Brief Introduction

1. Brief Introduction • 87y/o WF who presented for routine exam, evaluation of mild VA decline • Fell in Thompson Hall parking lot • On questioning, pt has frequent falls and dizzy spells • By our exam, pt was found to have changes consistent with glaucoma • Subsequently diagnosed with normal-tension glaucoma

2. Help…I’ve Fallen and I Can’t Get my IOP Up Laura S. Gilmore, MD Grand Rounds January 9, 2004 Texas Tech University HSC Lubbock, TX

3. History • CC: Mild VA decrease over past year • HPI: 87y/o WF who presented for routine exam, eval of mild VA decline • PMH: HTN, h/o breast cancer, hypothyroidism. • ROS: no h/o migraines, steroid use. +frequent falls/dizziness, but no known h/o head trauma or prior optic disc abnormalities • Ocular History: CE OU, 2002 • FH: no known h/o glaucoma • SH: has lived with daughter in Lubbock since 2/03 • Meds: Toprol, Amiodarone, Coumadin, Prinivil, Synthroid, Lasix, Hytrin

4. Physical Exam • VS: BP 87/55, 84/54, 88/49; P 50’s-60’s on 3 visits • Best Corrected VA: 20/40+2, 20/30-1 • IOP: 12 OU • PCIOL OU, with 2-3+ PCO OU • DFE: C/D 0.7 OU, with 2+ disc pallor, saucerization, and infero-temporal thinning OU • Gonioscopy: OD--angle recession 220o, 45o angle, configuration Q, 2+ pigment OS-- angle recession 90o, D, 45o angle config Q, 2+pigment

5. Visual Field

6. Findings in POAG • C/D ratio =/> 0.5 • C/D asymmetry >0.1 • deep cupping • neural rim thinning (notching) • peripapillary flame hemorrhages • nerve fiber layer dropout on red-free exam • normal gonioscopy • VF abnormalities including arcuate, nasal step, paracentral, and temporal wedge defects

7. Overview of NTG • Type of POAG • Mean IOP =/< 21mmHg • Glaucomatous optic disc damage and VF loss • Open drainage angle on gonioscopy • No secondary causes for optic disc damage • Prevalence of 0.2% in age group over 40 • Accounts for 25% of all POAG cases • Glaucomatous cupping is similar to that in pressure-dependent POAG

8. Characteristics of Glaucomatous Cupping

9. Distinguishing Clinical Features • IOP is usually in high teens, but can be in low-teens • ONH is larger than in POAG • Disc hemorrhages • Peripapillary atrophy more common • Inferior pitting of disc • VF defects similar, but may be closer to fixation, deeper, steeper and more localized in NTG • Due to delayed diagnosis, pt’s tend to present with more advanced damage than in POAG

10. Disc hemorrhages often seen in NTG

11. General Risk Factors • Age: Tends to occur in elderly • Gender: females at 2:1 risk over males • Race: More common in Japan than in Europe or North America

12. Common Associated Findings • Peripheral vascular spasm on cooling • Migraine headaches • Overtreated systemic hypertension • Nocturnal systemic hypotension • Reduced blood flow velocity in ophthalmic artery by transcranial Doppler • Paraproteinemia and serum autoantibodies

13. Differential Diagnosis • POAG presenting with normal IOP but with diurnal swing. Detect with diurnal IOP curve, looking for IOP spike >21mmHG • Congenital optic disc anomalies, like large optic disc pits or colobomas • Neurologic lesions causing compression of chiasm or nerve, resulting in misinterpretation of VF defects • Previous ischemic optic neuropathy • Vascular occlusion • Optic nerve head drusen • Chorioretinitis, RD, retinoschisis

14. Possible appearances of a normal cup

15. Congenital pit and coloboma of the optic disc, which could be mistaken for glaucomatous cupping

16. Theories • Elevated intraocular pressure (IOP) has long been considered the primary cause of glaucoma, but other factors contribute to susceptibility • Mechanical: Interruption of axoplasmic flow by compression of optic nerve fibers against lamina cribosa • Ischemic: Compromised blood supply to nerve • Autoregulation dysfunction (abnormal vasospasm, resistance to vasoactive substances, abnormal vessels) may contribute to nerve damage by increasing susceptibility to even normal IOPs

17. Major Vascular Risk Factors for Glaucoma • systemic hypotension • local vasospasm • aberrant autoregulation of blood flow in the optic nerve head and choroid • systemic hypertension-pt’s usually show large swings in BP, with an average of a 26% drop from day to night • hypertensives treated with beta blockers can have DBP during sleep of 50 mm Hg or less, and rarely down to 30 mm Hg or less. An abnormally deep dip may compromise local vascular supply

18. Diastolic perfusion pressure versus glaucoma risk. • diastolic perfusion pressure = diastolic blood pressure - IOP.Diastolic blood pressures of 30 to 40 mm Hg are low enough to seriously compromise blood flow to the eye • DPP (mmHg) ratio Glaucoma risk • > 50 1.00 • 40 - 49 1.72 • 30 - 39 2.14 • < 30 6.22

19. Management • Complete history-exclude episodes of high IOP, ocular trauma, chronic uveitis, topical steroid use, acute blood loss or shock, MI, carotid disease, vasculopathy • 24 hour BP monitoring-if significant nocturnal drop, modify/avoid antihypertensive therapy, esp. no bedtime dosing; exercise; salted diet; possible fludrocortisone tx to raise BP in normotensives? • PE, stereo photos, gonioscopy, baseline VF, blood workup, CT of orbits optic nerves and brain, carotid US • Reduction in IOP-of at least 30%, indicated only with progressive VF loss • Systemic calcium-channel blockers- not used much anymore; effect questionable, and, where low BP could be part of the equation, could make situation worse by lowering BP too much

20. Cantor, Louis, MD et al, Basic and Clinical Science Course 2003-2004: Section 10, Glaucoma, 2003, pp.42-44, 79-81.Kanski, Jack J., Clinical Ophthalmology, 4th Edition, 2000, pp209-211.Kanski, Jack J. and Ken K. Nischal, Ophthalmology: Clinical Signs and Differential Diagnosis, 2000, pp254-255.Mandava, Suresh et al, Color Atlas of Ophthalmology: The Manhattan Eye, Ear, and Throat Hospital Pocket Guide, 1999, pp242-243.