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© Borgis - Postępy Nauk Medycznych 1/2016, s. 64-70
Monika Kuźmińska1, Magdalena Walicka2, Ada Sawicka3, Wojciech Kukwa1, *Ewa Marcinowska-Suchowierska3
Średnia i minimalna saturacja jako wskaźnik ciężkości choroby u pacjentów z podejrzeniem zespołu zaburzeń oddychania w czasie snu o charakterze bezdechu obturacyjnego (OSA)
Average and minimum oxygen saturation in patients with suspected OSA as a disease severity index in polysomnographic evaluation
1Department of Otolaryngology, Faculty of Medicine and Dentistry, Medical University of Warsaw, Warszawa
Head of Department: prof. Antoni Krzeski, MD, PhD
2Department of Internal Diseases, Endocrinology and Diabetology, Central Clinical Hospital of the Ministry of Interior in Warsaw, Warszawa
Head of Department: prof. Edward Franek, MD, PhD
3Department of Geriatric, Internal Medicine and Metabolic Bone Disease, Centre of Postgraduate Medical Education, Warszawa
Head of Department: prof. Marek Tałałaj, MD, PhD
Streszczenie
Wstęp. Nocne niedotlenienie jest odpowiedzialne za wiele powikłań zespołu zaburzeń oddychania o charakterze bezdechu obturacyjnego (OSA), dlatego saturacja jako wykładnik wartości niedotlenienia jest istotna dla oceny ryzyka powikłań.
Cel pracy. Celem pracy było porównanie saturacji pacjentów z i bez OSA.
Materiał i metody. Do badania włączono 907 pacjentów. Na podstawie polisomnografii (PSG) podzielono ich wg AHI na 2 grupy: z OSA (AHI ≥ 5) i bez OSA (AHI < 5). Grupę OSA podzielono na 3 stadia: łagodne (5 ≤ AHI < 15), umiarkowane (15 ≤ AHI ≤ 30) i ciężkie (AHI > 30). U wszystkich pacjentów oceniano średnią (Av SaO2) oraz minimalną (Min SaO2) saturację. Wyniki analizowano za pomocą programu Statistica 6.0.
Wyniki. Grupa OSA (n = 557): Av SaO2 = 91,69%, Min SaO2 = 77,21%; grupa bez OSA (n = 350): Av SaO2 = 93,62%, Min SaO2 = 87,26%. Różnice te były statystycznie znamienne (p < 0,0001). Dla stadiów OSA saturacje wynosiły odpowiednio: łagodne – Av SaO2 = 92,93%, Min SaO2 = 81,83%; umiarkowane – Av SaO2 = 92,24%, Min SaO2 = 78.9%; ciężkie – Av SaO2 = 90,06%, Min SaO2 = 71,44%. Różnice istotne statystycznie stwierdzono między Av SaO2 (p < 0,05) i Min SaO2 (p < 0,0005) w łagodnym i umiarkowanym stadium OSA oraz między Av SaO2 i Min SaO2 w umiarkowanym i ciężkim stadium (p < 0,0001).
Wnioski. Niższe wartości Av SaO2 i Min SaO2 obserwowano w bardziej zaawansowanych stadiach OSA, może to być dodatkową obok AHI wskazówką do wdrożenia leczenia i w zapobieganiu powikłaniom.
Summary
Introduction. Nocturnal hypoxia is responsible for many obstructive sleep apnea syndrome (OSA) complications, therefore the saturation values-exponents of hypoxia are important for assessing the risk of complications.
Aim. Aim of this work was to compare the oxygen saturation in OSA vs non OSA patients.
Material and methods. We included 907 patients. On the basis of polysomnography (PSG) according to AHI (Apnea-Hypopnea Index) they were divided into 2 groups: OSA (AHI ≥ 5) and non OSA (AHI < 5). The OSA group was divided into 3 stages: mild (5 ≤ AHI < 15), moderate (15 ≤ AHI ≤ 30), and severe (AHI > 30). In all patients average (Av SaO2) and minimum (Min SaO2) oxygen saturation was evaluated. The outcomes were analyzed by Statistica 6.0.
Results. OSA group (n = 557): Av SaO2 = 91.69%, Min SaO2 = 77.21%; non OSA (n = 350): Av SaO2 = 93.62%, Min SaO2 = 87.26%. These differences were statistically significant (p < 0.0001). For each stage of OSA the mean saturations: mild – Av SaO2 = 92.93%, Min SaO2 = 81.83%; moderate – Av SaO2 = 92.24%, Min SaO2 = 78.9%; severe – Av SaO2 = 90.06%, Min SaO2 = 71.44%. Statistically significant differences were found between Av SaO2 (p < 0.05) and Min SaO2 (p < 0.0005) in the mild and moderate OSA stage and Av SaO2 and Min SaO2 in the moderate and severe stage (p < 0.0001).
Conclusions. We concluded in more advanced OSA lower Av SaO2 and Min SaO2 were observed which is additional to AHI hint to apply the treatment and prevent complications associated with hypoxia.
Słowa kluczowe: OSA, polisomnografia, hipoksja, saturacja, AHI.



Introduction
Obstructive sleep apnea (OSA) is an important problem of the developed world (affects more than 4% of male population and 2% women population) (1) and is characterized by repetitive upper airway obstruction during sleep that leads to intermittent hypoxia. Repetitive episodes of oxygen desaturation of 2-4% are a typical symptom of obstructive sleep apnea syndrome (OSA). They are the consequences of respiratory apnea and hypopnea incidents. A unique form of hypoxia with repetitive short cycles of desaturation followed by rapid reoxygenation is termed intermittent hypoxia (IH) and it probably plays a significant role in pathogenesis of cardiovascular complications in OSA (2, 3). In some studies intermittent hypoxia is considered as the main factor involved in cardiovascular remodelling in OSA (4, 5). It has also been noticed that in OSA patients, early signs of atherosclerosis are correlated with hypoxia severity even after adjustment for confounding factors (6). Average and minimum saturation is together with AHI (Apnea-Hypopnea Index) and ODI (Oxygen Desaturation Index) an important predictor of the severity OSA.
Obesity is closely associated with OSA. White adipose tissue is a major secretory and endocrine organ. Obesity induces a chronic low-grade inflammatory state and many of the inflammatory pathways proposed to be activated by intermittent hypoxia in OSA are also activated in adipose tissue (7-9).
In our opinion average and minimum oxygen saturation are indirect markers of hypoxia and help – in addition to AHI – to assess severity of OSA.
Aim
With regard to the important role of night hypoxia in OSA we wanted to compare the average and minimum oxygen saturation in OSA patients (AHI ≥ 5) vs non-OSA population (AHI < 5) during sleep in polysomnography (PSG) and see the differences in average and minimum oxygen saturation in these patients for different OSA stages. We also wanted to investigate a possible correlation between both mean values of saturations and AHI.
Material and methods
We examined retrospectively 907 (n = 907) polysomnograms recruited from patients (both sexes) referred to a sleep laboratory for suspected sleep apnea. We included bariatric patients, patients before laryngological procedures, and patients who snored regularly. Patients were referred to sleep laboratory by physicians of many specialties: family doctors, surgeons, internists, otolaryngologists.
The reasons for referring patients to clinical polysomnography were as follows:
– snoring,
– snoring with apnea observed by persons sleeping in one room with the patient,
– abnormal nasal patency, and throat – before any surgery,
– excessive daytime sleepiness,
– insomnia,
– heart problems, such as hypertension, resistant to treatment,
– obesity,
– prior to the surgery of obesity (bariatric surgery).
Anthropometric characteristics of the group are listed in table1.
Table1. Anthropometric characteristics of the group
ParametersWomen
(n = 271)
Men
(n = 636)
Total
(n = 907)
Mean age (SD)51.9 (14.7)51.9 (13.1)51.9 (13.6)
Mean BMI kg/m2 (SD)35.2 (10.5)31.3 (7.3)32.5 (8.6)
SD – standard deviation
Polysomnographic studies were performed and evaluated in accordance to current international standards (10-12).
PSG included the following variables: electroencephalograms, electrooculograms, electromyelograms of submental muscules, electrocardiogram, airflow (nasal and oral), chest and abdominal efforts, snoring (microphone) and arterial oxyhemoglobin saturation and pulse (finger probe).
Polysomnographic recordings were evaluated with respect to:
– amount of disordered breathing during sleep,
– type disorders: obstructive sleep apnea, mixed, central, hypopnea,
– AHI number of apnea/hypopnea incidents per one hour of sleep,
– disease severity based on AHI (a mild form of 5 ≤ AHI < 15, moderate 15 ≤ AHI ≤ 30; severe AHI > 30),
– the number of desaturations,
– the average oxygen saturation (Av SaO2),
– minimum oxygen saturation (Min SaO2),
– heart rate (HR),
– the length of non REM (non-rapid eye movement) sleep composed of light sleep stages 1 and 2 (1 + 2), and composed of deep sleep stages 3 and 4 (3 + 4),
– the length of REM sleep (rapid eye movement).
Statistical analysis included:
– descriptive statistic on the parameters (mean value, standard deviation),
– correlations between the assessed parameters (r-Pearson correlation),
– rate differences in the evaluated parameters (t-Student test for dependent and independent samples, Z-test, Ch2 NW test, Ch2 Pearson test, Ch2 with Yate’s correction),
– we considered statistically significant 95% confidence level (p < 0.05).
All statistical analyses were carried out using statistical software Statistica version 6.0.
Results
We analyzed 907 patients with suspected OSA. 557 patients with AHI ≥ 5 were treated as the OSA group, which was composed of 155 females and 402 males. The group with AHI < 5 named as the non-OSA group included 350 people consisting of 116 females and 234 males. We compared average (Av SaO2) and minimum (Min SaO2) saturation between the OSA group AHI ≥ 5 and the non-OSA AHI < 5 both in women and men.

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Piśmiennictwo
1. Young T, Palta M, Dempsey J et al.: The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993; 328: 1230-1235.
2. Ryan S, McNicholas WT: Intermittent hypoxia and activation of inflammatory molecular pathways in OSAS. Arch Physiol Biochem 2008 Oct; 114(4): 261-266.
3. Kimoff RJ: When to Suspect Sleep Apnea and What to Do About It. Can J Cardiol 2015 Jul; 31(7): 945-948. doi: 10.1016/j.cjca.2015.04.020. Epub 2015 Apr 28.
4. Dematteis M, Godin-Ribuot D, Arnaud C et al.: Cardiovascular consequences of sleep-disordered breathing: contribution of animal models to understanding the human disease. ILAR J 2009; 50: 262-281.
5. Bostanci A, Turhan M, Bozkurt S: Factors influencing sleep time with oxygen saturation below 90% in sleep-disordered breathing. Laryngoscope 2015 Apr; 125(4): 1008-1012. doi: 10.1002/lary.24942. Epub 2014 Sep 19.
6. Baguet JP, Hammer L, Lèvy P et al.: The severity of oxygen desaturation is predictive of carotid wall thickening and plaque occurrence. Chest 2005; 128: 3407-3412.
7. Hotamisligil GS, Spiegelman BM: Tumor necrosis factor α: a key component of the obesity-diabetes link. Diabetes 1994; 43: 1271-1278.
8. Mohamed-Ali V, Goodrick S, Rawesh A et al.: Subcutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor-α, in vivo. J Clin Endocrinol Metab 1997; 82: 4196-4200.
9. Coppack S: Pro-inflammatory cytokines and adipose tissue. Proc Nutr Soc 2001; 60: 349-356.
10. Iber C, Ancoli-Israel S, Chesson A et al.: The International Classification of Sleep Disorders Diagnostic and Coding Manual. American Academy of Sleep Medicine, Westchester 2001.
11. Iber C, Ancoli-Israel S, Chesson A et al.: The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. 1st ed., American Academy of Sleep Medicine, Westchester 2007.
12. Ruehland WR, Rochford PD, O’Donoghue FJ et al.: The new AASM criteria for scoring hypopneas: impact on the apnea hypopnea index. Sleep 2009; 32: 150-157.
13. Hedner J, Grote L, Bonsignore M et al.: The European Sleep Apnoea Database (ESADA): report from 22 European sleep laboratories. Eur Respir J 2011; 38: 635-642.
14. Landsberg R, Friedman M, Ascher-Landsberg J: Treatment of hypoxemia in obstructive sleep apnea. Am J Rhino 2001 Sept-Oct; 15(5): 311-313.
15. Kristiansen HA, Kværne KJ, Akre H et al.: Sleep apnea headache in general population. Cephalalgia 2012; 32(6): 451-458.
16. Amardottir ES, Maislin G, Schwab RJ et al.: The interaction of obstructive sleep apnea and obesity on the inflammatory markers C-reactive protein and interleukin-6: the Icelandic Sleep Apnea Cohort Study. Sleep 2012; 35(7): 921-932.
17. Al Lawanti N, Mulgrew A, Cheeema R et al.: Pro-atherogenic cytokine profile of patients with suspected obstructive sleep apnea. Sleep Breath 2009; 13(4): 391-395.
18. Kent BD, Ryan S, McNicholas WT: Obstructive sleep apnea and inflammation: relationship to cardiovascular co-morbidity. Respir Physiol Neurobiol 2011; 178(3): 475-481.
19. Gonzales C, Yubero S, Gomez-Nino MA et al.: Some reflections on intermittent hypoxia. Does it constitute the translational niche for caroid body chemoreceptors researchers? Adv Exp Med Biol 2012; 758: 333-342.
20. Ross R: The pathogenesis of atherosclerosis a perspective for the 1990s. Nature 1993; 362: 801-809.
21. Ohga E, Nagase T, Tomita T et al.: Increased level of circulating ICAM-1, VCAM-1, and L-selectin in obstructive sleep apnea syndrome. J Appl Physiol 1999; 87: 10-14.
22. Zieliński J, Pływaczewski R, Bednarek M: Zaburzenia oddychania w czasie snu. PZWL, Warszawa 2006: 15-23.
otrzymano: 2015-12-12
zaakceptowano do druku: 2016-01-04

Adres do korespondencji:
*Ewa Marcinowska-Suchowierska
Department of Geriatric, Internal Medicine and Metabolic Bone Disease Centre of Postgraduate Medical Education
ul. Czerniakowska 231, 00-416 Warszawa
tel. +48 (22) 584-11-01
marsu@cmkp.edu.pl

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