Sleep Apnea & The Eye - 2013


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A review of the impact of sleep apnea on ocular health

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  • Each nasal opening lets air in easily but then retards the flow of air coming out. Technically, airway resistance is very low going into the nose, very high exiting the nose. By increasing airway resistance on exhaling, the air pressure backs up in the throat and helps 'stent open' the airway, to keep it from collapsing. This is the same principle used in CPAP, which creates an increased pressure to keep the (otherwise collapsing) airway open.Does it work? In one large, controlled study published in the journal Sleep, about 250 patients were divided into a treatment group and a 'sham group'. The treatment group got the Provent device, which they used nightly. The sham group used something that looks just like Provent, but it did not offer any resistance on breathing out. The results? Sleep apnea was signficantly improved with Provent, but not with the sham device. Also, the amount of daytime sleepiness in the treatment group was much better compared to the sham group.Advantages of Provent include no tight-fitting mask or head straps required, no machine needed, and much easier portability. Disadvatages include the fact that it's not suitable for people who have low oxygen during sleep, and it's generally not as effective as CPAP. So in summary: not as good as CPAP, but much better than nothing. Expect more such devices to be developed and brought to market.
  • IF OSA IS IN THE MED HX - be on the lookout for sxs of fatigue - possibly due to poor compliance or residual fatigueIF OSA NOT IN THE MED HX - high index of suspicion for OSA whenever cc is fatigue or asthenopia - esp if habitus is pickwickian - screen for sleepinessIf the pt is dx with OSA and presents with these sxs - compliance? - residual fatigueIf pt is not dx with OSA - pickwickian? - sleepiness screening - question bed partner
  • One possible explanation why CPAP noncompliance increases risk of ocular discomfort is that CPAP helps decrease sxs associated with FES
  • We describe 3 patients with signs that were similar to the giant fornix syndrome. They also had chronic mucopurulentconjunctival discharge that was refractory to multiple courses of antibiotic therapy. Although the superior forniceal space is the site of involvement in patients with giant fornix syndrome, the anatomic sources of the persistent purulent discharge in our patients were the fistulous tracts within the upper eyelid tarsal conjunctiva. We have termed this condition tarsoconjunctival crypts.Clinically, all patients had purulent conjunctival discharge ranging from moderate (Case 1) to copious (Cases 2 and 3). The upper eyelid tarsal conjunctiva was the principal anatomic site of the pathologic features, and the eyelids were characterized by the retention of a yellowish coagulum within horizontally oriented epitarsal fistulous tracts. A Bowman probe was passed through the length of the tracts to confirm their epitarsal location, which also verified that the tarsal plate was not involved. All of the fistulous tracts were managed by marsupialization of the individual fistulous tracts with either a no. 11 Bard-Parker blade or sharp Westcott scissors.We postulate that the formation of the tarsoconjunctival crypts was initiated by trauma to the tarsal conjunctival epithelium by mechanical abrasion resulting from nocturnal lid eversion in the floppy eyelid syndrome in. Partial sloughing of the tarsal conjunctiva and subsequent re-epithelialization over a lamellar layer of epithelium formed an epithelialized tunnel to trap the bacterial.
  • We know from the CNTGS that decreasing IOP by at least 30% can help slow the progression of NTG
  • Sleep Apnea & The Eye - 2013

    1. 1. Sleep Apnea & the Eye Rick Trevino, OD, FAAO Rosenberg School of Optometry University of the Incarnate Word
    2. 2. Sleep Apnea & the Eye• Sleep Apnea • What it is • How it’s diagnosed & treated• Ocular Manifestations • Asthenopia • CPAP-assoc red eye • Floppy eyelid syndrome • Diabetic retinopathy • NAION • Papilledema • Normal tension glaucoma
    3. 3. Online ResourcesLecture Notes • http://richardtrevino.netPowerpoint Slides • Texts • (Aug 2008)
    4. 4. Sleep DisordersOSA 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 J Am Board Fam Med. 2007;20:392-398
    5. 5. Sleep Architecture
    6. 6. 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 Thorax 2004;59:73-78
    7. 7. Obstructive Sleep Apnea Polysomnography (PSG)
    8. 8. Obstructive Sleep Apnea Clinical CharacteristicsExcessive daytime Obesitysleepiness • 30% of pts with a BMI > 30 have OSA, and 50% of pts with a BMI• Most common symptom > 40 have OSA.Disruptive snoring Neck circumference• Also gasping/snorting during • ≥40 cm had a sensitivity of 61% arousals and a specificity of 93% for OSAApneic events • Correlates better than BMIwitnessed by bed Malepartner • 2-3x more common than female Family history of OSA• Disruptive snoring + witnessed apneas: 94% specificity • Relatives have 2-4 fold  risk
    9. 9. 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 Postgrad Med. 2002;111:70
    10. 10. Obstructive Sleep Apnea Clinical ConsequencesCardiovascular Disease Cognitive and Emotional• HTN, CAD/MI, CHF, • Impaired mental functioning Arrhythmia • Depression • Mood alterationStroke Effects on bed partnersObesity • Disruptive snoringMetabolic Syndrome Accidents • Drowsy drivingOther Diseases • Workplace• Morning headache, Eye, Liver, Kidney, others
    11. 11. Obstructive Sleep Apnea Clinical EvaluationHistory• Sleepiness assessment• Disruptive snoring• Witnessed apneasPhysical• Obesity• Neck circumference• Throat/Mouth examPSG• Gold Standard• Respiratory DisturbanceIndex; Apnea/Hypopnea Index J Fam Prac. 2008;57(8) Suppl (
    12. 12. Obstructive Sleep Apnea Epworth Sleepiness ScaleHow likely are you to doze off or fall asleep in the following situations? 0 = No chance, 1 = Slight chance, 2 = Moderate chance, 3 = High Chance1. Sitting and reading2. Watching TV3. Sitting inactive in a public place (theater, meeting)4. As a passenger in a car for an hour without a break5. Lying down to rest in the afternoon whencircumstances permit6. Sitting and talking to someone7. Sitting quietly after a lunch without alcohol8. In a car, while stopped for a few minutes in traffic Sleep 1994;17:160–167
    13. 13. Obstructive Sleep ApneaTreatment Options• Behavioral: Weight loss, EtOH avoidance, nonsupine position• Positive Airway Pressure: CPAP, Provent, others• Mandibular advancement device• Surgery: UPPP, Tonsillectomy, Tracheostomy J Fam Prac. 2008;57(8) Suppl (
    14. 14. ProventProvent is a relatively new nasalexpiratory positive airway pressure(EPAP) device• It is a one-way valve that is taped into the nostrils, so that the seal is airtight.• By inhibiting the outflow of air, positive pressure in the airway is achieved
    15. 15. OSA & the EyeOcular Manifestations ofSleep Apnea• Asthenopia• CPAP-associated Red Eye• Floppy Eyelid Syndrome• Diabetic Retinopathy• NAION• Papilledema• Normal Tension Glaucoma
    16. 16. AsthenopiaCommon OSA-associated asthenopicsymptoms• Unexplained symptoms of blur • Trouble “focusing eyes” • Vision is 20/20 but the patient is c/o blur• Misinterpreting what is seen • Incorrect recording or copying • Work-related errors• Eye strain and/or fatigue• Headaches • Worse in the morning
    17. 17. AsthenopiaIf OSA is in the medical history• Ask about sleepiness or fatigue• Possibly due to poor compliance or residual fatigue• Offer supportive management (eg. CPAP compliance)If OSA is not in the medical history• High index of suspicion whenever the chief complaint is fatigue or asthenopia• Especially if habitus is Pickwickian• Be prepared to screen for sleepiness
    18. 18. CPAP-associated Red EyeClinical Problems• Dry eye syndrome• EXW CL intolerance• Recurrent corneal erosion• Infectious conjunctivitisCauses• Air leaks• Retrograde air flow thru nasolacrimal apparatusTreatment• Lubricating ointments HS, punctal plugs• CPAP refitting: adjust headgear and pressure Optometry. 2007;78:352-355
    19. 19. CPAP-associated Red Eye
    20. 20. Persons with OSA generally have greater ocular discomfort than controls, but is greatest among persons that are noncompliant with CPAP Eye 2010;24:843–850
    21. 21. Floppy Eyelid SyndromeClinical 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 Clin Exp Ophthalmol 2005;33:117-125.
    22. 22. Floppy Eyelid SyndromeEyelash ptosis• Downward displacement of eyelashes• Lashes may point in various directions• Loss of parallelism• Pts may trim with scissors Ophthalmology 1998;105:165-169
    23. 23. Floppy Eyelid Syndrome
    24. 24. Fistulous tracts within the upper eyelid tarsal conjunctiva containingbacteria-laden protein coagulum may contribute to chronic conjunctivitis inpatients with FES that is refractory to antibiotic tx. Surgical evacuation ofthe conjunctival crypts can lead to resolution of the conjunctivitis AJO 2012;154:527
    25. 25. Floppy Eyelid SyndromeEtiopathogenesis• Loss of elastic fibers in tarsus• Likely caused by repeated mechanical trauma, possibly eye rubbing or sleeping with the face buried in the pillow• FES strongly associated with keratoconus, reinforcing suspected role of mechanical trauma Surv Ophthalmol 2010;55:35-46
    26. 26. Floppy Eyelid SyndromeTreatment• CPAP therapy • Treatment of OSA can improve sxs• Protect eye during sleep • Ointments HS • Patching, taping, sleep mask• Surgery isconsidered the definitive treatment • 25-50% failure rate within 2yrs Ophthalmology 2010;117:839-846
    27. 27. Floppy Eyelid SyndromeRelation to OSA• About 10-20% of OSA pts have FES• 40% of pts with severe OSA have FES• 96% pts with FES have OSA• FES strongly associated with OSA even after adjusting for weight Surv Ophthalmol 2010;55:35-46
    28. 28. OSA & the EyeOcular Manifestations ofSleep Apnea• Asthenopia• CPAP-associated Red Eye• Floppy Eyelid Syndrome• Diabetic Retinopathy• NAION• Papilledema• Normal Tension Glaucoma
    29. 29. Diabetic RetinopathyOSA increases risk of progression of retinopathy• Diabetic retinopathy is more common and severe in patients with OSA, independent of other risk factors• Risk of progression associated with severity of OSA• CPAP may prevent progression of diabetic retinopathy by minimizing nocturnal hypoxia• Diabetics with OSA should be screened for retinopathy and encouraged to be compliant with CPAP Am J Ophthalmol. 2010;149:959–963
    30. 30. Other Retinal Disorders Associated with OSACentral Serous Chorioretinopathy• OSA associated with increased catecholamine levels and sympathetic activation• CSCR has been associated with increased adrenergic and sympathetic activity• Treatment of OSA has been reported to hasten recovery of CSCR (Graefe’s 2010;248:1037)Retinal Vein Occlusion• OSA has been identified as an independent risk factor for RVO (hazard ratio: 1.94) (AJO 2012;154:20)
    31. 31. NAIONClinical 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
    32. 32. NAIONPathophysiology• 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
    33. 33. NAIONDiagnosis: Must exclude GCA inevery case• ESR• C-Reactive Protein • Levels increase in presence of inflammation • Upper limit normal does not rise with age• Platelets • Secondary thrombocytosis due to chronic inflammation
    34. 34. NAIONTreatment• Aspirin • Decreases incidence in fellow eye at 2 yrs, but not at 5 yrs• Surgical decompression • No benefit (Ischemic Optic Neuropathy Decompression Trial)• Control of predisposing systemic disease • May slow progression or reduce incidence in fellow eye • Hypertension, Diabetes, Hyperlipidemia, OSA• Avoidphosphodiesterase 5 inhibitors (Viagra, Cialis, etc) • May increase risk of NAION in fellow eye
    35. 35. NAIONMedicolegal obligation to inform pts of risk to fellow eye
    36. 36. NAIONRelation to OSANAION Patients with OSA Mojon (2002) 71% Controls: 18% Palombi (2006) 89% HTN: 59%, DM: 37% Li (2007) 30% Controls: 18% Arda (2013) 85% Controls: 65% (matched for DM, HTN)Conclusions• OSA may play an important role in pathogenesis of NAION• OSA may be the systemic disorder most frequently associated with NAION• Every patient newly diagnosed with NAION should be tested for OSA
    37. 37. PapilledemaClinical 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
    38. 38. PapilledemaWork-up• Urgent MRI or CT scan• Lumbar puncture if imaging normalIdiopathic IntracranialHypertension• “Pseudotumor cerebri”• Syndrome of elevated ICP, papilledema, normal MRI/CT, normal CSF• Secondary pseudotumor cerebri syndromes with an identifiable cause (venous sinus thrombosis, vitamin A toxicity, COPD, OSA)• Tx: Diamox 250mg po QID , Underlying cause if known
    39. 39. PapilledemaRelation to OSA• Stein (2011) • Reviewed 2.3 million insurance company billing records • Persons with OSA have 30% to 100% increased risk of developing papilledema• Parvin (2000) • 4 pts with unexplained papilledema that resolved with successful treatment of OSA • ICP is normal during the day but elevated at night • Intermittent (nocturnal) ↑ ICP can cause sustained papilledema • Hypercapnia-induced cerebral vasodilatation elevates ICP
    40. 40. OSA & the EyeOcular Manifestations ofSleep Apnea• Asthenopia• CPAP-associated Red Eye• Floppy Eyelid Syndrome• Diabetic Retinopathy• NAION• Papilledema• Normal Tension Glaucoma
    41. 41. Normal Tension GlaucomaClinical Characteristics• Probably a variant of POAG• 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
    42. 42. Normal Tension GlaucomaPathophysiology • IOP-independent factors predominate • Vascular insufficiency: CVD, HTN • Vasospasm: migraine, Raynauds phenomenon • Translaminar pressure difference: low ICP
    43. 43. Normal Tension GlaucomaDiagnosis• R/O other glaucomas • POAG with diurnal IOP fluctuation • IOP normalization (Burnt-out glaucoma, steroids)• R/Oother 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 Ophthalmology 1998;105:1866-1874
    44. 44. Normal Tension GlaucomaRelation to OSA Greater than general pop Glaucoma Patients with OSAPOAG Mojon (2000) 20%POAG Girkin (2006) 1%POAG Roberts (2009) 17%POAG Blumen (2010) 48%NTG Marcus (2001) 57%NTG Mojon (2002) 50-60% (varies with age)Conclusion • 50%-60% of NTG patients have OSA
    45. 45. Normal Tension GlaucomaRelation to OSA Greater than general popOSA Patients with Glaucoma POAG NTG Mojon (1999) 4% 3% Geyer (2003) 1% 1% About 5%-10% of OSA patients Sergi (2007) 6% have glaucoma Bendel (2008) 27% Karakuck (2008) 3% 10% Boonyaleephan (2008) 5% 9% NTG is at least Lin (2010) 6% as common as Kadyan (2010) 2% POAG in this patient population Boyle-Walker (2011) 8%
    46. 46. Normal Tension GlaucomaRelation to OSA • 6%-10% of OSA patients have NTG (0.5% general pop) • 50% of NTG patients have OSA • Treatment of OSA may help stabilize NTG (Kremmer, 2003) and improve VF performance (Sebastian, 2006)
    47. 47. Normal Tension GlaucomaCPAP Increases IOP• Kiekens (2008) • Diurnal IOP measured with and without CPAP • Average IOP and diurnal fluctuation higher with CPAP • 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 Invest Ophthalmol Vis Sci. 2008;49:934–940
    48. 48. Normal Tension GlaucomaCPAP Increases IOP• Pepin (2010) • Diurnal IOP measured with and without CPAP • CPAP caused a significant increase in nocturnal IOP • Speculate that some effects of untreated OSA may result in decreased nocturnal IOP and these are normalized by use of CPAP • Concludes that IOP changes induced by CPAP are explained by restoring normal IOP rhythm rather than by a deleterious effect of the device Arch Ophthalmol 2010;128:1257-1263
    49. 49. Normal Tension GlaucomaOSA May Cause NFL Loss Without Glaucoma• NFL thinning may represent preclinical NTG• Numerous studies (using both OCT and GDx) have found that NFL thickness is reduced in patients with OSA compared to healthy controls • Degree of thinning has been correlated with severity of OSA• Functional loss in these patients may be detected with mfVEP, but standard automated perimetry may still be normal• This “silent optic neuropathy” may in some patients evolve into NTG
    50. 50. Normal Tension GlaucomaOSA May Cause VF Loss Without Glaucoma• VF loss may occur due to optic nerve damage caused by cerebral ischemia and intermittent ICP elevation• Visual field indices are, on average, worse among patients with OSA, and the severity of the VF damage has been correlated with the severity of OSA
    51. 51. Normal Tension GlaucomaConclusions & Recommendations• Persons with OSA should be screened for glaucoma • Risk of glaucoma is correlated with severity of OSA• Patientswith NTG should be screened or at least questioned about OSA • Treatment of uncontrolled OSA may help stabilize glaucoma and improve VF performance• Initiation of CPAP therapy may increase nocturnal IOP • The clinical significance of this in unknown
    52. 52. Source: Can J Ophthalmol 2007;42:238–243
    53. 53. Thank You!