A 37-year-old female who suffers from recurrent corneal erosions due to EBMD recently presented with a red, painful, itchy rash covering her face. She has shown sensitivity to various things before that presented as a rash, such as various antibiotics, face cremes, soaps, and cleaning supplies. We went through the list, removing all facial cremes, makeup, perfumes, and treated with oral steroids.

It improved while taking the steroids, and immediately returned after discontinuation. At this point, I said, “I think it is your CPAP mask.” I instructed her to walk into the office of the doctor where she got the mask and ask to speak to the nurse. My goal was for them to see the rash. Instead of doing this, she called her regular doctor and got an appointment three days later. She got more steroids and it improved while on the steroids, and promptly returned after discontinuation.

She came back and I took photographs (see below). I again instructed her to go to the CPAP doctor’s office to show them the rash. She did and they told her she “must have had a reaction to something”. She discontinued wearing her mask for one week and convinced her doctor she needed a different mask when she presented with much clearer skin.

I have a love-hate relationship with CPAP masks. While they are important for those suffering from obstructive sleep apnea (OSA), it can make controlling ocular surface disease difficult. 

OSA is a chronic disorder affecting about 2–4% of the adult population, most commonly middle-aged men who are overweight. Patients suffer from repetitive episodes of complete or partial collapse of the upper airway (mainly the oropharyngeal tract) with a consequent cessation or reduction of airflow during sleep. The repetitive obstructive events cause a progressive asphyxia that increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened from sleep.2  Risk factors include snoring, obesity, male gender, age, post-menopausal women, a large neck circumference, nasal obstruction, enlarged tonsils or adenoids, macroglossia and low-lying soft palate.2  Over many years, recurrent episodes of intermittent hypoxia and sleep disruption affect the brain and the cardiovascular system among others, and alter metabolic balance, leading to  OSA syndrome. Daytime sleepiness resulting from nocturnal sleep fragmentation is a key symptom of OSA. It is reported in more than 80% of the patients.2 The sleepiness may be so severe that driving becomes dangerous and work is negatively affected.

Positive airway pressure (PAP) devices function as a pneumatic support to maintain upper airway patency by increasing the upper airway pressure above a ‘critical’ value. The critical value is the pressure value below which the airways collapse. The amount of pressure to apply varies with the severity of OSA. Higher pressures are needed to abolish apnoeas occurring during rapid eye movement sleep, as well as when the patient is supine or severely obese. 

Masks come in various forms, including nasal, pillow and full face masks. They typically include headgear to hold the mask in place, a nasal piece for delivery of oxygen and a hose. Think of a really expensive elephant costume. Nasal masks are the smallest and lightest devices with minimal facial contact. Pillow masks are nasal masks with cushions that keep the mask connected to the nostrils with movement and are designed for active sleepers. Full face masks cover the nose and mouth and may be an issue for those who like to read in bed.    

Machines also vary in the pressure delivered. Traditional Continuous Positive Airway Pressure provides one level of pressure to the upper airway during sleep. BiPAP machines provide two levels of pressure for those having trouble exhaling against a high positive pressure. A higher pressure is delivered on inhalation while a lower level is delivered on exhalation. Auto-adjusting machines provide variable pressures based on the patient’s needs and stages of sleep. 

Oral appliances (OAs), also called mandibular advancement devices or MADs, may also be used to treat OSA. Thankfully, my patient was a candidate for this type of treatment and will be free from the CPAP machine. These appliances maintain the airway by holding the mouth in a certain position and have been found to be effective in improving OSA. The forward inclination of the lower incisors can cause dental changes over time, but these devices are typically fitted by dentists who monitor these changes. Studies report that OAs are better for mild OSA, and while effective, their efficacy is more variable than that of traditional CPAP. While less effective, patients are more likely to use them every night because they are less cumbersome so compliance is better. And of course, they don’t cause dermatitis and they do not exacerbate ocular surface disease.

Sleep Apnea and Ocular Disorders

Ocular manifestations associated with sleep apnea include ocular surface disorders, keratoconus, normal tension glaucoma, papilledema, and Nonarteritic Anterior Ischemic Optic Neuropathy (NAION).

Studies have found OSA patients to suffer from increased ocular surface disease. Common associations include exposure keratopathy, floppy eyelid syndrome, recurrent erosions, and keratitis. Lower Schirmer and TBUT scores, and increased OSDI questionnaire scores have been reported. Conjunctival squamous metaplasia has also been reported. Years ago, I often had patients with what I thought was “intractable dry eye” suddenly announce after months of ineffective treatment that they were using a CPAP machine. Now I know to ask at the first visit.

Keratoconus has also been linked to OSA. Pedrotti, et al, found OSA was 10 to 20 times more prevalent among patients with KCN than the rate reported for the general population. Corneal hysteresis has been found to be lower in moderate to severe OSA patients compared to mild cases of OSA or normal (non-OSA) patients. Central corneal thickness has been reported to be inversely correlated with the severity of OSA.

Normal tension glaucoma is thought to result from a lack of oxygen to the optic nerve.  OSA may reduce optic nerve head perfusion, cause transient hypoxia and increased vascular resistance. A study by Bilgin found the prevalence of OSA was 29.2% higher in NTG patients than controls without glaucoma. Decreased RNFL was found in patients with severe OSA while those with mild to moderate OSA were not significantly different from normal. Thinning of the central subfoveal choroidal thickness and retinal nerve fiber layer was noted in severe cases of OSA using enhanced depth imaging optical coherence tomography (EDI-OCT). IOP fluctuations have been found during sleep in patients with moderate to severe OSA, with a mean lower IOP during apnea events versus non-apnea phases. Lower IOP may result in hypoxia.

An increase in CO2 concentrations can result from OSA. This may dilate blood vessels and increase pressure, leading to optic disc swelling. Patients with OSA have higher incidences of papilledema. CPAP therapy treatment has been shown to improve or even resolve papilledema.

Research has reported that 71% of patients with NAION have OSA. Patients with NAION should be referred for a polysomnogram test to rule out OSAPatients with severe OSA who are noncompliant with their CPAP treatment have an increased risk of second eye NAION vision loss.

These studies appear to indicate that ocular manifestations are more likely in severe OSA.   For this reason, I am now more likely to ask not only if my patients have OSA, but what their disease severity level is and the type of mask they are currently using.


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