Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_41_библиотеки_им_акад_М_И_Перельмана
.pdf
182
https://t.me/medicina_free
58. Marik PE, Desai H.Characteristics of patients with the “malignant obesity hypoventilation
syndrome” admitted to an ICU.J Intensive Care Med. 2013;28(2):124–30.
59. Quint JK, Ward L, Davison AG.Previously undiagnosed obesity hypoventilation syndrome.
Thorax. 2007;62(5):462–3.
60. Masa JF, Corral J, Romero A, etal. Protective cardiovascular effect of sleep apnea severity in
obesity hypoventilation syndrome. Chest. 2016;150(1):68–79.
61. Pelosi P, Croci M, Ravagnan I, Vicardi P, Gattinoni L.Total respiratory system, lung, and
chest wall mechanics in sedated-paralyzed postoperative morbidly obese patients. Chest.
1996;109(1):144–51.
62. Steier J, Jolley CJ, Seymour J, Roughton M, Polkey MI, Moxham J.Neural respiratory drive
in obesity. Thorax. 2009;64(8):719–25.
63. Lee MY, Lin CC, Shen SY, Chiu CH, Liaw SF.Work of breathing in eucapnic and hypercap-
nic sleep apnea syndrome. Respiration. 2009;77(2):146–53.
64. Lopata M, Onal E.Mass loading, sleep apnea, and the pathogenesis of obesity hypoventila-
tion. Am Rev Respir Dis. 1982;126(4):640–5.
65. Javaheri S, Simbartl LA. Respiratory determinants of diurnal hypercapnia in obesity
hypoventilation syndrome. What does weight have to do with it? Ann Am Thorac Soc.
2014;11(6):945–50.
66. Fernandez Alvarez R, Rubinos Cuadrado G, Ruiz Alvarez I, etal. Hypercapnia response
in patients with obesity-hypoventilation syndrome treated with non-invasive ventilation at
home. Arch Bronconeumol (Engl Ed). 2018;54(9):455–9.
67. Berger KI, Ayappa I, Sorkin IB, Norman RG, Rapoport DM, Goldring RM.Postevent venti-
lation as a function of CO
Physiol. 2002;93(3):917–24.
68. Redol S, Corda L, La Piana G, Spandrio S, Prometti P, Tantucci C.Long-term non- invasive
ventilation increases chemosensitivity and leptin in obesity-hypoventilation syndrome.
Respir Med. 2007;101(6):1191–5.
69. Lin CC, Wu KM, Chou CS, Liaw SF.Oral airway resistance during wakefulness in eucapnic
and hypercapnic sleep apnea syndrome. Respir Physiol Neurobiol. 2004;139(2):215–24.
70. Berger KI, Ayappa I, Sorkin IB, Norman RG, Rapoport DM, Goldring RM.CO(2) homeosta-
sis during periodic breathing in obstructive sleep apnea. J Appl Physiol. 2000;88(1):257–64.
71. Ayappa I, Berger KI, Norman RG, Oppenheimer BW, Rapoport DM, Goldring
RM. Hypercapnia and ventilatory periodicity in obstructive sleep apnea syndrome. Am J
Respir Crit Care Med. 2002;166(8):1112–5.
72. Berger KI, Goldring RM, Rapoport DM.Obesity hypoventilation syndrome. Semin Respir
Crit Care Med. 2009;30:253–61.
73. Phipps PR, Starritt E, Caterson I, Grunstein RR.Association of serum leptin with hypoventi-
lation in human obesity. Thorax. 2002;57(1):75–6.
74. Campo A, Fruhbeck G, Zulueta JJ, etal. Hyperleptinemia, respiratory drive and hypercapnic
response in obese patients. Eur Respir J. 2007;30:223–31.
75. Makinodan K, Yoshikawa M, Fukuoka A, etal. Effect of serum leptin levels on hypercapnic
ventilatory response in obstructive sleep apnea. Respiration. 2008;75(3):257–64.
76. Schwartz MW, Peskind E, Raskind M, Boyko EJ, Porte D Jr. Cerebrospinal uid leptin levels:
relationship to plasma levels and to adiposity in humans. Nat Med. 1996;2(5):589–93.
77. Polotsky M, Elsayed-Ahmed AS, Pichard L, etal. Effects of leptin and obesity on the upper
airway function. J Appl Physiol. 2012;112(10):1637–43.
78. Berger S, Pho H, Fleury-Curado T, etal. Intranasal leptin relieves sleep disordered breathing
in mice with diet induced obesity. Am J Respir Crit Care Med. 2019;199(6):773–83.
79. Ip MSM, Mokhlesi B.Activating leptin receptors in the central nervous system using intra-
nasal leptin. A novel therapeutic target for sleep-disordered breathing. Am J Respir Crit Care
Med. 2019;199(6):689–91.
80. Howard ME, Piper AJ, Stevens B, et al. A randomised controlled trial of CPAP versus
non-invasive ventilation for initial treatment of obesity hypoventilation syndrome. Thorax.
2017;72(5):437–44.
load during respiratory events in obstructive sleep apnea. J Appl
2
A. J. Piper

9
https://t.me/medicina_free
Sleep andHypoventilation
81. Masa JF, Mokhlesi B, Benitez I, et al. Long-term clinical effectiveness of continuous posi-
tive airway pressure therapy versus non-invasive ventilation therapy in patients with obesity
hypoventilation syndrome: a multicentre, open-label, randomised controlled trial. Lancet.
2019;393(10182):1721–32.
82. Piper AJ, Wang D, Yee BJ, Barnes DJ, Grunstein RR.Randomised trial of CPAP vs bilevel
support in the treatment of obesity hypoventilation syndrome without severe nocturnal desaturation. Thorax. 2008;63(5):395–401.
83. Royer CP, Schweiger C, Manica D, Rabaioli L, Guerra V, Sbruzzi G. Efcacy of bilevel
ventilatory support in the treatment of stable patients with obesity hypoventilation syndrome:
systematic review and meta-analysis. Sleep Med. 2018;53:153–64.
84. Soghier I, Brozek JL, Afshar M, etal. Noninvasive ventilation versus CPAP as initial treat-
ment of obesity hypoventilation syndrome. Ann Am Thorac Soc. 2019;16(10):1295–303.
85. Bouloukaki I, Mermigkis C, Michelakis S, etal. The association between adherence to posi-
tive airway pressure therapy and long-term outcomes in patients with obesity hypoventilation
syndrome: a prospective observational study. J Clin Sleep Med. 2018;14(9):1539–50.
86. Mokhlesi B, Tulaimat A, Evans AT, etal. Impact of adherence with positive airway pressure
therapy on hypercapnia in obstructive sleep apnea. J Clin Sleep Med. 2006;2(1):57–62.
87. Salord N, Mayos M, Miralda RM, etal. Continuous positive airway pressure in clinically sta-
ble patients with mild-to-moderate obesity hypoventilation syndrome and obstructive sleep
apnoea. Respirology. 2013;18(7):1135–42.
88. Masa JF, Mokhlesi B, Benítez I, etal. Echocardiographic changes with positive airway pres-
sure therapy in obesity hypoventilation syndrome. Long-term Pickwick randomized controlled clinical trial. Am J Respir Crit Care Med. 2020;201(5):586–97.
89. Banerjee D, Yee BJ, Piper AJ, Zwillich CW, Grunstein RR. Obesity hypoventila-
tion syndrome: hypoxemia during continuous positive airway pressure. Chest.
2007;131(6):1678–84.
90. Perez de Llano LA, Golpe R, Ortiz Piquer M, et al. Clinical heterogeneity among
patients with obesity hypoventilation syndrome: therapeutic implications. Respiration.
2008;75(1):34–9.
91. Masa JF, Benítez I, Sánchez-Quiroga M, etal. Long-term noninvasive ventilation in obesity
hypoventilation syndrome without severe OSA: the Pickwick randomized controlled trial.
Chest. 2020:S0012-3692(20)30711-X.; https://doi.org/10.1016/j.chest.2020.03.068.
92. Carrillo A, Ferrer M, Gonzalez-Diaz G, etal. Noninvasive ventilation in acute hypercapnic
respiratory failure caused by obesity hypoventilation syndrome and chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2012;186(12):1279–85.
93. Kakazu MT, Soghier I, Afshar M, et al. Weight loss interventions as treatment of obesity
hypoventilation syndrome. A systematic review. Ann Am Thorac Soc. 2020;17(4):492–502.
94. Borel J-C, Burel B, Tamisier R, et al. Comorbidities and mortality in hypercapnic obese
under domiciliary noninvasive ventilation. PLoS One. 2013;8(1):e52006.
95. Lo Coco D, Marchese S, Corrao S, etal. Development of chronic hypoventilation in amyo-
trophic lateral sclerosis patients. Respir Med. 2006;100(6):1028–36.
96. Prell T, Ringer TM, Wullenkord K, etal. Assessment of pulmonary function in amyotrophic
lateral sclerosis: when can polygraphy help evaluate the need for non-invasive ventilation? J
Neurol Neurosurg Psychiatry. 2016;87(9):1022–6.
97. Reyhani A, Benbir Senel G, Karadeniz D.Effects of sleep-related disorders on the prognosis
of amyotrophic lateral sclerosis. Neurodegener Dis. 2019;19(3-4):148–54.
98. Aboussouan LS.Sleep-disordered breathing in neuromuscular disease. Am J Respir Crit Care
Med. 2015;191(9):979–89.
99. Suresh S, Wales P, Dakin C, Harris MA, Cooper DG.Sleep-related breathing disorder in
Duchenne muscular dystrophy: disease spectrum in the paediatric population. J Paediatr
Child Health. 2005;41(9-10):500–3.
100. Georges M, Attali V, Golmard JL, et al. Reduced survival in patients with ALS with upper
airway obstructive events on non-invasive ventilation. J Neurol Neurosurg Psychiatry.
2016;87(10):1045–50.
183

184
https://t.me/medicina_free
101. Quaranta VN, Carratù P, Damiani MF, etal. The prognostic role of obstructive sleep apnea at
the onset of amyotrophic lateral sclerosis. Neurodegener Dis. 2017;17(1):14–21.
102. Bianchi ML, Losurdo A, Di Blasi C, etal. Prevalence and clinical correlates of sleep disor-
dered breathing in myotonic dystrophy types 1 and 2. Sleep Breath. 2014;18(3):579–89.
103. Laberge L, Dauvilliers Y, Bégin P, Richer L, Jean S, Mathieu J.Fatigue and daytime sleepi-
ness in patients with myotonic dystrophy type 1: to lump or split? Neuromuscul Disord.
2009;19(6):397–402.
104. van der Meche FG, Bogaard JM, van der Sluys JC, Schimsheimer RJ, Ververs CC, Busch
HF.Daytime sleep in myotonic dystrophy is not caused by sleep apnoea. J Neurol Neurosurg
Psychiatry. 1994;57(5):626–8.
105. Ono S, Takahashi K, Jinnai K, etal. Loss of catecholaminergic neurons in the medullary
reticular formation in myotonic dystrophy. Neurology. 1998;51(4):1121–4.
106. Atalaia A, De Carvalho M, Evangelista T, Pinto A.Sleep characteristics of amyotrophic lat-
eral sclerosis in patients with preserved diaphragmatic function. Amyotroph Lateral Scler.
2007;8(2):101–5.
107. de Carvalho M, Costa J, Pinto S, Pinto A.Percutaneous nocturnal oximetry in amyotrophic
lateral sclerosis: periodic desaturation. Amyotroph Lateral Scler. 2009;10(3):154–61.
108. Sancho J, Burés E, Ferrer S, Ferrando A, Bañuls P, Servera E.Unstable control of breathing
can lead to ineffective noninvasive ventilation in amyotrophic lateral sclerosis. ERJ Open
Res. 2019;5(3):00099-2019.
109. Benditt JO. Respiratory care of patients with neuromuscular disease. Respir Care.
2019;64(6):679–88.
110. McSharry DG, Ryan S, Calverley P, Edwards JC, McNicholas WT.Sleep quality in chronic
obstructive pulmonary disease. Respirology. 2012;17(7):1119–24.
111. Omachi TA, Blanc PD, Claman DM, etal. Disturbed sleep among COPD patients is longitudi-
nally associated with mortality and adverse COPD outcomes. Sleep Med. 2012;13(5):476–83.
112. Shorofsky M, Bourbeau J, Kimoff J, etal. Impaired sleep quality in COPD is associated with
exacerbations: the CanCOLD cohort study. Chest. 2019;156(5):852–63.
113. Jolley CJ, Luo YM, Steier J, et al. Neural respiratory drive in healthy subjects and in
COPD.Eur Respir J. 2009;33(2):289–97.
114. Kwon JS, Wolfe LF, Lu BS, Kalhan R.Hyperination is associated with lower sleep ef-
ciency in COPD with co-existent obstructive sleep apnea. COPD. 2009;6(6):441–5.
115. O’Donoghue FJ, Catcheside PG, Eckert DJ, McEvoy RD.Changes in respiration in NREM
sleep in hypercapnic chronic obstructive pulmonary disease. J Physiol. 2004;559(2):663–73.
116. Costello R, Deegan P, Fitzpatrick M, McNicholas WT.Reversible hypercapnia in chronic
obstructive pulmonary disease: a distinct pattern of respiratory failure with a favorable prognosis. Am J Med. 1997;102(3):239–44.
117. O'Donoghue FJ, Catcheside PG, Ellis EE, et al. Sleep hypoventilation in hypercap-
nic chronic obstructive pulmonary disease: prevalence and associated factors. Eur Respir
J. 2003;21(6):977–84.
118. Holmedahl NH, Overland B, Fondenes O, Ellingsen I, Hardie JA.Sleep hypoventilation and
daytime hypercapnia in stable chronic obstructive pulmonary disease. Int J Chron Obstruct
Pulmon Dis. 2014;9:265–75.
119. Kitajima T, Marumo S, Shima H, etal. Clinical impact of episodic nocturnal hypercapnia and
its treatment with noninvasive positive pressure ventilation in patients with stable advanced
COPD.Int J Chron Obstruct Pulmon Dis. 2018;13:843–53.
120. Kohnlein T, Windisch W, Kohler D, etal. Non-invasive positive pressure ventilation for the
treatment of severe stable chronic obstructive pulmonary disease: a prospective, multicentre,
randomised, controlled clinical trial. Lancet Respir Med. 2014;2(9):698–705.
121. Murphy PB, Rehal S, Arbane G, etal. Effect of home noninvasive ventilation with oxygen
therapy vs oxygen therapy alone on hospital readmission or death after an acute COPD exacerbation: a randomized clinical trial. JAMA. 2017;317(21):2177–86.
A. J. Piper

Sleep andHypoventilation
https://t.me/medicina_free
9
122. Struik FM, Lacasse Y, Goldstein RS, Kerstjens HAM, Wijkstra PJ.Nocturnal noninvasive
positive pressure ventilation in stable COPD: a systematic review and individual patient data
meta-analysis. Respir Med. 2014;108(2):329–37.
123. Windisch W, Geiseler J, Simon K, Walterspacher S, Dreher M.German national guideline
for treating chronic respiratory failure with invasive and non-invasive ventilation- revised
edition 2017: part 2. Respiration. 2018;96(2):171–203.
124. Ergan B, Oczkowski S, Rochwerg B, et al. European Respiratory Society guidelines
on long-term home non-invasive ventilation for management of COPD. Eur Respir
J. 2019;54(3):1901003.
125. Crummy F, Piper AJ, Naughton MT.Obesity and the lung: 2. Obesity and sleep-disordered
breathing. Thorax. 2008;63(8):738–46.
126. Marin JM, Soriano JB, Carrizo SJ, Boldova A, Celli BR.Outcomes in patients with chronic
obstructive pulmonary disease and obstructive sleep apnea. The overlap syndrome. Am J
Respir Crit Care Med. 2010;182(3):325–31.
127. Shawon MS, Perret JL, Senaratna CV, Lodge C, Hamilton GS, Dharmage SC.Current evi-
dence on prevalence and clinical outcomes of co-morbid obstructive sleep apnea and chronic
obstructive pulmonary disease: a systematic review. Sleep Med Rev. 2017;32:58–68.
128. Soler X, Gaio E.High prevalence of obstructive sleep apnea in patients with moderate to
severe chronic obstructive pulmonary disease. Ann Am Thorac Soc. 2015;12(8):1219–25.
129. He BT, Lu G, Xiao SC, etal. Coexistence of OSA may compensate for sleep related reduction
in neural respiratory drive in patients with COPD.Thorax. 2017;72(3):256–62.
130. Messineo L, Lonni S, Magri R, etal. Lung air trapping lowers respiratory arousal threshold
and contributes to sleep apnea pathogenesis in COPD patients with overlap syndrome. Respir
Physiol Neurobiol. 2020;271:103315.
131. Konikkara J, Tavella R, Willes L, Kavuru M, Sharma S.Early recognition of obstructive sleep
apnea in patients hospitalized with COPD exacerbation is associated with reduced readmission. Hosp Pract (1995). 2016;44(1):41–7.
132. Jaoude P, Kufel T, El-Solh A.Survival benet of CPAP favors hypercapnic patients with the
overlap syndrome. Lung. 2014;192(2):251–8.
133. Kuklisova Z, Tkacova R, Joppa P, Wouters E, Sastry M.Severity of nocturnal hypoxia and
daytime hypercapnia predicts CPAP failure in patients with COPD and obstructive sleep
apnea overlap syndrome. Sleep Med. 2017;30:139–45.
185

Chapter 10
https://t.me/medicina_free
Perioperative Care ofPatients
withObstructive Sleep Apnea Syndrome
KaraL.Dupuy-McCauley, HavenR.Malish, andPeterC.Gay
Keywords Perioperative complications · Postoperative monitoring · Obstructive
sleep apnea · Questionnaires · Perioperative guidelines · Sleep apnea guidelines ·
Postoperative CPAP · Hospital sleep apnea
Introduction
Obstructive sleep apnea (OSA) is a prevalent chronic condition, which is characterized by repeated episodes of collapse of the upper airway during sleep, leading to
episodic hypoxemia, sympathetic nervous system activation, and arousal from sleep
[1, 2]. Patients with obstructive sleep apnea have anatomical narrowing of the upper
airway (UA) leading to increased resistance, such that the force of the UA dilator
muscles is insufcient to prevent collapse [1]. As anesthesia, sedation, and analgesia can approximate certain aspects of the sleep state, patients with OSA are at risk
for worsening of disordered breathing events in the postoperative period and
increased postoperative cardiopulmonary complications.
Several anesthesia and sleep societies have proposed guidelines for the postoperative management of this patient population, aimed at reducing the risk of postoperative cardiopulmonary complications [3–8], although there are limited data
regarding the impact of implantation of these guidelines. This chapter will review
the most recent evidence regarding postoperative risks to the patient with OSA and
K. L. Dupuy-McCauley
Center for Sleep Medicine, Mayo Clinic, Rochester, MN, USA
H. R. Malish
Sleep Medicine, Mayo Clinic, Rochester, MN, USA
P. C. Gay (
Department of Medicine, Mayo Clinic, Rochester, MN, USA
e-mail: gay.peter@mayo.edu
M. S. Badr, J. L. Martin (eds.), Essentials of Sleep Medicine,
Respiratory Medicine, https://doi.org/10.1007/978-3-030-93739-3_10
*)
187© Springer Nature Switzerland AG 2022

188
https://t.me/medicina_free
the current recommendations regarding the care of patients with OSA during the
perioperative period.
K. L. Dupuy-McCauley et al.
Epidemiology andRisk Factors forOSA
The prevalence of OSA is thought to be 15–30% in males and 10–15% in females in
the general population of North America, but prevalence is increasing [9, 10] and
may vary based on population characteristics. For instance, OSA is more common in
older age, increased body mass index (BMI), and male gender [11]. Craniofacial
structure may also inuence the presence of OSA [12], as well as ethnicity with OSA
being more common in those of East Asian and African American descent [13, 14].
The association between obesity and OSA warrants special consideration owing
to the alarming increase in the prevalence of obesity in the United States. Obesity is
associated with increased risk of OSA [10, 15], and may account for 58% of cases
of OSA with an AHI≥15 [16]. In 2015–2016, the prevalence of obesity was 37.9%
in men and 41.1% in women [17]. The prevalence of severe obesity (BMI≥40kg/
m2) has increased from 5.7% to 7.7% from 2007 to 2016. Projections from this data
suggest that by 2030, almost half of United States adults will be obese and almost
one-fourth will be severely obese [17], and with this increase in weight, we will
certainly see an increase in prevalence of OSA.
In a population of patients presenting for bariatric surgery, prevalence of OSA
was very high and increased as BMI increased: For BMI 35–39.9kg/m2– 71%,
BMI 40–49.9kg/m2– 74%, and BMI>60kg/m2– 95% [18].
Postoperative Risks Associated withOSA
OSA is a well-established risk factor for increased complications after surgery [19–
35]. The most common of these would be respiratory-related adverse outcomes
including worsening of OSA, acute respiratory failure requiring non-invasive ventilation or tracheal intubation with mechanical ventilation, pulmonary edema, acute
respiratory distress syndrome (ARDS), and oxyhemoglobin desaturation [20, 24–26,
36–39]. Patients also may be at risk for cardiovascular complications including atrial
brillation, myocardial infarction, cardiac arrest, congestive heart failure (CHF),
cerebrovascular accident (CVA), venous thromboembolism (VTE), and shock [19,
20, 22, 24, 26, 39–41]. Several studies have shown increased risk of mortality, and
other miscellaneous complications such as acute renal failure, wound hematomas or
seromas, ICU transfer, and prolonged length of stay in hospital [24, 31].
Patients who have OSA overlapping with either obesity hypoventilation syndrome (OHS) or chronic obstructive pulmonary disease (COPD) have higher risk of
pulmonary and cardiac complications, ICU transfer, and increased length of stay
compared with OSA alone [23, 29].

10 Perioperative Care ofPatients withObstructive Sleep Apnea Syndrome
https://t.me/medicina_free
It is important to note that these studies are heterogeneous as far as surgical procedures performed, methods and statistical analysis, and the evidence is of varying
quality. In a more recent meta-analysis of the existing literature, OSA remained
associated with myocardial infarction, atrial brillation, pneumonia, respiratory
failure, oxygen desaturation, postoperative delirium, acute kidney injury, venous
thromboembolism, length of hospital stay, 30-day mortality, unplanned ICU admission, and increased hospital admission costs, but was not found to be associated
with CHF, CVA, risk of reintubation, in-hospital mortality, surgical site infection, or
postoperative bleeding [42]. As an example of variance between postoperative risk
and procedure performed, a meta-analysis examining outcomes after cardiac surgery specically determined OSA was associated with increased risk of pooled
major adverse cardiovascular and cerebrovascular events up to 30days after surgery
(all-cause mortality, myocardial infarction, myocardial injury, nonfatal cardiac
arrest, revascularization process, pulmonary embolism, deep venous thrombosis,
newly documented atrial brillation, CVA, and CHF), new-onset atrial brillation,
postoperative tracheal intubation and mechanical ventilation, but not with ICU or
hospital length- of- stay, infection, sepsis, or ICU readmission [43].
It is also important to acknowledge that some of these studies separate out mild,
moderate, and severe OSA, whereas others do not. This is an important consideration because mild OSA may not portend the same postoperative consequences as
moderate or severe disease. For instance, Chan and colleagues found in a post hoc
analysis of their study on OSA and postoperative cardiovascular complications that
severe OSA was associated with a higher risk of postoperative cardiac death, myocardial injury, CHF, new-onset atrial brillation, unplanned admission or readmission to the ICU, and unplanned tracheal intubation or lung ventilation, while
moderate OSA was associated with postoperative cardiac death, unplanned ICU
readmission, unplanned tracheal intubation, and infections, and mild OSA was only
associated with unplanned ICU admission or readmission to the ICU, unplanned
tracheal intubation or lung ventilation, and pneumonia [22].
Despite limitations in ability to determine precisely how severity of OSA, and
type of surgery being performed might inuence the risk of specic postoperative
outcomes, it is clear that OSA does lead to a general increased postoperative risk
and therefore it would follow that there may be a benet to identifying people with
OSA prior to surgery.
189
Preoperative Evaluation
Preoperative Risk Assessment andOSA Screening Protocols
Despite the increasing prevalence of OSA, many patients presenting for outpatient surgery (67%) remain undiagnosed [22]. In the case of elective, outpatient surgery, it may
be possible to capture this population of patients through routine screening during preoperative evaluation and refer for evaluation of sleep-disordered breathing in advance

190
https://t.me/medicina_free
of a planned surgical procedure if screening is positive. The American Society of
Anesthesiologists (ASA) recommends that screening for OSA, which is now encouraged in most US hospitals, should begin with a thorough history and physical exam [3].
The history should focus on eliciting any risk factors for OSA that the patient may have
including age, gender, ethnicity, presence of obesity, and common comorbid associated
conditions including hypertension, history of stroke, history of myocardial infarction,
diabetes mellitus, or abnormal cephalometric measurements. This would also include
assessment of any congenital conditions and disease states that may be associated with
OSA including Down’s syndrome, acromegaly, neuromuscular disease, and cerebral
palsy. Questions regarding the symptoms of OSA may include considering the presence of snoring, witnessed apneic episodes, frequent arousals during sleep, morning
headaches, and daytime somnolence. Other important aspects of the history may
include difculty with previous anesthetic administration or history of difcult intubation. The physical exam should include assessment of the craniofacial structure, nasal
passages, features of the posterior oropharynx (including tonsils and tongue size), and
neck circumference. A neck circumference of >17 inches (43cm) in men, and>16
inches (40cm) in women is a positive predictor for the presence of OSA [3, 7].
After preoperative evaluation, the decision may be made to manage the patient
expectantly despite suspected OSA, or to delay surgery and have the patient pursue
a more urgent evaluation and treatment for sleep disordered breathing.
K. L. Dupuy-McCauley et al.
Preoperative Screening forSuspected OSA
Several questionnaires have been developed for the purpose of screening for OSA
and most have been assessed for use in the preoperative population and compared
via meta-analysis [44, 45]. The ASA, Society of Anesthesia and Sleep Medicine
(SASM), and the American Academy of Sleep Medicine (AASM) recommend routine preoperative screening for OSA to identify patients at increased risk of perioperative complications [46–48]. While there is consensus that risk of OSA should be
evaluated and documented, this does not necessarily mean that the plan for surgery
must be altered. The SASM guidelines state that there is insufcient evidence to
advocate cancelling or delaying surgery with the intent of pursuing a sleep evaluation in patients with suspected OSA unless there is signicant evidence of serious
uncontrolled comorbid disease or gas exchange abnormality [5].
The Berlin Questionnaire
The Berlin Questionnaire was designed for use in an outpatient primary care setting
and assesses ve questions on snoring, three on excessive daytime sleepiness, one
on sleepiness while driving, and one on history of hypertension [49]. Age, gender,
weight, height, and neck circumference are also recorded. The Berlin Questionnaire’s
predictive performance is population dependent: In a primary care setting of 744
patients, it carried a sensitivity of 0.89, and specicity of 0.71. Half of high-risk

10 Perioperative Care ofPatients withObstructive Sleep Apnea Syndrome
https://t.me/medicina_free
patients it identies are subsequently found to have at least moderate OSA (at
AHI>15) by polysomnography. In the preoperative setting, one study found the
Berlin Questionnaire classied 24% of patients presenting for elective surgery as
high risk [50]. Another study of preoperative use of the Berlin Questionnaire determined it had a sensitivity and specicity of 69% and 56% respectively in detecting
OSA with AHI>5, 79% and 51% respectively in detecting OSA with AHI>15, and
87% and 46% respectively in detecting OSA with AHI>30 [51]. Despite its varied
performance in different patient populations, this data regarding use in the presurgical population suggests a moderately high sensitivity especially in moderateto- severe OSA, and therefore supports the Berlin Questionnaire as a reasonable tool
to rule out OSA in the preoperative setting [51].
191
The American Society ofAnesthesiologists’ Checklist
In the 2006 edition of the guidelines for the perioperative management of patients
with OSA, the ASA taskforce on OSA developed a 14-item, provider-administered
checklist to assist anesthesiologists in identifying OSA [52]. Patients endorsing
symptoms or signs in two or more of the three categories (physical characteristics,
history of airway obstruction during sleep, and complaints of somnolence) are considered high risk of having OSA.Like the Berlin Questionnaire and the STOP-Bang
Questionnaire, the ASA checklist exhibits a relatively good sensitivity in detective
OSA with an AHI of >5, >15, and> 30; 72%, 79%, and 87%, respectively. The
specicity remains rather low at 38%, 37%, and 36%, respectively, making is
another reasonable screening tool to rule out OSA [51].
The STOP Questionnaire
A condensed modication of the questions in the Berlin Questionnaire, the STOP
Questionnaire was developed and validated to facilitate widespread OSA screening
in surgical patients (S: Snore loudly, T: daytime Tiredness, O: Observed to stop
breathing during sleep, P: high blood Pressure). In the presurgical population, the
sensitivity of the STOP questionnaire at an AHI of >5, >15, and>30 events/h cutoff
levels was found to be 66%, 74%, and 80%, respectively, with a specicity of 60%,
53% and 49%, respectively [46].
The STOP-Bang Model
The STOP-Bang Questionnaire adds demographic and physical features (B: BMI
>35kg/m2, A: Age>50years, N: Neck circumference>40cm, G: male Gender) to
the STOP Questionnaire, and has the highest sensitivity in ruling OSA, especially in
moderate-to-severe disease.

192
https://t.me/medicina_free
A meta-analysis of the use of the STOP-Bang Questionnaire in the presurgical
population found a pooled prevalence of 68.4%, 39.2%, and 18.7% for any OSA,
moderate-to-severe OSA, and severe OSA respectively, with corresponding sensitivities of 84%, 91%, and 96% respectively and specicity of 43%, 32%, and
29%, respectively [53]. A recent prospective cohort study of preoperative patients
found that a STOP-Bang score of 5–8 may be signicantly more suggestive of
moderate- to- severe OSA than scores of 3–4: 78% prevalence versus 53% respective prevalence of moderate-to-severe OSA [54]. A study of an ethnically diverse
population of bariatric patients found that the STOP-Bang previously validated
cutoff of ≥4 achieved a sensitivity of >80% and specicity of 50–60%, which is
similar to other populations [55]. The STOP-Bang has also been assessed in a
variety of ethnic groups (Chinese, Indian, Malay, Caucasian) and there are recommendations in those groups for alternative BMI thresholds and STOP-Bang score
cutoffs for optimal sensitivity and specicity in these patient populations [56].
Taken together, these data suggest that the STOP-Bang may be an appropriate
assessment tool for a wide variety of patient populations but with alternative cutoffs for certain groups.
K. L. Dupuy-McCauley et al.
Sleep Apnea Clinical Score
The Sleep Apnea Clinical Score (SACS) was validated in the outpatient sleep laboratory environment and shown to have a high positive predictive value for OSA
[57]. The SACS score was initially validated in postsurgical patients to identify
patients who desaturated in the postoperative hospital ward area [58]. A large prospective study enrolled nearly 700 patients using the SACS and showed a higher
risk of OSA (32% of all patients) was associated with a much higher likelihood of a
postoperative 4% oxygen desaturation index (ODI) >10 events/h and recurrent post
anesthesia care unit (PACU) respiratory events [59]. Subsequent postoperative hospital ward episodes of respiratory complications were also associated with a high
SACS (odds ratio 3.5, P<0.001), especially if they also had recurrent respiratory
events in the PACU during 90min of observation, whereby the likelihood of a postoperative respiratory event was profoundly increased (odds ratio 21.0, P<0.001).
There was no signicant benet with the SACS questionnaire in predicting cardiac
complications or prolonged hospital stay.
Preoperative Screening inSuspected OSA
The use of one screening tool over another is not mandatory, and most guidelines
leave this decision of which tool to use up to the provider who is performing the
preoperative assessment. Optimal preoperative evaluation must also include consideration of the risk inherent to the particular type of surgery being performed, risk of
Соседние файлы в папке Библиотека им академика М.И. Перельмана
