Postoperative management of patients with obstructive sleep apnea: implications for the medical-surgical nurse.
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.sup.2]) 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 0-10 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[R]) 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[R]) prior to hospital discharge at 2:45 p.m. Later that evening, Mrs. Young's 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, 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 post-anesthesia care unit also should assess and screen for OSA.
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 in-depth screening by nurses thus is needed.
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, & O'Donnell, 2010; Kiyger 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.
The stereotypical person with OSA is an older, obese male. However, many factors are involved in a person's risk for OSA. Cranio-facial 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).
Persons with OSA can vary widely in the number and severity of symptoms as well as in their clinical presentation. The most typical symptom 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 medical-surgical 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 electroencephalogram 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 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 (Cronbach's 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 sensitivity 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 one's 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 questionnaire's 10 items focus on common symptoms of sleep apnea (Netzer, Stoohs, Netzer, Clark, & Strohl, 1999). The first question asks the patient to self-report 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 Cronbach's 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:
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 patient's 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). Bi-level 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 patient's mouth and over the teeth to reposition the patient's 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 device's effectiveness in treating OSA (Ahrens, McGrath, & Hagg, 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, 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, maxillo-mandibular 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).
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" 0arzyna 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 patient's risk factors for respiratory 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 doses-paring 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" Oarzyna 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 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" Qarzyna 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).
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).
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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.
TABLE 1. General Overview of OSA Common Signs and Symptoms Common Treatment for Characteristics of of OSA OSA Affected Individual Obesity Apnea CPAP Craniofacial Snoring or gasping EPAP malformation during sleep Nasal deformities Daytime sleepiness BiPAP Positive family Night awakenings MAD history of OSA Recurrent alcohol Surgical intervention ingestion (e.g., Sedative use uvulopalatophrayngoplasty, tracheostomy) (Gutierrez & Brady, (Gutierrez & Brady, (Epstein et al., 2009; 2013; Krygeretal., 2013; Krygeretal., Gutierrez & Brady, 2013) 2011) 2011) Common Common Complications of OSA Characteristics of Affected Individual Obesity Fatigue Craniofacial Poor daytime function malformation Nasal deformities Cognitive impairment Positive family Hypertension history of OSA Recurrent alcohol Cardiovascular disease ingestion Sedative use Type 2 diabetes Depression (Gutierrez & Brady, (Bucks, Olaithe, & Eastwood, 2013; Krygeretal., 2013; Douglas et al., 2013; 2011) 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 TABLE 2. Common Screening Tools Name General Number of Time for Purpose Questions Completion of Tool Epworth Sleepiness Assess level 8 1-2 minutes Scale (ESS) (Johns, of day-time 1991) sleepiness Wisconsin Sleep Assess risk 5 0-1 minute Questionnaire for OSA (Young et al., 2008; Young et al., 2009) Berlin Questionnaire Assess risk 10 1-2 minutes (Netzer et al., for OSA 1999) STOP Questionnaire Assess signs 4 0-1 minute (Chung et al., 2008) of OSA STOP-BANG Assess signs 8 1-2 minutes Questionnaire of OSA (Chung et al., 2008) Name Reliability and Validity Epworth Sleepiness Cronbach's alpha 0.88 for patients with Scale (ESS) (Johns, sleep disorders. 1991) 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. Wisconsin Sleep Validity is reported with sensitivity Questionnaire between 79% and 95% for mild OSA, (Young et al., 2008; with specificity between 46% and 64%. Young et al., 2009) Berlin Questionnaire Cronbach's alpha 0.92 for items in (Netzer et al., category 1 (snoring characteristics and 1999) breathing pauses), 0.86 for items in category 2 (daytime sleepiness excluding the question regarding falling asleep while driving). Sensitivity 86% for detecting mild OSA. STOP Questionnaire Sensitivity 65.6% in mild OSA, 74.3% in (Chung et al., 2008) moderate OSA, 79.5% in severe OSA. STOP-BANG Sensitivity 83.6% in mild OSA, 92.9% in Questionnaire moderate OSA, 100% (Chung et al., 2008) in severe OSA.
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|Title Annotation:||Clinical Practice|
|Author:||Helvig, Ashley W.; Minick, Ptlene; Patrick, David|
|Date:||May 1, 2014|
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