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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4538_Библиотеки_им_академика_М_И_Перельмана
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Ophthalmology:
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Neuro- Ophthalmological
AraceliNogueira, GabrielaBosco, NuriaPérez-Martín,
MartaMorato, CarlosS.Fernández-Escámez,
NicolásToledano, CarlosO’Connor-Reina,
andGuillermoPlaza
19.1 Introduction
Obstructive sleep apnea (OSA) does have an impact on ocular health. McNab [1, 2],
Waller et al. [3], and Nieto Enriquez et al. [4] summarized the different ocular
pathology that can be found in OSA patients more than a decade ago. Since then,
several extensive studies and novel ndings on this issue have been reported. These
ndings have been recently reviewed in several systematic reviews and metaanalysis [5–9].
Several pathways have been proposed to explain the association between OSA
and different ocular diseases, including damage to the vessels and optic nerve that
may cause glaucoma progression or retinal deterioration, but also having hypoxia,
endothelial proliferation, angiogenesis and oxidative stress, promoting the development of keratoconus and proliferative diabetic retinopathy (Fig.19.1).
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A. Nogueira · C. S. Fernández-Escámez · N. Toledano
Department of Ophthalmology, Hospital Universitario de Fuenlabrada, Madrid, Spain
G. Bosco · N. Pérez-Martín · G. Plaza (*)
Department of Otolaryngology, Hospital Universitario Sanitas La Zarzuela, Madrid, Spain
Department of Otolaryngology, Hospital Universitario de Fuenlabrada, Universidad Rey Juan
Carlos, Madrid, Spain
e-mail: guillermo.plaza@salud.madrid.org
M. Morato
Department of Otolaryngology, Hospital Universitario de Fuenlabrada, Universidad Rey Juan
Carlos, Madrid, Spain
C. O’Connor-Reina
Department of Otolaryngology, Hospital Quiron Salud Marbella, Hospital Quiron Salud
Campo de Gibraltar, Spain, Marbella, Spain
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
P. M. Baptista et al. (eds.), Obstructive Sleep Apnea,
https://doi.org/10.1007/978-3-031-35225-6_19
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Fig. 19.1 Obstructive sleep apnea-related ocular pathology
19.2 Floppy Eye Syndrome
A. Nogueira et al.
In 1981, two ophthalmologists, Culbertson and Ostler [10], described for the rst
time an unusual entity characterized by “oppy” and redundant upper eyelids with
marked papillary conjunctivitis in obese middle-aged and older men (Fig.19.2).
They coined the term “oppy eyelid syndrome.” The affected eye corresponded to
the side the patient preferentially slept on and if both eyes were affected, the patient
alternated sides they slept on, or they slept face down. Some were noted to sleep
with the affected upper eyelid spontaneously everted and rubbing on the pillow. The
patients typically complained of symptoms of watering, stickiness, discomfort, and
blurred vision in the affected eye(s), and these symptoms were typically worse
on waking.
Since the rst description of oppy eye syndrome in an OSA patient by Woog
[11], several series and reviews [12–29] have been reported including, many patients
with oppy eye syndrome related to OSA.It affects primarily middle-aged obese
men with a diagnosis of OSA.However, only a small minority of patients (2%–5%)
with OSA have oppy eye syndrome, although two series have reported higher incidence, up to 50% of OSA patients [22–24, 29].
Two recent meta-analyses showed that oppy eyelid syndrome is more common
in OSA patients. Huon etal. [6]. found it in 312 of 690 patients with OSA and in 25
of 212 patients without OSA.The overall pooled (odds ratio) OR for oppy eyelid
syndrome was 3.126 (P<0.001) in the OSA group versus the non-OSA group.
Wang etal. [30] found pooled OR for oppy eye syndrome in OSA of 4.12in a total
of 767 participants (Fig.19.3), and such OR increased up to 7.64in severe cases.
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Fig. 19.2 Floppy eyelid, showing increased upper eyelid laxity with easy eversion of the eyelid
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Fig. 19.3 Forest plot of oppy eyelid syndrome (FES) prevalence in OSA.CI, condence interval. From Wang etal. [30]
Mild ptosis, downward-pointing eyelashes, or inversion may also be present.
Papillary conjunctivitis is apparent in the involved eye. Corneal involvement is
common and may include punctuate keratopathy, gross surface scarring, ulceration,
or increased vascularization.
Patients with suspected oppy eyelid syndrome should be referred for a full ophthalmologic evaluation. If oppy eyelid syndrome is conrmed, patients should
strongly be considered in OSA assessment. Treatment of oppy eyelid syndrome
can consist of conservative measures, including weight loss, eye shields or other
protective devices, lubricants, and occasionally corticosteroids or antibiotics based
on ophthalmologic ndings. Resolution after treatment of OSA has been well
documented.
Viera etal. [31] observed that oppy eye syndrome reversed in about half of 34
patients after 6months of CPAP therapy. However, Kadyan etal. [17] failed to nd
any signicant difference in upper or lower lid laxity between CPAP-treated and
untreated patients. Bayir et al. [32] have shown how surgical treatment of OSA
through anterior palatoplasty improved oppy eyelid in 50%–60% of the patients.
Surgical tightening of the eyelids can be performed in medically refractory cases,
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but high recurrence rates after surgery have been documented in patients with
untreated OSA.This observation further stresses the importance of managing OSA
in these patients.
19.3 Keratoconus
Corneal changes occurring with oppy eye syndrome, such as reduced corneal hysteresis and increased tendency to eye rubbing, have been suggested to predispose to
keratoconus [9, 33, 34]. Keratoconus is a noninammatory thinning and bulging of
the cornea, causing a distortion of the normal shape of the cornea and resulting in
extreme myopia and/or astigmatism. It has been described in OSA patients
(Fig.19.4).
A case–control study further reported that patients with OSA had thinner corneas
by 20μm compared to controls, with increased severity of OSA associated with
thinner corneas [35].
Several studies have also reported that patients with keratoconus have a high
prevalence of OSA (18%–20%) or are at high risk of OSA (12%–53%) as assessed
by the Berlin Questionnaire [36–40]. A meta-analysis estimated that patients with
OSA have an OR of 1.84 (95% condence interval, 1.163–2.914; P=0.009) for
keratoconus compared to controls (Fig.19.5) [41]. Thus, there is signicant evidence that OSA is associated with keratoconus. Therefore, proper screening for
OSA is warned for keratoconus patients to prevent various cardiovascular
comorbidities.
Fig. 19.4 Keratoconus
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Fig. 19.5 Forest plot of the association between obstructive sleep apnea and keratoconus. Squares
represent study-specic odds ratio (size of the square reects the study weight), horizontal lines
represent 95% condence intervals (CIs), and the diamond represents the pooled odds ratio, which
was computed by using random-effects model. From Pellegrini etal. [41]
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19.4 Ocular Surface Inflammation
The rst line of treatment for OSA is CPAP because of both its efcacy and its
safety. However, common complications of CPAP treatment are nasal irritation and
dryness, skin irritation, skin breakdown, and ulceration secondary to pressure from
the mask. Ophthalmologic problems or complications after CPAP are also occasionally seen [3, 4]. In 1984, Stauffer etal. [42] described a patient with bacterial conjunctivitis after CPAP use. In 2006, Ely and Khorfan [43] reported a case of a
woman with OSA who developed unilateral periorbital swelling with CPAP treatment that resolved when she stopped CPAP treatment. Harrison etal. [44] reported
three patients with eye complications while undergoing CPAP treatment.
Eye complications from CPAP treatment may arise from two possible mechanisms. The rst, and probably most common, is from an air leak around the superior
portion of the mask, resulting in the air blowing into the eye. The second may be
retrograde movement of air and mucus from the nasal passage through the nasolacrimal duct and into the eye. Furthermore, CPAP increases ocular irritation, tear
evaporation, and squamous metaplasia in the conjunctiva of the patients’ right and
left eyes [45].
Nocturnal lubrication or articial tears relieve to patients who develop morning
eye dryness while receiving CPAP treatment. Proper mask t should be veried to
prevent air leaks. Switching from a nasal mask to an intranasal interface may alleviate areas of pressure and air leakage near the eyes Early ophthalmologic consultation is required to exclude corneal disease if a patient develops substantial eye
irritation that persists into the day or has signs of infection. However, given the
possibility of increased risk of eye infections, it is reasonable to advise against
extended-wear contacts. In patients who develop recurrent eye infections or depend
on contact lenses and cannot tolerate CPAP treatment secondary to eye irritation,
alternative therapy to CPAP treatment may need to be considered.
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19.5 Glaucoma
Glaucoma is a progressive optic neurodegenerative disease characterized by progressive loss of optic nerve bers with corresponding visual eld defects (Fig.19.6).
Since the rst description by Mojon etal. [46] in 1999, a possible link between
OSA and glaucoma, mainly primary open-angle glaucoma, has been established in
the last two decades [7–9], with four meta-analyses published that conrmed this
association [6, 47–49] nding a pooled OR for glaucoma in patients with OSA
ranging from 1.4 to 2.5. However, more recent and larger, well-designed cohort or
population-based studies have failed to nd signicant associations between OSA
and glaucoma, especially after accounting for comorbidities [9, 50–53]. A very
recent meta-analysis including 16 case–control studies (233,273 patients with OSA
and 4802,386 subjects without OSA) has conrmed that OSA is associated with a
signicantly increased risk of glaucoma (Fig.19.7), with a pooled OR of 1.50 (CI:
1.25–1.80; p<0.001) [8].
Instead of relying on the presence of glaucoma, some studies explored associations of OSA with measures of glaucoma-related endophenotypes, such as the peripapillary retinal nerve ber layer (pRNFL) thickness measured through optical
coherence tomography (OCT) (Fig.19.8), intraocular pressure (IOP), and visual
eld defects. Findings from most of these studies supported a link between OSA
and thinner pRNFL, higher IOP, or poorer visual elds morbidities [54–59].
However, these studies have failed to nd a relationship between IOP and apneahypopnea index (AHI) [8]. Five meta-analyses [60–64] further noted thinner global
pRNFL by 2–4μm in patients with OSA compared to controls. These results are
less signicant when adjusted for potential confounders [9].
Fig. 19.6 Optic nerve
showing glaucomatous
cupping
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Fig. 19.7 Forest plot of cross-sectional studies showing the odds ratios (OR) with 95% condence intervals (95% CI) of glaucoma for participants with and without OSA.The squares and
horizontal lines represent the study-specic OR and 95% CI.The sizes of the squares reect the
statistical weights of the studies. The pooled OR is indicated by a diamond (random-effect model).
From Garcia-Sanchez etal. [8]
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Fig. 19.8 OCT showing thinning of the retinal nerve ber layer around the optic nerve
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Given the presumptive ischemia of the optic disc induced by OSA, we may
expect glaucoma progression to be faster in patients with OSA than in those without
respiratory disease. Indeed, studies have reported that patients with OSA tend to
have more rapid glaucoma progression than those without OSA.In a retrospective
study comprising 32 patients with glaucoma, Fan etal. [65] reported that those with
moderate or severe had an eight-fold increase in the risk of pRNFL thinning than
those with no or mild OSA, after adjusting for age, sex, body mass index (BMI), and
co-morbidities. Over 3-years, Wozniak etal. [66] similarly reported that the rate of
global pRNFL loss in glaucoma patients with OSA was almost double the rate in
those without OSA (−1.1 vs. −0.6 μm/year), after adjustments for potential
confounders.
OSA treatment has a great potential indeed to slow glaucoma progression [67–
74]. CPAP therapy is highly effective in alleviating upper airway collapse and
improves optic nerve perfusion and reduces glaucoma risk. Himori et al. [68]
reported that patients with OSA and glaucoma had slower rates of visual eld loss
after undergoing an initial CPAP therapy. Other studies [69–73] also reported
increases in pRNFL thickness, macular thickness, or visual eld sensitivity after
3–6months of CPAP therapy. However, these studies lacked control groups, and the
improved measures, especially in visual elds, could be due to a learning effect.
Zengin etal. [70] studied 44 OSA patients treated with CPAP, who were followed for a whole year with OCT examinations every 3months, and compared
those results to healthy subjects. Baseline OCT data showed no differences between
both samples; however, following 1year of CPAP therapy, a lower average peripapillary RNFL, and nasal, inferior, and superior quadrant thicknesses were described
in the patients with OSAS group as compared to the control group. They also studied the correlation between the AHI and the RNFL thickness, observing a weak
negative correlation. Similarly, Lin etal. [71] presented a prospective study on 32
OSA patients treated with CPAP who underwent an OCT 3months after treatment.
They found that the inferior quadrant and nasal-inferior sector of the RNFL thickness signicantly improved after treatment. In addition, the macula layer thickness
in the superior-inner sector, inferior-outer sector, nasal-outer sector, superior hemisphere, and inferior hemisphere was also signicantly improved after treatment.
The improvement of macular layer thickness in the superior-inner sector positively
correlated with the AHI and desaturation index correction. Naranjo-Bonilla etal.
[72] have recently reported a prospective study including 28 patients treated with
CPAP and 12 untreated, again showing normalization of the choroidal thickness
measured by OCT in treated patients.
While CPAP therapy potentially improves optic disc perfusion, its use is known
to elevate IOP [74–76], which may paradoxically increase the risk of glaucoma or
worsen existing disease. As a result, some authors have suggested that patients with
glaucoma or those at high risk of glaucoma using CPAP therapy should be closely
monitored.
Surgical treatment of OSA has also shown to improve glaucoma in OSA patients
[77–81]. In a retrospective study involving over 12,000 patients, Chen etal. [81]
reported that CPAP-treated and untreated patients with OSA had similar levels of
increased glaucoma risk relative to a comparison cohort (HR = 1.65 and 2.15,
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respectively). However, those who had undergone surgical treatment did not have an
elevated risk of glaucoma compared to the controls, suggesting that surgical treatment for OSA may be more benecial than CPAP therapy regarding glaucoma risk.
In 108 patients with OSA, Lin etal. [77] noted improvements in visual elds measures and thickening of the macula 6 months after surgical treatment for
OSA.However, this study lacked a control group like the CPAP studies above. On
the contrary, Kaya etal. [78] presented a prospective study on 34 OSAS patients
treated with expansion sphincter pharyngoplasty. After 6months, the preoperative
and postoperative AHI scores and average oxygen saturation values were signicantly different, but there was no signicant disparity between the preoperative and
postoperative RNFL thicknesses.
Jayakumar etal. [79] published a prospective study including 36 patients, comparing CPAP, uvulopalatopharyngoplasty, and no treatment. They showed that choroidal thickness and vascularity improved after surgery and CPAP for 6months.
Tejero-Garcés etal. [80] also found an improvement in OCT ndings in severe OSA
patients after CPAP or surgical treatment. However, they did not obtain any correlation between changes in the AHI and changes in the OCT after surgical treatment.
The most relevant nding in their study was that the foveal thickness and retinal
nerve bers’ (RNFL) average thickness improved after 6months of treatment in
severe cases.
19.6 Nonarteritic Anterior Ischemic Optic Neuropathy
Nonarteritic anterior ischemic optic neuropathy (NAION) is an ischemic disorder of
the anterior portion of the optic nerve (Fig.19.9), characterized by sudden, and
painless unilateral visual loss, altitudinal visual eld defects and optic disc swelling
Fig. 19.9 Nonarteritic
anterior ischemic optic
neuropathy (NAION)
showing edema of optic
nerve bers and splinter
hemorrhages
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A. Nogueira et al.
[82]. It is the most frequent acute optical neuropathy after the age of 50, with an
incidence of 2–10 per 100,000 people per year. It is classically associated with several risk factors, particularly cardiovascular, such as hypertension, diabetes, dyslipidemia, ischemic heart disease, or cerebrovascular disease. Moreover, NAION
patients have a 15% risk for contralateral eye involvement within 5years [8, 83].
The presumed optic nerve vascular dysregulation, including hypercapnia,
induced by OSA has also been suggested to increase the risk of NAION, with a
meta-analysis estimating that the odds of NAION are increased six-fold in those
with OSA, compared to controls [84]. In addition, two recent large studies, which
reported HRs of 1.7–3.8 for NAION in patients with OSA have reinforced such
association [85, 86].
Evidence that treatment for OSA using CPAP therapy may reduce the risk of
incident NAION is promising. In a retrospective review of over two million clinical
records, Stein et al. [52] reported that untreated patients with OSA had a 16%
increased risk of developing NAION relative to those without OSA, after adjusting
for potential confounders, including age and co-morbidities. Those treated with
CPAP therapy, on the other hand, did not have elevated NAION risk relative to controls. In another small study of 67 patients with unilateral NAION and OSA, Aptel
etal. [87] reported that those with poor compliance to CPAP therapy had a signicantly higher risk of second eye involvement, with an HR of 5.5. A recent metaanalysis evaluating seven studies (Fig.19.10), including 9571 patients with OSA
and 43,296 subjects without OSA, showed that patients with OSA are more at risk
of NAION than nonapneic subjects, with a pooled OR of 3.62 (CI 1.94–6.76;
p<0.001) [8].
Given the importance of preserving the fellow eye in patients with NAION, it
may be prudent to consider addressing any undiagnosed or untreated OSA in all
patients with NAION.
Fig. 19.10 Forest plot of cross-sectional studies showing the odds ratios (OR) with 95% condence intervals (95% CI) of nonarteritic anterior ischemic optic neuropathy (NAION) for participants with and without OSA.The squares and horizontal lines represent the study-specic OR and
95% CI.The sizes of the squares reect the statistical weights of the studies. The pooled OR is
indicated by a diamond (random-effect model). From Garcia-Sanchez etal. [8]
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