Transcript Slide 1
Sleep Apnea
& the Eye
Rick Trevino, OD
VA Outpatient Clinic
Evansville, IN
[email protected]
Sleep Apnea & the Eye
Sleep Apnea
Sleep physiology
Clinical consequences
Diagnosis
Treatment
Ocular
Manifestations
Asthenopia
CPAP-assoc red eye
Floppy eyelid syndrome
NAION
Papilledema
Normal tension glaucoma
Online Resources
Lecture Notes
Powerpoint Slides
http://richardtrevino.net/sleepapnea
http://www.slideshare.net/rhodopsin
Free Texts
http://jfponline.com (Aug 2008)
http://pubs.nrc-cnrc.gc.ca/cjo
Can J Ophthalmol 2007;42(2):238-43
Sleep Cycle
Sleep Cycle
Polysomnography
EEG channels
EOG channels
EMG channel
Nasal air current channel
Thoracic motion channel
Abdominal motion channel
Oximeter channel
Leg movement channels
Microphone
Video recording
Source: Graefes Arch Clin Exp Ophthalmol 2008;246:129–134
Sleep Cycle
Polysomnogram
Source: N Engl J Med 2007;356:1751-1758
Sleep Disorders
OSA is the “most physiologically disruptive and dangerous
of the sleep-related disorders.”
Sleep apnea
Insomnia
Narcolepsy
Restless leg syndrome
Parasomnias
Circadian disorders
Drug side effects
Shift work
Source: J Am Board Fam Med. 2007;20:392-398
Obstructive Sleep Apnea
Obstructive Sleep Apnea
Any Condition that
Causes or Contributes
to Upper Airway
Narrowing is a Risk
Factor for OSA
Obesity
Enlarged Tonsils
Anatomical Malformations
Neoplasms
Edema of the pharynx
Lymphoid Hypertrophy
Pharyngeal Muscle
Weakness
Dyscoordination of
Respiratory Muscles
Source: Thorax 2004;59:73-78
Obstructive Sleep Apnea
Clinical Characteristics
Excessive daytime
sleepiness
Also gasping/snorting during arousals
Apneic events
witnessed by bed
partner
Obesity
Most common symptom
Disruptive snoring
Disruptive snoring + witnessed
apneas: 94% specificity
Neck circumference
≥40 cm had a sensitivity of 61% and a
specificity of 93% for OSA
Correlates better than BMI
Male
30% of pts with a BMI > 30 have OSA,
and 50% of pts with a BMI > 40 have
OSA.
2-3x more common than female
Family history of OSA
Relatives have 2-4 fold risk
Source: eMedicine (http://www.emedicine.com/med/topic163.htm)
Obstructive Sleep Apnea
Pickwickian Syndrome
Obesity, daytime
somnolence, loud snoring
Charles Dicken’s “Pickwick
Papers” (1837)
Prevalence increasing in
parallel with prevalence of
obesity
30-60yo: 9%F, 24%M
Under-diagnosed
Source: Postgrad Med 2002;111(3):70-6.
Obstructive Sleep Apnea
Clinical Consequences
Cardiovascular Disease
HTN, CAD/MI, CHF,
Arrhythmia
Stroke
Obesity
Metabolic Syndrome
Other Diseases
Morning headache, Eye,
Liver, Kidney, others
Cognitive and Emotional
Effects on bed partners
Impaired mental
functioning
Depression
Mood alteration
Disruptive snoring
Accidents
Drowsy driving
Workplace
Source: How Stuff Works (http://healthguide.howstuffworks.com/sleep-apnea-in-depth.htm)
Obstructive Sleep Apnea
Source: Hypertension. 2003;42:1067-1074
Obstructive Sleep Apnea
Clinical Evaluation
History
Physical
Sleepiness assessment
Disruptive snoring
Witnessed apneas
Obesity
Neck circumference
Throat/Mouth exam
PSG
Gold Standard
Respiratory Disturbance Index
Source: J Fam Prac. 2008;57(8) Suppl (http://www.jfponline.com)
Obstructive Sleep Apnea
Epworth Sleepiness Scale
How likely are you to doze off or fall asleep in the following situations?
0 = No chance, 1 = Slight chance, 2 = Moderate chance, 3 = High Chance
1. Sitting and reading
2. Watching TV
3. Sitting inactive in a public place (theater, meeting)
4. As a passenger in a car for an hour without a break
5. Lying down to rest in the afternoon when
circumstances permit
6. Sitting and talking to someone
7. Sitting quietly after a lunch without alcohol
8. In a car, while stopped for a few minutes in traffic
Source: Sleep 1994;17:160–167
Obstructive Sleep Apnea
Treatment Options
Behavioral: Weight loss, EtOH avoidance, nonsupine position
Positive Airway Pressure: CPAP, others
Mandibular advancement device
Surgery: UPPP, Tonsillectomy,
Tracheostomy
Source: J Fam Prac. 2008;57(8) Suppl (http://www.jfponline.com)
OSA & the Eye
Obese middle-aged men
Excessive sleepiness
Disruptive snoring
Witnessed apneas
Ocular Manifestations
Asthenopia
CPAP-associated red eye
Floppy Eyelid Syndrome
NAION
Papilledema
Normal Tension Glaucoma
Asthenopia
Common OSA Symptoms Include:
“Tiredness”
“Fatigue”
“Lack of energy”
Morning headache
These OSA symptoms
may be misinterpreted
as “eye strain”
Source: J Fam Prac. 2008;57(8) Suppl (http://www.jfponline.com)
Asthenopia
Common OSA-associated asthenopic symptoms
Unexplained symptoms of blur
Vision is 20/20 but the
patient is c/o blur
Misinterpreting what is seen
Incorrect recording or
copying
Eye strain and/or fatigue
Headaches
Worse in the morning
Asthenopia
42yo WM presents with c/o eye fatigue at near.
LEE: <1yr with current eyeglasses
MH:
1.
2.
3.
4.
5.
6.
OSA (noncompliant with CPAP)
Frequent HA
Overweight
Hyperlipidemia
GERD
Smokes 1PPD
Optometric Exam: Unremarkable
Plan:
1. OSA management
2. Visual hygiene
3. Smoking cessation
Asthenopia
OSA Supportive Management
Encourage compliance with CPAP
Quit smoking
10% increase in weight results in 6x greater risk of developing OSA
Weight loss decreases OSA severity
Avoid sleeping on back
Smokers 3 times more likely to have OSA
Reversible with smoking cessation
Weight reduction
50% compliance rate, high drop-out rate
Sew golf ball into pocket on back of shirt
Avoid alcohol within 4 hours of bedtime
Avoid sleeping pills
Source: JAMA 2004;291:2013-2016
OSA & the Eye
Obese middle-aged men
Excessive sleepiness
Disruptive snoring
Witnessed apneas
Ocular Manifestations
Asthenopia
CPAP-associated red eye
Floppy Eyelid Syndrome
NAION
Papilledema
Normal Tension Glaucoma
CPAP-associated Red Eye
Clinical Problems
Dry eye
EXW CL intolerance
Conjunctivitis
Reactivation of RCE
Causes
Air leaks
Retrograde air flow
thru nasolacrimal apparatus
Treatment
CPAP refitting: adjust headgear and pressure
Ointments HS, punctal plugs
Source: Optometry. 2007;78:352-355
OSA & the Eye
Obese middle-aged men
Excessive sleepiness,
disruptive snoring, witnessed
apneas
Ocular Manifestations
Asthenopia
CPAP-associated red eye
Floppy Eyelid Syndrome
NAION
Papilledema
Normal Tension Glaucoma
Floppy Eyelid Syndrome
Clinical Characteristics
Eyelid hyperlaxity
Rubbery, easily everted upper
eyelids
Eyelash ptosis with loss of
parallelism
Papillary conjunctivitis
Chronic ocular irritation, worse
upon waking
SPK, mucoid discharge common
Rubbing on pillow case
Should be suspected in any obese
pt with a chronic red eye
Source: Clin Exp Ophthalmol 2005;33:117-125.
Floppy Eyelid Syndrome
Eyelash ptosis
Downward displacement
of eyelashes
Lashes may curl toward
the globe
Lashes may point in
various directions - loss
of parallelism
Pts may trim with
scissors
Source: Ophthalmology 1998;105:165-169
Floppy Eyelid Syndrome
Floppy Eyelid Syndrome
Pathophysiology
Loss of elastic fibers in
tarsus and skin of lid
Upregulation of elastindegrading enzymes (matrix
metalloproteinases)
Caused by repeated
mechanical trauma, possibly
eye rubbing or sleeping with
the face buried in the pillow
Source: Ophthalmology. 2005;112:694-704
Floppy Eyelid Syndrome
Treatment
Lubrication therapy
Protect eye during sleep
Poor lid-eye contact
Inadequate tear distribution
Ointments HS
Fox shield, patching, taping
May improve or resolve
with CPAP
Surgical therapy deferred until OSA treated
Horizontal lid shortening
Source: Curr Opin Ophthalmol. 2007;18:430-433
Floppy Eyelid Syndrome
Relation to OSA
Pts with FES are a subset
of all OSA pts
96% pts with FES have
OSA (almost 100%!)
5-15% pts with OSA have
FES
OSA tends to be more
severe in pts with FES
Source: Clin Exp Ophthalmol 2005;33:117–125
OSA & the Eye
Obese middle-aged men
Excessive sleepiness
Disruptive snoring
Witnessed apneas
Ocular Manifestations
Asthenopia
CPAP-associated red eye
Floppy Eyelid Syndrome
NAION
Papilledema
Normal Tension Glaucoma
NAION
Clinical Characteristics
Most common acute optic
neuropathy in pts >50yo
Sudden painless visual loss,
usually upon awaking
Nerve fiber bundle VF defects
Diffuse or sectoral disc edema
Disc at risk: small, crowded
Mean C/D = 0.2
All ≤ 0.4
Source: Rev Ophthalmol (http://www.revophth.com/index.asp?page=1_13156.htm)
NAION
Pathophysiology
Idiopathic ischemic process
Disorder of posterior ciliary artery circulation
Transient poor circulation in the ONH
Trigger Event: Fall in blood pressure below a critical
level?
There is no actual blockage of the posterior ciliary arteries
Cascade Effect
Mechanical crowding caused by small crowded disc
Ischemia Swelling Compression Ischemia
Source: http://webeye.ophth.uiowa.edu/dept/AION/Index.htm
NAION
Diagnosis: Must exclude GCA in every case
ESR
C-Reactive Protein
Positive acute-phase protein
Levels increase in presence of
inflammation
Upper limit normal does not
rise with age
Platelets
Secondary thrombocytosis
due to chronic inflammation
NAION
Treatment
Aspirin
Surgical decompression
No benefit (Ischemic Optic Neuropathy Decompression Trial)
Control of predisposing systemic disease
Decreases incidence in fellow eye at 2 years, but not at 5 years
May slow progression or reduce incidence in fellow eye
Hypertension, Diabetes, Hyperlipidemia
Avoid phosphodiesterase 5 inhibitors (Viagra,
Levitra, Cialis)
May increase risk of NAION in fellow eye
NAION
Medicolegal obligation to inform pts of risk to fellow eye
NAION
Relation to OSA
Mojon (2002)
Behbehani (2005)
Palombi (2006)
Li (2007)
NAION
Mojon (2002)
Matched case-control study
with 17 NAION cases and
17 controls
71% of patients with
NAION have OSA
compared with 18% of
controls
Can CPAP prevent NAION
in predisposed individuals
with OSA?
Source: Arch Ophthalmol 2002;120:601-605
NAION
Behbehani (2005)
Report of 3 patients that
developed NAION while
using CPAP for OSA
Concluded that CPAP does
not prevent NAION in
patients with OSA
Questions role of OSA in
development of NAION
Source: Am J Ophthalmol 2005;139:518–521
NAION
Palombi (2006)
24 of 27 (89%) NAION
patients had OSA
OSA was the most frequent
disorder associated with
NAION
HTN: 59%
DM: 37%
Recommend all NAION
pts be screened for OSA
Daytime sleepiness, noisy sleep, witnessed apneas
Pickwickian habitus (obese middle-aged men)
Source: Br J Ophthalmol 2006;90:879–882
NAION
Li (2007)
Matched case-control study
of 73 NAION cases and 73
controls
Administered questionnaire
that included the SA-SDQ
22 (30.1%) cases and 13
(17.8%) controls had scores
consistent with OSA
Conclude that patients with
OSA are at increased risk
of NAION
Source: Br. J. Ophthalmol. 2007;91:1524-1527
OSA & the Eye
Obese middle-aged men
Excessive sleepiness
Disruptive snoring
Witnessed apneas
Ocular Manifestations
Asthenopia
CPAP-associated red eye
Floppy Eyelid Syndrome
NAION
Papilledema
Normal Tension Glaucoma
Papilledema
Clinical Characteristics
Disc swelling associated
with increased ICP
Symptoms of elevated
ICP: Headache, tinnitus,
TOV
Chronic papilledema
(months) may lead to optic
atrophy and vision loss
Papilledema
Work-up
Urgent MRI or CT scan
Lumbar puncture if imaging normal
Idiopathic Intracranial
Hypertension
“Pseudotumor cerebri”
Syndrome of elevated ICP,
papilledema, normal MRI/CT,
normal CSF
Secondary pseudotumor cerebri
syndromes
Venous sinus thrombosis,
vitamin A toxicity, COPD, OSA
Tx: Diamox 250mg po QID , Underlying cause if known
Source: Arch Ophthalmol 2000;118:1626-1630
Papilledema
Relation to OSA
4 pts with vision loss,
unexplained disc edema and
OSA
ICP is normal during the day
but elevated at night
Hypercapnia-induced cerebral
vasodilatation elevates ICP
Apneas were occurring despite
CPAP – require surgical tx
Intermittent ↑ ICP can cause
sustained papilledema
Papilledema resolved with
successful tx of OSA
Source: Arch Ophthalmol 2000;118:1626-1630
OSA & the Eye
Obese middle-aged men
Excessive sleepiness
Disruptive snoring
Witnessed apneas
Ocular Manifestations
Asthenopia
CPAP-associated red eye
Floppy Eyelid Syndrome
NAION
Papilledema
Normal Tension Glaucoma
Normal Tension Glaucoma
Clinical Characteristics
Probably a variant of COAG
IOP is never documented above
21 mmHg
Peripapillary hemorrhages may
be more frequent
Peripapillary atrophy may be
more marked
VF defects tend to be deeper
and more localized
Source: Shield's Textbook of Glaucoma, 2005
Normal Tension Glaucoma
Pathophysiology
NTG differs from NAION only in that the latter is a
more acute process. (Hayreh, 1975)
Role of IOP unclear
Proven value of aggressive
IOP lowering (CNTGS, 1998)
Pressure-independent
component also exists
(LoGTS, 2007)
Source: Ophthalmology 2007;114:460–465
Normal Tension Glaucoma
Diagnosis
R/O other glaucomas
Diurnal IOP fluctuation
IOP normalization (Burnt-out
glaucoma, pseudophakia, steroids)
R/O other optic neuropathies
NAION, space-occupying lesions,
congenital anomalies
When to order neuroimaging:
Younger age (<50 yrs)
Reduced VA (< 20/40)
Vertically aligned VF defects
Neuroretinal rim pallor
Source: Ophthalmology 1998;105:1866-1874
Normal Tension Glaucoma
Relation to OSA
Glaucoma Patients with OSA
(50-60% NTG pts have OSA)
Mojon (2000)
20% (POAG)
Marcus (2001)
57% (NTG)
Mojon (2002)
50-60% (NTG, varies with age)
OSA Patients with Glaucoma
(5-10% OSA pts have NTG)
Mojon (1999)
7%
Geyer (2003)
2%
Sergi (2007)
6% (NTG)
Bendel (2007)
27%
Karakuck (2008)
10% (NTG), 3% (POAG)
Normal Tension Glaucoma
OSA May Cause VF Loss Without Glaucoma
VF loss may occur due to optic nerve damage caused by cerebral
ischemia and intermittent ICP elevation
Batisse (2004)
Tsang (2006)
Eye exam on 35 consecutive patients undergoing PSG
VF mean deviation correlated with RDI
Compared VF and ONH changes between 41 pts with moderate-severe
OSA with 35 age-matched controls
In OSA pts the VF indices were significantly subnormal
Karakucuk (2008)
Eye exams and orbital blood flow studies on 31 pts with OSA and 25
normal control subjects
VF defects were detected in 10 pts despite normal eye exam.
Normal Tension Glaucoma
CPAP Increases IOP
Kiekens (2008)
Diurnal IOP in 21 OSA
pts with and without CPAP
Average IOP and diurnal
fluctuation higher with CPAP
30 min after CPAP cessation
a significant decrease in IOP
was recorded
Speculate that CPAP elevates intrathoracic pressure, leading to higher
central venous pressure, and ultimately higher IOP
Recommend regular screening of VF and the optic disc for all patients
with OSA, especially those treated with CPAP
Source: Invest Ophthalmol Vis Sci. 2008;49:934–940
Source: Can J Ophthalmol 2007;42:238–243
Thank You!