Download Epiretinal Membranes in Macular Dysfunction

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 normaltension glaucoma
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
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
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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
Physical Exam
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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
Visual Field
Findings in POAG
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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
Overview of NTG
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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 pressuredependent POAG
Characteristics of Glaucomatous Cupping
Distinguishing Clinical Features
• IOP is usually in high teens, but can be in lowteens
• 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
Disc hemorrhages often seen in NTG
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
Common Associated Findings
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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
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
Possible appearances
of a normal cup
Congenital pit and
coloboma of the optic
disc, which could be
mistaken for
glaucomatous cupping
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
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
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
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
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.