenital Glaucoma Incidence: 1 in 10,000 births Usually identified in 1 st year of life 75% %bl bilateral l Due to abnormal development of trabecular meshwork Barkan s membrane Male>female Presenting Symptoms Watery eye Photophobia Blepharospasm Signs Enlarged eyeball (bupthalmos) Hazy enlarged cornea Corneal Opacity Facial hemangioma Facial Neurofibromatosis 7

8 Congenital Glaucoma Congenital Glaucoma Enlarged Eyeball Corneal Opacity Examination under anesthesia Surgical management Goniotomy/trabeculotomy Trabeculectomy Glaucoma Drain Surgery Medical management plays supporting role Corneal diameter >12 mm in 1 st year of life is strongly suggestive of congential glaucoma Relatively poor prognosis with higher incidence of amblyopia and visual impairment Steroid Induced OAG Traumatic Glaucoma Any route though higher incidence with topical and oral steroid use Ocular damage similar to OAG Usually takes 3-4 weeks of steroid use but can occur within hours IOP normalization on stopping steroids 3-4% need long term treatment Blunt trauma or penetrating/perforating trauma Direct damage to trabecular meshwork/angle stuctures Secondary inflammation, hyphema Can have delayed presentation Difficult to treat When to suspect glaucoma Systemic medications to avoid in patients with glaucoma Family history African-american>40 years, white/hispanic> 60 years Steroid use Transient blurring of vision, haloes, headaches/periorbital aches Eye trauma Vigabatrin Bilateral irreversible visual field loss Topiramate Bilateral angle closure Sildenafil Orthostatic hypotension, may impact NTG Steroid 8

9 Summary Thank you 9