Ocular Manifestations Of Sleep Apnea

Written by Larry J Alexander OD FAAO, Brad Sutton, OD FAAO Tuesday, 18 December 2012

Ocular Manifestations Of Sleep Apnea

Sleep apnea is a systemic disorder in which breathing repeatedly stops and starts during sleep, usually with 10 to 60 second interruptions. “Apnea” is Greek for “without breath.” Each pause in breathing is an “apnea”, and each low breathing event is referred to as a hypopnea. When oxygen saturation in the blood drops below a critical level, the brain signals the body to “wake up” and take a deep breath, thus preventing deep sleep. While seemingly innocuous and more annoying to the bed partner than the patient (the sufferer is almost never aware during sleep), sleep apnea represents a genuine threat to both systemic and ocular health because of the associated compromise of oxygen flow to end organs.

Of historic interest is the association of Sleep Apnea to the term “Pickwickian Syndrome.”  The Pickwickian syndrome is also called Obesity Hypoventilation Syndrome and is characterized by body mass index above 30 kg/m2, hypoxia, hypercapnia, and hypoventilation. 1 The reference is to the “fat boy” character in the Charles Dickens novel, “The Pickwick Papers.”  It refers to the character traits and general habitus of Obstructive Sleep Apnea (OSAS) patients, which evolves around excessive obesity. Sleep apnea is far more common than most clinicians realize, and the potential for ocular and systemic damage is an issue. 2 Obstructive sleep apnea and ocular disorders.  Perfusion is altered during the sleep apnea and can impact on all tissues dependent on active oxygen flow.  The inherent low oxygenation of blood associated with uncontrolled A1C levels in diabetes increases the risk of compromise.  There are three basic types of sleep apnea; 1. Obstructive (OSAS) which occurs when throat muscles relax and the soft palate collapses, 2. Central:  caused by a stroke, tumor of the brainstem, or heart disease- which occurs when your brain doesn’t send proper signals to breathing muscles, and 3. Complex or mixed which is a combination of both types. OSAS accounts for 84% of cases, mixed for 15%, and pure central (also known as Cheyne-Stokes syndrome) for .4%. 3  Obstructive sleep apnea occurs two to three times more often in older adults and two times more often in men compared to women.It is estimated that over 11,000,000 Americans are affected, with up to 24% of Caucasian males and 9% of Caucasian females.4 Sleep apnea appears to affect African Americans more often than whites, at a rate of approximately 2.5 to 1. In addition to multiple ocular conditions, sleep apnea is highly associated with heart disease, hypertension due to increased epinephrine and norepinephrine production, and stroke.

SLEEP APNEA STATISTICS AND FACTS (www.medcinenet.com/sleep_apnea/page4.htm):

  • 70% of Obese Individuals Have OSAS
  • 50% of Heart Disease Patients Have OSAS
  • 60% of Stroke Patients Have OSAS
  • 80% of Patients with Difficult to Control Hypertension Have OSAS
  • 34% of NFL Lineman Have OSAS
  • 80% or More of Individuals with OSAS are Undiagnosed
  • 10% of Individuals with OSAS are actually treated

SIGNS AND SYMPTOMS OF SLEEP APNEA

Attention to the signs and symptoms of sleep apnea are important in the practice of primary eye care.  While the signs and symptoms may be mixed, the more common include:

http://www.mayoclinic.com/health/sleep-apnea/DS00148

  • Excessive Daytime Sleepiness and Fatigue
  • Trouble Concentrating (Altered Cognitive Function) 5
  • Memory Loss and Forgetfulness
  • Loud Snoring (Obstructive) With Gasps and Typically No Report of Dreams
  • Snoring that Stops and Restarts (This is Practically Diagnostic of the Condition)
  • Observed (Usually by Partner) Episodes of Cessation of Breathing During Sleep-Often Obstructive
  • Abrupt Awakening With Dry Mouth and/or Sore Throat - Often Central Causation
  • Morning Headaches
  • Difficulty Staying Asleep
  • Irritability
  • Rapid Weight Gain
  • Mood and Behavior Changes
  • Cognitive impairment possibly related to decreased blood serum Brain Derived Neurotrophin Factor(BDNF), which also has an association to glaucoma. 6
  • Anxiety and/or Depression

SLEEP APNEA CAUSES, RELATED SYSTEMIC CONDITIONS AND RISK FACTORS

  • Sleep apnea is commonly associated with obesity, but you don’t have to be obese to be afflicted.  34% of NFL Lineman Have OSAS.  Related conditions include: 7

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TAKEO SPIKES Credit: Photograph by NFL via Getty Image

http://www.slate.com/slideshows/sports/the-nfls-widest-necks.html

  • Neck Circumference over 17 Inches (43cm) 8
  • Gastro Esophageal Reflux disease (50%) GERD
  • Excessive weight
  • Being older
  • Prolonged sitting
  • Males twice as likely
  • Hypertension
  • Inherited Narrow Airway
  • Irregular Sleep Hours
  • Polycystic Ovary Syndrome
  • Alcohol or Sedatives Before Bedtime
  • Smoking
  • Nasal Congestion
  • Asthma and Chronic Bronchitis
  • Family History
  • Diabetes
  • Hypothyroidism
  • Neuromuscular Disorders
  • Sleeping at a Higher Altitude Than You are Used To

Cystic fibrosis 9

http://www.mayoclinic.com/health/sleep-apnea/DS00148 is an excellent online reference for patients

There are multiple approaches utilized to assist in the diagnosis of sleep apnea. These include, but are not limited to the following:

  • Epworth Sleepiness Scale (self reported questionnaire). Dr Murray Johns owns the copyright in the ESS (Copyright © M.W.Johns 1990-1997).  Dr Johns permits personal, non-commercial use to be made of the ESS (but excluding by governmental agencies) at no charge, so long as Dr Johns’ ownership of copyright in the ESS is acknowledged when the ESS is referenced.   The acknowledgment should be as follows: “Copyright © MW Johns 1990-1997.  Used under license.”  Visit the following website for information: www.epworthsleepinessscale.com.
  • Pulse Oximetry (at-home measurement of blood oxygen levels overnight) 10
  • Polysomnography Sleep Study (the gold standard: includes EEG, EOG, EMG, measurement of air flow, measurement of chest movement, audio snoring recording, oximetry, and video surveillance. 11
  • Apnea Hypopnea Index (AHI) During Sleep Study
  • Respiratory Disturbance Index (RDI) During Sleep Study

MANAGEMENT OF SLEEP APNEA

Like diagnosis, there are multiple approaches to the management of obstructive sleep apnea. They are all designed to maintain the patency of the airway during sleep. These treatment approaches include, but are not limited to, the following:

  • Weight Loss
  • Discontinuing Smoking
  • Sleeping on Side
  • Acetazolamide lowers blood pH and encourages respiration
  • Avoidance of Alcohol
  • Avoidance of Sleeping Pills
  • Dental Appliances (move lower jaw forward to open airway: can worsen TMJ)
  • Pillar Procedure (Dacron strips inserted in to soft palate: performed in office)
  • BiPAP and automated continually adjusting CPAP
  • 50% of patients discontinue CPAP use, and many others do not comply with nightly use. The machines can be noisy, the masks can be uncomfortable, and they are difficult to travel with.
  • Play the didgeridoo to strengthen muscles in the throat. 15
  • Adherence to a Mediterranean diet and regular physical exercise.  12

  • Surgical Procedures (Maxillo-Mandibular Enhancement, Tongue reduction, tonsillectomy ) 13

  • CPAP (Continuous Positive Airway Pressure. Uses continuous positive airflow to keep the airway open) with the caution that often there are POTENTIAL side effects on the ocular surface.  14

http://www.garyradler.com/photos/i-vL7KLVJ/0/Th/i-vL7KLVJ-Th.jpg" >

image5

OCULAR SIDE EFFECTS OF SLEEP APNEA

SIDE EFFECTS OF CPAP USE

Use of a CPAP apparatus and mask can be associated with ocular side effects.

It is not uncommon for a small amount of forced air to escape around the edge of the mask. This forced airflow can lead to ocular dryness and irritation. Patients utilizing CPAP therapy also experience a higher rate of bacterial conjunctivitis, possibly due to air being forced through the nose and lacrimal system in to the eye. CPAP use has also been shown to elevate intraocular pressure. It has accounted for elevation up to 5-8 mm hg in some studies. 16  This elevation, however, was found in patients who were not taking glaucoma medications. The effect of medication may prevent, or significantly decrease, this phenomenon.

FLOPPY EYELID SYNDROME

image6 

Floppy Eyelid Syndrome (FES) was first described by Culberston and Ostler in 1981. 17 While less than 5% of people with OSAS have FES, essentially 100% of patients with FES have OSAS. 18  The relationship remains unclear at this point, but the associated oxygen deprivation in the lid tissue may lead to increased matrix metalloproteinase, which in turn decreases tissue elasticity. 19 Floppy Eyelid Syndrome and sleep apnea is most commonly encountered in obese men, and it is also associated with a higher incidence of keratoconus. 20-21   Patients with FES have very loose, rubbery eyelids that evert easily with minimal pressure. During sleep, contact between the lids and the pillow can lead to opening or complete eversion of the lids. This, in turn, results in exposure related complications and mechanical abrasions. Depending upon an individual’s preferred sleeping position and degree of night-time movement, one or both eyes may be affected.  Patients report significant discomfort through the night and upon awakening that improves throughout waking hours. Lash ptosis, or the downward pointing of the upper eyelashes, is also commonly encountered with FES. Eyes with FES can be prone to excessive mucous production, which may then result in mucous fishing syndrome.

Floppy eyelid syndrome should alert the clinician to question the likelihood of sleep apnea syndrome. 22

Treatment of FES is multifactoral. Use of a night-time lubricant ointment helps to protect the ocular surface during sleep. Use of a cylindrical pillow instead of a standard pillow may allow the cheek but not the eyelids to contact the sleeping surface. Use of a stiff sleep mask that covers the eyes can also help to prevent eversion of the lids. The lids can be taped closed at night, but compliance with this therapy is often very poor. Surgical procedures can be undertaken to tighten the lids, and management of the underlying OSAS frequently decreases the severity of the disease.

OPTIC DISC EDEMA (ODE) SECONDARY TO INCREASED INTRACRANIAL PRESSURE (PAPILLEDEMA)

BILATERAL ODE SECONDARY TO SLEEP APNEA

image7image8

Patients with OSAS may experience increased intracranial pressure (Idiopathic Intracranial Hypertension) at night, leading to papilledema. 23-24  This can be difficult to appropriately diagnosis because lumbar taps performed on these individuals during waking hours typically yield normal results. Use of effective CPAP therapy often decreases the ICP, thus eradicating the problem. Because obesity is highly associated with both OSAS and Idiopathic Intracranial Hypertension, there is certainly overlap. OSAS related elevations of ICP should be strongly suspected in obese males with papilledema, normal MRI’s, and normal opening pressures on day- time lumbar taps. In fact, OSAS should be a consideration in the evaluation of any patient presenting with papilledema. 25

NON-ARTERITIC ISCHEMIC OPTIC NEUROPATHY (NA-AION)

NA-ION OD WITH DISC PALLOR INFERIOR

image9image10

CORRESPONDING THINNING OF RNFL ON SDOCT

image11

CORRESPONDING THINNING OF GANGLION CELL COMPLEX ON SDOCT

image12

NAION represents hypo-perfusion induced ischemic damage to the anterior optic nerve head. The visual loss or disturbance experienced by the patient is typically noted upon awakening. NAION is most commonly encountered in small nerves with little to no cupping. As it relates to NAION, this anatomical configuration is frequently referred to as a “disc at risk”. Many systemic conditions and certain medications are associated with NAION, but OSAS has risen to the top of the list. 26-29 Multiple studies have shown a substantial link between OSAS and NAION. Patients that have suffered an NAION event have a five times greater risk of having OSAS than the general population. In one recent study, 24 of 27 NAION patients had sleep apnea. 30 In another, 12/17 NAION patients had OSAS, while only 3/17 controls had the disease. 31  The OSAS associated night-time drop in oxygen perfusion is believed to trigger the acute ischemic event. This may be exacerbated by use of antihypertensive medications before bed, or by the use of erectile dysfunction drugs. It also appears that treatment of OSAS with continuous positive airway pressure does not necessarily prevent development of NA-AION. 32  It has also been reported that  the diameter and blood flow of OA, PCA and CRA change in OSAS patients. Compared with non-OSAS patients, the auto-regulation function of PCA and CRA is weakened in OSAS patients. 33

Obstructive sleep apnea syndrome (OSAS) and nocturnal hypotension have an intimate association. In one study up to 89 % of patients with NA-ION had associated sleep apnea.  In that same study, it was reported that approximately 75% of all patients with NA-AION discovered visual loss on first awakening. 34

GLAUCOMA [(BOTH PRIMARY OPEN ANGLE GLAUCOMA(POAG) AND NORMAL TENSION GLAUCOMA(NTG)]

The link between glaucoma and obstructive sleep apnea syndrome is a bit controversial but certainly offers a potential association. 35-39  Patients with OSAS demonstrated significant 24-hourIOP fluctuations, with the highest values at night. CPAP therapy causes an additional IOP increase, especially at night. Regular screening of visual fields and the optic disc is warranted for all patients with OSAS, especially those treated with CPAP.40  There are enough reports to create a potential link, and the investigation of normal tension glaucoma should include OSAS. Persons with either normal tension glaucoma or primary open angle glaucoma should be questioned regarding sleep apnea syndrome.

It has been reported that there is a proportional decrease in the retinal nerve fiber layer (RNFL) measurement of patients with OSAS, even in the absence of glaucoma. 41  It appears that moderate to severe OSAS is more likely to attenuate the RNFL. 42-43 Coincident with the attenuated RNFL is a concurrent reduction in visual field sensitivity. 44-46 The measurement of the Ganglion Cell Complex with SDOCT affords the clinician another opportunity to assess the OSAS patient as the inner retinal layer is the diseased structure.

The other associations with OSAS of non-arteritic ischemic optic neuropathy (NAION) and papilledema also implicate some alteration occurring within the architecture of the optic nerve head. 47  The alteration may either be pure alteration of perfusion or an association with increased cerebrospinal fluid pressure (CSFP) actually compressing and altering blood flow.  In patients under age 50, there is also a strong link between NAION and an underlying anomalous or small disc (92%) and an increased likelihood of involvement of the fellow eye.  48  One issue of primary concern is the fact that in our typical case history form, Sleep Apnea is often not addressed and we as clinicians are usually unaware of the condition.

The issue of sleep apnea should be addressed in patients with signs or symptoms of OSAS and likewise deserves investigation in patients presenting with any potential vascular flow issues to the optic nerve.

RETINAL VASCULAR DISEASE

OSAS also plays a significant role in retinal vascular disease. OSAS is reported to be associated with increases in microvascular complications with diabetes. 49-50 Recent reports have shown that diabetic patients with OSAS have a significantly higher risk of developing Proliferative Diabetic Retinopathy (PDR) than those without OSAS. 51 Likewise, in patients with PDR, OSAS increases the risk of iris neovascularization. 52  In addition, another report examining patients with retinal vein occlusions found 23 of 30 patients to suffer from OSAS. 53

IDIOPATHIC CENTRAL SEROUS CHORIORETINOPATHY

image13

Idiopathic Central Serous Chorioretinopathy (ICSC) has been reported as the first sign of onset of sleep apnea syndrome. 54  The etiopathogenesisis thought to be related to increased epinephrine and norepinephrine occurring with sleep apnea increasing the catecholamine levels. 55   It is reported that the treatment of OSAS results in rapid resolution of the ICSC. 56  

Patients with Idiopathic Central Serous Chorioretinopathy should be questioned regarding symptoms of sleep apnea syndrome. 57

CONCLUSION

Consideration of, and investigation for, the presence of sleep apnea in the population seeking eye care is of paramount importance.  It is estimated that over 11,000,000 Americans are affected, with up to 24% of Caucasian males and 9% of Caucasian females. The dominant cause is obstructive in nature.  Sleep apnea causes nocturnal hypoxia and has very strong association to systemic disease.  Likewise there are implications of sleep apnea in eye care.  The strong association of sleep apnea to the following ocular conditions illustrates that point.

Ocular Conditions Associated with Sleep Apnea and Hypopnea

  • Floppy Eyelid Syndrome
  • Keratoconus
  • Normal Tension Glaucoma
  • Primary Open Angle Glaucoma
  • Non-Arteritic Ischemic Optic Neuropathy
  • Enhancement of `Retinal Vascular Disease
  • Enhancement of Developing Diabetic Retinopathy
  • Idiopathic Central Serous Chorioretinopathy
  • Optic Disc Edema Associated with Increased Intracranial Pressure

It is then incumbent upon eye care providers to be aware of the signs and symptoms of sleep apnea and to apply appropriate questioning and investigation of sleep apnea when the conditions present in the office.  Simple observation and questioning of the patient would start the process and perhaps precipitate the appropriate sleep studies.  Ask the patient or the patient’s significant other about:

  • Reports of Difficulty Sleeping and Staying Asleep
  • Excessive Daytime Sleepiness and Fatigue and Trouble Concentrating
  • Use the Epworth Sleepiness Scale
  • Memory Loss and Forgetfulness
  • Loud Snoring That Stops and Starts With No Report of Dreams
  • Observed Episodes of Cessation of Breathing During Sleep-Often Obstructive
  • Abrupt Awakening With Dry Mouth and/or Sore Throat and Morning Headaches
  • Irritability, Anxiety and/or Depression, Moodiness
  • Rapid Weight Gain, Obesity and a Very Large Neck Over 17 Inches

The general physician caring for the patient with sleep apnea should likewise be aware of the ocular side effects of the disorder and request appropriate consultation from the local eye care provider.  A baseline should be obtained with regard to optic nerve health including an SD-OCT assessment of the retinal nerve fiber layer and the ganglion cell complex.

The eye care practitioner is a very important player in the detection of sleep apnea and the subsequent management of resulting ocular disorders.

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About the Author(s)

Larry J Alexander OD FAAO

Larry J Alexander OD FAAO

Dr. Alexander (1948-2016) was a 1971 graduate of Indiana University School of Optometry. He served in the US Navy then served as a Professor at the University of Alabama Birmingham School of Optometry. Larry contributed to a number of chapters in textbooks and has published three editions of Primary Care of the Posterior Segment, as well as contributed to the professional literature. He also lectured extensively in the area of ocular and systemic disease. His areas of special interest included dysfunctional tear syndrome, glaucoma and macular degeneration.  His lessons are the basis for this site and he will be dearly missed. 

Brad Sutton, OD FAAO

Dr. Brad Sutton received his Bachelor of Arts degree in Psychology from Indiana University in 1989 and his Optometry Doctorate from IU in 1993. His main areas of clinical interest include ocular disease and surgical management. He has given over 100 continuing education lectures on topics related to ocular disease at the local, state, national, and international level. He has also published numerous journal articles and a book chapter. Dr. Sutton is a member of the American Optometric Association and a fellow in The American Academy of Optometry. He has also served as an examiner for the National Boards on multiple occasions and has been an assistant chief examiner four times. He was named the Young Optometrist of the Year for the state of Tennessee in 1997-1998 and received the same award (President's Citation) for the state of Indiana in 2001.

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