Clinical Practice

Postoperative Management
of Patients with Obstructive
Sleep Apnea: Implications
for the Medical-Surgical Nurse
Ashley W. Helvig, Ptlene Minick, and David Patrick
Case Presentation #1
Mr. Franks, a 58-year-old male convenience store manager, has a medical history of obesity (body mass
index [BMI] 37 kg/m) and hypertension (managed with hydrochlorothiazide 25 mg daily). The patient was
admitted to a medical-surgical unit
after an uncomplicated partial colon
resection at 1:30 p.m. Mr. Franks was
alert and oriented after surgery but
complained of severe pain (8 on a 010 pain-intensity scale). Pulse oximetry was 95% or greater, and he was
able to tolerate clear liquids. The
nurse administered morphine sulfate
4 mg IV as ordered. At 3:45 p.m., Mr.
Franks continued to complain of pain
and was given an additional 4 mg of
morphine per order. He remained
alert throughout the evening and
received two more 4-mg doses of
morphine due to severe pain. At
11:30 p.m., the nurse found Mr.
Franks difficult to arouse; his oxygen
saturation was 75%. After successful
administration of naloxone (Narcan)
and oxygen, Mr. Franks was admitted
to the intensive care unit and stabilized. Mrs. Frank threatened to sue
the hospital for overmedicating her
husband with morphine.

Case Presentation #2
Mrs. Young, a 42-year-old female
elementary school principal with no
reported medical history and a BMI
of 22.5, was discharged home after
an uncomplicated cholecystectomy.
Mrs. Young took two tablets of
oxycodone with acetaminophen
(Percocet) prior to hospital discharge at 2:45 p.m. Later that

Obstructive sleep apnea (OSA) affects up to 7% of Americans, and

those undergoing surgery are at risk for complications. Medical-surgical nurses should be knowledgeable regarding this common disorder and understand how to screen effectively and monitor
patients with OSA.
evening, Mrs. Youngs pain returned;
she took two more tablets of oxycodone at 7:00 p.m. and went to bed
at 9:00 p.m. Her husband checked on
her at 9:45 p.m. and discovered her
color was ashen and she appeared
to not be breathing. Mrs. Young
aroused after her husband yelled her
name and shook her, and they both
decided she should be evaluated in
the emergency room. The physician
discontinued the oxycodone and
ordered non-opioid analgesia.
Both these patients were assumed
to have opioid-induced respiratory
depression; neither patient was
screened for obstructive sleep apnea
(OSA). General anesthesia can lead
to respiratory complications even in
the otherwise uncompromised
patient (Cereda, Neligan, & Reed,
2013). Nurses have an opportunity
to prevent adverse or sentinel events
by identifying patients who are at
high risk for undiagnosed OSA. In
this article, the pathophysiology of
OSA, treatment, and nursing care of
affected patients is discussed. In
addition, a summary of screening

questionnaires that can be used to

identify undiagnosed OSA in the
postoperative period is included.

Definition and
Epidemiology of OSA
Obstructive sleep apnea is the
most common form of sleep-disordered breathing. This disorder causes
recurrent partial or complete collapse
of the upper airway during sleep,
resulting in periods of apnea (cessation of breathing) lasting over 10 seconds (Kryger, Roth, & Dement,
2011). These apneic periods lead to
fragmented sleep, hypoxemia, hypercapnia, marked variations in intrathoracic pressure, and increased sympathetic activity (Epstein et al., 2009).
Obstructive sleep apnea is associated with significant harmful effects.
Intermittent airway obstruction and
apnea lead to repeated arousals
throughout the night, resulting in
poor sleep quality, significant daytime sleepiness, and fatigue (Kryger
et al., 2011). Untreated, OSA can lead
to cognitive dysfunction (Bucks,

Ashley W. Helvig, PhD, RN, CNE, is Assistant Professor, Tanner Health System School of
Nursing, University of West Georgia, Carrollton, GA.
Ptlene Minick, PhD, RN, is Associate Professor, Byrdine F. Lewis School of Nursing, Georgia
State University, Atlanta, GA.
David Patrick, MSN, RN, NP-C, is Nurse Practitioner, Heart Failure Clinic, Piedmont Hospital,
Atlanta, GA.

May-June 2014 Vol. 23/No. 3

171

Clinical Practice
Olaithe, & Eastwood, 2013), impaired
work performance, increased risk of
motor vehicle accidents (Sanna,
2012), and decreased quality of life
(Dutt, Janmeja, Mohapatra, & Singh,
2013; Patidar, Andrews, & Seth,
2011). OSA is associated with the
development of hypertension (Young
et al., 2009), cardiovascular disease
(Shah, Yaggi, Concato, & Mohsenin,
2010), heart failure (Gottlieb et al.,
2010), stroke (Kendzerska, Gershon,
Hawker, Leung, & Tomlinson, 2014),
type 2 diabetes (Botros et al., 2009),
and depressive symptoms (Douglas et
al., 2013). In a meta-analysis by Ge
and colleagues (2013), a significantly
high mortality risk was associated
with untreated sleep-disordered
breathing. Liao, Yegneswaran, Vairavanathan, Zilberman, and Chung
(2009) found greater complications
(44% in the OSA group vs. 28% in the
non-OSA group) among postoperative patients, with most complications occurring after transfer from
postanesthesia care to the general
medical-surgical unit. Because the
patient with undiagnosed OSA is at
greatest risk for complications, the
medical-surgical nurse must be
knowledgeable about risk factors as
well as the signs, symptoms, and
potential treatments of OSA.
Mild OSA is a somewhat common
condition in the United States, with
24% of men and 9% of women
affected; in addition, approximately
4% of women and 9% of men have
severe OSA (Young et al., 2009).
However, up to 90% of men and 98%
of women with OSA are undiagnosed
(Patil, Schneider, Schwartz, & Smith,
2007). The prevalence of OSA is higher in patients with a history of hypertension, stroke, coronary artery disease, heart failure, and diabetes;
patients with any of these conditions
should be screened for OSA prior to
surgery. Almost 70% of patients
undergoing bariatric surgery have
OSA (Ravesloot, Van Maanen,
Hilgevoord, van Wagensveld, & de
Vries, 2012), with the majority undiagnosed. While patients typically are
screened pre-operatively, the nurse
receiving patients from the postanesthesia care unit also should
assess and screen for OSA.

172

If Mr. Franks had been screened

for OSA before and after surgery, the
health care team would have learned
he had a 30-year history of snoring,
making it difficult for his wife to
sleep in the same room because of
his snoring severity. Although Mrs.
Young did not complain of snoring
(nor did her husband complain), she
had a 5-year history of daytime
sleepiness which she attributed to
stress of work and family. Mrs.
Young also had a family history of
OSA. Nurses have the prime opportunity to initiate screening for OSA
to prevent adverse outcomes. Many
patients do not recognize symptoms
such as daytime sleepiness as signs of
OSA (Kryger et al., 2011); more indepth screening by nurses thus is
needed.

Pathophysiology
Neurological as well as structural
factors contribute to OSA. Previously,
sleep experts differentiated between
OSA caused by central nervous system problems (central sleep apnea)
and peripheral problems such as collapse of the upper airway (Kryger et
al., 2011). More recently, experts suggested OSA occurs as a result of both
central and peripheral problems
(Dempsey, Veasey, Morgan, &
ODonnell, 2010; Kryger et al., 2011).
During wakefulness, the body
responds to hypoxia and hypercapnia via peripheral chemoreceptors
that communicate with the brain to
initiate a breath. Additionally, during wakefulness, a person who has
an easily collapsible airway experiences central nervous system (CNS)
compensation that helps to stabilize
the airway; thus there is no impairment during waking hours. Peripheral chemoreceptors are not as
sensitive during sleep. With sleep
apnea, CNS control of airway stability is lost during the transition into
sleep as well as during non-rapid eye
movement sleep and rapid eye
movement sleep. These factors lead
to hypopneic or apneic episodes
(Dempsey et al., 2010). Dempsey
and colleagues (2010) described how
a loss of central nervous system excitatory inputs can cause hypotonia of

muscles in the respiratory system,

leading to less diaphragmatic control
of breathing as well as collapse of the
upper airway. This collapse is
thought to be the major cause of
OSA. The majority of the pharynx
has no skeletal support, and its opening is affected easily by the pressure
created during breathing. Dempsey
and colleagues also suggested multiple regions of the pharynx may be
subject to hypotonia, thereby contributing to OSA. Once the airway
closes, or a major resistance in the
airway occurs, continued diaphragmatic movements may increase
intrathoracic negative pressure and
further worsen airway collapse.

Risk Factors
The stereotypical person with
OSA is an older, obese male.
However, many factors are involved
in a persons risk for OSA. Craniofacial malformation retrognathia
(recession of the chin), nasal deformities, positive family history, recurrent alcohol ingestion, sedative use,
and minority race also have been
associated with OSA (Kryger et al.,
2011). Decreased lung volume, airway edema, increased surface tension of the upper airway, and injury
of airway muscles also are associated
with OSA (Dempsey et al., 2010).
Children are also at risk for OSA; the
incidence of OSA in children has
risen over the past decade and is
attributed to increasing childhood
obesity (Chang & Chae, 2010;
Dempsey et al., 2010). Although
obesity is considered a major risk factor of OSA and more persons who
are obese have OSA than persons
with healthy weights, not everyone
with OSA is obese (Gutierrez &
Brady, 2013). The wide variation in
obvious risk factors emphasizes the
importance of postoperative assessment and potential OSA screening
for everyone (see Table 1).

Clinical Presentation
Persons with OSA can vary widely
in the number and severity of symptoms as well as in their clinical presentation. The most typical symptom

May-June 2014 Vol. 23/No. 3

Postoperative Management of Patients with Obstructive Sleep Apnea: Implications for the Medical-Surgical Nurse

TABLE 1.
General Overview of OSA
Common Characteristics
of Affected Individual

Signs and Symptoms

of OSA

Common Treatment
for OSA

Common Complications
of OSA

Obesity
Craniofacial malformation
Nasal deformities
Positive family history of OSA
Recurrent alcohol ingestion
Sedative use

Apnea
Snoring or gasping during
sleep
Daytime sleepiness
Night awakenings

CPAP
EPAP
BiPAP
MAD
Surgical intervention (e.g.,
uvulopalatophrayngoplasty,
tracheostomy)

Fatigue
Poor daytime function
Cognitive impairment
Hypertension
Cardiovascular disease
Type 2 diabetes
Depression

(Gutierrez & Brady, 2013;

Kryger et al., 2011)

(Gutierrez & Brady, 2013;

Kryger et al., 2011)

(Epstein et al., 2009; Gutierrez (Bucks, Olaithe, & Eastwood,

& Brady, 2013)
2013; Douglas et al., 2013;
Dutt et al., 2013; Kendzerska
et al., 2014; Sanna, 2012)

Notes:
CPAP = continuous positive airway pressure
EPAP = expiratory positive airway pressure
BiPAP = bi-level positive airway pressure
MAD = mandibular advancement device

is upper airway obstruction during

sleep. Although this cannot be
detected visually without specialized
diagnostic equipment, a person with
airway obstruction during sleep may
appear to have abdominal movements mimicking breathing without
air passing through the nose or
mouth. Other common signs and
characteristics are excessive daytime
sleepiness, insomnia or nighttime
awakenings, obesity, snoring, gasping while sleeping, macroglossia
(enlarged tongue), retrognathia (recession of the chin), and tonsillar
hyperplasia (Gutierrez & Brady,
2013; Krug, 1999). Another common
characteristic is a familial history
of OSA (Lundkvist, Sundquist, &
Friberg, 2012) (see Table 1).

Diagnostic and Screening

Tools
Due to the high number of people
with undiagnosed OSA, the medicalsurgical nurse should be aware of the
tools used to screen patients, especially postoperatively. The gold standard for diagnosis of OSA is polysomnography (PSG), which is conducted during sleep to assess elec-

troencephalogram activity, leg movements, eye movements, breathing,

and other diagnostic assessments,
such as heart rate and pulse oximetry (Epstein et al., 2009). The diagnosis of OSA is based on the number of
apneic or hypopneic episodes per
hour of sleep, a measure called the
apnea hypopnea index (AHI) (Kryger
et al., 2011). OSA is classified as mild
(AHI 5-15), moderate (AHI 15-30), or
severe (AHI >30) (Epstein et al.,
2009). Although PSG testing is ideal,
it is time consuming and expensive,
and the demand for testing exceeds
the availability of sleep laboratories
(Whitelaw & Burgess, 2010). Polysomnography is conducted based on
clinical evaluation by a physician; it
requires advance notice and specialized equipment to be completed.
Due to issues of cost, access, and timing, multiple screening questionnaires have been developed to help
practitioners identify patients at risk
for OSA. These tools (see Table 2) are
easy to use and require very little
time for the nurse or patient. The
results can alert nurses to high-risk
patients so that postoperative complications can be prevented. Readers
should note these tools are for
screening purposes only and not

May-June 2014 Vol. 23/No. 3

intended for diagnosis or determination of treatment (Gutierrez & Brady,

2013).
The Epworth Sleepiness Scale
(ESS) was designed in 1991 as a simple, cost-effective method to determine daytime sleepiness by asking
individuals how likely they would be
to fall asleep if they encountered
eight different situations (Johns,
1991). They are asked to think only
of how likely they would be to fall
asleep, not how likely they are to be
tired or fatigued in those situations.
Anyone with a score greater than 10
is considered to have excessive daytime sleepiness and a possible sleep
disturbance. Johns (1991) explained
carefully that a score greater than 10
does not diagnose a sleep disorder.
The ESS is to be used as an assessment tool and screening for potential sleep problems. Although this
tool does not screen specifically for
OSA, it does screen for the most
common symptom of OSA: daytime
sleepiness. Johns (1992) reported an
acceptable internal consistency
(Cronbachs alpha 0.88) for the ESS.
However, the validity of ESS (when
compared to polysomnography) as a
tool for OSA was reported by Ulasli
and colleagues (2014) with a sensi-

173

Clinical Practice
TABLE 2.
Common Screening Tools
Name

General Purpose

Number of
Questions

Time for
Completion of Tool

1-2 minutes

Reliability and Validity

Epworth Sleepiness
Scale (ESS) (Johns,
1991)

Assess level of daytime sleepiness

Cronbachs alpha 0.88 for patients with

sleep disorders.

Wisconsin Sleep
Questionnaire
(Young et al., 2008;
Young et al., 2009)

Assess risk for OSA

0-1 minute

Validity is reported with sensitivity

between 79% and 95% for mild OSA,
with specificity between 46% and 64%.

Berlin Questionnaire
(Netzer et al., 1999)

Assess risk for OSA

10

1-2 minutes

Cronbachs alpha 0.92 for items in category 1 (snoring characteristics and

breathing pauses), 0.86 for items in category 2 (daytime sleepiness excluding
the question regarding falling asleep
while driving).

Sensitivity for detecting mild OSA is

46.9% and 52.8% for detecting severe
OSA. Specificity for ruling out OSA is
60% for mild OSA and 58.2% for
severe OSA.

Sensitivity 86% for detecting mild OSA.

STOP Questionnaire
(Chung et al., 2008)

Assess signs of OSA

0-1 minute

Sensitivity 65.6% in mild OSA, 74.3% in

moderate OSA, 79.5%
in severe OSA.

STOP-BANG
Questionnaire
(Chung et al., 2008)

Assess signs of OSA

1-2 minutes

Sensitivity 83.6% in mild OSA, 92.9% in

moderate OSA, 100%
in severe OSA.

tivity for detecting mild OSA at only

46.9% and 52.8% for detecting
severe OSA. Specificity for excluding
OSA was 60% for mild OSA and
58.2% for severe OSA.
The Wisconsin Sleep Questionnaire is a tool used to detect persons
at risk for OSA. Although it is difficult to find reliability data for this
questionnaire conducted with the
English version, the five questions
are direct, simple, and specific
regarding the most common clinical
features of OSA (snoring, holding
ones breath, daytime sleepiness,
medical symptoms associated with
OSA such as acid reflux or hypertension, and obesity) (Benca, n.d.).
Validity is reported with sensitivity
between 79% and 95% for mild OSA
and specificity between 46% and
64% (Abrishami, Khajehdehi, &
Chung, 2010).
The Berlin Questionnaire also
was designed to screen for symptoms of OSA. The questionnaires 10

174

items focus on common symptoms

of sleep apnea (Netzer, Stoohs,
Netzer, Clark, & Strohl, 1999). The
first question asks the patient to selfreport height and weight. The first
category of questions focus on snoring (such as snoring frequency and
intensity, and breathing pauses).
The second category focuses on
sleepiness (daytime sleepiness,
falling asleep while driving). The
final question asks about diagnosis
of hypertension. Netzer and colleagues reported an internal consistency Cronbachs alpha 0.92 for
items in category 1 (snoring characteristics and breathing pauses) and
0.86 for items in category 2 (daytime sleepiness excluding the question regarding falling asleep while
driving). It was hoped the Berlin
Questionnaire would be able to distinguish between low-risk (persons
presenting with symptoms less than
3-4 times per week) and high-risk
groups (persons presenting with

symptoms greater than 3-4 times

per week in two different categories). Sensitivity of the questionnaire compared to portable monitoring was reported as 86%; however, this was only for detecting mild
OSA as defined by a Respiratory Disturbance Index (this is the number
of respiratory events per hour)
greater than five (greater than five is
considered mild and greater than 30
is considered severe) (Netzer et al.,
1999). Ulasli and colleagues (2014)
compared the Berlin Questionnaire
to PSG and reported sensitivity for
detecting mild OSA as 73.1% and
80.3% for severe OSA, with a specificity of 44.5% and 35.3%, respectively. These reports of validity
emphasize the use of these instruments only as screening tools.
The STOP Questionnaire, developed by Chung and colleagues
(2008), is a self-report scale that contains simple yes-no questions. The
questions are:

May-June 2014 Vol. 23/No. 3

Postoperative Management of Patients with Obstructive Sleep Apnea: Implications for the Medical-Surgical Nurse

1.

S Do you Snore loudly

(Louder than talking or loud
enough to be heard through
closed doors)?
2. T Do you often feel Tired,
fatigued, or sleepy, during daytime?
3. O Has anyone Observed you
stop breathing during your
sleep?
4. P Do you have or are you
being treated for high blood
Pressure?
A person with a score of two or more
is considered to be at high risk for
OSA.
To improve the sensitivity of the
questionnaire, Chung and colleagues (2008) developed the STOPBANG model. The STOP-BANG
model combines the STOP questionnaire with additional yes-no questions. These questions are as follows:
1. B Is the BMI more than 35
kg/m2?
2. A Is the Age over 50?
3. N Is the Neck circumference
greater than 40 cm?
4. G Is the Gender male?
A person with three or more positive answers is considered at high
risk for OSA. By adding these questions, the sensitivity of the scale
improved. Chung and colleagues
(2008) reported a sensitivity of
83.6% for mild OSA and 100% for
severe OSA. Additionally, the specificity is 56.4% for mild OSA and 37%
for severe OSA. Although these questionnaires do not diagnose a person
with OSA, they are extremely useful
in screening persons at risk for OSA.
These questionnaires are inexpensive, easy to use, and readily available, and could lead to better postoperative outcomes for patients at risk
for OSA.

Management of OSA
Management for OSA encompasses a variety of noninvasive methods,
such as weight loss or oral devices
(Epstein et al., 2009; Gutierrez &
Brady, 2013). Surgical intervention
may be necessary if the patients
anatomy is causing severe obstruction (Epstein et al., 2009) or if primary noninvasive therapy is not

adequate (Epstein et al., 2009;

Gutierrez & Brady, 2013). In persons
with OSA that can be attributed to
obesity or enlarged neck circumference from adipose tissue, weight loss
might be the least invasive and most
cost-effective choice for management (Epstein et al., 2009; Gutierrez
& Brady, 2013).
Positive airway pressure is considered the ideal treatment for OSA and
can be delivered through the nose or
mouth, or via oronasal device
(Epstein et al., 2009). A continuous
positive airway pressure (CPAP)
device is used commonly in the
management of OSA; however,
adherence to device use is poor. The
CPAP device uses a mouthpiece that
covers the nose or oronasal area, and
continually pushes air through the
airway to keep it open. Poor treatment adherence usually is attributed
to the loud noise of the machine,
uncomfortable device, irritation
around the mouth or nose, and
movement of the device into an
improper position (Shapiro &
Shapiro, 2010). A new device, the
expiratory positive airway pressure
(EPAP) device, is gaining popularity.
EPAP uses a smaller piece that covers
the nose; it has greater treatment
adherence and improved results over
the CPAP device (Walsh, 2011). Bilevel positive airway pressure (BiPAP)
also could be considered helpful in
patients who do not tolerate CPAP
(Epstein et al., 2009; Gutierrez &
Brady, 2013); however, there are very
few studies examining the effectiveness of BiPAP.
An alternative to CPAP may be an
oral device such as a mandibular
advancement device (MAD). These
devices are inserted into the patients
mouth and over the teeth to reposition the patients jaw and help keep
the upper airway open (Woodson,
2010). Several different types of
MADs are available, with material
and design playing a part in the
devices effectiveness in treating OSA
(Ahrens, McGrath, & Hgg, 2011).
Surgical intervention is not recommended routinely and is contraindicated in persons with collapse
in certain areas of the upper airway
(e.g., the base of the tongue) (Powers,

May-June 2014 Vol. 23/No. 3

Allan, Hayes, & Michaelson, 2010).

Surgical procedures include nasal airway repair (functional septorhinoplasty), retro-palatal airway repair
(e.g., uvulopalatopharyngoplasty),
and maxilla and/or mandibular
repair (e.g., anterior horizontal
mandibular osteotomy, maxillomandibular advancement) (Colin &
Duval, 2005; Powers et al., 2010).
Persons with severe OSA that does
not respond to CPAP may be treated
with a tracheostomy. This surgical
intervention is an elective treatment,
and patients must meet strict criteria
(Browaldh, Markstrom, & Friberg,
2009) (see Table 1).

Nursing Implications
When a postoperative patient is
transferred from the post-anesthesia
care unit (PACU), the receiving nurse
should investigate if the patient was
screened pre-operatively for OSA. If
no screening has occurred, the
receiving nurse could screen the
patient quickly using any of the
tools described in Table 2. If the postoperative patient has a positive
screening result, or has a questionable or definitive history of OSA, the
nurse should monitor the patient
very closely, especially if the patient
is drowsy or sleeping. Patients receiving opioid analgesics are at higher
risk for respiratory depression and
should be monitored frequently
whether or not they have a positive
screening or history of OSA (Jarzyna
et al., 2011). The American Society
for Pain Management Nursing
(ASPMN) suggested nurses should
assess, identify, and document
patients with factors that may place
patients at risk for unintended
advancing sedation and respiratory
depression with opioid therapy
(Jarzyna et al., 2011, p. 127). In addition, patients with sleep-disordered
breathing are at increased risk during
the postoperative period. The
ASPMN (Jarzyna et al., 2011) also
indicated nurses should communicate between shifts and during transitions of care within the hospitalization to ensure other nurses and
health care providers understand a
patients risk factors for respiratory

175

Clinical Practice
depression. Cardiac and respiratory
monitoring or pulse oximetry are
useful in detecting apneic episodes
or early oxygen desaturation (Seet &
Chung, 2010a, 2010b). Close cardiac
and pulse oximetry monitoring will
allow the nurse to administer appropriate analgesia while ensuring adequate circulation and oxygenation.
The ASPMN (Jarzyna et al., 2011)
noted information obtained from
patient assessments and available
clinical information should be used
to formulate individualized plans of
care for the level, frequency, and
intensity of patient monitoring of
sedation and respiratory status during opioid therapy (p. 129).
Because many postoperative
patients have opioid analgesics
ordered, respiratory depression is a
potential concern. The ASPMN
(Jarzyna et al., 2011) recommended
nurses should act as strong advocates for pain management plans
that incorporate opioid dose-sparing
strategies initiated early in the course
of treatment, e.g., on admission,
before surgery, during surgery, and
early after surgery (p. 131). Authors
also stated that even if opioid dosesparing strategies are used, nurses are
still responsible for assessment and
monitoring of sedation and respiratory depression. More intensive and
frequent observation of patients and
assessment of sedation and respiratory status are recommended when
sedating agents are administered
concomitantly with opioids, especially during the postoperative period (Jarzyna et al., 2011. p. 133).
Recommendations include regular
assessment of sedation (using a reliable and valid sedation scale) during
sleep and wakefulness. If a patient is
increasing in sedation (a risk for respiratory depression), the frequency
of monitoring needs to increase as
well. Additionally, while the patient
is resting quietly or sleeping, respiratory assessment needs to include a 1minute count of respirations with
identification of the rhythm and
depth as well. Nurses also should
avoid transferring patients to different units when the effects of analgesics may be at the highest level.
Patients found to have signs of respiratory depression (e.g., rate defined
176

as <8 or <10 breaths per minute

and/or paradoxic rhythm with little
chest excursion), evidence of advancing sedation, poor respiratory effort
or quality, snoring or other noisy respiration, or desaturation should be
aroused immediately and instructed
to take deep breaths. Intervene and
communicate with other team members per practice policy and continue
patient monitoring until patient
recovers (Jarzyna et al., 2011, p.
139). During times when patients are
at greater risk for sedation and/or respiratory depression (first 24 hours
post-operative; after increases in opioid dose; recent or rapid change in
liver, kidneys, or lung function; or
changing opioid medication or
route), nurses should be monitoring
patients more frequently and vigilantly (Jarzyna et al., 2011).

Conclusion
The prevalence of sleep-disordered breathing is somewhat high in
the United States, with the vast
majority of persons going undiagnosed (Patil et al., 2007; Young et al.,
2009). Postoperative complications
in the patient with OSA can be
severe; most complications occur
after the patient has been transferred
from the PACU to the general medical-surgical unit (Chung, Liao,
Yegneswaran, Shapiro, & Kang,
2014). While many patients with
OSA have classic risk factors, such as
obesity and snoring, many patients
do not exhibit the classic signs
(Kryger et al., 2011). The use of simple screening tools, such as the
Berlin Questionnaire or STOP-BANG
questionnaire, could lead to identification of patients at risk for OSA.
This screening during the postoperative period could help to prevent
severe respiratory complications
(Setaro, 2012).
REFERENCES
Abrishami, A., Khajehdehi, A., & Chung, F.
(2010). A systematic review of screening
questionnaires for obstructive sleep
apnea. Canadian Journal of Anesthesia,
57(5), 423-438. doi:10.1007/s12630010-9280-x
Ahrens, A., McGrath, C., & Hgg, U. (2011). A
systematic review of the efficacy of oral
appliance design in the management of

obstructive sleep apnoea. The European

Journal of Orthodontics, 33(3), 318-324.
doi:10.1093/ejo/cjq079
Benca, R. (n.d.). Wisconsin sleep. Retreived
from http://wisconsinsleep.org/sleepapnea/
Botros, N., Concato, J., Mohsenin, V., Selim,
B., Doctor, K., & Yaggi, H.K. (2009).
Obstructive sleep apnea as a risk factor
for type 2 diabetes. The American
Journal of Medicine, 122(12), 11221127.
Browaldh, N., Markstrom, A., & Friberg, D.
(2009). Elective tracheostomy is an alternative treatment in patients with severe
obstructive sleep apnoea syndrome and
CPAP failure. Acta Oto-laryngologica,
129(10), 1121-1126.
Bucks, R.S., Olaithe, M., & Eastwood P.
(2013). Neurocognitive function in
obstructive sleep apnoea: A metareview. Respirology, 18(1), 61-70.
doi:10.1111/j.1440-1843.2012.02255.x
Cereda, M., Neligan, P.J., & Reed, A.J. (2013).
Noninvasive respiratory support in the
perioperative period. Current Opinion in
Anesthesiology, 26(2), 124-140. doi:
10.1097/ACO.0b013e32835e8002
Chang, S., & Chae, K. (2010). Obstructive
sleep apnea syndrome in children:
Epidemiology, pathophysiology, diagnosis and sequelae. Korean Journal of
Pediatrics, 53(10), 863-871.
Chung, F., Liao, P., Yegneswaran, B., Shapiro,
C., & Kang, W. (2014). Postoperative
changes in sleep-disordered breathing
and sleep architecture in patients with
obstructive sleep apnea. Anesthesiology,
120(2), 287-298. doi: 10.1097/ALN.
0000000000000040
Chung, F., Yegneswaran, B., Liao, P., Chung, S.,
Vairavanathan, S., Islam, S., Shapiro,
C.M. (2008). STOP Questionnaire: A tool
to screen patients for obstructive sleep
apnea. Anesthesiology, 108(5), 812-821.
Colin, W., & Duval, D. (2005). Home study program. Surgical treatment of obstructive
sleep apnea. AORN Journal, 82(3), 371374. doi:10.1016/S0001-2092(06)603347
Dempsey, J.A., Veasey, S.C., Morgan, B.J., &
ODonnell, C.P. (2010). Pathophysiology
of sleep apnea. Physiological Reviews,
90(1), 47-112.
Douglas, N., Young, A., Roebuck, T., Ho., S.,
Miller, B.R., Kee, K., Naughton, M.T.
(2013). Prevalence of depression in
patients referred with snoring and
obstructive sleep apnoea. Internal
Medicine Journal, 43(6), 630-634.
doi:10.1111/imj.12108
Dutt, N., Janmeja, A.K., Mohapatra, P.R., &
Singh, A.K. (2013). Quality of life impairment in patients of obstructive sleep
apnea and its relation with the severity of
disease. Lung India, 30(4), 289-294.
doi:10.4103/0970-2113.120603

May-June 2014 Vol. 23/No. 3

Postoperative Management of Patients with Obstructive Sleep Apnea: Implications for the Medical-Surgical Nurse
Epstein, L.J., Kristo, D., Strollo, P.J., Friedman,
N., Malhotra, A., Patil, S.P., Weinstein,
W.M. (2009). Clinical guideline for the
evaluation, management and long-term
care of obstructive sleep apnea in adults.
Journal of Clinical Sleep Medicine, 5(3),
263-276.
Ge, X., Han, F., Huang, Y., Zhang, Y., Yang, T.,
Bai, C., & Guo, X. (2013). Is obstructive
sleep apnea associated with cardiovascular and all-cause mortality? PLOS
ONE, 8(7), e69432. doi:10.1371/jour
nal.pone.0069432
Gottlieb, D., Yenokyan, G., Newman, A.B.,
OConnor, G.T., Punjabi, N.M., Quan,
S.F., Shahar, E. (2010). Prospective
study of obstructive sleep apnea and
incident coronary heart disease and
heart failure: The sleep heart health
study. Circulation, 122(4), 352-360.
Gutierrez, C., & Brady, P. (2013). Obstructive
sleep apnea: A diagnostic and treatment
guide. The Journal of Family Practice,
62(10), 565-572.
Jarzyna, D., Jungquist, C.R., Pasero, C.,
Willens, J.S., Nisbet, A., Oakes, L.,
Polomano, R.C. (2011). American Society
for Pain Management Nursing guidelines
on monitoring for opioid-induced sedation
and respiratory depression. Pain Management Nursing, 12(3), 118-145.e10.
doi:10.1016/j.pmn.2011.06.008
Johns, M.W. (1991). A new method for measuring daytime sleepiness: The Epworth
Sleepiness Scale. Sleep, 14(6), 540.
Johns, M.W. (1992). Reliability and factor
analysis of the Epworth Sleepiness
Scale. Sleep, 15(4), 376-381.
Kendzerska, T., Gershon, A.S., Hawker, G.,
Leung, R.S., & Tomlinson, G. (2014).
Obstructive sleep apnea and risk of cardiovascular events and all-cause mortality: A decade-long historical cohort study.
PLOS Medicine, 11(2), e1001599. doi:
10.1371/journal.pmed.1001599
Krug, P. (1999). Snoring and obstructive sleep
apnea. AORN Journal, 69(4), 792-801.
doi:10.1016/S0001-2092(06)62352-1
Kryger, M.H., Roth, T., & Dement, W.C. (2011).
Principles and practice of sleep medicine. Philadelphia, PA: Elsevier
Saunders.
Liao, P., Yegneswaran, B., Vairavanathan, S.,
Zilberman, P., & Chung, F. (2009).
Postoperative complications in patients
with obstructive sleep apnea: A retrospective matched cohort study.
Canadian Journal of Anesthesia, 56(11),
819-828.
Lundkvist, K., Sundquist, K., Li, X., & Friberg,
D. (2012). Familial risk of sleep-disordered breathing. Sleep Medicine, 13(6),
668-673. doi:10.1016/j.sleep.2012.01.
014
Netzer, N.C., Stoohs, R.A., Netzer, C.M.,
Clark, K., & Strohl, K.P. (1999). Using the
Berlin Questionnaire to identify patients
at risk for the sleep apnea syndrome.
Annals of Internal Medicine, 131(7), 485491.
Patidar, A.B., Andrews, G.R., & Seth, S.
(2011). Prevalence of obstructive sleep
apnea, associated risk factors, and qual-

ity of life among Indian congestive heart

failure patients: A cross-sectional survey.
Journal of Cardiovascular Nursing,
26(6), 452-459.
Patil, S., Schneider, H., Schwartz, A.R., &
Smith, P.L. (2007). Adult obstructive
sleep apnea. Chest, 132(1), 325-337.
Powers, D.B., Allan, P.F., Hayes, C.J., &
Michaelson, P.G. (2010). A review of the
surgical treatment options for the
obstructive sleep apnea/hypopnea syndrome patient. Military Medicine, 175(9),
676-685.
Ravesloot, M.J., van Maanen, J.P., Hilgevoord,
A.A., van Wagensveld, B.A, & de Vries,
N. (2012). Obstructive sleep apnea is
underrecognized and underdiagnosed in
patients undergoing bariatric surgery.
European Archives of Oto-RhinoLaryngology, 269(7), 1865-1871.
Sanna, A. (2012). Obstructive sleep apnoea,
motor vehicle accidents, and work performance. Chronic Respiratory Disease,
10(1), 29-33.
Seet, E., & Chung, F. (2010a). Management of
sleep apnea in adults - functional algorithms for the perioperative period:
Continuing professional development.
Canadian Journal of Anesthesia, 57(9),
849-864.
Seet, E., & Chung, F. (2010b). Obstructive
sleep apnea: Preoperative assessment.
Anesthesiology Clinics, 28(2), 199-215.
Setaro, J. (2012). Obstructive sleep apnea: A
standard of care that works. Journal of
Perianesthesia Nursing, 27(5), 323-328.
doi:10.1016/j.jopan.2012.06.005
Shah, N.A., Yaggi, H.K., Concato, J., &
Mohsenin, V. (2010). Obstructive sleep
apnea as a risk factor for coronary events

May-June 2014 Vol. 23/No. 3

or cardiovascular death. Sleep &

Breathing, 14(2), 131-136.
Shapiro, G.K., & Shapiro, C.M. (2010). Factors
that influence CPAP adherence: An
overview. Sleep & Breathing, 14(4), 323335.
Ulasli, S.S., Gunay, E., Koyuncu, T., Akar, O.,
Halici, B., Ulu, S., & Unlu, M. (2014).
Predictive value of Berlin Questionnaire
and Epworth Sleepiness Scale for
obstructive sleep apnea in a sleep clinic
population. The Clinical Respiratory
Journal. [Epub ahead of print.]
doi:10.1111/crj.12070
Walsh, J.K. (2011). A convenient expiratory
positive airway pressure nasal device for
the treatment of sleep apnea in patients
non-adherent with continuous positive
airway pressure. Sleep Medicine, 12(2),
147-152.
Whitelaw, W.A., & Burgess, K.R. (2010).
Diagnosis of sleep apnoea: Some critical
issues. Indian Journal of Medical
Research, 131, 217-229.
Woodson, B.T. (2010). Non-pressure therapies
for obstructive sleep apnea: Surgery and
oral appliances. Respiratory Care,
55(10), 1314-1321.
Young, T., Finn, L., Peppard, P., Szklo-Coxe,
M., Austin, D., Nieto, F.J., Hla, K.M.
(2008). Sleep disordered breathing and
mortality: Eighteen-year follow-up of the
Wisconsin sleep cohort. Sleep, 31(8),
1071-1078.
Young, T., Palta, M., Dempsey, J., Peppard,
P.E., Nieto, J.F., & Hla, K.M. (2009).
Burden of sleep apnea: Rationale,
design, and major findings of the
Wisconsin Sleep Cohort study.
Wisconsin Medical Journal, 108(5), 246.

177

Reproduced with permission of the copyright owner. Further reproduction prohibited without
permission.